Karena Pengaruh Alergi atau Hipersensitif Makanan ?

• Banyak orang tua mengeluh bahwa anaknya seringkali sulit tidur malam atau gangguan tidur yang lain. Hal itu biasa terjadi sejak bayi hingga usia di atas 5 tahun. Hal itu sering dikeluhkan kepafda dokter tetapi saat ini jarang sekali bisa dijelaskan dengan baik mengapa hal itu terjadi. Penyebab gangguan tidur sangat banyak dan bervariasi. Ternyata sebagian besar penyebab gangguan tidur pada anak disebabkan karena pengaruh alergi dan hipersensitifitas makanan. Setelah dilakukan penghindaran makanan tertentu gangguan anak yang selama ini menjadi membaik.
• Insomnia Alergi makanan adalah gangguan untuk memulai tidur dan mempertahankan kualitas tidur yang disebabkan akibat manifestasi atau respon karena alergi makanan. The International Classification of Sleep Disorders mencamtukan Food Allergy Insomnia dengan klasifikasi ICSD : 780.52-2, sedangkan ICD 10 menggolongkan dalam G47.0+T78.4 sebagai Disorders of Initiating and Maintaining Sleep (Insomnias), sedangkan DSM IV menggolongkan dalam kelompok 780.52 sebagai Sleep Disorder Due to a General Medical Condition: Insomnia Type
• Angka kejadian insomnia alergi makanan masih belum diketahui pasti, tetapi tampaknya gangguan ini sering dialami terutama pada usia anak dibawah usia 5 tahun terutama usia 2 tahun
• Manifestasi klinis gangguan insomnia karena alergi makanan, masih belum terungkap jelas. Beberapa penelitian mengatakan beberapa gangguan tidur lainnya ternyata sering dikaitkan dengan insomnia alergi makanan.
• Penelitian yang telah dilakukan dr Widodo Judarwanto SpA tahun 2004 yang telah diajukan dalam acara ilmiah internasional 24TH INTERNATIONAL CONGRESS OF PEDIATRICS CANCÚN MÉXICO AUGUST 15TH – 20TH 2004, menunjukkan bahwa dari 64 anak dengan gangguan alergi makanan dan gangguan tidur, setelah dilakukan eliminasi makanan penyebab alergi selama 3 minggu didapatkan perbaikan. Didapatkan 97% anak perbaikkan dari pola tidurnya. Didapatkan 42 (66%) anak mengalami insomnia food allergy, 12 (19%) anak dengan somnambulisme, 8 (13%) anak dengan night terror, 32(50%) anak dengan nocturnal myoclonus.

Amati Tanda Dan Gejala Gangguan tidur pada anak anda 

• Pada bayi : malam sering terbangun sering dikira haus atau sering dikira ASI ibu kurang sehingga minum ASI berlebihan, akibatnya BB anak naik berlebihan karena terlalu banyak minum.
• Sulit untuk memulai tidur malam atau tidur larut malam
• Tidur bolak-balik dari ujung ke ujung tempat tidur
• Berbicara,tertawa,berteriak atau berjalan saat tidur
• Mendadak terbangun duduk saat tidur kemdian tidur lagi
• Mimpi buruk
• “beradu gigi”  atau gigi gemeretak atau bruxism

Amati Tanda dan gejala gangguan saluran cerna yang disebabkan karena alergi dan hipersensitif makanan (Gastrointestinal Hipersensitivity)

(Gejala Gangguan Fungsi saluran cerna yang ada selama ini sering dianggap normal)

• Pada Bayi  : GASTROOESEPHAGEAL REFLUKS ATAU GER, Sering MUNTAH/gumoh, kembung,“cegukan”, buang angin keras dan sering, sering rewel gelisah (kolik) terutama malam hari, BAB > 3 kali perhari, BAB tidak tiap hari. Feses warna hijau,hitam dan berbau.  Sering “ngeden & beresiko Hernia Umbilikalis (pusar), Scrotalis, inguinalis. Air liur berlebihan. Lidah/mulut sering timbul putih, bibir kering
• Pada anak yang lebih besar :

1. Mudah MUNTAH bila menangis, berlari atau makan banyak. MUAL pagi hari.
2. Sering Buang Air Besar (BAB)  3 kali/hari atau lebih, sulit BAB sering ngeden kesakitan saat BAB (obstipasi). Kotoran bulat kecil hitam seperti kotoran kambing, keras, warna hitam, hijau dan bau tajam. sering buang angin, berak di celana. Sering KEMBUNG, sering buang angin dan bau tajam. Sering NYERI PERUT, tidur malam nungging (biasanya karena perut tidak nyaman)
3. Nyeri gigi, gigi berwarna kuning kecoklatan, gigi rusak, gusi mudah bengkak/berdarah. Bibir kering dan mudah berdarah, sering SARIAWAN, lidah putih & berpulau, mulut berbau, air liur berlebihan.

• KULIT : sering timbul bintik kemerahan terutama di pipi, telinga dan daerah yang tertutup popok. Kerak di daerah rambut. Timbul bekas hitam seperti tergigit nyamuk. Kotoran telinga berlebihan & berbau. Bekas suntikan BCG bengkak dan bernanah. Timbul bisul.
• SALURAN NAPAS : Napas grok-grok, kadang disertai batuk ringan. Sesak pada bayi baru lahir disertai kelenjar thimus membesar (TRDN/TTNB)
• HIDUNG : Bersin, hidung berbunyi, kotoran hidung banyak, kepala sering miring ke salah satu sisi karena salah satu sisi hidung buntu, sehingga beresiko ”KEPALA PEYANG”.
• MATA : Mata berair atau timbul kotoran mata (belekan) salah satu sisi.
• KELENJAR : Pembesaran kelenjar di leher dan kepala belakang bawah.
• PEMBULUH DARAH :  telapak tangan dan kaki seperti pucat, sering terba dingin
• GANGGUAN HORMONAL : keputihan/keluar darah dari vagina, timbul bintil merah bernanah, pembesaran payudara, rambut rontok.
• PERSARAFAN : Mudah kaget bila ada suara keras. Saat menangis : tangan, kaki dan bibir sering gemetar atau napas tertahan/berhenti sesaat (breath holding spells)
• PROBLEM MINUM ASI : minum berlebihan, berat berlebihan krn bayi sering menangis dianggap haus (haus palsu : sering menangis belum tentu karena haus atau bukan karena ASI kurang.). Sering menggigit puting sehingga luka. Minum ASI sering tersedak, karena hidung buntu & napas dengan mulut. Minum ASI lebih sebentar pada satu sisi,`karena satu sisi hidung buntu, jangka panjang bisa berakibat payudara besar sebelah.

• SALURAN NAPAS DAN HIDUNG : Batuk / pilek lama (>2 minggu), ASMA, bersin, hidung buntu, terutama malam dan pagi hari. MIMISAN, suara serak, SINUSITIS, sering menarik napas dalam.
• KULIT : Kulit timbul BISUL, kemerahan, bercak putih dan bekas hitam seperti tergigit nyamuk. Warna putih pada kulit seperti ”panu”. Sering menggosok mata, hidung, telinga, sering menarik atau memegang alat kelamin karena gatal. Kotoran telinga berlebihan, sedikit berbau, sakit telinga bila ditekan (otitis eksterna).
• SALURAN CERNA : Mudah MUNTAH bila menangis, berlari atau makan banyak. MUAL pagi hari. Sering Buang Air Besar (BAB)  3 kali/hari atau lebih, sulit BAB (obstipasi), kotoran bulat kecil hitam seperti kotoran kambing, keras, sering buang angin, berak di celana. Sering KEMBUNG, sering buang angin dan bau tajam. Sering NYERI PERUT.
• GIGI DAN MULUT : Nyeri gigi, gigi berwarna kuning kecoklatan, gigi rusak, gusi mudah bengkak/berdarah. Bibir kering dan mudah berdarah, sering SARIAWAN, lidah putih & berpulau, mulut berbau, air liur berlebihan.
• PEMBULUH DARAH Vaskulitis (pembuluh darah kecil pecah) : sering LEBAM KEBIRUAN pada tulang kering kaki atau pipi atas seperti bekas terbentur. Berdebar-debar, mudah pingsan, tekanan darah rendah.
• OTOT DAN TULANG : nyeri kaki atau kadang  tangan, sering minta dipijat terutama saat malam hari. Kadang nyeri dada
• SALURAN KENCING : Sering minta kencing, BED WETTING (semalam  ngompol 2-3 kali)
• MATA : Mata gatal, timbul bintil di kelopak mata (hordeolum). Kulit hitam di area bawah kelopak mata. memakai kaca mata (silindris) sejak usia 6-12 tahun.
• HORMONAL : rambut berlebihan di kaki atau tangan, keputihan, gangguan pertumbuhan tinggi badan.
• Kepala,telapak kaki/tangan sering teraba hangat. Berkeringat berlebihan meski dingin (malam/ac). Keringat  berbau.
• FATIQUE :  mudah lelah, sering minta gendong

• SUSUNAN SARAF PUSAT : sakit kepala, MIGRAIN, TICS (gerakan mata sering berkedip), , KEJANG NONSPESIFIK (kejang tanpa demam & EEG normal).
• GERAKAN MOTORIK BERLEBIHAN Mata bayi sering melihat ke atas. Tangan dan kaki bergerak terus tidak bisa dibedong/diselimuti. Senang posisi berdiri bila digendong, sering minta turun atau sering menggerakkan kepala ke belakang, membentur benturkan kepala. Sering bergulung-gulung di kasur, menjatuhkan badan di kasur (“smackdown”}. ”Tomboy” pada anak perempuan : main bola, memanjat dll.
• AGRESIF MENINGKAT sering memukul kepala sendiri, orang lain. Sering menggigit, menjilat, mencubit, menjambak (spt “gemes”)
• GANGGUAN KONSENTRASI: cepat bosan sesuatu aktifitas kecuali menonton televisi,main game, baca komik, belajar. Mengerjakan sesuatu  tidak bisa lama, tidak teliti, sering kehilangan barang, tidak mau antri, pelupa, suka “bengong”, TAPI ANAK TAMPAK CERDAS
• EMOSI TINGGI (mudah marah, sering berteriak /mengamuk/tantrum), keras kepala, negatifisme
• GANGGUAN KESEIMBANGAN KOORDINASI DAN MOTORIK : Terlambat bolak-balik, duduk, merangkak dan berjalan. Jalan terburu-buru, mudah terjatuh/ menabrak, duduk leter ”W”. 
• GANGGUAN SENSORIS : sensitif terhadap suara (frekuensi tinggi) , cahaya (silau), raba (jalan jinjit, flat foot, mudah geli, mudah jijik)
• GANGGUAN ORAL MOTOR : TERLAMBAT BICARA, bicara terburu-buru, cadel, gagap. GANGGUAN MENELAN DAN MENGUNYAH, tidak bisa  makan makanan berserat (daging sapi, sayur, nasi) Disertai keterlambatan pertumbuhan gigi.
• IMPULSIF : banyak bicara,tertawa berlebihan, sering memotong pembicaraan orang lain
• AUTIS dan ADHD (Alergi dan hipersensititas makanan bukan penyebab Autis atau ADHD tetapi hanya memperberat gejalanya)

• Diagnosis insomnia alergi atau hipersensitif makanan dibuat bukan dengan tes alergi tetapi berdasarkan diagnosis klinis, yaitu anamnesa (mengetahui riwayat penyakit penderita) dan pemeriksaan yang cermat tentang riwayat keluarga, riwayat pemberian makanan, tanda dan gejala alergi makanan sejak bayi dan dengan eliminasi dan provokasi.
• Untuk memastikan makanan penyebab alergi harus menggunakan Provokasi makanan secara buta (Double Blind Placebo Control Food Chalenge = DBPCFC). DBPCFC adalah gold standard atau baku emas untuk mencari penyebab secara pasti alergi makanan. Cara DBPCFC tersebut sangat rumit dan membutuhkan waktu, tidak praktis dan biaya yang tidak sedikit.
• Beberapa pusat layanan alergi anak melakukan modifikasi terhadap cara itu. Children Allergy clinic Jakarta melakukan modifikasi dengan cara yang lebih sederhana, murah dan cukup efektif. Modifikasi DBPCFC tersebut dengan melakukan “Eliminasi Provokasi Makanan Terbuka Sederhana”. Bila setelah dilakukan eliminasi beberapa penyebab alergi makanan selama 3 minggu didapatkan perbaikan dalam gangguan muntah tersebut, maka dapat dipastikan penyebabnya adalah alergi makanan.
• Pemeriksaan standar yang dipakai oleh para ahli alergi untuk mengetahui penyebab alergi adalah dengan tes kulit. Tes kulit ini bisa terdari tes gores, tes tusuk atau tes suntik. PEMERIKSAAN INI HANYA MEMASTIKAN ADANYA ALERGI ATAU TIDAK, BUKAN UNTUK MEMASTIKAN PENYEBAB ALERGI. Pemeriksaan ini mempunyai sensitifitas yang cukup baik, tetapi sayangnya spesifitasnya rendah. Sehingga seringkali terdapat false negatif, artinya hasil negatif belum tentu bukan penyebab alergi. Karena hal inilah maka sebaiknya tidak membolehkan makan makanan penyebab alergi hanya berdasarkan tes kulit ini.  
• Dalam waktu terakhir ini sering dipakai alat diagnosis yang masih sangat kontroversial atau ”unproven diagnosis”. Terdapat berbagai pemeriksaan dan tes untuk mengetahui penyebab alergi dengan akurasi yang sangat bervariasi. Secara ilmiah pemeriksaan ini masih tidak terbukti baik sebagai alat diagnosis. Pada umumnya pemeriksaan tersebut mempunyai spesifitas dan sensitifitas yang sangat rendah. Bahkan beberapa organisasi profesi alergi dunia tidak merekomendasikan penggunaan alat tersebut. Yang menjadi perhatian oraganisasi profesi tersebut bukan hanya karena masalah mahalnya harga alat diagnostik tersebut tetapi ternyata juga sering menyesatkan penderita alergi yang sering memperberat permasalahan alergi yang ada
• Namun pemeriksaan ini masih banyak dipakai oleh praktisi kesehatan atau dokter. Di bidang kedokteran pemeriksaan tersebut belum terbukti secara klinis sebagai alat diagnosis karena sensitifitas dan spesifitasnya tidak terlalu baik. Beberapa pemeriksaan diagnosis yang kontroversial tersebut adalah Applied Kinesiology, VEGA Testing (Electrodermal Test, BIORESONANSI), Hair Analysis Testing in Allergy, Auriculo-cardiac reflex, Provocation-Neutralisation Tests, Nampudripad’s Allergy Elimination Technique (NAET), Beware of anecdotal and unsubstantiated allergy tests.

 PENATALAKSANAAN 

• Penanganan gangguan tidur karena alergi makanan pada anak haruslah dilakukan secara benar, paripurna dan berkesinambungan. Pemberian obat terus menerus bukanlah jalan terbaik dalam penanganan gangguan tersebut tetapi yang paling ideal adalah menghindari penyebab yang bisa menimbulkan keluhan alergi tersebut.    
• Penghindaran makanan penyebab alergi pada anak harus dicermati secara benar, karena beresiko untuk terjadi gangguan gizi. Sehingga orang tua penderita harus diberitahu tentang makanan pengganti yang tak kalah kandungan gizinya dibandingklan dengan makanan penyebab alergi. Penghindaran terhadap susu sapi dapat diganti dengan susu soya, formula hidrolisat kasein atau hidrolisat whey., meskipun anak alergi terhadap susu sapi 30% diantaranya alergi terhadap susu soya. Sayur dapat dipakai sebagai pengganti buah. Tahu, tempe, daging sapi atau daging kambing dapat dipakai sebagai pengganti telur, ayam atau ikan. Pemberian makanan jadi atau di rumah makan harus dibiasakan mengetahui kandungan isi makanan atau membaca label makanan.  
• Obat-obatan simtomatis, anti histamine (AH1 dan AH2), ketotifen, ketotofen, kortikosteroid, serta inhibitor sintesaseprostaglandin hanya dapat mengurangi gejala sementara, tetapi umumnya mempunyai efisiensi rendah. Sedangkan penggunaan imunoterapi dan natrium kromogilat peroral masih menjadi kontroversi hingga sekarang.  

Obat

• Pengobatan gangguan tidur karena alergi makanan yang baik adalah dengan menanggulangi penyebabnya. Bila insomnia yang dialami disebabkan karena gangguan alergi makanan, penanganan terbaik adalah menunda atau menghindari makanan sebagai penyebab tersebut.    
• Konsumsi obat-obatan, konsumsi susu formula yang mengklaim bisa membuat nyenyak tidur, terapi tradisional ataupun beberapa cara dan strategi untuk membuat tidur nyenyak pada anak tidak akan berhasil selama penyebab utama gangguan tidur pada anak karena alergi dan hipersensitifitas makanan tidak diperbaiki.

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Prevent Depression While You Sleep

Researchers have known for years that depression can cause insomnia, trouble falling asleep or staying asleep. But new research on the connection between sleep and depression finds that the opposite is true as well: Chronic insomnia may increase your risk of becoming clinically depressed.

The details

In a study of sleep and depression published in the American Journal of Epidemiology, researchers at Old Dominion University in Norfolk, Va., identified 555 people who suffered from chronic insomnia. Four years later, the researchers found that this group was up to five times more likely to be depressed than those without insomnia. It should be noted that no one in the group of insomniacs suffered from depression at the beginning of the study period, suggesting that it was indeed the insomnia that led to the depression, rather than the other way around.

What it means

A third of Americans report occasional bouts of insomnia, while 10 percent to 15 percent suffer from a chronic form of the condition. The consequences are not limited to daytime drowsiness. Insomnia can affect your physical health, work performance, and quality of life. And as this study makes clear, the condition can increase your risk of depression. The good news is that the research points to an interesting new strategy for preventing depression and helping people who are depressed. “Our results suggest that recognition and treatment of insomnia by healthcare providers may be critical for preventing or mitigating the occurrence of depression,” write the study authors.

This study doesn’t prove that insomnia directly causes depression; it may be an early marker, or the two conditions may be linked in some other way. But, along with the other effects of sleep loss, it’s a good reason to take insomnia seriously. If you have chronic insomnia, meaning at least three nights a week for a month or longer, ask your doctor about behavioral therapies and/or medications that might work. And here some strategies you can try:

1. Practice good sleep hygiene: While medication can help you sleep in the short term, many people can get lasting relief from insomnia by practicing good sleep hygiene—behaviors and habits that cue your body that it’s time to shut down for the night. See how some people are getting more sleep with skills, not pills.
2. Stick to a sleep schedule: Keep your bedtime and wake time consistent from day to day, including on weekends. It may be tempting to sleep in on a Saturday, but a recent study found that doing so sets you up for a cumulative sleep deficit.
3. Make the sun work for you: Sunlight can have a powerful effect on our sleep schedules, and not only when it’s peeking through the blinds in the morning. Some people are particularly sensitive to changes in day length, or to the dip in sun exposure that most of us experience in wintertime. Read about healthy effects of bright light

source : http://health.msn.com/

Supported  by

 CHILDREN SLEEP CLINIC  Yudhasmara Foundation

 Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210 

phone : 62(021) 70081995 – 5703646 email : judarwanto@gmail.com, http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :WIDODO JUDARWANTO, pediatrician 

email : judarwanto@gmail.com

curriculum vitae  

Copyright © 2010, Children Sleep Clinic  Information Education Network. All rights reserved

Scientists Unravel Secrets of Sound Sleep

Ever wonder how some people can sleep through thunderstorms and traffic noise, while others wake up at the slightest sound? Differences in people’s brain rhythms during sleep may hold the answer, scientists say.

While treatments based on the findings remain a long ways off, “by knowing this information, we will better understand what can be done to enhance natural sleep,” said study senior author Dr. Jeffrey Ellenbogen, chief of the division of sleep medicine at Massachusetts General Hospital and assistant professor of neurology at Harvard Medical School.

Reporting in the Aug. 10 issue of Current Biology, Ellenbogen and his colleagues studied how sensitivity to noise during sleep is associated with a type of brain activity called sleep “spindles” — bursts of fast brain rhythms that punctuate the otherwise slow-wave patterns characteristic of sleep.

These spindle rhythms are generated by a structure in the brain called the thalamus, which is responsible for relaying sensory information from the outside world to other parts of the brain. It’s thought that the thalamus might generate these sleep spindles as a way to prevent sensory input (such as loud noise) from reaching the sleeping brain.

To see if spindles might shield the brain from sound in the environment, the researchers first measured spindle production in the brains of 12 healthy adult volunteers during a quiet night of sleep. On the next two nights, they evaluated the volunteers’ sleep behavior in the presence of noises like road and air traffic or a ringing telephone.

The researchers found that people with higher rates of spindle rhythms were consistently less likely to awake in response to these noises.

“Spindles have previously been associated with suppression of incoming stimuli during sleep, so the results are logical,” said one expert, Torbjorn Akerstedt, director of the Stress Research Institute at Stockholm University in Sweden.

It’s not completely clear if sleep spindles are directly interfering with sound transmission to the brain, although that’s the current hypothesis, Ellenbogen said. “If a spindle occurs at the same time as a sound, then the sound is likely blocked from perception, keeping the person asleep. More spindles makes it more likely that noises will collide with this sleep-protecting rhythm,” he said. Alternatively, it’s possible that the spindle is simply a sign of an as-yet-unknown brain process that controls noise sensitivity.

Each person’s spindle rate was similar across all three nights, suggesting that it’s a stable trait for an individual across time, although “little is known about what makes one person produce more spindles than another,” Ellenbogen said.

Understanding sleep spindle production may someday help researchers devise behavioral or pharmaceutical methods of increasing resilience to noise during sleep, although such applications remain far off, he noted.

“Certain drugs make sleep spindles more prominent, particularly those that are considered sleep drugs,” Ellenbogen said. “It is not known, however, whether these synthetically made spindles behave similarly to those naturally occurring. We are currently investigating that important question.”

Studies of sleep spindles may also have implications for other aspects of sleep besides noise sensitivity, Akerstedt said. “Spindles may be a good new physiological indicator of sleep quality,” he said. “This may be important, since we lack consensus on what constitutes physiologically good sleep.”

source : http://health.msn.com/   By Melissa Lee Phillips HealthDay Reporter

Supported  by

 CHILDREN SLEEP CLINIC  Yudhasmara Foundation

 Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210 

phone : 62(021) 70081995 – 5703646 email : judarwanto@gmail.com, http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :WIDODO JUDARWANTO, pediatrician 

email : judarwanto@gmail.com

curriculum vitae  

Copyright © 2010, Children Sleep Clinic  Information Education Network. All rights reserved

Menguak Misteri Tidur

Dewasa ini sering kita dengan bahwa rekomendasi tidur yang ideal pada orang dewasa adalah  6-8 jam  sehari. Tetapi nyatanya, tak sedikit orang yang cuma tidur 4 jam setiap harinya namun tetap sehat dan bugar. Sebenarnya, berapa lama durasi tidur yang paling tepat?

Pada dasarnya waktu tidur sangat individual. Ini berarti, tidak ada “takaran” yang sama untuk semua orang. “Boleh-boleh saja tidur 4 jam, asalkan saat bangun di pagi hari kita merasa segar dan terpulihkan. Kalau kita justru merasa lesu dan tak ada semangat, itu artinya kita memang kurang tidur.

Lamanya durasi tidur ternyata juga tak akan memberi pengaruh pada kesehatan bila tidak memiliki kualitas yang baik. “Agar tetap sehat, yang perlu diperhatikan adalah kualitas tidurnya. Tidur yang dalam NREM (non rapid eye movement) sangat esensial untuk kelangsungan hidup. Dalam tahap NREM, akan dihasilkan hormon pertumbuhan yang berguna untuk regenerasi sel-sel dan meningkatkan imunitas tubuh. Saat tidur NREM, seseorang akan sulit dibangunkan dan jika bermimpi saat bangun, kita sudah tidak mengingat isi mimpinya.

“Hormon pertumbuhan dan perbaikan sel ini hanya dikeluarkan tubuh di malam hari dan tidak bisa digantikan dengan tidur siang,” ujar dr Nurmiati. Ia menambahkan, suasana gelap di malam hari ikut membantu pengeluaran hormon melatonin lebih cepat sehingga secara alami kita akan mengantuk.

Untuk mendapatkan tidur yang berkualitas, ada beberapa hal yang perlu diperhatikan, yakni membiasakan diri untuk bangun pagi secara teratur, menghindari stres emosi dan pekerjaan di tempat tidur, melatih relaksasi, dan baru pergi tidur setelah mengantuk. “Idealnya tidak ada orang yang perlu obat untuk tidur.

Infant Insomnia
Chronic insomnia in infants has been linked to allergies to cow’s milk proteins. In one study, a group of children with known allergies to cow’s milk proteins, as well as a group of children with chronic insomnia but undiagnosed allergies to milk, slept well when milk was removed from their diet and slept poorly when milk was reintroduced. Those children in the chronic insomnia group were tested and found to have allergies to cow’s milk proteins. So if your child has chronic insomnia, think about getting him or her tested for allergies.


Not only does the sheer misery induced by allergy symptoms keep you awake at night, but your body’s immunological response to those allergens disrupts the systems set up to regulate your sleep. So the key to a good night’s sleep is to keep allergens at bay—or, when that’s simply impossible, find a way to minimize your body’s reaction to them. Here’s how to do it.

1. MAKE A BATTLE PLAN. Get an ID on the allergens that are driving you crazy, find out when and how they appear, then formulate a battle plan with your doctor. Include everything from reducing contact with the allergen to treating it with medication.

If your allergies aren’t immediately obvious to you and your doctor, ask your doctor for a referral to an allergist in your community. Or go to www.aaaai.org, click on “patients and consumers,” then click on “find an allergist.” Your allergist will run a series of skin or blood tests to reveal specific allergens.

2. WASH. When allergens, dust, and mold enter your nasal passages, they tend to get stuck in the membrane lining those passages. Inflammation sets in, your nose becomes swollen and clogged, and a nasty sinus infection can be the result.

Fortunately, however, “nasal irrigation, if it is done correctly and gently, can remove allergens, irritants, and inflammatory mucus,” says William H. Anderson, M.D., a member of the American Academy of Allergy, Asthma, and Immunology. Doing this is helpful for everyone, he adds, but for those with a tendency toward sinus infections, it’s particularly recommended.

To wash out your nasal passages, stand by the bathroom sink first thing in the morning, wash your hands with soap and water, then fill a bowl with 2 cups of water that feels as though it’s around body temperature. Mix in 12 teaspoon salt and stir to dissolve. (If you are sensitive to iodine, use non-iodized salt.) Then pick up a small bulb syringe (available from your local drugstore) and squeeze out all the air. Put the narrow end into the saltwater solution and release the bulb to suck up the saltwater into the bulb. Squirt the water into the sink.

Now bend over the sink, squeeze the air out of the bulb once again, put the narrow end into the saltwater, release the bulb, and suck up the saltwater. Insert the tip of the syringe into one nostril—no farther than the width of your fingertip—and tilt the syringe tip toward the outer corner of your eye. Gently release the bulb and allow the water to gently squirt into your nose as you continue to lean over the sink.

Let the water drain out of your nostril back into the sink. Don’t be alarmed if it comes out of your other nostril or your mouth. Both nostrils and the back of your mouth are all connected.

Repeat the procedure, switch nostrils, and then wash the second nostril twice. Wash out the bulb with fresh clean water several times, then store it, tip down, in a cup.

3. SQUIRT. “Nasal saline sprays can be very helpful,” says Dr. Anderson. Use them throughout the day and particularly at night before bed. Avoid daily use of nasal vasoconstricting nose sprays, such as Afrin. If you use them for more than three days, you will become addicted. The nasal passages will swell and obstruct airway passages until the effect wears off—another three days.

4. FORGET OTC DECONGESTANTS. Over-the-counter decongestants can cause insomnia, says Dr. Anderson. If sleep is your objective, forget about taking ’em.PRETREAT.

5. PRETREAT. Since your immune system responds to the allergen with inflammation and that’s what swells shut your nasal passages, prevent the inflammation by using a prescription anti-inflammatory nasal spray, says Dr. Anderson. Brands inlclude Flonase, Nasonex, Veramyst, and Nasacort. All are effective.

6. LOOK FOR THE NEWER ANTIHISTAMINES. Older antihistamines can cause dry mouth or, when sold combined with decongestants, prevent sleep. “Newer antihistamines—including loratadine (generic Claritin), fexofenadine (generic Allegra), prescription Zyrtec, and prescription Clarinex don’t interfere with sleep like some of the older ones do,” says Dr. Anderson. Check with your doctor to see if one of them is right for you.

7. SHOWER WITH EUCALYPTUS. Head into the bathroom, turn on the shower, and fill the room with steam. Then sprinkle a half-dozen drops of essential oil of eucalyptus on your wet bath mitt, lather the mitt with an unscented soap, and wash your entire body from top to bottom. By the time you hit your feet, your nose will be breathing freely, your sinuses will be clear, and your throat will feel soothed and moisturized

For an extra treat after you shampoo, use a few drops of eucalyptus in the final rinse for your hair. Keep it out of your eyes.

8. RINSE OFF. To keep pollen out of the bedroom, shower right before bed, use a dryer-dried towel, and don dryer-dried bedclothes.

9. HIDE OUT. Hot, dry, and windy weather can each send dust, pollen, and molds skittering through your windows at home, work, in your car—virtually everywhere. So stay indoors with windows closed when those conditions are present during your allergy season. Schedule shopping and outdoor activities when it’s windless, cloudy, or even rainy. There’s less pollen in the air.

10. CHECK THE POLLEN COUNT. If you have a pollen allergy, go to www.aaaai.org, click on “patients and consumers,” then click on “pollen count” and follow the prompts to see what’s pollinating in your area and how heavy the levels are. Plan outdoor activities when the counts are low; schedule indoor activities when the counts are high.

11. CLOSE WINDOWS IN THE EARLY MORNING. Pollen is usually emitted between 5:00 and 10:00 A.M. To avoid giving yourself a big dose before you even open your peepers, close windows the night before.
 

12. EXERCISE AFTER 10:00 A.M.. You’ll breathe better and get a better workout if you exercise after that 5:00 to 10:00 A.M. blast of pollen.
 

13. SCHEDULE VACATIONS DURING YOUR ALLERGY SEASON. Why not skip your allergy season altogether? Try vacationing in another part of the world while your allergens are blooming at home.

14. HIRE A LAWN PERSON. Mowing the grass stirs up a textbook’s worth of pollens and molds, and raking leaves does the same thing. Hire a professional to do both—and suggest they wear a mask.

The Truth About Allergies

Increased Cerebral Blood Flow Velocity in Children with Mild Sleep-Disordered Breathing

A Possible Association with Abnormal Neuropsychological Function

Catherine M. Hill, BM, MSc, MRCP, FRCPCH,a Alexandra M. Hogan, PhD,b Nwanneka Onugha, BM,a Dawn Harrison, BSc,b Sara Cooper, MSc(Med),c Victoria J. McGrigor, MBBS, DCH, FRCPCH,d Avijit Datta, BSc, MD, MRCP,e and Fenella J. Kirkham, MBBChir, FRCPCHaf

aDivision of Clinical Neurosciences, University of Southampton, Southampton, United Kingdom

bDevelopmental Brain-Behaviour Unit, University of Southampton, Southampton, United Kingdom

cChildren’s Sleep Disorders Unit, Sydney Adventist Hospital, New South Wales, Australia

dChildren’s Sleep Disorder Service, Southampton City Primary Care Trust, Southampton, United Kingdom

eInstitute of Biomedical and Biomolecular Sciences, University of Portsmouth, Portsmouth, United Kingdom

fInstitute of Child Health, University College London, London, United Kingdom

Address correspondence to Catherine M. Hill, BM, MSc, MRCP, FRCPCH, University of Southampton-Child Health, Mail Point 803, Southampton General Hospital, Southampton, Hampshire SO16 6YD, United Kingdom. Email: cmh2/at/soton.ac.uk

The authors have indicated they have no financial relationships relevant to this article to disclose.

The publisher’s final edited version of this article is available free at Pediatrics.

See commentary “Increased cerebral blood flow velocity in children with sickle cell disease: adenotonsillectomy or transfusion regimens?” in Pediatrics, volume 120 on page 235.

See other articles in PMC that cite the published article.

Abstract

Objective

Sleep-disordered breathing describes a spectrum of upper airway obstruction in sleep from simple primary snoring, estimated to affect 10% of preschool children, to the syndrome of obstructive sleep apnea. Emerging evidence has challenged previous assumptions that primary snoring is benign. A recent report identified reduced attention and higher levels of social problems and anxiety/depressive symptoms in snoring children compared with controls. Uncertainty persists regarding clinical thresholds for medical or surgical intervention in sleep-disordered breathing, underlining the need to better understand the pathophysiology of this condition. Adults with sleep-disordered breathing have an increased risk of cerebrovascular disease independent of atherosclerotic risk factors. There has been little focus on cerebrovascular function in children with sleep-disordered breathing, although this would seem an important line of investigation, because studies have identified abnormalities of the systemic vasculature. Raised cerebral blood flow velocities on transcranial Doppler, compatible with raised blood flow and/or vascular narrowing, are associated with neuropsychological deficits in children with sickle cell disease, a condition in which sleep-disordered breathing is common. We hypothesized that there would be cerebral blood flow velocity differences in sleep-disordered breathing children without sickle cell disease that might contribute to the association with neuropsychological deficits.

Design

Thirty-one snoring children aged 3 to 7 years were recruited from adenotonsillectomy waiting lists, and 17 control children were identified through a local Sunday school or as siblings of cases. Children with craniofacial abnormalities, neuromuscular disorders, moderate or severe learning disabilities, chronic respiratory/cardiac conditions, or allergic rhinitis were excluded. Severity of sleep-disordered breathing in snoring children was categorized by attended polysomnography. Weight, height, and head circumference were measured in all of the children. BMI and occipitofrontal circumference z scores were computed. Resting systolic and diastolic blood pressure were obtained. Both sleep-disordered breathing children and the age- and BMI-similar controls were assessed using the Behavior Rating Inventory of Executive Function (BRIEF), Neuropsychological Test Battery for Children (NEPSY) visual attention and visuomotor integration, and IQ assessment (Wechsler Preschool and Primary Scale of Intelligence Version III). Transcranial Doppler was performed using a TL2-64b 2-MHz pulsed Doppler device between 2 PM and 7 PM in all of the patients and the majority of controls while awake. Time-averaged mean of the maximal cerebral blood flow velocities was measured in the left and right middle cerebral artery and the higher used for analysis.

Results

Twenty-one snoring children had an apnea/hypopnea index <5, consistent with mild sleep-disordered breathing below the conventional threshold for surgical intervention. Compared with 17 nonsnoring controls, these children had significantly raised middle cerebral artery blood flow velocities. There was no correlation between cerebral blood flow velocities and BMI or systolic or diastolic blood pressure indices. Exploratory analyses did not reveal any significant associations with apnea/hypopnea index, apnea index, hypopnea index, mean pulse oxygen saturation, lowest pulse oxygen saturation, accumulated time at pulse oxygen saturation 80% of the preceding breath for ≥2 breaths. Hypopneas were classified as for apneas but where the reduction in flow was 50%-80% of the previous breath. Oxygen desaturation was classified by a 3% or more decrease in Spo2 from the baseline. The apnea/hypopnea index was defined as the number of obstructive apneas, hypopneas, and mixed apneas per hour of total sleep time. Central apneas could be confidently identified from the respiratory inductance plethysmography bands and were separately scored. There is currently no consensus for respiratory scoring criteria in children.34 These criteria were selected to discriminate obstructive respiratory events in sleep. Studies were independently scored by an experienced sleep technician (S.C.) and a pediatrician (C.M.H).

In addition to polysomnography, which is a single time point measure of SDB severity, the duration of exposure to SDB was estimated based on parental report, recorded as the number of years that the child had snored multiplied by the mean days per week of snoring during the previous year. Parents were asked 2 questions: (1) “How many years has your child snored?” and (2) “During the past year, on average how many days per week has your child snored?” There are no validated measures of snoring exposure in children, although previous studies have addressed this issue indirectly by asking how often the child snores35 or if the child snored between the ages of 2 and 6 years.36

Blood Pressure and Anthropometric Measures

Children were weighed, and height and occipitofrontal circumference were measured. BMI and occipitofrontal circumference z scores were computed. Resting systolic and diastolic blood pressure were obtained using Dinamp technology (Dash 3000 GE Health care). To control for influence of age and height on blood pressure,37 a blood pressure index was computed as described by Amin et al.23



where BP is blood pressure. Blood pressure centiles were derived from standard published values.37

TCD

TCD was performed using a TL2-64b 2-MHz pulsed Doppler device between 2 PM and 7 PM in all of the patients and in the majority of controls. The operator (N.O.) was blinded to the neuropsychological, behavioral, and SDB status of the child but was aware of their patient/control status. The child remained awake but was encouraged to lie quietly. Time-averaged mean of the maximal CBFV of the left and right middle cerebral artery (henceforth simply referred to as CBFV) was measured through the temporal ultrasound “acoustic window” above the zygomatic arch and anterior to the ear. All of the studies started at a depth of 45 mm, and identification of the maximum velocity envelope in the terminal internal cerebral artery/middle cerebral artery was confirmed by following the vessel to a shallow depth of 35 to 40 mm and a deeper depth of 50 to 55 mm, the middle cerebral artery/anterior cerebral artery bifurcation. CBFV was recorded bilaterally for the middle cerebral artery,38 responsible for ≥80% of cerebral blood flow. Attempts to additionally insonate the anterior cerebral artery and basilar arteries were rarely tolerated by these young children. For 5 cases (2 controls), similar CBFV recordings were obtained by one of the principal investigators (A.M.H.) immediately after the first recording (r = 0.996; P 0.33 is considered to be abnormal (R. D. Chervin, MD, MS, written communication, 2005). None of the controls scored within the abnormal range (group mean: 0.1; SD: 0.1; t36 = 10.4; P < .001), further validating their allocation to a nonsnoring group.

Polysomnography

Polysomnography in the snoring children demonstrated that all of the children had some episodes of upper airway obstruction during sleep. The majority of these episodes were hypopneas. Mean oxygen levels were in the reference range for all of the children, although some children experienced episodic desaturations associated with obstructive events (Table 2). The duration of parental estimated exposure of snoring for those with SDB was 18.8 (SD: 8.0).



Time-Averaged Mean of the Maximum Blood Flow Velocities in the Middle Cerebral Artery

TCD recordings from ≥1 side were obtained in 18 of 21 and 17 of 17 of the mild SDB and control groups, respectively. As illustrated in Fig 1, CBFV was significantly increased in the mild SDB group compared with controls (t27.7 = 8.3; P < .001). Posthoc analyses addressed the possibility that systemic hypertension might account for the group differences in CBFV. However, the majority of children were normotensive according to age-, gender-, and height-adjusted values: systolic blood pressure index was raised in 1 SDB child (7.8) and diastolic in 1 control child (1.4). There was no significant correlation between blood pressure indices and CBFV, and the inclusion of this covariate did not alter the significant CBFV group difference (P < .001).



We were interested to know whether the variance in CBFV might be explained by specific polysomnographic variables. Exploratory analyses did not reveal any significant associations with apnea/hypopnea index, apnea index, hypopnea index, mean Spo2, lowest Spo2, accumulated time at Spo2 .1), the significant group differences did not remain when CBFV was entered as a covariate (analysis of covariance). This indicates that a proportion of the variance in processing speed and visual attention scores may be explained by factors associated with increased CBFV.



Parental Ratings of Executive Function Behavior

All of the executive function behaviors assessed by the BRIEF were significantly worse in mild SDB children compared with controls (see Table 4). As before, there were no direct correlations between BRIEF subscales or total score and CBFV in the mild SDB group (P > .1). For the majority of indices, analysis of covariance tests revealed a residual difference between groups when controlling for CBFV, although the significance of this difference slightly decreased suggesting that there may be some partial association between CBFV and parental report of executive function behaviors.



DISCUSSION

The finding of significant differences between otherwise healthy children with mild SDB and controls on neuropsychological and behavioral measures of executive function replicates the findings of previous studies.9,10 We also provide novel preliminary evidence of abnormal cerebral hemodynamics in a nonobese population of young children with mild SDB of a severity below the conventional treatment threshold. The fact that adjusting for CBFV reduces group differences in neuropsychological measures suggests that factors associated with cerebral hemodynamics may contribute to the relationship between SDB and neuropsychological impairment.

Children with a history of snoring obtained a mean value for CBFV (120 cm/second) that was intermediate between that obtained from healthy controls (84 cm/second) and the threshold for moderate stroke risk in children with sickle cell disease (>170 cm/second).40 Even African children, with a high prevalence of anemia secondary to iron deficiency and sickle trait, have mean CBFV values of 92 cm/second (+2 SDs = 142 cm/second)41; in comparison, 1 of the SDB children in the current series had a CBFV of 147 cm/second. The CBFV values for control children are very similar to those published previously in healthy children of similar age42 and before sleep in 5 children aged 5 to 13 years.43 There were no previous studies of CBFV in SDB children on which to base a power calculation, but in this sample of 21 with mild SDB, in 18 of whom we managed to obtain a TCD study, and 17 controls, the effect of snoring was large (d = 2.79). Raised CBFV is likely to be attributable either to increased cerebral blood flow or narrowing of the cerebral vessels or a combination of these factors. A number of physiologic changes might alter cerebral blood flow and/or vessel diameter and, therefore, affect CBFV. We were able to study several potential confounding influences on CBF. First, there were no differences in systolic and diastolic blood pressure indices between SDB children and controls. Second, although CBFV increases with increasing partial pressure of carbon dioxide44,45 and hypoxia,46 it is unlikely that observed differences could be accounted for by arterial blood gas tensions, because all of the children in the study were healthy with no cardiorespiratory disease, other than SDB in the snoring group. Although arterial partial pressure of oxygen and partial pressure of carbon dioxide were not monitored during CBFV measurement, assessment was undertaken during the afternoon/early evening when the child was awake, and all of the SDB children had normal resting oxyhemoglobin saturation at the outset of their subsequent sleep studies that day.

Finally, there is an inverse linear relationship between CBF and hematocrit in adults,47 and it is known that iron-deficient erythropoiesis is associated with chronic infection, such as recurrent tonsillitis, a clinical feature of many of the snoring children in the study.48 Increased CBFV might reflect increased CBF as an adaptation to anemia and reduced arterial oxygen content. Blood tests were not routinely performed on these children. However, a hemoglobin measure was obtained from 4 children immediately preoperatively and within 6 months of the TCD study after advice to the otolaryngologist that the child’s CBFV was raised. Normal hemoglobin levels (lower reference limits: 11.1g/dL at <5 years and 11.5 g/dL at 5-8 years) were found in 2 children with CBFV measures of 130 and 137 cm/second, respectively. Borderline low hemoglobin levels in 2 children (case 1 [3 years]: 10.9 g/dL; and case 2 [6 years]: 10.2 g/dL) were associated with CBFV values, respectively, of 131 and 130 cm/second.

Thus, there was no apparent relation between hemoglobin concentration and CBFV within the ethical constraints limiting blood tests to only a proportion of symptomatic children undergoing adenotonsillectomy. It will be important to explore the association between iron-deficient erythropoiesis and CBFV in future studies, because chronic anemia could, in part, explain both the observed neurocognitive deficits49-51 and increased CBFV in children with SDB.

Our data suggest a relationship between snoring, increased CBFV, and indices of cognitive (visual attention and processing speed), and perhaps behavioral (BRIEF) function, but this finding is preliminary and requires replication; a causal relationship is not established, and the physiologic mechanisms underlying such a relationship are not clear. However, evidence obtained from young children with sickle cell disease suggests that increased CBFV may represent generalized increased CBF, as an adaptation to chronic-intermittent hypoxemia, or cerebrovascular disease.52 It is important to note that whereas the SDB group did not exhibit significant hypoxia at the time of study, it was unclear to what extent this may have been a feature of their SDB in the past.

Despite the specific cognitive and behavioral deficits observed, there was no apparent impact on more general intellectual function (VIQ, PIQ, and FSIQ) or visuomotor integration, perhaps because of the young age of these children in whom intellectual function is still emerging. This finding is consistent with previous studies showing that intellectual deficit may not be expected in children with SDB53,54; however, it is possible that intellectual and cognitive deficit may become increasingly apparent with age and academic progression.36 The results of repeat measures in these children after adenotonsillectomy and longitudinal studies extending into adolescence will be of interest.

In this study, we found that as-yet unconfirmed factors associated with cerebral hemodynamic derangement may explain a proportion of the variance in visual attention and processing speed functions, both skills that are already known to be vulnerable to chronic-intermittent hypoxia associated with SDB in adults55 and with chronic hypoxia associated with cardiac abnormalities in children.56 Prospective studies that quantify cumulative exposure to the physiologic consequences of SDB, such as hypoxia, would be informative.

CONCLUSIONS

Noninvasive transcranial Doppler measurement of CBFV may provide an important marker of brain vulnerability in children with SDB. The relevance of these findings to clinical practice requires additional study. It will be important to establish whether increased CBFV is a transient adaptive response to SDB or is indicative of a permanent alteration of cerebral hemodynamics with implications for future health. Additional studies in larger samples may clarify whether correlations can be demonstrated with measurable alternations in the systemic vasculature, as well as with polysomnographic indices of hypoxia and sleep arousals.

Abbreviations

SDB

sleep-disordered breathing

OSA

obstructive sleep apnea

TCD

transcranial Doppler

CBFV

cerebral blood flow velocity

PSQ

pediatric sleep questionnaire

Wechsler Preschool and Primary Scale of Intelligence Version III

VIQ

visual IQ

PIQ

performance IQ

FSIQ

full-scale IQ

NEPSY

Neuropsychological Test Battery for Children

BRIEF

Behavior Rating Inventory of Executive Function

Spo2

pulse oxygen saturation

Footnotes

Drs Hill and Hogan contributed equally to this work and share first authorship.

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CHILDREN SLEEP CLINIC

http://childrensleepclinic.wordpress.com

Sleep. 2007 June 1; 30(6): 683–702.

Copyright © 2007 Associated Professional Sleep Societies, LLC.

Carlos H. Schenck, MD,1 Isabelle Arnulf, MD, PhD,*2 and Mark W. Mahowald, MD3

Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center, University of Minnesota Medical School, Departments of Psychiatry 1 and

Neurology 3 Minneapolis, MN

2Center for Narcolepsy, Stanford University School of Medicine, Palo Alto, CA

Address correspondence to: Carlos H. Schenck, MD, Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center (Psychiatry R7), 701 Park Avenue South, Minneapolis, MN 55415, Phone: (612) 873-6288, Fax: (612) 904-4207, ; Email: schen010/at/umn.edu

*Current Affiliation

Fédération des Pathologies du Sommeil, Hôpital Pitié-Salpêtrière, Assistance Publique – Hôpitaux de Paris

Received October 2006; Accepted February 2007.

This article has been cited by other articles in PMC.

Abstract

Study Objectives:

To formulate the first classification of sleep related disorders and abnormal sexual behaviors and experiences.

Design:

A computerized literature search was conducted, and other sources, such as textbooks, were searched.

Results:

Many categories of sleep related disorders were represented in the classification: parasomnias (confusional arousals/sleepwalking, with or without obstructive sleep apnea; REM sleep behavior disorder); sleep related seizures; Kleine-Levin syndrome (KLS); severe chronic insomnia; restless legs syndrome; narcolepsy; sleep exacerbation of persistent sexual arousal syndrome; sleep related painful erections; sleep related dissociative disorders; nocturnal psychotic disorders; miscellaneous states. Kleine-Levin syndrome (78 cases) and parasomnias (31 cases) were most frequently reported. Parasomnias and sleep related seizures had overlapping and divergent clinical features. Thirty-one cases of parasomnias (25 males; mean age, 32 years) and 7 cases of sleep related seizures (4 males; mean age, 38 years) were identified. A full range of sleep related sexual behaviors with self and/or bed partners or others were reported, including masturbation, sexual vocalizations, fondling, sexual intercourse with climax, sexual assault/rape, ictal sexual hyperarousal, ictal orgasm, and ictal automatism. Adverse physical and/or psychosocial effects from the sleepsex were present in all parasomnia and sleep related seizure cases, but pleasurable effects were reported by 5 bed partners and by 3 patients with sleep related seizures. Forensic consequences were common, occurring in 35.5% (11/31) of parasomnia cases, with most (9/11) involving minors. All parasomnias cases reported amnesia for the sleepsex, in contrast to 28.6% (2/7) of sleep related seizure cases. Polysomnography (without penile tumescence monitoring), performed in 26 of 31 parasomnia cases, documented sexual moaning from slow wave sleep in 3 cases and sexual intercourse during stage 1 sleep/wakefulness in one case (with sex provoked by the bed partner). Confusional arousals (CAs) were diagnosed as the cause of “sleepsex” (“sexsomnia”) in 26 cases (with obstructive sleep apnea [OSA] comorbidity in 4 cases), and sleepwalking in 2 cases, totaling 90.3% (28/31) of cases being NREM sleep parasomnias. REM behavior disorder was the presumed cause in the other 3 cases. Bedtime clonazepam therapy was effective in 90% (9/10) of treated parasomnia cases; nasal continuous positive airway pressure therapy was effective in controlling comorbid OSA and CAs in both treated cases. All five treated patients with sleep related sexual seizures responded to anticonvulsant therapy. The hypersexuality in KLS, which was twice as common in males compared to females, had no reported effective therapy.

Conclusions:

A broad range of sleep related disorders associated with abnormal sexual behaviors and experiences exists, with major clinical and forensic consequences.

Citation:

Schenck CH; Arnulf I; Mahowald MW et al. Sleep and sex: what can go wrong? A review of the literature on sleep related disorders and abnormal sexual behaviors and experiences. SLEEP 2007;30(6):683-702.

Keywords: Sleep, sleep disorders, sexual behavior/experience, parasomnias, sleep related/nocturnal seizures, NREM sleep parasomnias, confusional arousals, Kleine-Levin Syndrome, polysomnography/sleep EEG, forensic medicine

INTRODUCTION

THE RECENTLY REVISED INTERNATIONAL CLASSIFICATION OF SLEEP DISORDERS-2ND EDITION (ICSD-2) CONTAINS A SUBSTANTIALLY UPDATED SECTION ON THE parasomnias, which encompass sleep related behaviors, emotions, perceptions, dreaming, and autonomic nervous system events during entry into sleep, within sleep, or during arousals from sleep.”1 Instinctual behaviors are often released inappropriately, as seen with sleepwalking (locomotion), REM sleep behavior disorder (aggression), sleep related eating disorder (feeding), and confusional arousals (sexual behaviors).

A classification of sleep related disorders associated with abnormal sexual behaviors and experiences, to our knowledge, has not been published. We now present such a classification for several reasons. First, there is growing awareness that abnormal sexual behaviors can emerge during sleep, described as “sleepsex,” “atypical sexual behavior during sleep” and “sexsomnia.”2–4 The ICSD-2 recognized this phenomenon as a parasomnia classified as a variant of confusional arousals (and sleepwalking).1 Second, there is an expanding set of sleep disorders and other nocturnal disorders known to be associated with abnormal sexual behaviors, or the misperception of sexual behaviors. Third, the cause of sleepsex can often be identified after clinical and polysomnographic (PSG) evaluations, and can then be effectively treated. Fourth, the forensic aspects of abnormal sleep related sexual behavior have commanded increasing attention. Fifth, new data on periodic hypersomnia (Kleine-Levin syndrome), including its range and frequency of abnormal sexual behaviors have recently been published. The question of how to distinguish normal from abnormal sleep related sexual activity also needs to be considered.

METHODS

Computerized literature searches were conducted for English language publications, including foreign language publications with English abstracts. Old Medline (1950–1965), and Medline, Embase, and PsycInfo searches (1966–2006) used the following key words, restricted to humans: Sleep and sex/sexual behavior; parasomnia and sex/sexual behavior; epilepsy/seizures and sexual behavior/hypersexuality; nocturnal frontal lobe epilepsy and sexual behavior; Kleine-Levin syndrome (KLS) and sexuality/hypersexuality. In addition, information on sleep and sexual, or pseudo-sexual (“sexualized”) behavior from peer-reviewed journal articles that were not detected by the computerized literature searches was gathered by the authors. Data were analyzed to categorize and describe the known associations between sleep, sleep related disorders, and abnormal sexual behaviors and experiences. Data on patients with sleepsex parasomnias and with sexual seizures were also tabulated.

Current textbooks on sleep medicine were reviewed for descriptions and citations related to sexual activity during sleep or sexual behaviors associated with sleep disorders. Additionally, the large-scale Kinsey and Hite reports were reviewed.5–9 The Kinsey reports, conducted more than 50 years ago, remain the most comprehensive, systematic studies on sexual behavior in males (n=5,000) and females (n=6,000) that utilized direct person-to-person interviews with a semi-structured format.5,6 A subsequent book, with a question-and-answer format, was published by the Kinsey Institute in 1991.7 The Hite reports, from 30 and 25 years ago, gathered extensive data on the sexual behavior and experiences of thousands of women and men in the general population by means of mailed anonymous essay questionnaires.8–9

The table of contents and the index in each of the 3 Kinsey reports and the 2 Hite reports (containing only a table of contents) were reviewed to identify all sleep and dream entries related to sexual behavior and experience, including orgasm.

Finally, a comprehensive review of the world literature on KLS, including its association with hypersexuality and deviant sexuality during recurrent hypersomnia phases, was gathered by one of the authors (IA), as described in a separate section on KLS.

RESULTS

Kinsey and Hite Reports

The topic of sleep and sexual behavior was not specifically covered in either of the 2 Kinsey books on males and females5,6 or in the subsequent Kinsey Institute book,7 apart from considerable attention being paid to “nocturnal emissions” or “wet dreams” in males (Chapter 15: Nocturnal Emissions).5 These events were described as being “generally accepted as a usual part of the sexual picture.”5 It was also acknowledged that nocturnal emissions, i.e., spontaneous ejaculations during sleep, could be strongly associated with sexual dreams in some people, but rarely or never accompanied by dream recall in other people. Sleep ejaculations were sometimes reported to occur from daytime naps.

There was no mention of any elicited or spontaneous reports of either sleep masturbation, sleepsex with a bed partner, or sexual sleeptalking in the Nocturnal Emissions chapter. In a discussion of the physiologic origins of the nocturnal emissions, sleep related mechanisms were not mentioned.5

Chapter 14 on male masturbation did not cover sleep related (i.e., involuntary) masturbation.5 The observation was made that “human sexual behavior represents one of the least explored segments of biology, psychology, and sociology.” Kinsey described his study as a “fact-finding survey” to discover what people do sexually (given the lack of adequate scientific information). First-hand interviews were used to obtain the data. However, sleep related sexual behavior was not addressed (other than nocturnal emissions), despite the claim that “all kinds of persons and all aspects of human sexual behavior are being included in this survery… [without] preconception of what is rare or what is common…the story of the sexual behavior of the American male, as we find him.” The following sexual outlets were systematically addressed in Part III (“Sources of sexual outlet”): masturbation, heterosexual petting, pre-marital intercourse, marital intercourse, extra-marital intercourse, intercourse with prostitutes, homosexual outlet, and animal contacts. Although Part II addressed the topic of “Factors affecting sexual outlet,” in which nine factors were discussed in separate chapters, sleep was not discussed, apart from nocturnal emissions. In the section on “Individual Variation,” Kinsey commented on the broad range of variation in human sexual behavior, which from our current-day perspective most likely also applies to human sexual behavior during sleep.

In Kinsey’s book on female sexual behavior,6 the entry for sleep in the index pertained to nudity and also to sexual responses, with the latter referring only to nocturnal sexual dreams and to orgasms; 99% of sleep orgasms in females were associated with sexual dreams.

In the Kinsey Institute New Report on Sex,7 a question-and-answer format was used, based on letters containing questions sent to the Kinsey Institute. The topic of sleep was not addressed in the title of any of the 19 chapters. In the “involuntary sexual behaviors” section of Chapter 6 (“The Sexual Adult”), the topic of spontaneous nocturnal orgasms in males and females, described to occur during REM sleep, was restricted to five questions and the corresponding answers. The index did not have an entry for “sleep,” but did have 4 entries for “Rapid Eye Movement (REM) sleep, sexual arousal during”; 5 entries for “nocturnal emissions (wet dreams)”; and 3 entries for “nocturnal penile tumescence (NPT).” No question or answer addressed the topic of any other sexual behavior during sleep (involving either an individual alone or together with a bed partner), or sleep vocalizations with sexual content.

The Hite Reports, like the Kinsey Reports, had no information on sleep and sexual behavior in women or men, and did not cover the topic of nocturnal emissions.8,9 Sleep was not included among the six questions that discussed the context for achieving orgasms in women. No write-in question discussed orgasm during sleep or dreams. At the end of the questionnaire for women, respondents were asked “is there anything on your mind you would like to speak about which was left untouched by this questionnaire?” Similarly, male respondents were asked at the end of their questioning: “please add anything you would like to say that was not mentioned.”9 There was no response in which sleepsex was reported.

Other Reports

Data from a 28-item internet survey of sexual behavior in sleep were gathered over a 3-month period, as recently reported.10 There were 219 respondents (69% male; mean age, 30.4 yrs, range 15–67 yrs), 92% of whom reported multiple episodes of sexsomnia. Sexual intercourse during sleep was reported by 48%. Precipitating factors for sexsomnia included physical contact with another person in bed (64%), stress (52%), fatigue (41%), alcohol use (14.6%), and drug use (4.3%). Sexsomnia with minors during sleep was reported by 5.9% (10 males, 3 females), with legal repercussions occurring in most cases. Almost half (47%) reported having another sleep disorder. No information on degree of recall or amnesia for the sexsomnia was provided.

The relationship between specific sexual activity (i.e., masturbation) and its subsequent effect on sleep has been explored with PSG monitoring in one study.11 This study involved 10 volunteers (5 men, 5 women; mean age, 25.1 years) without sleep complaints, psychopathology, or sexual dysfunction. Three conditions were examined: sleep following masturbation with or without orgasm, and sleep after reading neutral material. The PSG sleep parameters did not reveal any effect of masturbation on sleep. The authors pointed out that a significant sleep effect might have occurred after masturbation or coitus in a more natural (i.e., nonlaboratory) setting, or among older subjects, insomniacs, or people experiencing tension/anxiety before sexual activity, with sexual activity then serving an anxiolytic, and perhaps sleep-enhancing, role. (On the other hand, coitus can also promote difficulty in falling asleep.12) The authors also called attention to an anecdotal literature without PSG monitoring that revealed wide individual differences after orgasm, particularly among women, ranging from enhanced sleepiness to hyperarousal. Another study examined the effects of viewing an erotic film during the day-time on the subsequent night’s sleep and dreams in 10 young adult men.13 No sleep disturbance was documented, but reduced dream recall was found, along with other dream changes. A third study examined the effects of a brief period of sexual arousal, without climax, on sleep related erections (SREs) in 12 men who viewed a sexually explicit video (with associated erections) for 5 minutes before sleep.14 No adverse effects on SREs were found.

The effect on nocturnal penile tumescence (NPT) and sleep architecture from 10 consecutive days of sexual abstinence followed by a night of sexual intercourse was evaluated in 10 married men, 22–32 years old.15 No increase in NPT or sleep disturbance was found.

A questionnaire study of nocturnal orgasm in college women focused only on spontaneous sleep orgasms and “sexual excitement in dreams” without any mention of self-induced sleep orgasm (i.e., sleep masturbation) observed by a bed partner or roommate.16

Among the current sleep medicine textbooks, one has the following listings in the index17: 1) sexual activity, in arousal disorders and in hypnagogic hallucinations; 2) sexual content of dreams; sex hormones; penile erections; penile tumescence; penis. Another book18 has one listing for nocturnal penile tumescence (NPT), but no listing for sex/sexual behavior or orgasm. A third book19 has a listing for sexual activity, sleep related; two listings for sexual abuse, dissociated memories; one listing for NPT; and no listing for orgasm.

Table 1 contains a classification linking sleep related disorders with a broad range of abnormal sexual behaviors and experiences. Each category will be presented, with a focus on objective data, experiential aspects, clinical and legal consequences, and response to treatment.



Parasomnias With Abnormal Sleep Related Sexual Behaviors And Sleep Related Sexual Seizures

Table 2 contains data on 31 published cases of parasomnias and 7 published cases of epilepsy with abnormal sleep related sexual behaviors and experiences. Eight peer-reviewed journal articles and one peer-reviewed abstract were the sources of the 31 parasomnia cases,2–4,20–25 and seven peer-reviewed articles were the sources of the 7 sleep related seizure cases.3,26–31 Two parasomnia articles were published in a foreign language (German,22 Dutch23), each with an English abstract. These two articles were translated into English (courtesy of R. Ghedini [German to English] & M. Corner [Dutch to English]).



Both the parasomnia and seizure groups had notable findings; caution, however, should be taken when comparing the data between the two groups, since the latter had a small size. The parasomnia group has a strong male predominance. Age of onset of “sleepsex” in both groups was during early adulthood. Sleepsex had been a longstanding problem in 8 parasomnia patients and 4 epilepsy patients prior to clinical intervention.

Four categories of sleepsex behaviors were found in the parasomnia group, and 5 categories of sleepsex behaviors and/or experiences were found in the sleep epilepsy group. In the parasomnia group, females almost exclusively engaged in masturbation and sexual vocalizations, whereas males commonly engaged in sexual fondling and sexual intercourse with females. There were 2 cases of sleep related homosexual behavior: i) A 16-year-old male (without reported sexual orientation) went sleepwalking into the bedroom of his aunt and uncle (who slept in the same bed) and started fondling his uncle’s genitals.4 ii) A heterosexual Dutch man had a history of multiple forms of interpersonal sleepsex, involving sexual initiatives towards his brother, current wife, and ex-wife; he was also accused of fondling his 15-year-old daughter on one occasion.23 Therefore, in at least one of these two cases, homosexual sleep behavior diverged from customary (wakeful) sexual orientation.

Memory recall after sleepsex diverged between the two groups: all 31 parasomnia patients had full amnesia for their sleepsex episodes, whereas there was recall of sleepsex episodes in 5 of 7 patients with sleep related seizures.

Agitated or assaultive sleepsex behaviors, sleepsex with minors, and legal consequences affected a substantial number of parasomnia patients. Sleepsex was far more injurious to the bed partner than to the affected person in the parasomnia group. However, adverse psychosocial consequences were quite common in both patients and bed partners. In contrast, pleasurable experiences from the sleepsex were reported by 3 patients with sleep related seizures, and by the bed partners of 4 parasomnia patients and 1 sleep related seizure patient.

In the parasomnia group, histories of multiple NREM sleep parasomnias were common, with confusional arousals being predominant. Sleepsex was rarely the only parasomnia behavior in the longitudinal histories of these patients. Two cases also involved sleepwalking with “sleep driving”4 and one case also involved sleep related eating disorder.2 Besides a clinical evaluation, PSG monitoring (without penile tumescence monitoring) took place in the preponderance of cases. OSA comorbidity that promoted sleepsex was present in 3 cases, with snoring during sleepsex being a prominent feature. (The authors of one report4 commented on an additional case of sexsomnia with OSA that resolved with CPAP therapy).

Although 26 parasomnia patients with sexsomnia had PSG studies, sometimes on multiple nights, only 4 (15.4%) demonstrated sexual behaviors during sleep: 3 patients had sexual moaning during slow wave sleep (with one patient also attempting to remove his pajamas3); one patient, who slept with his wife during the PSG study, had the following event occur: “the video surveillance showed Mrs. D. initiating sexual foreplay, which led to intercourse, performed by Mr. D. while he was ‘drifting’ between stage 1 and wakefulness. The patient was not aware of this in the morning.”4 Therefore, the only parasomnia sleepsex behaviors documented by PSG in the published literature involves sexual moaning, and one case of sexual intercourse initiated by the bed partner.

The apparent association of sexsomnia with alcohol use/abuse and drug abuse was as follows: limited use of alcohol on the night of sleepsex (therefore, no presumed link), n=1; sufficient alcohol use or abuse on the night of sleepsex (therefore, possible or probable contributing factor), n=8 (with n=1 also smoking marijuana, and n=1 also taking “speed”). In addition 3 had past histories of drug abuse, with established remission at the time of sleepsex. A total of 8 patients had identified psychiatric disorders, but without any presumed link with the sexsomnia. Another patient was experiencing “stress” and sleep deprivation on the night of committing sexual assault during sexsomnia.

Parasomnias, OSA, and seizure-induced sleepsex appeared readily amenable to therapy. The benzodiazepine clonazepam was effective in almost all treated parasomnia cases, CPAP was effective in all 3 treated OSA cases, and anticonvulsant medication was effective in all 5 treated seizure cases.

Abnormal Sleepsex Behaviors Found with Parasomnias and Sleep Related Seizures

Masturbation:

In the parasomnia group, 4 patients masturbated to climax on a recurrent basis during sleep, whereas three patients did not climax during recurrent episodes of sleep masturbation. In the nocturnal seizure group, one man had longstanding, recurrent episodes of “violent masturbation.”

Parasomnia masturbation had various clinical manifestations:

A 34-year-old married man would spontaneously masturbate to ejaculation every night after he had been asleep 2–3 hours, and was not arousable. Nightly sleep masturbation occurred while he continued to engage in sexual intercourse with his wife every night before falling asleep.20

A 27-year-old man “usually ‘awoke’ with an ejaculation between 02:00 and 06:00 during the preceding 5 years. He broke 2 fingers when he tore off the restraints he used to avoid moving in bed. He also slept in a different bed or on the floor in futile attempts to avoid the undesired masturbation.3

A 26-year-old married woman had a history of abruptly tearing off her clothing and masturbating violently during the first half of the night. Her masturbation was associated with soft to loud vocalization and occasional vaginal discharge. If her husband interrupted the episode of masturbation, it might recur a second or a third time during the night. Any attempt to initiate intercourse after she was awakened was rejected, and she denied the behavior.3

A 38-year-old woman “asked for professional help after her husband, to whom she was married for 2 months, had awoken repeatedly at night only to find his wife apparently masturbating in her sleep.”4

The one patient with sleepsex masturbation associated with nocturnal seizures was a 31-year-old man with a 12-year history of masturbating while asleep.3 Episodes lasted from 3 to 15 minutes, and movements became increasingly violent the longer the episodes lasted. Bed partners would hear inarticulate moaning sounds together with movements of the feet or legs. There was confusion and disorientation whenever he awakened during an episode. Timing of these events was variable. No ejaculation was reported by the patient or the bed partner. Because of his sleep masturbation, the patient avoided sexual relationships for more than 8 years. During that time, he was aware of repeated bruising of the penis, along with a sore groin.

Sexual Vocalizations and Talking:

In the parasomnia group, sleeptalking and sleep vocalizations (brief or prolonged) affected 48.4% (15/31) of patients, with 19.4% (n=6) having sexual sleeptalking and vocalizations, and 29.0% (n=9) having nonsexual sleeptalking and vocalizations. Some examples include:

A 26-year-old woman had soft to loud vocalizations during sleep masturbation.3

A 27-year-old woman had sexual moaning during sleep at least three nights weekly for 15 years that would emerge within 15–20 minutes of sleep onset.3

A 28-year-old woman had nightly sexual moaning and sexual fondling during sleep for 16 years that would appear within 20 minutes of falling asleep and disturb the sleep of her husband and children.3

A 26-year-old woman would initiate foreplay with her bed partner while they were both asleep between 02:00 and 05:00 and would utter sexually provocative phrases while fondling him. Whenever he responded positively to her involuntary sexual overtures during sleep, she would then awaken and accuse him of forcing sex on her while she slept.3

Uttering profanities and sexually provocative phrases, or engaging in “dirty talk” accompanied sleepsex fondling or intercourse in three patients. In the sleep related epilepsy group, previous bed partners of one patient had noted inarticulate sexual moaning during sleep together with movement of the feet and legs. Another patient shouted while engaging in sleepsex.

Sexual Fondling:

Some examples include the following:

A 23-year-old man would attempt to remove his girlfriend’s clothing and fondle her, without ejaculating, during the first part of the night. When he was awakened, he would be confused and disoriented.3

An 18-year-old male was accused of putting his finger into the vagina of a nearby teenager at 6 a.m. while he was asleep with recent sleep deprivation. 3

A man would grab his wife’s buttocks during sleep while “grinding her from behind” with rhythmic pelvic movements. 22

A 22-year-old man on two occasions within a month, while presumably asleep, fondled the breasts of one woman (before initiating intercourse), and inserted his fingers into the vagina of another woman (and when she asked him to stop, “he did so and left the room without incident”).25

A 27-year-old man would frequently engage in cunnilingus on his wife while they both were asleep.4

Sexual Intercourse:

A diverse set of clinical presentations was reported:

“During the episodes, the [27-year-old] patient typically procured his wife, achieving complete sexual intercourse with total amnesia…His wife remained in bed with him after the episodes.”24

A 43-year-old man engaged in nightly episodes of amnestic sleepsex along with amnestic eating in his sleep. His current and previous girlfriends had sexual intercourse with him every night while he would be snoring and sound asleep for up to 30 minutes before ejaculation. Furthermore, “the repertoire of unconscious sexual activity by the patient was varied and included intercourse in different body positions, as well as oral sex, both given and received.”2

A 38-year-old man for 12 years had sexually assaulted his spouse during sleep between 03:00 and 05:00 at irregular intervals, but at least once every 15 days. He would tear off his wife’s clothes, fondle her, and initiate sexual intercourse. His wife observed that he was “not present” and “unresponsive” while acting violently, and one time attempted to choke her.3

A 33-year-old man one night grabbed his wife in his sleep, tore off her bed clothes, and forced intercourse. Despite her active resistance, she could not “reach” him. He seemed “far away” and appeared “glassy-eyed.”3

A woman whose husband would initiate and consummate sexual intercourse with her while asleep also described his total disregard for her menstrual status while engaging in sexsomnia; they never had engaged in sex during wakefulness while she was menstruating.4

A woman described her husband as being more amorous and more aggressive during episodes of sexsomnia than during his wakeful sexual activity. On some nights “there is no stopping him.” Once when he grabbed her around the neck, she slapped him hard, which awakened him, and he immediately let go.4

A man had his two current girlfriends independently confirm that he frequently engaged in sexsomnia. One girlfriend commented that he was a “different person” during sexsomnia, being a more amorous and gentle lover, and more oriented in sexually satisfying her.2

A 29-year-old man for at least six years had sexually assaulted his bed partner and uttered profanities between 03:00 and 06:00 while he was asleep. He also moved his arms and legs excessively in sleep when he dreamt of fighting against “intruders.” 4

A 22-year-old man “after a night out drinking” fell asleep on the sofa in a separate room from a female (platonic) friend who an hour later “was woken suddenly feeling a hand fondling her breasts and then, in rapid succession, she felt his erect penis penetrating her anally, vaginally, and then being forced orally.”25

Sleepsex Behaviors and Experiences Found Exclusively with Sleep Related Seizures

Sexual Hyperarousal.

i) A 38 year-old man had a right temporal lobectomy one year earlier after a 19 year history of intractable complex partial seizures that were devoid of any sexual manifestations.26 One year after surgery, complex partial seizures reemerged at a rate of 2–3 times monthly, with 2 de novo forms of sexual behaviors and experiences coming from sleep and wakefulness. He would “occasionally wake up during the night with a strong sexual desire, and he believed that this was brought about by a seizure.” An immediate post-awakening, post-ictal sexual hyperarousal was considered to be the most likely explanation. The second form of abnormal sexual behavior occurred while he was awake, about 20 minutes after the onset of a complex partial seizure. He would approach his wife to have sex, but he would not be insistent nor would he proceed if their children were present. If a seizure occurred after sex with his wife, 20 minutes later he would again desire sex with his wife. ii) A 32-year-old woman developed sleep related hypersexuality 3 weeks after undergoing removal of a right inferior temporal lobe lesion, for an 18-year history of intractable bitemporal complex partial seizures.27 “She would wake in the middle of the night with intense sexual desire and rouse her husband. She stated a wish for her husband to have the same operation…The hypersexuality subsided 18 months after surgery.” The histopathology of the resected tissue identified a dysembryonic neuroepithelial tumor.

Ictal Orgasm.

A 41-year-old woman developed frequent, brief episodes of sleep related somatosensory seizures that responded to phenobarbital therapy for 2 years. One night 5 months after discontinuing phenobarbital she “was awakened by the electrical [seizure] discharge, now with paresthesia in the right lateral abdominal and pubic regions and about her genitalia.28 A sensation of vaginal dilatation ensued immediately afterward, which inevitably brought about an orgasm, either pleasant or painful. During these episodes there was no confusion or memory loss…Normal marital sexual behavior was reported.” PSG with extensive sleep EEG documented 8 clinical seizures, with the first 4 emerging from slow wave sleep, and the remainder emerging from stages 1 and 2 sleep. The central-parietal regions exhibited sharp wave and spike paroxysmal activity followed by the patient awakening, with electrical sensations. Orgasm immediately ensued, with persistence of generalized paroxysmal EEG activity. Resumption of phenobarbital therapy immediately conrolled her seizures.

A 55-year-old woman had a 12-year history of “paroxysmal nymphomania” arising from sleep, when she awakened with “a feeling of being hot all over as if she were having coitus.”29 She also had left somatosensory seizures and developed left hemiplegia.

A 31-year-old man with temporal lobe epilepsy had nocturnal attacks in which he would awaken with a stereotyped sequence of motor, sensory, and experiential symptoms that began with twitching of the forehead and face which progressed down to the neck and left arm, followed by the sensation of “being just like an orgasm” and “sexual and intensely pleasurable,” but never associated with ejaculation.30 There was a dramatic response to diphenylhydantoin therapy, with total cessation of nocturnal attacks and orgasmic sensations.

Ictal Sexual Automatisms:

A 36-year-old man with a 16-year history of complex partial seizures with sexual automatisms underwent sleep EEG monitoring with sphenoidal leads.31 Sleep related seizures “consisted of the patient suddenly seizing the groin area with both hands, turning and thrashing about, and uttering obscenities. He continued to manipulate his penis and then had lip smacking, snorting noises, and intermittent grimaces for 2 minutes, with postictal confusion for 5 minutes. EEG during the attack showed rhythmic slowing bilaterally.”

Other cases of nocturnal seizures associated with various nocturnal sexual automatisms and experiences have been published, but without mention of whether they were sleep related, and neither sleep EEG or PSG were performed.32–34 In another case, a 51-year-old man with a 21-year seizure history was documented to have genital automatisms arising from a wakeful complex partial seizure, but genital automatisms were not present during a documented sleep related seizure.35 However, given his long and intractable seizure history, it is possible that some of his sleep related seizures involved genital automatisms.

Sleep Related Hyperkinetic Seizures with Sexualized Pelvic Thrusting

Repetitive pelvic thrusting that often resembles sexual (coital) behavior is a prominent feature of sleep related hyperkinetic seizures that are found most commonly in nocturnal frontal lobe epilepsy (NFLE), but also in nocturnal temporal lobe epilepsy (NTLE).36–40 In a study of 442 surgically treated epileptic patients, 5.6% (n=25) had exclusively sleep related hyperkinetic seizures.40 These 25 patients reported sensory-experiential (nonsexual) auras emerging from sleep that immediately preceded the hyperkinetic automatisms. These 25 treatment-resistant patients underwent surgical resections of their epileptogenic zones; 18 were diagnosed with NFLE and 7 with NTLE. The 16 patients with Taylor’s dysplasia, as demonstrated by histopathology, were all free of their sleep related seizures after one year; the status of the other 9 patients was not reported. In contrast to the sleep related, sexualized, hyperkinetic seizures that are predominantly due to NFLE, discrete epileptic genital automatisms without a hypermotoric component is generally due to NTLE.35

Legal Consequences, Including Sleepsex with Minors, in the Parasomnia Group

The legal outcome from the accusations and legal charges of sleepsex with minors were acquittal, N=2 (on the basis of sexsomnia); long-term probation, N=2 (including outpatient psychiatric monitoring); and unknown, N=6 (outcome from legal charges and completion of child protection agency investigations were still pending). Sexsomnia was the medical diagnosis that was also used as a legal defense in the cases involving minors. The following are pertinent examples:

A 45-year-old man with lifelong sleepwalking was awakened one night around 02:00 by the screaming of his 14-year-old daughter’s girlfriend who was sleeping over at their home. She accused him of sexually fondling her while she was asleep. He was arrested that night, and claimed to be entirely amnestic for the episode.2

An 18-year-old male with longstanding sleep terrors and sleepwalking was accused of placing his finger into the vagina of a female teenager who was sleeping in the vicinity.4

A 39-year-old married man was charged with sexually touching his 9-year-old daughter while she was sleeping one night in bed with her parents, after leaving her own bed because of a nightmare. He claimed to have been sleeping at the time. He and his wife would often initiate sex with each other during sleep.4

A 32-year-old man was accused of inserting a finger into the vagina of a 10-year-old girl, after falling asleep in bed with her (and another child) subsequent to drinking alcohol excessively and smoking marijuana. He had a history of sleeptalking, had one known episode of sleepwalking, and had a family history of parasomnia.4

A man was accused by his 15-year-old daughter of kissing her breasts and penetrating her vagina with his finger while he was asleep, which his wife and ex-wife also reported his doing to them while he was asleep.23

A 35-year-old man was accused by his 11- and 8-year-old daughters of touching their genitalia (without penetration) while they were all apparently asleep.21

Another category of child molestation involving sexual fondling during sleep was reported in a 27-year-old man with severe obstructive sleep apnea.21 While napping on two separate days, his young daughter jumped into bed with him and fondled his genitalia until ejaculation, when he then awakened and became alarmed.

In one of the two adult cases with forensic consequences, a 27-year-old man faced criminal charges initiated by his wife because she claimed that he frequently assaulted her sexually while she was asleep by attempting cunnilingus and sexual intercourse. He was amnestic for these episodes, had a history of sleepwalking and sleep terrors, and had a family history of sleepwalking.4 In the other adult case, a 22-year-old man was acquitted “on the basis of automatism” that presumably occurred during sleep.25

Physical and Psychosocial Consequences

In the parasomnia group, the bed partners often experienced physical injuries (ecchymoses, lacerations) from the sexual assaults, and to a lesser extent the patients were also physically injured (bruised penis; fractured digits). Moreover, both the patients and bed partners often experienced an array of adverse psychosocial consequences involving bewilderment, embarrassment, shame, guilt, despair, “shock,” alarm, anger, worry, annoyance, denial, feelings of inadequacy/low self-esteem, and reactive emotional distancing that led to some marital estrangement with marriage counseling sometimes being sought. In some cases, there was “low-grade guilt” over disturbing the sleep of family members from sexual moaning.3 One man was not convinced that he engaged in any sleep masturbation (that occurred nightly), but then became worried “about the effect of excessive drainage of seminal fluid on his health.”20 His wife, on the other hand, was quite concerned about his sleep masturbation and “felt sexually redundant, inadequate, ‘cheated’ of her husband’s confidence.” Interestingly, they regularly engaged in sexual intercourse before falling asleep.

On the other hand, in 4 parasomnia cases, pleasurable aspects of the sleepsex were reported by the bed partners, with negative aspects also acknowledged:

One woman commented that her boyfriend’s sleepsex was more “aggressive and dominant” than his waking sexual behavior, and she “found some aspects of the sleepsex pleasurable…and a little kinky,” such as “forceful albeit playful biting and ‘talking dirty,‘ but “nonetheless she requested that the patient incorporate some of the nighttime sexual practices…into their conscious daytime lovemaking.” 2

Another woman “reported infrequent and hurried sex with her husband, whom she described as distant and reluctant during wakefulness. Nocturnal sex was more satisfactory to her, even if associated with bruises at times.”3

A woman who slept with a sexsomniac boyfriend commented on how he was a “different person during these activities—apparently, he is a more amorous and gentle lover and more oriented toward satisfying his partner when he is asleep.”4

A wife reported that her husband would initiate sex in his sleep about once monthly, during which times he would be “more aggressive and more amorous… than when he is awake.”4

Likewise, in 4 epilepsy cases, pleasurable aspects of sleep related sexual seizures were reported by the three patients and one bed partner:

A 41-year-old woman with nocturnal somatosensory seizures would experience pleasurable (or painful) orgasms together with vaginal dilatation during her seizures.28

A 31-year-old man with temporal lobe epilepsy would experience a sleep related “sensory phenomenon along with the twitching [that] was described as ‘being just like an orgasm…sexual and intensely pleasurable,” but without ejaculation being achieved.30

A 32-year-old woman with an 18-year history of complex partial seizures developed sleep related hypersexuality arising from sleep that began 3 weeks after surgery. “She would wake in the middle of the night with intense sexual desire and rouse her husband. She stated a wish for her husband to have the same operation.”27

A “wife had started to look forward to this happening,” referring to her husband’s post-ictal (psychomotor attacks) hypersexuality that occasionally emerged from sleep.31

Finally, it should be emphasized that in the parasomnia and epilepsy cases just described, psychopathology was uncommonly present and was not an identified contributing factor to the abnormal sleep related sexual behaviors and experiences. Furthermore, neither sexual deprivation/frustration nor a previous history of paraphilia or criminal sexual misconduct were reported.

Experiences with sleepsex, including psychosocial problems in both initiators and recipients of sleepsex, have been categorized in a web-based survey involving 121 respondents (mean age, 37 yrs; 65% female).41 Six distinct themes stemming from the problematic sleepsex, affecting the “initiators” and the “recipients”, were identified: (1) fear and a lack of emotional intimacy; (2) guilt and confusion; (3) a sense of repulsion and feelings of sexual abandonment; (4) shame, disappointment, and frustration; (5) annoyance and suspicion; (6) embarrassment and a sense of “self-incrimination.” Various methodologic limitations of this study were acknowledged by the author, such as lack of longitudinal information on sleepsex, absence of clinical evaluation and PSG, and the anonymous and non-verified nature of the reporting. Also, amnesia or recall for the sleepsex was not systematically addressed; there were comments of complete amnesia in some people, others “often had no recollection,” and others had “a high level of amnesia for the events.”

Sleep Disorders with Abnormal Sexual Behaviors During Wakefulness and Wake-Sleep Transitions

Sexual Disturbances in Kleine-Levin Syndrome (KLS) (Isabelle Arnulf)

KLS is a rare sleep disorder characterized by recurrent and unusually long episodes of hypersomnia.1 Sleep episodes last 16–24 hours per day for days or weeks, and during periods of wakefulness are associated with behavioral and cognitive disturbances, often including megaphagia and to a lesser extent sexual disinhibition. These symptomatic episodes alternate with periods in which patients have normal sleep and behavior that usually last for months to years.

Herein are presented the results of an extensive meta-analysis of all 195 articles published about KLS in the Medline database (1962–2004). After having removed duplicate and doubtful cases, reviews and points of view, information about 186 patients from 139 articles were compiled.42 KLS affected mainly males (68% of the group), with a median age of onset of 15 years. The disease was self-limiting, but usually lasted between 4 and 8 years.

Data on KLS was also gathered using a standardized questionnaire and interview of 108 new patients and their parents taking part in a prospective research program on KLS at Stanford University (Arnulf I, et al. submitted manuscript).

Frequency of Hypersexuality

In the meta-analysis of the literature, we found that 41.9% (n=78) of patients had symptoms of hypersexuality, while 57.5% (n=106) did not report these symptoms and a single patient had decreased libido during his episodes.42 In contrast with other symptoms, that were equally frequent in both sexes (such as megaphagia, 75% in women vs. 82% in men; or cognitive disturbances, 93% in women vs. 95% in men), hypersexuality was twice as frequent in men (51%) as in women (24%, odds ratio: 3.4, P = 0.002). The age at KLS onset was not different with (16±7 y) and without (17±10 y) sexual disinhibition. The presence of hypersexuality did not predict a worse prognosis (such as a longer disease course, or longer episodes) than its absence. This symptom was also present in 28% of 12 patients with KLS symptoms secondary to various brain lesions. Plasma levels of testosterone, measured in 16 of 186 KLS patients, were normal in 14 patients and mildly decreased in 2 patients, but never increased.

In the prospective KLS series involving 108 cases in which interviews used a structure questionnaire, 53% reported increased sexual drive, while 6% had decreased sexuality at least during an episode. Hypersexuality was more frequent in boys (58%) than in girls (35%).

Symptoms

Hypersexuality was briefly described in the second KLS patient of Kleine43 in 1925. Later, Robinson and McQuillan, in 1951, reported on a 19-year-old officer-cadet who had disinhibited behavior during a KLS episode: “He indecently exposed himself in the ward, and while lying unclothed on the bed he masturbated, grinning broadly. Lewd remarks were made to the nursing staff. Once he urinated in the garden in the presence of a sister.”44 In our meta-analysis, we observed that the changes in sexual behavior shared some similarities with the disturbed eating behavior, such as increased quantities (increased frequency of masturbation or of sexual intercourse, demanding intercourse several times daily45), compulsions (with active and uncontrolled research of sex), lack of judgment in the choice of sexual partner (sexual advances were made to religious sisters, to the patient’s daughter46 or sister,47–49 to a nurse “who is said to have been old enough to be his grandmother,”44 and in three cases to other males by otherwise non-homosexual male patients46,50,51), inattention to the environment (such as masturbating in public), and absence of self-awareness of the inappropriateness of the behavior.

Garland, in 1965, reported that a 16-year-old teenager made “frequent and vigorous attempts at masturbation, whether or not the curtains round his bed were drawn, and this would be continued during questioning. He never achieved either orgasm or ejaculation.”50 In our own prospective program on KLS, a young adolescent went to the beach with his family, and started to masturbate ostentatiously on the beach, to the great embarrassment of the grandparents, parents, and sister. Another reported masturbating 3 to 5 times a day, while one reported: “I masturbated excessively, to the point of bleeding.” A typical example of the compulsive component of KLS was observed a 39 year-old man, who, during his third episode of KLS, attacked 2 women sexually, and the same day attacked his daughter sexually. He showed exhibitionistic behavior and ran naked in the ward, threatening to attack the nurses sexually and fondled the female patients. During the sixth episode, he undressed himself, exposing himself to other patients, made advances to the nurses and patients, and threatened to sleep with them. During the seventh episode, he was confined to a male-only, locked psychiatric ward for 5 months, where he approached a male patient to have relations with him.46

Intensity of Symptoms

The intensity of the abnormal sexual behavior may vary. Some behaviors were considered as mildly inappropriate in a given context of education or culture: patients used obscene words in front of the parents and doctors.52 One mother told us his son was “cursing like a trooper”; a 14-year-old teenager answered to the female doctor that his three wishes were: “1- to go to sleep; 2-money; 3: to have a ‘dick’ as long as the width of the bed.” A usually extremely polite, 13-year-old teenager answered the doctor asking him what he would be doing during the course of summer: “fuck, fuck girls.” Patients can demonstrate inappropriate sexual behavior in the clinical setting while transgressing interpersonal boundaries: the aforementioned 14-year-old teenager also put his hand on the female doctor’s thigh, while another patient fondled the female nurse during his EEG recording. Another had increased interested in pornographic magazines,53 and one patient stared at a nurse’s body in tactless way.54 In our prospective series, several teenagers reported that they frequently accessed pornographic material via phone services or the internet, leading one of them to spend more than $500 in phone bills during an episode. A mother reported to us that her 15-year-old son, during the first episode, started masturbating when the urinary catheter was inserted in the emergency room, so everybody believed the catheter was responsible for the odd behavior. Even after the catheter had been removed, he continued to masturbate several times a day in front of people and used sexually explicit language with a curiously desperate voice (e.g., “I want to fuck you, I want to screw your ass, I want a blow-job”) without directing his comments at anyone in particular. A young father in India had a severe fever for 13 days, and after the fever subsided, he had an increased sexual urge and began using profanity.55 The sexual disinhibition was obvious as “he would drag away his wife, and would start undressing her in the presence of everybody, unconcerned and completely oblivious of their great horror and embarrassment. Not only that, he made amorous advances to other females too.”55 In another case, behaviors caused a disruptive and potentially dangerous, nuisance, involving a school boy who went to a neighbor’s house, masturbated into his neighbor’s underwear, stole football match tickets, and set fire to the drapes.46

Associated Symptoms

Sexual disinhibition sometimes occurred simultaneous with other repetitive, stereotypical behaviors compulsions such as setting fire,46 or with the compulsion to repeatedly turn the light switch on and off.47 Patients with KLS also frequently experience a disturbed state of consciousness that they struggle to describe as “being between dream and reality.” One of them “admitted he had vivid dreams, or rather fantasies, of a violent sexuo-sadistic character.”44 In almost all cases, however, the abnormal sexual behavior did not stem from sleep, as with sleepsex, but occurred during wakefulness in the daytime.

Hypersexuality in Women With KLS

The symptoms of sexual disinhibition were reported in women58–60 and in 3 prepubescent children.61–63 One young lady was hospitalized because she was somnolent and for the two previous days had been “scratching her genitals in public, lifting her clothes over her head to warm her buttocks at the fire.”58 During that KLS episode, she also made advances to male patients and staff. In our case series, the parents of a senior high school teenager noted a change in her daughter’s clothing choices. The teenager purchased tube tops, playboy tank tops, and thong swimwear; these choices were was completely out of character for her. One woman reported that during her KLS episodes: “remember, this experience was in the early 1950s, a more innocent time than today. I usually wanted to masturbate. In junior high school, riding in car with several kids, I sat on a boy’s lap and kissed him and have no idea what things I was saying to him. At the same time I asked myself, ‘What am I doing here? This isn’t me.’ Feelings were flat, no embarrassment or shame, though I was aware of the disapproval of others.”

Hypersexuality and the Longitudinal Course of KLS

In a recent prospective study of 108 KLS patients (76% male), the presence of hypersexuality in 53% (n=57; 48 [84%] males) of cases conferred a two-fold lengthening of the median KLS clinical course (21.2 + 1.7 yr vs. 10.2 + 1.9 yr) (P = 0.01) (Arunulf I, et al. submitted manuscript). Age of KLS onset did not differ between the hypersexual and non-hypersexual KLS groups: 16.2 +4.1 vs. 15.5 + 7.9 yr. This finding suggests that hypersexuality is associated with KLS disease severity.

Pathophysiology of KLS

The cause of KLS is unknown. Scarce neuropathological evidence and a possible association with HLA DQB1-20164 suggests it could be an autoimmune encephalitis restricted to the hypothalamus and adjacent areas. While brain computed tomography and magnetic resonance imaging were normal in all reported patients with primary KLS, diffuse brain hypoperfusion, mostly focused on the thalamic and frontotemporal areas, has been reported.65 It is therefore difficult to correlate the symptoms of hypersexuality in KLS with a precise anatomical location. KLS is strongly associated with male sex and puberty. Hypersexuality affects more than half of the patients and is associated with a much longer disease course. This suggests that boys are more vulnerable to the disease and may suffer from more extensive or severe brain lesions than girls. Eventually, the association of instinctive behaviors (sleep, sex, aggression and eating) being intensively released (hypersomnia, hypersexuality, overeating) in the same patients points at a common origin from brain structures driving archaic behaviors. Similar symptoms of hypersexuality are observed in various neurological diseases, such as in the Kluver-Bucy syndrome, caused by lesions of the temporal lobes (and associated with increased oral exploration) in humans66 and nonhuman primates,67 of the paramedian thalamus or subthalamus nucleus,68 of the orbitofrontal and medial frontal area.69 Hypersexuality may also complicate the course of the disease in patients with Alzheimer disease or mania, and as a side effect of dopaminergic agents in Parkinson disease.70 Some KLS behaviors, such as singing loudly while playing and banging on a piano continuously, are also observed in manic states. Finally, both deviant sexuality (including paraphiliac behaviors, e.g., exhibitionism) and hypersexuality are prominent manifestations of altered sexuality in KLS during its hypersomnia phases.

Sleep Disorders With Abnormal Sexual Behaviors During Wakefulness and Wake-Sleep Transitions

Severe Chronic Insomnia:

A published case described a 39-year-old woman who presented to a sleep disorders center with a lifelong history of severe insomnia associated with motor restlessness.71,72 She would sleeplessly walk around her house on most nights until 01:00–03:00 and rarely slept for more than 5 hours. In early adulthood, the insomnia became progressively worse. She felt that every day in her life there was “a motor running inside me all the time, revved up, with surges of electricity and high energy going all over me.” During the daytime, her mind and body felt speeded up, but she felt physically exhausted.

Beginning with puberty, she experienced problems with an excessive libido and genital hyperarousal that bothered her nearly every day. There were strong sexual sensations in the vulva, and general sexual heightening without erotic thoughts or altered consciousness that would only partly and briefly be relieved by having sex with her husband. Sometimes they had sex multiple times daily on many consecutive days. She could readily distinguish between this type of “hyper sex” (mechanical physical discharge, “pure lust,” devoid of emotion) from “emotional sex” which was intimate and pleasurable with her husband.

Successful control of her severe insomnia was only achieved with bedtime opiate therapy that also controlled her motor restlessness, along with her excessive libido and genital hyperarousal, without interfering with normal sexual relations with her husband. Remission of her insomnia, excessive libido, and genital hyperarousal has been maintained during more than 20 years of nightly opiate therapy, with relapses of these problems occurring whenever she did not take the medication.

Three additional cases of hypersexuality emerging during exacerbations of chronic insomnia in young adults (2 males; 1 disabled from insomnia) involved persistently heightened libido and increased sexual behavior that lasted for days to weeks until the insomnia had subsided sufficiently (CHS & MWM, unpublished data).

Restless Legs Syndrome (RLS)

A case has been reported involving a 72-year-old man with a 4-year history of RLS (with abnormal sensations originating in the lower abdomen), who was documented by PSG to engage in rhythmic, pelvic, coital-like movements during relaxed wakefulness, at the wake-sleep transition, during infrasleep awakenings, and after the final morning awakening.73 There were “intermittent periods (1–6 minutes) of stereotyped, repetitive, rhythmic body movements with side-to-side trunk motions or, when in a prone position, rhythmic pelvis forward and backward rocking, resembling coital movements, at a frequency between 2 and 3 per second.” The concurrent EEG showed alpha or alpha-theta activity, and the patient complained of typical restlessness in the lower abdomen. He could voluntarily suppress the pelvic movements for only brief periods of time. Pramipexole therapy at bedtime promptly controlled all sleep related sensory and motor symptoms, including the coital-like pelvic movements, which was sustained at one month follow-up. This case illustrates the convergence of RLS with a rhythmic movement disorder, both in the linked symptomatology and in the shared response to monotherapy. It also exemplifies how sexualized behavior can be linked with negative somatic sensations.

Another male patient with severe RLS, aged 64 yr, reported that he usually used masturbation at night to alleviate the painful sensation of RLS. He found long-lasting relief that could extend for the entire night (IA, personal communication). It is possible that orgasm-associated dopamine and opioid release mediated the therapeutic effect on RLS.

A study of 930 patients with moderate-to-severe RLS found that ropinerole-treated patients had significantly less disturbance in sexual activity than placebo-treated patients.74 The mechanisms of efficacy were postulated to involve a direct dopaminergic effect and/or an effect derived from the control of RLS symptoms.

Special Clinical Considerations

Narcolepsy:

Hypnagogic and hypnopomic hallucinations (HH), often occurring with sleep paralysis (SP), can incorporate sexual content, with serious consequences. A series of four cases with PSG/MSLT confirmed narcolepsy, with the narcoleptic tetrad, was reported in three females aged 31–42 years and a man 39 years old.75 In all four cases, compelling recurrent experiences of sexual molestation and rape began early in the course of their narcolepsy. One woman with the narcoleptic tetrad complained that after getting married, her father-in-law had continually molested her sexually in a bizarre manner. She also reported a history of HH without sexual content, recurrent sleep paralysis (including hypnopompic SP), and cataplexy. A second woman had SP and multi-sensory HH, including “astral travel experience” and paranoia about poisonings and plots. She described being raped by a policeman after going to bed, with detailed accounting of her state of undress and the sexual positions used. Following the rape, the policeman made her take drugs and then left. The patient saw a psychiatrist for rape counseling. She described another rape that had taken place five years after the first rape. Her manager at work gave a party, and after she drank alcohol and went to a bedroom, her chairman came in and raped her—while she reported being paralyzed and mute. Other men were then let in her room and they silently raped her. When she “recovered her senses” she found that the rapists had put her clothes back on. She “permanently” lost respect for her supervisors and retired early from her position. She reported being raped on other occasions. She was eventually correctly diagnosed to have narcolepsy, and responded well to amphetamine therapy.

A third woman with severe HH had her narcolepsy substantially controlled with amphetamine therapy, but had a persistent belief that she had previously been repeatedly raped. The fourth patient was a 39-year-old man with lifelong HH who recalled being repeatedly fondled sexually by a friend when he was a young man. During naps he would partially awaken and feel he was elsewhere, “paralyzed by drugs,” while his friend was fondling him. When he was awake, he found that his friend always acted appropriately. Amphetamine therapy completely controlled his narcolepsy. However, he persisted in regarding his previous sexual molestations were real and wondered what drug was used to paralyze him.

Two other cases of recurrent sleep related sexual hallucinations in undiagnosed narcolepsy have been reported.76 A 23 year old female vividly recalled being sexually assaulted in a car and went to the police to file charges, but then “she slowly realized that her experience of violation was a hallucination.” She then retracted her charges, and a sleep evaluation with PSG and MSLT confirmed narcolepsy-cataplexy. Clomipramine therapy, together with modafinil, fully suppressed the hallucinations. A 45 year old man had vivid experiences of sexual relations with the wife of his chief, and he told his colleagues about this, but they were skeptical. This led him to consider the possibility of hallucinations. After PSG-confirmed narcolepsy, clomipramine therapy, together with modafinil, fully suppressed the sexual hallucinations and their delusional interpretations.

In a study on SP associated with hypnagogic or hypnopompic hallucinations, in which the Waterloo Unusual Sensory Experiences Survey was administered to 1,273 undergraduate students, 13 respondents (all female) reported their SP experiences “as feeling very much like being sexually assaulted or raped.”77

In the original description and naming of narcolepsy by Gélineau in 1881, the patient was a 38-year-old man with a two year history of very frequent sleep attacks, totaling up to 200 attacks daily.78 This patient could not speak with Dr. Gélineau for even 30 minutes without falling asleep, and constantly needed his 13-year-old son at his side to keep awakening him, so he could attend to his successful business. A wide array of intense emotional states played a prominent role in triggering his sleep attacks. Gélineau’s male patient also spontaneously reported that his infant child “was conceived in a moment when the illness came over him.” He was convinced that sexual intercourse took place during one of his sleep attacks, which resulted in the conception of his child. This is an unlikely possibility, since even if he did have a REM-onset penile erection, the atonia of REM sleep would not have allowed him to initiate or participate in sexual intercourse. Gélineau’s patient most likely experienced either peri-orgasmic cataplexy, or he had a HH or vivid dream involving sexual intercourse with his wife during REM-onset sleep, which later became linked with his firm belief that the conception of their baby had also taken place during that sleep attack or HH.

Sleep Exacerbation of Persistent Sexual Arousal Syndrome (PSAS)

PSAS, also called recurrent sexual arousal syndrome, is a rare condition with widely diverse causes. Recently, a unique case involving exacerbation of PSAS with genital arousal during drowsiness and sleep onset was reported.79 A 66-year-old sexually active woman presented with a 5-year history of persistent, unpleasant, “overwhelming” internal sensations of the vagina and pelvis. These genital sensations became worse whenever she felt vibrations while riding in a car, or while reclining or falling asleep; these sensations would often disrupt her sleep several times nightly. Erotic thoughts did not accompany the genital arousal either while falling asleep, upon awakening, or during the daytime.

When she awakened after being asleep for less than an hour, lying in bed would become intolerable because of the insatiable urge for sexual release, always being on the verge of achieving orgasm. The genital sensations and urges were not accompanied by any subjective sexual desire (libido), and so a form of “mechanical sex” was recurring. The genital arousal “felt intrusive and unwanted.”

Sex with her male partner would reduce her symptoms for only 2–3 minutes after orgasm. Physical activity, cold compresses, and distraction techniques helped reduce her symptoms, as did overuse of analgesics. The longitudinal course of her PSAS was marked by progressive severity; after five years, more than 80% of her waking time was disturbed by her genital symptoms. The intensity of symptoms, however, had not changed in 3 years.

She had gone through menopause 14 years previously (9 years before developing PSAS), and hormone replacement therapy was discontinued after 4 years. There was no abnormal menstrual history and no psychiatric history. During drowsiness and sleep onset, vaginal pulse amplitudes increased by 95% of basal values, which together with other findings documented increased vaginal blood flow and congestion and corroborated the patient’s complaint of sleep exacerbation of her PSAS. Genito-sensory testing of the vaginal and clitoral areas documented reduced sensory function, pointing to an organic basis for her genital arousal disorder. The brain, spinal cord, and pelvic regions were intact upon testing. PSG was not performed.

Olanzapine, carbamazepine, clomipramine, paroxetine, and various other remedies had been ineffective; risperidone was effective upon initiation of therapy.

This case may represent a dissociated sleep state in which REM sleep genital arousal with increased vaginal blood flow inappropriately intruded into this woman’s hypnapgogic and hypnopompic states. Alternatively, this case may represent a “restless vagina syndrome” akin to RLS, consisting of abnormal vaginal sensations while resting before sleep onset associated with the “urge” to have sex, with sexual activity transiently reducing the unpleasant vaginal sensations.

Sleep Related Painful Erections (SRPE) and Increased Sexual Activity

SRPE is an obscure parasomnia in which painful erections occur during sleep and disappear upon awakening. Increased sexual activity can emerge during the course of SRPE as a (futile) form of self-therapy, as reported in a 65-year-old man who presented with a 10-year history of SRPE.80 He would experience 3–5 painful erections nightly, and over time the pain spread over surrounding areas. As soon as he awakened, the erection and pain completely ceased.

Two years after SRPE onset, he sought urologic consultation and underwent a transurethral prostatic resection, despite a negative history for urinary retention. SRPE did not improve after the surgery. He eventually resorted to “increased sexual activity” (details were not provided) in an effort to avert or diminish painful nocturnal erections. When relief from SRPE was not obtained with increased sexual activity, the patient presented for sleep and medical evaluation. PSG monitoring with SRE monitoring demonstrated nocturnal sleep disruptions associated with 3 REM sleep erections lasting 3–8 minutes before culminating in full awakenings with prompt cessation of erections. Brain MRI revealed a left posterior cerebral artery compression on the anterolateral surface of the left hypothalamus, an area which when stimulated (in rats and presumably in humans) induces erections and disinhibits penile reflexes. The location of the vascular compression was thus implicated in the pathophysiology of this case of SRPE.

Another recently reported case involved a 45-year-old man who developed SRPE 2 years after surgical excision of a thoracic ependymoma.81 Various measures were successfully used to relieve the pain, such as urination and cold water application, along with “physical maneuvers,” but it is unclear whether the latter referred to masturbation or other sexual activity. He was reported to be satisfied with his sex life with normal erections, ejaculations, and orgasm during sexual intercourse 1–4 times weekly. Amitryptyline therapy was not effective, and the patient refused other therapies.

SRPE has been described in over 35 publications, including a controlled study of 10 patients,81 raising the possibility of sexual overactivity in some of these other cases of SRPE.

Sleep Related Dissociative Disorders

Sexualized (repetitive behavior without affect) and frankly sexual behaviors (with affect) can emerge with sleep related dissociative disorders.83 A particularly striking episode was demonstrated by video-PSG in a 22-year-old woman, with a duration of seven minutes during well-defined EEG wakefulness.83 She quietly lay awake in bed with eyes closed just prior to falling asleep. Then she gradually began jerking her head side-to-side, which proceeded to squirming in bed followed by a crescendo progression of pelvic thrusting, side-to-side movements, and other thrashing behaviors, along with moaning and groaning. Defensive, pained behaviors and moaning often accompanied the sexualized behaviors, and comprised a reenactment of a past abuse scenario that she later believed she had been dreaming about, when in fact she had been awake and remembering in a dissociated state. In her “dream” that she was acting out in bed, her older sister was repeatedly shoving a ruler into her vagina, stomach, and legs, which hurt her but sometimes also sexually aroused her.

In a case of animalistic nocturnal personality involving a 19-year-old male who would prowl around the house on all 4 limbs while growling for approximately 30–60 minutes per episode twice weekly while occasionally chewing on a piece of uncooked bacon,82 a thinly disguised recurrent sexualized “dream” during his nocturnal dissociated states of wakefulness consisted of his being a large jungle cat approaching a female zookeeper who held a piece of raw meat in her hand which he wanted to pounce on and “snatch” it from her hand and eat it. However, “an invisible force field” prevented him from getting near to her, and he felt “frustrated” by being kept away and not having the raw meat. He would then “wake up” (i.e., snap out of his dissociated wakeful state) and be confused and groggy, and would only gradually reestablish contact with reality.

Nocturnal Psychotic Disorders

At least 2 categories associated with sexual delusions and hallucinations that may or may not be sleep related have been documented in the literature, one associated with a primary psychiatric disorder, such as schizophrenia, and the other with Parkinson disease (PD). A vivid example from the first category, involving schizophrenia, is found in the book, The Professor and the Madman: A Tale of Murder, Insanity, and the Making of the Oxford English Dictionary.84 Dr. William Chester Minor, an American Civil War veteran who was committed to the Broadmoor Criminal Lunatic Asylum in Great Britain for more than 2 decades for committing murder while under the influence of (subsequently diagnosed) schizophrenia, provided more than 10,000 entries for the Oxford English Dictionary. Examples of nocturnal sexual delusions are contained in excerpts taken from the book:

“Already at the time he was admitted he had a detailed awareness of the curious happenings that plagued him at night—always at night. Small boys, he believed, were put up in the rafters above his bed; they came down when he was fast asleep, chloroformed him, and then forced him to perform indecent acts…” It is a very dirty business,” he screamed one morning, standing now only in his drawers…“He made a pimp of me!”

“…fears that he would be transported from his room at night and made to perform “deeds of the wildest excess” in “dens of infamy” before being returned to his cell by dawn. Once airplanes were invented…he incorporated them into his delusions. Men would then break into his rooms, place him in a flying machine, and take him to brothels in Constantinople, where he would be forced to perform acts of terrible lewdness with cheap women and small girls.”

PSG-documented, immediate post-REM sleep nocturnal delusions, including sexual delusions, were first documented by Arnulf et al. in 2000.85 Ten patients with PD and visual hallucinations, 7 of whom also had delusions, were studied. Two of the patients had sexual delusions about the spouse being unfaithful. All had received long-term treatment with dopaminergic drugs, and 5 also with benzodiazepines, but none with anticholinergics or neuroleptics. (Of further interest is one patient with possible sexual RBD whose spouse observed aggressive sleep behaviors associated with moaning and penile erection). A subsequent report by Pacchetti et al. in 2005 on a consecutive series of treated PD patients found that 6 patients suffered from “erotomanic-type delusions” that often emerged in the evening or after nocturnal awakenings in association with aggressive behaviors and clouded sensorium.86 Nocturnal hallucinations were observed in 62 patients, but the content was not described, apart from distinguishing “minor” from “formed” hallucinations. Presence of RBD increased the risk of delusions and hallucinations, with an odds ratio of 2.73.

Hypersexuality After Nocturnal Awakenings

A case has been reported of a 57-year-old man with PD who underwent a pallidotomy, followed 2 years later by deep brain stimulation (DBS) therapy; within 5 months his wife noticed inappropriate hypersexuality, including when he “awoke in the middle of the night demanding sexual intercourse…”87 No further sleep related details were given and PSG was not performed. Hypersexuality can be triggered by a variety of brain insults,88 but apart from the case just cited, and the epileptic cases previously cited, we are not aware of any other descriptions of nocturnal or sleep related hypersexuality in neurologic patients with wakeful hypersexuality.

Miscellaneous Sleep and Sex Associations

Naps:

One of the authors (IA, unpublished case) evaluated a patient with PD being treated with dopaminergic therapy who reported various types of pleasant kinesthetic experiences and visual hallucinations upon awakening from both nocturnal sleep and daytime naps, associated with sleep paralysis. This 54-year-old woman had a mild, de novo form of PD. She reported out of body experiences, with her body floating above her bed, then moving downstairs up to the entrance door, and then being suddenly projected back in the bed. She also saw colorful sceneries, including blue skies and green landscapes, having the feeling of standing on the top of a church, and wonderful golden horses surrounding a chimney. During one early morning while sleeping in bed with her husband, and having her back turned to him, she suddenly woke with the internal sensation that he had just penetrated her from behind with his penis. She couldn’t move because of her SP, but after a while she could turn and was surprised to see him sleeping. Also, after awakening from afternoon naps, she regularly experienced a man making love to her. Although she could not see his face, she had the feeling that it was someone familiar, but not her husband. She sometimes reached orgasm. An overnight PSG and next-day MSLT indicated SOREMPs and short sleep latency, indicative of “narcolepsy-like” phenotype, as described in several other PD patients. During wakefulness, the woman, who had menopause 4 years before, had regular, satisfying sex with her husband, and had no lover.

In another recent case (JE Tatman, unpublished data), a 32-year-old divorced male presented to sleep disorders center with the complaint of excessive sleepiness, nocturnal awakenings, and intermittent RLS. He underwent a PSG followed by a MSLT the next day. The PSG was abnormal for poor sleep efficiency and a prolonged >2 hour awakening. Sleep during his third MSLT nap was immediately preceded by masturbation that was recorded on videotape. He did not sleep during any of the 3 other MSLT nap opportunities. During 2 subsequent interviews he confirmed the masturbation incident during the MSLT and related it to being “very frustrated” about his poor nocturnal sleep the preceding night and the lack of sleep during the preceding 2 nap opportunities. He also reported frequent difficulty in initiating sleep or returning to sleep at home without prior sexual activity, either by masturbating or by having sex with a female partner. His ex-wife complained about his frequent insistence on having sex as soon as they got into bed at night in preparation for sleep.

Sleep Erections and Sexual Vulnerability:

An example is contained in a report of a study on men who reported being pressured or forced to have sex.89 One man wrote that he came home “drunk from the bars” and passed out in a friend’s bunk bed. He awoke to find an acquaintance—who wanted to date him—“riding” him in order to “get off.” Presumably these were REM sleep erections, and given the customary atonia of REM sleep, a male in REM sleep is in a demonstrated state of sexual vulnerability, with an involuntary physiologic penile erection accompanied by generalized muscle paralysis and an increased sensory threshold.

The above scenario has been played out with forensic consequences, as reported in 2001.90 The report, translated from French by one of the authors (IA), reads thusly: “An unusual case of ‘rape by surprise’ during sleep without the victim being aroused was recently arbitrated in France. A 24-year-old man woke up a Saturday morning with painful anal lesions that made him suspect he had been raped during his sleep the night before. The legal medicine examination indeed reported on visibly recent tears of the anal margin. The young man described himself as heterosexual, a deep sleeper and not an alcohol drinker. On the preceding Friday afternoon, he was invited by his boss to have a sauna, then go swimming and finally to drink 7 beers (11.4 grams pure alcohol) between 9 p.m. and 1 a.m. As his boss had no access to public transportation at that time, the young man proposed for him to sleep in his sofa, while he slept in his mezzanine. The boss (who stayed in jail for 2 years before the judgment) reported that he indeed had anal sex with the young man soon after going to bed on that ‘alcoholic night,’ but felt he was a willing participant in having sex because he had a penile erection and did not react to his anal penetration…. The court finally arbitrated that both the victim and the defendant were right, and the defendant was released.” Therefore the visible sexual arousal (penile erection, presumably during REM sleep) and lack of resistance to anal penetration convinced the boss that this was consensual sex on the part of the 24-year-old man.

Medication-Induced States:

In a report on amnestic sleep related eating associated with zolpidem therapy of insomnia,91 4 additional patients were mentioned who had engaged in non-eating amnestic parasomnias induced by zolpidem, 2 of whom had engaged in sleepsex with their usual partners. The unusual feature of these two cases was that sleepsex had not occurred in their lives prior to the initiation of zolpidem therapy. In a third case involving zolpidem, a 43-year-old woman developed de novo sleepsex together with morbid sleep related eating (requiring bariatric surgery).92 During sleep medicine consultation prompted by progressive weight gain after the bariatric surgery, this was attributed to the initiation of nightly zolpidem therapy 4 years previously. Her husband observed not only the new-onset sleepsex but also her unprecedented sexual behaviors, such as being the initiator of sex and being aggressive, with groping and biting, for which she had no recall.92 In addition, in a series of 54 patients with narcolepsy-cataplexy treated with sodium oxybate, two male patients had to be withdrawn from the drug because of hypersexuality. In one case the patient was craving for the drug as its consumption was associated with enhanced erotic fantasy thinking. The other patient reported he was running around in his house, naked, sexually aroused, with an erection after he took the drug. He was concerned it could embarrass his young daughter to see him in this state. Both patients had this sexual arousal while fully awake (Geert Mayer, cases presented during the symposium, “Narcolepsy: multi-symptoms therapeutic approach,” at the European Sleep Research Society meeting, Innsbrück, Austria, September 13, 2006).

Forensic Considerations

Although an in-depth analysis of this topic is beyond the scope of this review, some clinical and medicolegal points pertinent to sexsomnia can be addressed. Sleepwalking with lewd behavior in public that prompted several arrests (from exposing, fondling, masturbating himself, but never in front of another person) was reported in a 21-year-old man with childhood-onset sleepwalking, and without any history of unusual, problematic or criminal sexual behavior during the daytime.92 Charges were dropped because of the apparent sleepwalking. Clinical and PSG evaluations later supported the diagnosis of sleepwalking with pseudo-paraphilia (i.e. pseudo-psychosexual disorder).

In regard to sleepwalking and the “sleepwalking defense,” 2 additional medico-legal categories have been proposed, including their use in cases with sexual charges involving adults or minors: “Parasomnia with continuing danger as a non-insane automatism,” and “Parasomnia with (intermittent) state-dependent continuing danger as a non-insane automatism.”93 The first category was proposed in response to a report entitled “Sleepwalking and Indecent Exposure.”93 A sleepwalker (or any other type of “parasomniac”) who intentionally engages in any behavior that for him is known to trigger sleepwalking should be recognized as “carrying de facto full legal culpability for the consequences of any subsequent actions promoted by such behavior.” The behavior in question was excessive alcohol consumption, and the case involved a 27-year-old man convicted of indecent exposure despite evidence indicating that he had been sleepwalking. Both this man and his mother reported that excessive use of alcohol was known to trigger his sleepwalking. The scientific evidence and forensic considerations of alcohol-induced sleepwalking or confusional arousals as a defense to criminal behavior have recently been critically reviewed.94 In addition, factors that can predispose, prime and precipitate NREM parasomnias in adults have been recently reviewed, with forensic (including sexsomnia) implications.95

Another proposed medicolegal category was contained in the report “An analysis of a recent criminal trial involving sexual misconduct with a child, alcohol abuse and a successful sleepwalking defence: arguments supporting two proposed new forensic categories.”96 This report was prompted by a Vancouver, British Columbia case in 1996 involving a 26-year-old man who drank 36 beers with a friend over a 10-hour period, and then—after his friend was injured and taken to a hospital, where the friend’s wife joined him—he ended up in the same bed as his friend’s 4-year-old daughter, who later was found “upset and crying…and saying, ‘he took my panties off and he hurt me.’” Medical examination revealed an abrasion in the little girl’s vagina. Therefore, there was no medical-legal doubt that the girl was “interfered with” by the defendant, who then invoked the sleepwalking defense. He had an observed history of childhood onset, recurrent sleepwalking, as did his mother and sister. In one prior dramatic episode, “the night before his marriage, when after he had been out drinking…he…got up and urinated in a basket next to his sister’s bed, splashing her…he had no recall of this…” In the subsequent forensic case, both the prosecution and defense agreed that there was no prior history of pedophilia, no prior criminal history, and the defendant was not faking sleep or amnesia. However, there was no mention of whether he had been evaluated or diagnosed with alcoholism, or whether he had received any DWI (driving while intoxicated) citations.

The court identified 5 additional factors, besides the personal and family history of sleepwalking, that supported the defendant’s sleepwalking defense:

disorientation upon awakening from sleep, as determined by the arresting police officers. (However, this could have been lingering intoxication after sharing 36 beers with his friend)

amnesia for the event (this also could have been due to intoxication)

presence of factors known to trigger sleepwalking—alcohol; fatigue; stress

no apparent attempt to conceal the crime

the crime was out of character for this person.

The court acquitted the defendant because he “was not conscious of what he was doing” at the time of the sexual misconduct. By legal criteria, he was not found to have any internal disease of the brain or mind. Rather, “fleeting disturbances of consciousness which are external to the person’s individual, emotional and psychological make-up do not fall within the concept of a disease of the mind. The evidence is that this episode was triggered by external cause.” The identified “external causes” consisted of (excessive) alcohol consumption, stress, and sleep deprivation.

This trial is of medical-legal importance because it raised the issue of whether a sleepwalker with a prior sleepwalking episode(s) provoked by alcohol excess should be held legally culpable for any subsequent alcohol-provoked sleepwalking with criminal misconduct. In our opinion, the Vancouver court did not adequately address the issue of alcohol use in this case, since we believe that it should have played a crucial role in determining whether the defendant’s sleepwalking posed a “continuing danger.” Instead, the final judgment considered the set of circumstances resulting in sexual misconduct during presumed sleepwalking to be so extraordinary and unique that the risk of recurrence was found to be negligible, and he was thus granted an outright acquittal. There was no mention of future culpability were he to once again drink alcohol excessively and engage in sleepwalking with criminal misconduct, either sexual or nonsexual. Furthermore, there was no recommendation for the defendant to obtain clinical consultations for possible alcohol abuse disorder and/or for his sleepwalking, and how to minimize its recurrence.

As a result of this Vancouver case, in 1998 an expanded category of “(Intermittent) State-Dependent Continuing Danger” was introduced with a focus on the legal consequences of behaviors willfully engaged in by a person who already knows that such behavior carries a definite risk for triggering a parasomnia recurrence (including criminal sleepsex).96 The acquitted person, as part of the final judgment, would be informed that the “SW defense” would be unacceptable for any future SW episode resulting from such high-risk behavior. Guidelines for the proper methods for evaluating forensic parasomnia cases, including those involving presumed sexsomnia, have been developed and refined.97 Finally, malingering should always be considered in clinical and medicallegal cases.98

DISCUSSION

A broad set of problematic and clinically consequential sexual behaviors can be associated with parasomnias and other sleep disorders, and emerge during vulnerable sleep states, sleep-wake transitional states, or wakeful states. Furthermore, seizure disorders and other neurologic and medical disorders can manifest with abnormal sleep related sexual behaviors and experiences. A classification of these associations, as shown in Table 1, provides a framework for expansion and refinements as more cases (preferably from large case series) are published and further knowledge is gained in this area. Clinicians across various specialties should be informed about the clinical and medical-legal aspects of “sleep and sex” and consider questioning their patients about any sexual problems associated with their sleep disorders, or about any sleep and sexual problems associated with their neurologic or medical disorders. The latter comment has already been well-recognized in regards to the adverse (i.e., suppressing) effects on libido and sexual activity resulting from a range of chronic sleep disorders, such as OSA, RLS, insomnia, etc. This is a related but separate issue from the focus of this report. Questioning on altered sexuality (libido and behavior) related to a sleep complaint or disorder is strongly encouraged.

The striking male predominance in the published cases of sleepsex, as shown in Table 2, underscores the major sex discordances often found with adult parasomnias.1 RBD is also male-predominant,1 along with OSA “pseudo-RBD,”99 and injurious sleepwalking and sleep terrors.1 In contrast, sleep related eating disorder and sleep related dissociative disorders are female-predominant.1 The basis for the male predominance in the reported cases of sleepsex is not known. The data in Table 2 indicate that sleepsex is often a longstanding disorder that carries major adverse physical, psychosocial, and legal consequences. However, 5 of the bed partners and 3 of the patients reported pleasurable aspects to the sleepsex. Fortunately, the reported sexual parasomnias have been very responsive to standard therapy, consisting of clonazepam for NREM parasomnias and presumed RBD, or CPAP therapy of OSA precipating confusional arousals with sexual behaviors.

The complete amnesia for the sleepsex reported in all 31 parasomnia cases is contrasted by only 2 of the 7 sleep related epilepsy patients having amnesia for their nocturnal sexual episodes, suggesting that their memory systems were either activated and/or not suppressed by the seizure-related episodes. However, the very small sample size precludes any generalizations. Also, selection bias for complete amnesia in the 31 published parasomnia cases may have been present, for several reasons: only the most severe cases may have presented clinically with profound confusional arousals or sleepwalking linked with prominent sexual disinhibition; embarrassment in recalling sleepsex would lead to no reported recall; and in medicolegal cases, claiming amnesia for sleepsex would carry secondary gain. Therefore, the issue of amnesia or recall of sleepsex related to parasomnias or epilepsy remains an open question and more data need to be gathered.

Terminology

Based on current knowledge reflected in the published literature to date, as already cited in this report, we would advocate the use of the terms pertaining to abnormal sleep and sex listed in Table 3 in future reports in the sleep medicine and other clinical-scientific literature. These terms, as indicated in the table, cover both etiologic and purely behavior-experiential descriptors. These terms should be considered sufficiently clear to be used in patient-related medicolegal reports. Further subtyping is facilitated by Table 3, such as identifying whether problematic events (presumably) occurred within NREM or REM sleep, during arousals from these sleep stages, during wake-sleep transitions, or during established wakefulness. Additionally, specific sexual behaviors and experiences can be listed under each term, as shown in Table 2, with further elucidations possible, such as describing seizurerelated sexual automatisms (e.g., paroxysmal nymphomania). On the other hand, terms such as “restless vagina syndrome” as a variant of RLS should be avoided unless future reported cases justify the use of this term with sufficient documentation.


The topic of “sexualized” movements or behaviors, particularly repetitive pelvic thrusting, was discussed in relation to nocturnal frontal lobe or temporal lobe seizures, RLS, and sleep related dissociative disorders. These types of “sexualized” activity reflect restricted components of the sexual repertoire expressed in a repetitive manner and often without an affective component. The use of the term “sexualized” should be reserved for these behavioral phenomena that appear to be expressions of “central pattern generator” activity originating in the brainstem, as elucidated by Tassinari and colleagues.100

The Evaluation and Management of Sleep Related Sexual Complaints

Patients with parasomnias, OSA, and RLS should be questioned (with their bed partners) about any associated sleepsex. We believe that a sleep-wake questionnaire for patients presenting to a sleep center should now include 2 questions on the topic of sleep and sex: “Has your libido or sexual activity changed, either while you are awake, or falling asleep, or during your sleep? Has your bed partner observed any sexual vocalizations or sexual behaviors on your part while you are asleep?” For those patients having sleepsex, the frequency, severity, longitudinal course, and predisposing and precipitating factors should be identified, along with any psychosocial and physical consequences. Covering the problematic sleepsex experiences identified by Mangan41 can be useful in distinguishing between sleepsex “initiator” and “recipient” problems: the initiators often feel “guilt, confusion, shame, disappointment, frustration, embarrassment and self-incrimination,” whereas the recipients often feel “fear, lack of emotional intimacy, repulsion, sexual abandonment, annoyance and suspicion.”

Screening psychological testing, e.g. Minnesota Multiphasic Personality Inventory, Beck Depression Inventory, should be administered, and formal psychiatric consultation should be considered on a case-by-case basis.

Time-synchronized video-PSG with seizure-montage and fast EEG speeds, and upper/lower limb EMG monitoring are strongly recommended in evaluating the complaint of sleepsex. At present SRE monitoring is not recommended, for the reasons given in the next section. Although the yield in identifying parasomnia behaviors and confirming the diagnosis by PSG is substantial, sexual behaviors during sleep have rarely been documented, as already described. Similarly, with epileptic sexual seizures, only 2 cases have documented sleepsex during PSG or sleep EEG monitoring, as described.

Management of this problem can occur along 2 dimensions: the medical management of any identified underlying sleep, medical, neurologic, or psychiatric disorder (or their therapies) promoting the problematic sexuality; individual and/or couple’s psychotherapy to address any predisposing issues and/or to address the consequences of the problematic sexuality.

SRE Monitoring

The lack of SRE monitoring during PSG in any of the published sexsomnia cases allows only for speculation at present. Given the preponderance of published cases of sleepsex involving males diagnosed with a disorder of arousal from NREM sleep, the question of penile erections emerging during NREM sleep or immediately after an arousal from NREM sleep must be considered. A problematic issue is that penile erections during sleep in humans are predominantly, but not exclusively, a REM sleep phenomenon,101–103 as erections can emerge for minutes during transitional NREM-REM sleep periods and be sustained during REM-NREM transitional sleep periods.101 Furthermore, medications such as trazodone can accelerate the onset of tumescence in NREM sleep prior to REM sleep, and also prolong erections into NREM sleep after cessation of REM sleep.104 Various conditions, such as spinal cord injury, other neurogenic problems, and other disorders or medications can be associated with NREM erections representing dissociations of SRE from REM sleep.101,105 Therefore, the interpretation of NREM sleep erections may be the indeterminate. Penile erections may also emerge during partial arousals from NREM sleep as a manifestation of emerging wakefulness with sexual arousal. However, it is unlikely that full wakefulness is established, since complete amnesia occurred in all reported cases of sleepsex. There is precedent in the animal literature for penile erections during NREM sleep, as documented in the armadillo, which also had the absence of penile erections during REM sleep.106 Rats, in contrast, demonstrate a pattern identical to humans with REM sleep penile erections.107

Adults Co-sleeping with Teens and Children

A recommendation based on the published data is that adults or teens with NREM sleep parasomnias should be informed about the risks of co-sleeping, including co-sleeping with minors, especially after drinking alcohol or after sleep deprivation. There may be inadvertent touching during sleep that could precipitate sexual behaviors, resulting in legal and psychosocial consequences. A notable example is contained in the report on “sexsomnia,”3 in which a 32-year-old male shared a bed with 2 children during a nap at a friend’s home, “and was subsequently awakened by a friend who said that one of the children, a 10-year-old girl, claimed that he had inserted a finger into her vagina. Mr. F. could not recall the event, saying he had been asleep at the time.”

Does “Sexual RBD” Exist?

The issue of “sexual RBD” is problematic, since sexual behaviors during REM sleep have not yet been documented by PSG, and the 3 reported cases of sexual RBD did not involve any dream-enacting behaviors.3 This is atypical for RBD, for which “dream-enacting behaviors” is a virtual hallmark.1 Hundreds of RBD cases have been reported in the peer-reviewed literature, but apart from these 3 cases, none has involved sexual behaviors.

An experimental animal model of RBD involving cats does not include sexual behavior.108 In fact among a large series of cats with experimental RBD, no sexual behavior was ever observed during REM sleep, apart from one case of a female cat demonstrating the characteristic meowing while in heat (J-P Sastre, personal communication).

However, 2 additional cases support the possibility of sexual RBD. An elderly man with a typical history of RBD sodomized his wife in bed one night while he was clearly asleep, but it was not known whether he was dreaming at the time, and he later denied recall of the event. The presence of an erection suggests a REM sleep event (sexual RBD), which was a singular event for this man and his wife (CHS, MWM, unpublished case). The other case involved a previously described man with PD treated with dopaminergic therapy whose wife observed an erection while he moaned and moved side-to-side in bed.84 It is known that patients with PD receiving dopaminergic therapy are prone to sexual and other forms of disinhibited behaviors during wakefulness.109 Furthermore, male PD patients carry an elevated risk for subclinical and clinical RBD.110 The available clinical evidence would thus suggest that the most likely clinical scenario for identifying “sexual RBD” would be middle-aged and older male patients with PD and subclinical or clinical RBD, who are receiving dopaminergic therapy, and who also have waking hallucinations and delusions (a recognized complication of PD86), particularly if erotic content is present.

Concluding Comments

The first synthesis of the literature assessing the effects of neurologic insults on human sexual behavior has recently been published, with six key brain regions (including the hypothalamus, also a key sleep center) being identified as mediating specific aspects of sexual behavior.88 Although sleep was not specifically addressed in this review, the various conditions identified with hypersexuality in wakefulness or after awakenings (e.g. after pallidotomy and deep brain stimulation therapies of PD)87 may be relevant to problematic sleep and sex.

A broad set of research studies should be encouraged by this review, such as obtaining normative data on the range of nonproblematic and problematic sexual behaviors during sleep in both the general population and various clinical populations, particularly those patients who appear to be at highest risk, i.e., those with NREM parasomnias, OSA, other sleep disorders, nocturnal seizures, and PD. Nocturnal epilepsy monitoring should include not only a comprehensive EEG montage but also PSG with timesynchronized audio-videotaping of sleep behaviors. Finally, a review of the clinical correlates of erectile-sexual dysfunction, as detected during sleep with SRE monitoring, is beyond the scope of this review, but has recently been addressed comprehensively, with a proposed set of clinical indications for formal SRE monitoring in a sleep laboratory.107,111

ACKNOWLEDGEMENTS

Emmanuel Mignot collaborated with Isabelle Arnulf in the KLS study. Isabelle Arnulf, Michael Corner, and Rolando Ghedini translated foreign language reports to English where indicated. Kathleen Warner and the Health Sciences Library staff at the Hennepin County Medical Center provided excellent ongoing assistance.

APPENDIX

I) Confusional Arousal With Sleepsex In Literature

In Tess of the d’Urbervilles (1891), a confusional arousal with sleepsex and rape comprises the pivotal point in Thomas Hardy’s novel. The protagonist Tess had always rebuffed the persistent advances of a man named Alec. He finally was able to take advantage of his base desires when an exhausted Tess fell asleep rapidly and deeply inside a forest late at night, and forced himself on her, raped her and made her pregnant, with tragic consequences: “She was sleeping soundly, and upon her eyelashes there lingered tears. Darkness and silence ruled everywhere around…But, might some say, where was Tess’s guardian angel? Where was the providence of her simple faith? Perhaps, like that other god of whom the ironical Tishbite spoke, he was talking, or he was pursuing, or he was in a journey, or he was sleeping and not to be awaked. Why it was that upon this beautiful feminine tissue, sensitive as gossamer and practically blank as snow as yet, there should have been traced such a coarse pattern as it was doomed to receive… many thousand years of analytical philosophy have failed to explain to our sense of order.” Later Hardy referred to that sleep scene in which Tess “had been stirred to confused surrender…” and had acted with “inadvertence.”

Tess had six risk factors that night promoting confusional arousals: her youth (the younger the age, the greater the risk for confusional arousals); acute sleep deprivation (waking up early and falling asleep at a “late hour” that night); physical exhaustion from walking many miles across changing terrain that day; forced awakening by her assailant; acute stress from being confronted by a jealous female who wanted to fight with her earlier in the evening; and major, longstanding emotional stress—her family and Alec (her assailant) were pressuring her to marry a man (i.e., Alec) she didn’t love.

Strong homeostatic and circadian factors were thus promoting precipitous and deep sleep, and Tess collapsed on the ground in the forest and quite probably rapidly fell into delta sleep. Shortly afterwards a confusional arousal was elicited during a forced awakening when Alec rapes her. She does not resist him in her state of profound sleepiness, a stark contrast to her unwavering rejection of his advances while being awake.

II) Sleepsex in Movies

Two prominent examples, one comedic and the other dramatic, are contained in the following Hollywood feature films: i) Planes, Trains and Automobiles (1987, starring John Candy and Steve Martin). After an exhausting and aggravating day of not getting anywhere with any mode of transport, two strangers then have to share a hotel room with only one bed. John Candy and Steve Martin did manage to fall asleep. The next morning, John Candy has a confusional arousal and initiates sexual foreplay with a surprised and resistant Steve Martin. When John Candy finally awakens, he is shocked to realize what he had inadvertently done, and repeatedly denies any intentional wrongdoing. ii) Brokeback Mountain (2005, Oscar-nominated film directed by Oscar-winning best director Ang Lee, starring Heath Ledger and Jake Gyllenhaal). The first moment of physical and sexual intimacy between the two cowboy leads came suddenly out of sleep. While asleep in their sleeping bags inside a tent, Jake’s character suddenly roused from sleep, turned over and lurched over his partner who was sleeping with his back towards him, who then also roused and they clasped their hands and then sat up and were kneeling in front of each other when they began passionate kissing.

Note Added in Proof

Two cases of sexual behaviors in sleep (SBS) associated with PSG-confirmed parasomnia overlap disorder have been identified in a 41 y.o. man and 61 y.o. woman (Cicolin A, et al., personal communication & submitted manuscript). During the first SWS period in the PSG study, the woman attempted to remove her pyjamas and began to masturbate while moaning, and was amnestic for the episode. In both cases, SBS were diagnosed as NREM parasomnias, and RBD was considered to be a separate parasomnia in both cases of parasomnia overlap disorder.

A case of hypersexuality induced by dopaminergic therapy of RLS has been identified in a 54 y.o. married man who developed new-onset, longstanding, compulsive (multiple times daily) masturbation after starting pramipexole therapy that effectively controlled his RLS, in contrast to prior therapy with levodopa that had been ineffective for RLS and had not induced any change in sexual arousal or behavior. Discontinuation of pramipexole immediately eliminated the compulsive masturbation. (Ramseyer J, et al., manuscript in preparation).

Footnotes

Disclosure Statement

This was not an industry supported study. Dr. Mahowald has received research support from Advanced Medical Electronics, Kyowa Pharmaceuticals, Merck, Schwarz Pharmaceuticals, and Xenoport. Dr. Arnulf has participated in clinical studies funded by Bioprojet, Boehringer Ingelheim, and GlaxoSmithKline and has participated in a speaking engagement for UCB Pharma. Dr. Schenck has indicated no financial conflicts of interest.

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CHILDREN SLEEP CLINIC

http://childrensleepclinic.wordpress.com

Evid Based Complement Alternat Med. 2006 September; 3(3): 373–377.

Tim I. Williams

School of Psychology, University of Reading and Berkshire Healthcare NHS Trust, UK

Abstract

Previous studies have found beneficial effects of aromatherapy massage for agitation in people with dementia, for pain relief and for poor sleep. Children with autism often have sleep difficulties, and it was thought that aromatherapy massage might enable more rapid sleep onset, less sleep disruption and longer sleep duration. Twelve children with autism and learning difficulties (2 girls and 10 boys aged between 12 years 2 months to 15 years 7 months) in a residential school participated in a within subjects repeated measures design: 3 nights when the children were given aromatherapy massage with lavender oil were compared with 14 nights when it was not given. The children were checked every 30 min throughout the night to determine the time taken for the children to settle to sleep, the number of awakenings and the sleep duration. One boy’s data were not analyzed owing to lengthy absence. Repeated measures analysis revealed no differences in any of the sleep measures between the nights when the children were given aromatherapy massage and nights when the children were not given aromatherapy massage. The results suggest that the use of aromatherapy massage with lavender oil has no beneficial effect on the sleep patterns of children with autism attending a residential school. It is possible that there are greater effects in the home environment or with longer-term interventions.

Keywords: Aromatherapy, massage, autism, sleep, children

What is the Evidence for Aromatherapy?

A recent review of the evidence for sensory stimulation in dementia care suggests that aromatherapy with lemon balm or lavender oil decreases agitation in patients with dementia (1). In other populations there are anecdotal reports of the effectiveness of aromatherapy in calming people with autistic spectrum disorders (2) and helping people sleep (3) and relax (4), although a systematic review of the field found little satisfactory evidence for the claims (5). Nevertheless, one of the review authors claimed that there was good evidence for a relaxing effect (6).

The situation is complicated by the fact that aromatherapy is often delivered as a massage, and research studies have not identified clearly which is the active ingredient (7,8). Trials of massage interventions alone have clearly established beneficial effects in chronic pain and situations where muscle relaxation is required (9). In an experimental study published last year, Kuriyama and co-workers were unable to identify psychological effects of aroma over that of the massage alone, but did find physiological effects of aromatic oils over and above that of the carrier oil massage (9). In this investigation we sought to demonstrate the effects of an aromatherapy massage.

How could Aromatherapy Massage help Children with Autism?

Children with autism have problems establishing a regular diurnal pattern and in remaining asleep through the night (11–13). Some of these difficulties may be owing to over arousal or agitation. Given the effects of aromatherapy massage in dementia and the wider claims of the effects of aromatherapy on sleep and arousal, we sought to examine whether aromatherapy massage enabled an improved sleep pattern in children with autism. During waking hours the behavior of children with autism is characterized by repetitive activities such as stereotyped behavior, which are thought to be the result of non-optimal levels (over and under arousal) of arousal (Fig. 1). The putative mode of action of aromatherapy would be that it enabled an arousal level closer to the optimal, and hence, made sleep both easier to achieve and to maintain. The aims of the study were therefore to examine whether aromatherapy delivered through massage resulted in faster sleep onset, longer sleep durations or fewer sleep interruptions.



Methods

Participants

All 12 children (2 girls and 10 boys) aged between 12 years 2 months to 15 years 7 months (mean age 14 years 1 month) from one unit of a residential school for children with autism were selected as participants for a trial of aromatherapy. The school checks diagnoses of autism against DSM-IV criteria before the children are admitted. One boy had a diagnosis of Down’s syndrome in addition to the diagnosis of autism. One girl was on carbamazepine and topiramate for control of her epilepsy and one of the boys was taking risperidone for control of behavior. All the children had severe learning difficulties and exhibited multiple repetitive behaviors. No children in the unit were excluded from entry to the trial, and the medication taken by the children did not change during the trial.

All the children lived in one residential unit of the school from Sunday to Thursday night inclusive. Only three of the children remained at the school for any of the Friday and Saturday nights during the study. Owing to these small numbers it has not been possible to estimate the effect of remaining for the weekend. Each child slept in a separate bedroom. Although 12 children were considered as participants for the trial, one became ill before the trial and remained at home for 10 of the possible 17 nights. His data has therefore been excluded from the analysis.

Design

A within subjects design was used. Aromatherapy massage was administered on Thursday nights. The period of the study was 24 days, beginning on the first night of the term and finishing after three administrations of aromatherapy. The first night of the study was a Tuesday night, and aromatherapy was provided on the second, third and fourth Thursday nights. This corresponds to an ABABAB design in which the A refers to nights when no aromatherapy was provided, and B refers to those nights when aromatherapy was provided. Nights without aromatherapy can be regarded as baseline nights. The design does carry with it the risk of improvements in sleep over time (a shifting baseline) if the effects of aromatherapy are cumulative.

Procedure

An experienced and trained aromatherapist delivered the aromatherapy as a foot and leg massage using 2% lavender oil in grapeseed oil on three separate evenings during the study period at the school. The timing of each child’s aromatherapy was variable owing to other activities undertaken by the child, but was always in the last 2 h before going to bed. All the children were free to leave the aromatherapy sessions, although none did so. In order to accustom the children to aromatherapy massage, it had been used as a leisure activity at various times during the school day in the previous term. This ceased once the trial started. Thus, the intervention was not anxiety provoking for them.

Measures

Sleep onset, sleep duration and wakings from sleep are routinely recorded by waking night staff who checks each child every 30 min throughout the night from 9 p.m. to 6 a.m. Sleep onset time is the time at which the children were first recorded as being asleep. Sleep duration was calculated as the difference between the time the children were first recorded as being asleep and the time the children woke up minus the time periods the children were awake. The number of wakings from sleep was identified from the sleep records. Consecutive records of being awake were counted as a single waking.

Results

Complete data were available for 11 children. The analyses reported below are for Sunday through Thursday nights of 3 weeks. Data from 17 nights of a possible 24 nights were examined, of which 3 nights included aromatherapy massage as part of the evening schedule. From the 24 possible nights, 3 Fridays and Saturdays were excluded because only 3 children stayed for those nights; a further one night was excluded from analysis because 2 children had been at home on that night (Fig. 2).



There was little variability in the average time the children fell asleep (Fig. 2). The children fell asleep on average between 10:30 p.m. and 11:15 p.m. A repeated measures analysis of variance comparing nights with and without aromatherapy revealed that there was no night with a statistically significant different sleep onset time (Greenhouse–Geisser corrected F = 1.27; df = 4.15, 41.5; P = 0.30). There was however a significant participant effect suggesting that there were systematic differences in the times at which individual children fell asleep (F = 59.83; df = 1, 10; P < 0.001; meansleep onset time range 9:30 p.m. and 11:40 p.m. Table 1).



In total only 22 sleep interruptions were recorded. Seven of the children slept through all the nights without any interruptions. Of the four remaining children, there were between 0.11 and 0.5 interruptions per night (i.e. between one awakening every nine nights and one every other night). There were no significant differences between the nights with and without aromatherapy (Friedman test χ2 = 20.19; df = 16; P = 0.21).

The length of time the children were asleep was also subject to a repeated measures analysis of variance which showed that there was no significant difference between the nights with and without aromatherapy (F = 0.59; df = 16, 160; P = 0.89). The children slept on average between 7.25.and 8.25 h per night (Fig. 2). There was however a statistically significant child effect suggesting that different children had significantly different sleep durations (F = 1411.4; df = 1, 10; P < 0.001; Table 1). The average number of hours slept per child ranged between 6.85 and 8.88 h.

Discussion

What did we Learn?

The results show that there were no statistically significant differences in the time the children went to sleep, the number of times they woke in the night and the length of time the children slept that could be ascribed to the aromatherapy massage. It was well tolerated by the children. Each child's sleep pattern seemed to be stable although there were marked inter-individual differences in both the duration of sleep and the sleep onset time. In summary, where children with autism and severe learning difficulties sleep well, aromatherapy massage does not appear to offer benefits for sleep patterns.

Limitations of the Study

A better study would have allowed for evaluation of the introduction of the intervention. Our results also suggest that the sample size may have been too small to detect a significant effect. Power calculations suggest that for an increase in sleep duration of 30 min, a sample of 160 children would need to be recruited. Alternatively, aromatherapy would need to produce an increase in sleep duration of about 1 h 6 min to reach a power of 0.80 at the 0.05 significance level. Our estimates of effect sizes may however have been skewed by the relatively good sleep pattern the children showed. While it is possible that a more sensitive measure of sleep would enable smaller effects on sleep to be detected, the inter- and intra-individual variability is so great that this seems unlikely.

Does this Study Agree with Others on Aromatherapy Massage?

This study offers evidence on the effects of aromatherapy massage on sleep patterns in children with comorbid learning disabilities and autism. To our knowledge this article represents the first attempt to evaluate the effects of aromatherapy massage on the sleep of people with autistic spectrum disorders. It differs from previous studies by virtue of considering sleep. A previous study with adults with learning disabilities similarly noted little change in communication skills, as a result of the use of aromatherapy massage (14). In contrast, the literature on agitation in the elderly suggests that there are benefits of the combined aromatherapy massage procedure, although these may not extend to pure aromatherapy [i.e. administration of the oil without massage or skin contact (8)].

These results are concordant with the systematic review of aromatherapy interventions reported by Cooke and Ernst (5). They concluded that the effects on anxiety were small and transient, but cautioned that the trials were conducted with participants for whom conventional anxiolytic treatment was not warranted. Similarly, the sleep patterns of the participants in this study did not warrant the use of medication. Indeed, the sleep pattern of the children is better than that of children in the community studied using actigraphic measures (13). The children in this study went to sleep at about the same time as the sleepless group in Wiggs and Stores (13), but showed rather less waking in the night. It might be better, therefore, to research aromatherapy massage in community samples where sleep problems are more prevalent.

What are Future Concerns for Analyses of Aromatherapy?

The fact that the children tolerated the aromatherapy massage suggests that further investigations of aromatherapy massage could be undertaken with this group. Future studies will have to take into account general concerns about the most appropriate design for a trial of aromatherapy massage. Any treatment that involves bodily contact cannot easily be subject to a double blind trial because the recipient will inevitably be aware that they are being touched. The materials used also leave traces on the skin of the recipient, and the aromatic constituent is easily detected. In order to ensure adequate blinding of the assessors, video or automated data gathering methods (e.g. actimeters, which are small devices the size of a wrist watch) would be useful. Alternatively, researchers might wish to consider the possibility of separating the aromatherapy and massage constituents of this intervention, since lavender oil mist has already been shown to have beneficial effects on agitation in the elderly (8) and there is some research showing better immune responses when aromatic essential oils are added to massage procedures (9). There may be a priori reasons for considering that some types of touch or aroma are non-therapeutic for this population, which would enable a comparative trial of different types of touch or aroma. Some consideration should also be given to the possibility that this population might choose to have aromatherapy massage because it is a pleasant sensation regardless of its effects on sleep, behavior or learning. Further trials should therefore consider the implications for the quality of life of the participants, by measuring behavioral disturbances, learning or quality of life in this population.

Finally, consideration should be given to the optimum duration of the intervention. The use of an ABABAB design requires both that aromatherapy has a rapid mode of action and that it does not continue to have effects for more than a few hours after it was administered. Support for this assertion comes from studies on sleep in the elderly (15) and joint attention in children with autism (16). However, one study has reported effects lasting several days for anxiety in children with autism (16). A further risk is that the effect of aromatherapy is cumulative, and becomes evident only after several administrations. As Fig. 2 shows that there appeared to be no significant gradient as would occur if a shifting baseline was involved. A much longer series of repeated administrations might enable a more thorough investigation of these effects.

Acknowledgments

The author is grateful to all the children and staff at Priors Court School, who gave of their time to make this project successful.

REFERENCES

1. Burns A, Byrne J, Ballard C, Holmes C. Sensory stimulation in dementia: an effective option for managing behavioural problems. Br Med J. 2002;325:1312–3.

2. Ellwood J. Aromatherapy and autism. Available at: http://www.aromacaring.co.uk/aromatherapy_and_autism.htm (last accessed 1 July 2005).

3. McCutcheon L. What's that I smell? The claims of aromatherapy. Skeptical Inquirer May 1996. Available at: http://www.csicorp.org/si/9605/aroma.html (last accessed 1 July 2005).

4. Maddocks-Jennings W, Wilkinson JM. Aromatherapy practice in nursing: literature review. J Adv Nurs. 2004;48:93–103. [PubMed]

5. Cooke B, Ernst E. Aromatherapy: a systematic review. Br J Gen Pract. 2000;50:493–6. [PubMed]

6. Ernst E. The role of complementary and alternative medicine. Br Med J. 2000;321:1133–5. [PubMed]

7. Holmes C, Hopkins V, Hensford C, MacLaughlin V, Wilkinson D, Rosenvinge H. Lavender oil as a treatment for agitated behaviour in severe dementia: a placebo controlled study. Int J Geriatr Psychiatry. 2002;17:305–8. [PubMed]

8. Snow AL, Hovanec L, Brandt J. A controlled trial of aromatherapy for agitation in nursing home patients with dementia. J Altern Complement Med. 2004;10:431–7. [PubMed]

9. Fellows D, Barnes K, Wilkinson S. Aromatherapy and massage for symptom relief in patients with cancer. Cochrane Database Syst Rev. 2004 CD002287.

10. Kuriyama H, Watanabe S, Nakaya T, Shigemori I, Kita M, Yoshida N, et al. Immunological and psychological benefits of aromatherapy massage. Evid Based Complement Alternat Med. 2005;2:179–84. [PubMed]

11. Diomedi M, Curatolo P, Scalise A, Placidi F, Caretto F, Gigli GL. Sleep abnormalities in mentally retarded autistic subjects: Down's syndrome with mental retardation and normal subjects. Brain Dev. 1999;21:548–53. [PubMed]

12. Patzold LM, Richdale AL, Tonge BJ. An investigation into sleep characteristics of children with autism and Asperger's Disorder. J Paediatr Child Health. 1998;34:528–33. [PubMed]

13. Wiggs L, Stores G. Sleep patterns and sleep disorders in children with autistic spectrum disorders: insights using parent report and actigraphy. Dev Med Child Neurol. 2004;46:372–80. [PubMed]

14. Lindsay WR, Black E, Broxholme S, Pitcaithly D, Hornsby N. Effects of four therapy procedures on communication in people with profound intellectual disabilities. J Appl Res in Intellect Disabil. 2001;14:110–9.

15. Connell FEA, Tan G, Gupta I, Gompertz P, Bennett GCJ, Herzberg JL. Can aromatherapy promote sleep in elderly hospitalized patients. J Can Geriatr Soc. 2001;4:191–5.

16. Solomons S. Using aromatherapy massage to increase shared attention behaviours in children with autistic spectrum disorders and severe learning difficulties. Br J Spec Educ. 2005;32:137.

17. Wilkinson S, Aldridge J, Salmon I, Cain E, Wilson B. An evaluation of aromatherapy massage in palliative care. Palliat Med. 1999;13:409–17. [PubMed]

Supported by
Dr Widodo Judarwanto SpA

http://childrenspeechclinic.wordpress.com

Ravi Singareddy, M.D.1; Sumana Moole, M.D.2; Susan Calhoun, Ph.D.1; Peter Vocalan, M.D.1; Marina Tsaoussoglou, B.S.1; Alexandros N. Vgontzas, M.D.1; Edward O. Bixler, Ph.D.1

1Sleep Research & Treatment Center, Department of Psychiatry and 2Division of Gastroenterology & Hepatology, Penn State College of Medicine, Hershey, PA

Objective: Studies in adults have found significant association between sleep disturbances and various medical symptoms/disorders. However, in children, few studies have explored this complex association in clinical samples. In this study, we examined prevalence of medical complaints in children with insomnia symptoms in a large general population of school aged children.

Methods: We conducted a cross sectional study of 700 children, ages 5–12 years, from the Penn State Children’s Cohort. All children underwent a medical and psychiatric history, physical examination, 9-h overnight polysomnography, and neuropsychological testing. Comprehensive sleep and development questionnaires were completed by a parent. We compared 135 (19.3%) children with parent-reported sleep disturbances to 565 (80.7%) children with no parent-reported sleep disturbances.

Results: Insomnia symptoms were significantly associated with gastrointestinal regurgitation and headaches after controlling for demographic variables, apnea hypopnea index, ADHD, learning disorder or other psychiatric/behavioral disorder, socioeconomic status, and minority status. Children with gastrointestinal regurgitation and headaches compared to children without these symptoms were 3.3 times and 2.3 times as likely to suffer from sleep disturbances, respectively. Objectively, sleep latency increased in the sleep disturbance group, and there were significant differences between groups in REM latency, slow wave, and stage 2 sleep.

Discussion: These results underscore the importance of inquiring about insomnia symptoms when children present with medical complaints particularly gastrointestinal regurgitation or headaches and taking a comprehensive medical history when children present with sleep complaints. Future studies are needed to replicate these findings and explore the possible underlying pathophysiological abnormalities of such comorbidity between insomnia symptoms and medical symptoms in children.

Keywords: Insomnia, insomnia symptoms, medical complaints, gastrointestinal regurgitation, headaches, pediatric sleep disorders

Supported by
Dr Widodo Judarwanto SpA

http://childrensleepclinic.wordpress.com

Louise M. O’Brien, Ph.D.1,2; Julie Koo, B.S.1; Ludi Fan, M.S.3; Jocelynn T. Owusu, B.A.1; Wattanachai Chotinaiwattarakul, M.D.1; Barbara T. Felt, M.D.4; Ronald D. Chervin, M.D., M.S.1

1Sleep Disorders Center and Department of Neurology, 2Department of Oral and Maxillofacial Surgery, 3Department of Biostatistics, 4Center for Human Growth and Development and Division of Child Behavioral Health, Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI

Study Objectives: Most clinical sleep studies are performed for suspected obstructive sleep apnea (OSA), yet one-quarter to one-half show periodic leg movements (PLMs), for reasons that remain unknown. Several other disparate sleep disorders also increase the risk for PLMs. We examined the novel hypotheses that OSA as a representative sleep disorder could promote lower body iron stores, as reflected by serum ferritin levels, and, through downstream effects on dopaminergic transmission, increase PLMs and daytime sleepiness.

Methods: Subjects were recruited as they underwent laboratory-based polysomnography for suspected OSA. Serum ferritin levels were measured the next morning. Each subject completed an Epworth Sleepiness Scale and a brief questionnaire to assess for restless legs syndrome (RLS).

Results: The frequency of apneic events showed no association with serum ferritin levels, before or after adjustment for age, sex, body mass index, and likely RLS (each p value > 0.3). Serum ferritin levels did not predict the frequency of PLMs (p = 0.7) or Epworth scores (p = 0.8). Iron deficiency as a dichotomous variable, determined by ferritin levels less than < 50µg/L or in combination with low transferrin saturation or mean corpuscular volume, showed similar results. In exploratory analyses, contrary to expectations, lower minimum oxygen saturation and increased sleep-stage shifts predicted increased rather than decreased ferritin levels (p = 0.03 and p = 0.02, respectively).

Conclusions: Results of this study, powered to detect small to moderate effect sizes, strongly suggest that OSA does not cause lower serum ferritin levels, which, in turn, cannot explain PLMs or daytime sleepiness in these patients.

Keywords: Ferritin, PLMs, sleepiness, OSA, iron

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Dr Widodo Judarwanto
Children Sleep Clinic

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Physician Practice Information: The Practice Expenses and Characteristics of Sleep Medicine as Compared with Other AMA-Recognized Medical Specialties

Caroline Blehart

Special Projects, American Academy of Sleep Medicine.

Summary: This report introduces the Physician Practice Information (PPI) Survey and its findings. Background information on the PPI Survey is explained, as is the Survey’s importance to the field of sleep medicine. Statistics reported by the Survey regarding Practice Expenses per Hour (PE/HR) for various specialties are analyzed in comparison with those reported specifically for sleep medicine. The similarities and differences between sleep medicine and all other medical specialties surveyed in terms of practice characteristics are also discussed.

Analysis of PE/HR data found that sleep medicine payroll practice expenses are closest to those of obstetrics/gynecology, likely due to the employment of technologists in both fields. Regarding supplies and equipment expenses, sleep medicine is most similar to radiology, cardiology, and spine surgery, probably due to the use of disposable medical supplies. In terms of total PE/HR (less separately billable), sleep medicine is most like obstetrics/gynecology, orthopedic surgery, and otolaryngology. The full cause of this is undeterminable from the PPI Survey.

Some areas of dissimilarity in regard to the practice characteristics of sleep physicians and all physicians surveyed across all specialties were found. Most of these fell in the area of “practice size and function of non-physician personnel.” Overall, the results of this section of the PPI Survey show that sleep medicine is practiced in a manner similar to that of the various specialty fields of all physicians surveyed across all specialties but still maintains some unique practice characteristics.

Keywords: Practice expenses; practice characteristics; medical specialties; sleep medicine; practice information

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CHILDREN SLEEP CLINIC

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Modafinil Improves Functional Outcomes in Patients with Residual Excessive Sleepiness Associated with CPAP Treatment 
Terri E. Weaver, Ph.D., R.N.1; Eileen R. Chasens, D.S.N.2; Sanjay Arora, Ph.D.†

A Multicenter, Prospective Study of a Novel Nasal EPAP Device in the Treatment of Obstructive Sleep Apnea: Efficacy and 30-Day Adherence 
Leon Rosenthal, M.D.1; Clifford A. Massie, Ph.D.2; Diana C. Dolan, B.S.1,3; Bryan Loomas, B.S.5; Jerrold Kram, M.D.4; Robert W. Hart, M.D.2

Differences in the Association Between Obesity and Obstructive Sleep Apnea Among Children and Adolescents. 506-511. 
Mark J. Kohler, Ph.D.1; Swetlana Thormaehlen2; J. Declan Kennedy, M.D.1,3; Yvonne Pamula, Ph.D.3; Cameron J. van den Heuvel, Ph.D.1; Kurt Lushington, Ph.D.4; A. James Martin, MBChB1,3

Gender Differences in Obstructive Sleep Apnea and Treatment Response to Continuous Positive Airway Pressure. 512-518.
Lichuan Ye, Ph.D., R.N.1; Grace W. Pien, M.D.2; Sarah J. Ratcliffe, Ph.D.3; Terri E. Weaver, Ph.D., R.N.2,4

Marked Reduction in Obstructive Sleep Apnea Severity in Slow Wave Sleep. 519-524.
Rajeev Ratnavadivel, M.B.Ch.B.1,2; Nuy Chau, B.Med.Sci.2; Daniel Stadler, B.Sci. (Hons)1,3; Aeneas Yeo, M.B.B.S.1; R. Doug McEvoy, M.D.1-3; Peter G. Catcheside, Ph.D.1-3

Iron Stores, Periodic Leg Movements, and Sleepiness in Obstructive Sleep Apnea. 525-531.
Louise M. O’Brien, Ph.D.1,2; Julie Koo, B.S.1; Ludi Fan, M.S.3; Jocelynn T. Owusu, B.A.1; Wattanachai Chotinaiwattarakul, M.D.1; Barbara T. Felt, M.D.4; Ronald D. Chervin, M.D., M.S.1

A Multicenter, Prospective Study of a Novel Nasal EPAP Device in the Treatment of Obstructive Sleep Apnea: Efficacy and 30-Day Adherence. 532-537. 
Leon Rosenthal, M.D.1; Clifford A. Massie, Ph.D.2; Diana C. Dolan, B.S.1,3; Bryan Loomas, B.S.5; Jerrold Kram, M.D.4; Robert W. Hart, M.D.2

Memory Before and After Sleep in Patients with Moderate Obstructive Sleep Apnea. 540-548.
Corinna Kloepfer, Ph.D.1; Dieter Riemann, Ph.D.1; Eric A. Nofzinger, M.D.2; Bernd Feige, Ph.D.1; Josef Unterrainer, Ph.D.3; Ruth O’Hara, Ph.D.4; Stephan Sorichter, M.D.5; Christoph Nissen, M.D.1

Medical Complaints Are More Common in Young School-Aged Children with Parent Reported Insomnia Symptoms. 549-553.
Ravi Singareddy, M.D.1; Sumana Moole, M.D.2; Susan Calhoun, Ph.D.1; Peter Vocalan, M.D.1; Marina Tsaoussoglou, B.S.1; Alexandros N. Vgontzas, M.D.1; Edward O. Bixler, Ph.D.1

Polysomnographic Findings are Associated with Cephalometric Measurements in Mouth-Breathing Children. 554-561.
Maria Ligia Juliano, D.D.S., Ph.D.1; Marco Antonio Cardoso Machado, D.D.S., Ph.D.1; Luciane Bizari Coin de Carvalho, Ph.D.1; Edilson Zancanella, M.D.1; Gianni Mara Silva Santos2; Lucila Bizari Fernandes do Prado, M.D., Ph.D.1; Gilmar Fernandes do Prado, M.D., Ph.D.3

Idiopathic Hypersomnia: Clinical Features and Response to Treatment. 562-568. 
Mohsin Ali, M.B.B.S.1; R. Robert Auger, M.D.2,3; Nancy L. Slocumb2; Timothy I. Morgenthaler, M.D.2,4

Obstructive Sleep Apnea and Risk of Motor Vehicle Crash: Systematic Review and Meta-Analysis
Stephen Tregear, Ph.D.1; James Reston, Ph.D., M.P.H.2; Karen Schoelles, M.D., S.M.2; Barbara Phillips, M.D., M.S.P.H.3

Supported by
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CHILDREN SLEEP CLINIC

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Bradley T. Martin, MB.BS., FRACP,1 Bruce D. Williamson, B.Sc.,2 Natalie Edwards, Ph.D.,3 and Arthur Y Teng, MB.BS.4

1Department of Sleep Medicine, Sydney Children’s Hospital, Randwick, NSW, Australia; School of Women’s and Children’s Health, University of New South Wales, NSW, Australia

2Department of Sleep Medicine, Sydney Children’s Hospital, Randwick, NSW, Australia

3Department of Sleep Medicine, Sydney Children’s Hospital, Randwick, NSW, Australia; Department of Medicine, University of Sydney, Australia

4Department of Sleep Medicine, Sydney Children’s Hospital, Randwick, NSW, Australia; School of Women’s and Children’s Health, University of New South Wales, NSW, Australia

Address correspondence to: Dr. Bradley T Martin, Department of Sleep Medicine, Sydney Children’s Hospital, High St, Randwick, NSW, 2031, Australia, Phone: (612) 9382 1210, Fax: (612) 9382 0399, ; Email: btmartin/at/optusnet.com.au

Received May 2007; Accepted October 2007.

Abstract

Study Objectives:

To examine the prevalence of raised periodic limb movements of sleep (PLMS) index in children referred for polysomnography (PSG) and whether parental report of symptoms correlates with objective measurement during PSG.

Methods:

Records of children undergoing PSG from January 2006 to July 2006 were retrospectively reviewed. At their initial sleep clinic visit, parents had been asked whether their child was restless or moved their legs excessively during sleep. Their response to these questions was compared to the child’s PLMS index (number of periodic limb movements per hour) during a full PSG. PLMS were scored according to internationally accepted criteria.

Results:

Data were examined for 101 children (60 male) with mean age 6.5 years (range 1.2 to 17.6 years). Excessive leg movements were reported by parents in 50% and restlessness in 73%. A raised PLMS index (defined as >5 per hour) was noted in 10 cases (prevalence 10%). Asking parents about whether their child kicks their legs excessively in sleep had sensitivity 50%, specificity 51%, positive predictive value (PPV) 10%, negative predictive value (NPV) 90% and positive likelihood ratio (LR+) 1.02 when compared to objective analysis. Asking parents about whether their child is restless in sleep had sensitivity 70%, specificity 26%, PPV 9%, NPV 89% and LR+ 0.95.

Conclusions:

Asking parents about their child’s symptoms is not an accurate predictor of raised PLMS index. We recommend that leg electromyography be used in all pediatric sleep studies to record PLMS.

Citation:

Martin BT; Williamson BD; Edwards N; Teng AY. Parental symptom report and periodic limb movements of sleep in children. J Clin Sleep Med 2008;4(1):57-61.

Keywords: Periodic limb movements of sleep, child, questionnaires, polysomnography, sensitivity and specificity, likelihood ratio

Periodic limb movements of sleep (PLMS) are recognized as stereotyped, repetitive movements of the limbs during sleep. Movements described include extension of the great toe (similar to the Babinski response), flexion of the foot and lower leg or abrupt extension of the lower leg.1 Movements of the upper limbs may also occur. PLMS occur most commonly in light sleep (stage 1 and 2) and are scored according to internationally accepted criteria originally developed by Coleman2 and recently updated by the American Academy of Sleep Medicine.3 An index of 5 or more PLMS per hour is considered abnormal, although data supporting this figure are limited.4 PLMS in children have been associated with iron deficiency,5–7 symptoms of attention deficit hyperactivity disorder (ADHD)8–12 and “growing pains.”1,13

In periodic limb movement disorder (PLMD), a rate of 5 or more PLMS per hour is accompanied by clinical sleep disturbance with a further diagnostic criterion that the leg movements cannot be accounted for by sleep disordered breathing (SDB) or medication such as antidepressants.4 The condition may be due to underactive dopaminergic pathways in the central nervous system.14–16 PLMD is a well-recognized but controversial phenomenon in adults but is thought to be under-recognized in children.17 PLMS index >5 has been noted to be uncommon in children and adolescents compared to adults aged >40 years.18 A large European survey reported a prevalence of 3.9% in the general population including 3.2% in adolescents aged 15 to 19 years, but polysomnography (PSG) data did not form part of the study.19 Studies including PSG have quoted prevalence in children ranging from 5.6% to 26% in several general and referred populations.10,17,20,21

Restless legs syndrome (RLS), which can be considered a separate but related condition to PLMD, is diagnosed clinically by the presence of uncomfortable sensations in the legs which tend to be worse in the evening or night and are relieved by movement. Most people with PLMS do not have clinical symptoms of RLS but up to 80% of RLS sufferers have significant PLMS noted during PSG.22 PLMS do not form part of the essential diagnostic criteria for RLS but they do provide supportive evidence.4

The prevalence of PLMS in children is not well defined23 and symptoms are often not well reported by children or their parents. Furthermore, PLMS are not routinely recorded and scored in all pediatric sleep laboratories. We sought to examine the prevalence of raised PLMS index in a population of children referred for PSG. We also examined whether parental report of symptoms predicted presence of PLMS on objective measurement. To limit confusion among PLMS, PLMD, and RLS, which often arises in the literature, we primarily examined PLMS as a PSG finding rather than PLMD or RLS as clinical disorders.

METHODS

Subjects

Records of children who underwent PSG at Sydney Children’s Hospital, Randwick, NSW, Australia between January and July 2006 were examined. At their initial clinic appointment with one of the authors (AYT), a standard questionnaire had been administered. This included asking parents whether their child was restless or moved their legs excessively during sleep. From the patient records, data were obtained for the following parameters: age; sex; indication for PSG; parental report of restlessness in sleep; parental report of excessive leg movements in sleep; PLMS index (number of PLMS per hour); and mixed/obstructive apnea/hypopnea index (MOAHI: number of mixed or obstructive apneas and hypopneas per hour of sleep). Children were excluded if they were younger than one year of age, did not have a complete diagnostic PSG, or had a neuromuscular or severe neurodevelopmental condition which could interfere with estimation of PLMS. We included studies supervised by a single physician to ensure consistency in questioning about symptoms.

Polysomnography

PSG was performed using Compumedics S or E Series (Compumedics, Melbourne, Australia). Studies were scored by the authors according to the criteria of Rechtschaffen and Kales.24 Sleep stages were scored manually using electroencephalography, electro-oculography, and submental electromyography (EMG). Audio and video were digitally recorded. Respiratory efforts were measured by respiratory bands as well as EMG of diaphragm and abdominal muscles. Nasal airflow was recorded using nasal cannulae with a pressure transducer and oronasal flow was measured by thermistor. Oxygen saturation (SpO2) was measured by pulse oximetry (Nellcor 595, Nellcor Puritan Bennett, Pleasanton, CA, USA) and electrocardiogram was recorded continuously. Carbon dioxide was recorded continuously by a transcutaneous electrode (Radiometer, Copenhagen, Denmark). Bilateral anterior tibialis EMG signals were calibrated at commencement of recording by voluntary movement in older children and as part of general calibration in younger children.

Respiratory Event Scoring

Central apnea was defined as cessation of airflow and effort for two or more respiratory cycles with SpO2 decrease of >3% from baseline. Obstructive apnea was defined as cessation of oronasal airflow with continuing respiratory effort regardless of SpO2. Hypopnea was defined as airflow 20% to 50% of baseline amplitude and as central or obstructive according to associated absence or presence of respiratory effort. Events with both central and obstructive components were scored as mixed apneas. MOAHI was calculated as the total number of mixed apneas, obstructive apneas and obstructive hypopneas per hour of sleep. MOAHI ≥1 is considered abnormal in children.25

PLMS Scoring

Periodic limb movements were scored according to accepted criteria as follows: (1) movements 0.5 s to 5 s in duration; (2) interval between movements 5 s to 90 s; (3) ≥4 movements in sequence; (4) movement at least 25% of calibrated magnitude.3 Movements following arousals due to respiratory events were not scored.

Statistical Analysis

Data were compiled in Microsoft Excel (Microsoft Corporation, Redmond, WA, USA) and analysed using SPSS Version 12.0 (SPSS Inc, Chicago, IL, USA). PLMS data were dichotomised into categories of 5 was taking fluoxetine, which may have exacerbated the condition.26 Parents of this child had reported both restlessness and excessive leg movements in sleep. This child was also the only one of the 10 with raised PLMS index to have reported “growing pains.”

Association of PLMS with Symptoms

Excessive leg movements in sleep were reported by 50 parents (50%) and restlessness was reported by 74 parents (73%). Parental report rate was significantly higher than the rate obtained by objective recording for excessive leg movements (McNemar χ21df = 30.4, p < 0.001) and for restlessness (McNemar χ21df = 56.7, p 5 of 10% in our referred population is similar to that reported by Crabtree et al of 11.9% in a community sample (χ21df = 0.33; p = 0.57) and 8.4% in a referred population (χ21df = 0.24; p = 0.63).17 It is also not statistically different from the rate of 5.6% reported by Kirk and Bohn in a referred population (χ21df = 2.76; p = 0.10).20 Traegar et al performed PSG on a group of children specifically excluding those likely to have OSA and reported a similar rate to ours of 8% (χ21df = 0.26; p = 0.61).21 Our rate, however, was lower than the 26% reported by Chervin and Archbold in children referred for suspected sleep disordered breathing (χ21df = 8.89; p = 0.003).10 Chervin and Archbold used slightly broader criteria for scoring PLMS (periodicity of 5 s to 120 s and sequence ≥3 movements), which may have resulted in more children being classified with raised PLMS index. It is important to note, however, that study populations and referral patterns are likely to have differed between the above studies so it is difficult to draw firm conclusions from these comparisons.

Chervin et al examined symptoms useful in predicting PLMD in order to compile a questionnaire.13 Asking about restlessness of the legs, growing pains in bed, insomnia, and morning headache were moderately predictive; but questions about leg movements during sleep, daytime sleepiness, and daytime behavior were not. Overall sensitivity and specificity of the final questionnaire based on symptoms associated with PLMS ≥5 per hour were only 79% and 56% respectively. Receiver-operator analysis suggested only moderate utility of their PLMS score as a diagnostic tool. This implies, as does our study, that clinical suspicion cannot be relied upon in the diagnosis of PLMS.

Martinez and Guilleminault noted that the report of leg pains at morning waking was associated with PLMS of any degree but that other symptoms such as sleep initiation problems, sleep maintenance problems, and daytime tiredness were not specific.1 Reporting of leg pains had sensitivity 80% and specificity 82% and may be a more useful symptom about which to enquire than leg movements in sleep or restlessness, although only one of the 10 subjects with raised PLMS index in our study reported such pain.

Picchietti and Walters, in a study of 129 children with PLMS index >5, reported that parents had noted the presence of PLMS in only 25 cases (19%), and even after being asked to look for leg movements did not notice them in 39 cases (30%).27 Furthermore, symptoms were only reported in 3 of 16 children considered severe cases with PLMS index >25. Another study noted substantial disparity between parental symptom report and PLMS index in a study of children with ADHD.9 Crabtree also noted no significant difference in reported symptoms by parents of children with and without PLMD,17 again highlighting the difficulty in using parental reports for diagnosis.

PLMD is an important diagnosis to consider as patients may be misdiagnosed with conditions such as ADHD and seizures if the diagnosis is not considered.26 Normal phenomena such as body shifts, hypnic jerks and phasic REM twitches may also be misinterpreted as PLMS.9 The condition is also potentially treatable, particularly if associated with SDB or low ferritin levels.1 Unfortunately, we were not able to perform repeat PSG on all of our patients to examine the effect of treatments such as adenotonsillectomy, CPAP, or iron therapy on PLMS index.

Six of the 10 subjects with raised PLMS index in our study also showed evidence of SDB. As leg movements directly following arousal due to respiratory events were not scored, we feel that PLMS can be considered a separate but perhaps related phenomenon in these children. Kirk and Bohn20 (60%), and Martinez and Guilleminault1 (50%) have reported similar comorbidity rates. Martinez and Guilleminault noted similar rates of SDB in children with and without PLMs, again implying independence of the conditions. They also noted that in 15 of 29 comorbid children treated for SDB, PLMs also resolved, but PLMs persisted or increased in the others.1 Chervin and Archbold found that PLMS index was related to hyperactivity scores in children with SDB—but not those without—and hypothesized that SDB may act as an effect modifier of PLMS.10 These and other studies highlight the difficulty in assessing the relationship between PLMS and SDB and the necessity to exclude movements associated with SDB-related arousals from scoring of PLMS. Regarding other comorbidities, none of our subjects was diagnosed with narcolepsy or REM sleep behavior disorder; these disorders are also commonly associated with PLMS. As data were not available for specific symptoms of RLS, we were not able to assess accurately the presence of this associated condition in our study sample.

PSG is widely recognized as the gold standard for diagnosis of PLMS as well as many other sleep disorders, but its complexity and expense limit its use in many environments. Actigraphy has been assessed as a more economical, less labor-intensive alternative method of diagnosis, but results have been conflicting.28–30 PSG, therefore, remains essential in the recording of PLMS.

As this was a retrospective study, PSGs had been reported in a clinical context and hence the reporter was not necessarily blinded to the symptom reports of the parents. We feel, however, that the use of standard, validated criteria to score PLMS counterbalanced this potential bias. Our sample size was based on pragmatic considerations, but we feel it compares well with other studies on this topic. Our use of a population referred for investigation of sleep problems, primarily snoring, also means that our results cannot be extrapolated to the general population but should be relevant for the practice of sleep medicine in most pediatric units.

CONCLUSION

Parental report of excessive leg movements or restlessness in sleep is not an accurate predictor of raised PLMS index compared with objective measurement during PSG. A negative report of symptoms is fairly likely to exclude significant PLMS but overall these symptoms perform poorly as diagnostic tools. As PLMS represent a potentially treatable condition in children which is associated with significant comorbidities, we recommend objective scoring of PLMS during PSG for all children over the age of one year.

REFERENCES

1. Martinez S, Guilleminault C. Periodic leg movements in prepubertal children with sleep disturbance. Dev Med Child Neurol. 2004;46:765–70. [PubMed]

2. Coleman RM, Pollak CP, Weitzman ED. Periodic movements in sleep (nocturnal myoclonus): relation to sleep disorders. Ann Neurol. 1980;8:416–21. [PubMed]

3. American Academy of Sleep Medicine. International classification of sleep disorders, second edition: Diagnostic and coding manual. Westchester, IL: American Academy of Sleep Medicine; 2005.

4. Allen RP, Picchietti D, Hening WA, Trenkwalder C, Walters AS, Montplaisir J. Restless legs syndrome: diagnostic criteria, special considerations, and epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop at the National Institutes of Health. Sleep Med. 2003;4:101–19. [PubMed]

5. Kryger MH, Otake K, Foerster J. Low body stores of iron and restless legs syndrome: a correctable cause of insomnia in adolescents and teenagers. Sleep Med. 2002;3:127–32. [PubMed]

6. Simakajornboon N, Gozal D, Vlasic V, Mack C, Sharon D, McGinley BM. Periodic limb movements in sleep and iron status in children. Sleep. 2003;26:735–8. [PubMed]

7. Kotagal S, Silber MH. Childhood-onset restless legs syndrome. Ann Neurol. 2004;56:803–7. [PubMed]

8. Picchietti DL, England SJ, Walters AS, Willis K, Verrico T. Periodic limb movement disorder and restless legs syndrome in children with attention-deficit hyperactivity disorder. J Child Neurol. 1998;13:588–94. [PubMed]

9. Picchietti DL, Underwood DJ, Farris WA, et al. Further studies on periodic limb movement disorder and restless legs syndrome in children with attention-deficit hyperactivity disorder. Mov Disord. 1999;14:1000–7. [PubMed]

10. Chervin RD, Archbold KH. Hyperactivity and polysomnographic findings in children evaluated for sleep-disordered breathing. Sleep. 2001;24:313–20. [PubMed]

11. Chervin RD, Archbold KH, Dillon JE, et al. Associations between symptoms of inattention, hyperactivity, restless legs, and periodic leg movements. Sleep. 2002;25:213–8. [PubMed]

12. Cortese S, Konofal E, Lecendreux M, et al. Restless legs syndrome and attention-deficit/hyperactivity disorder: a review of the literature. Sleep. 2005;28:1007–13. [PubMed]

13. Chervin RD, Hedger KM. Clinical prediction of periodic leg movements during sleep in children. Sleep Med. 2001;2:501–10. [PubMed]

14. Staedt J, Stoppe G, Kogler A, et al. Nocturnal myoclonus syndrome (periodic movements in sleep) related to central dopamine D2-receptor alteration. Eur Arch Psychiatry Clin Neurosci. 1995;245:8–10. [PubMed]

15. Turjanski N, Lees AJ, Brooks DJ. Striatal dopaminergic function in restless legs syndrome: 18F-dopa and 11C-raclopride PET studies. Neurology. 1999;52:932–7. [PubMed]

16. Ruottinen HM, Partinen M, Hublin C, et al. An FDOPA PET study in patients with periodic limb movement disorder and restless legs syndrome. Neurology. 2000;54:502–4. [PubMed]

17. Crabtree VM, Ivanenko A, O’Brien LM, Gozal D. Periodic limb movement disorder of sleep in children. J Sleep Res. 2003;12:73–81. [PubMed]

18. Pennestri MH, Whittom S, Adam B, Petit D, Carrier J, Montplaisir J. PLMS and PLMW in healthy subjects as a function of age: prevalence and interval distribution. Sleep. 2006;29:1183–7. [PubMed]

19. Ohayon MM, Roth T. Prevalence of restless legs syndrome and periodic limb movement disorder in the general population. J Psychosom Res. 2002;53:547–54. [PubMed]

20. Kirk VG, Bohn S. Periodic limb movements in children: prevalence in a referred population. Sleep. 2004;27:313–5. [PubMed]

21. Traegar N, Scgultz B, Pollock AN, Mason T, Marcus CL, Arens R. Polysomnographic values in children 2-9 years old: additional data and review of the literature. Pediatr Pulmonol. 2005;40:22–30. [PubMed]

22. Montplaisir J, Boucher S, Poirier G, Lavigne G, Lapierre O, Lesperance P. Clinical, polysomnographic, and genetic characteristics of restless legs syndrome: a study of 133 patients diagnosed with new standard criteria. Mov Disord. 1997;12:61–5. [PubMed]

23. Simakajornboon N. Periodic limb movement disorder in children. Paediatr Respir Rev. 2006;7(Suppl 1):S55–7. [PubMed]

24. Rechtschaffen A, Kales A. A manual of standardized terminology, techniques and scoring systems for sleep stages of human subjects. Washington, DC: National Institutes of Health; 1968.

25. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomnographic values for children and adolescents. Am Rev Respir Dis. 1992;146:1235–9. [PubMed]

26. Dorsey CM, Lukas SE, Cunningham SL. Fluoxetine-induced sleep disturbance in depressed patients. Neuropsychopharmacology. 1996;14:437–42. [PubMed]

27. Picchietti DL, Walters AS. Moderate to severe periodic limb movement disorder in childhood and adolescence. Sleep. 1999;22:297–300. [PubMed]

28. Shochat T, Oksenberg A, Hadas N, Molotsky A, Lavie P. The KickStrip: a novel testing device for periodic limb movement disorder. Sleep. 2003;26:480–3. [PubMed]

29. King MA, Jaffre MO, Morrish E, Shneerson JM, Smith IE. The validation of a new actigraphy system for the measurement of periodic leg movements in sleep. Sleep Med. 2005;6:507–13. [PubMed]

30. Montgomery-Downs HE, Crabtree VM, Gozal D. Actigraphic recordings in quantification of periodic leg movements during sleep in children. Sleep Med. 2005;6:325–32. [PubMed]

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G Stores, A Ellis, L Wiggs, C Crawford, and A Thomson

University of Oxford Section of Child and Adolescent Psychiatry, Park Hospital for Children, Headington, UK.

This article has been cited by other articles in PMC.

Abstract

Subjective and objective sleep disturbance was studied in children with nocturnal asthma. Relations between such disturbance and daytime psychological function were also explored, including possible changes in learning and behaviour associated with improvements in nocturnal asthma and sleep. Assessments included home polysomnography, parental questionnaires concerning sleep disturbance, behaviour, and mood and cognitive testing. Compared with matched controls, children with asthma had significantly more disturbed sleep, tended to have more psychological problems, and they performed less well on some tests of memory and concentration. In general, improvement of nocturnal asthma symptoms by changes in treatment was followed by improvement in sleep and psychological function in subsequent weeks. The effects of asthma on sleep and the possible psychological consequences are important aspects of overall care.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

Strachan DP, Anderson HR, Limb ES, O’Neill A, Wells N. A national survey of asthma prevalence, severity, and treatment in Great Britain. Arch Dis Child. 1994 Mar;70(3):174–178.

Janson C, De Backer W, Gislason T, Plaschke P, Björnsson E, Hetta J, Kristbjarnarson H, Vermeire P, Boman G. Increased prevalence of sleep disturbances and daytime sleepiness in subjects with bronchial asthma: a population study of young adults in three European countries. Eur Respir J. 1996 Oct;9(10):2132–2138.

Kales A, Beall GN, Bajor GF, Jacobson A, Kales JD. Sleep studies in asthmatic adults: relationship of attacks to sleep stage and time of night. J Allergy. 1968 Mar;41(3):164–173.

Montplaisir J, Walsh J, Malo JL. Nocturnal asthma: features of attacks, sleep and breathing patterns. Am Rev Respir Dis. 1982 Jan;125(1):18–22.

Fitzpatrick MF, Engleman H, Whyte KF, Deary IJ, Shapiro CM, Douglas NJ. Morbidity in nocturnal asthma: sleep quality and daytime cognitive performance. Thorax. 1991 Aug;46(8):569–573.

Kales A, Kales JD, Sly RM, Scharf MB, Tan TL, Preston TA. Sleep patterns of asthmaticchildren: all-night electroencephalographic studies. J Allergy. 1970 Nov;46(5):300–308.

Avital A, Steljes DG, Pasterkamp H, Kryger M, Sanchez I, Chernick V. Sleep quality in children with asthma treated with theophylline or cromolyn sodium. J Pediatr. 1991 Dec;119(6):979–984.

Dunleavy RA, Baade LE. Neuropsychological correlates of severe asthma in children 9-14 years old. J Consult Clin Psychol. 1980 Apr;48(2):214–219.

McNichol KN, Williams HE, Allan J, McAndrew I. Spectrum of asthma in children. 3. Psychological and social components. Br Med J. 1973 Oct 6;4(5883):16–20.

Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung. 1981;159(5):275–287.

Stradling JR, Thomas G, Warley AR, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet. 1990 Feb 3;335(8684):249–253.

Stores G. Investigation of sleep disorders including home monitoring. Arch Dis Child. 1994 Sep;71(3):184–185.

Coble PA, Kupfer DJ, Taska LS, Kane J. EEG sleep of normal healthy children. Part I: Findings using standard measurement methods. Sleep. 1984;7(4):289–303.

Simonds JF, Parraga H. Prevalence of sleep disorders and sleep behaviors in children and adolescents. J Am Acad Child Psychiatry. 1982 Jul;21(4):383–388.

Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991 Dec;14(6):540–545.

Stores G, Williams PL, Styles E, Zaiwalla Z. Psychological effects of sodium valproate and carbamazepine in epilepsy. Arch Dis Child. 1992 Nov;67(11):1330–1337.

Kovacs M. Rating scales to assess depression in school-aged children. Acta Paedopsychiatr. 1981 Feb;46(5-6):305–315.

Saunders KJ. Early refractive development in humans. Surv Ophthalmol. 1995 Nov–Dec;40(3):207–216.

Stores G. Practitioner review: assessment and treatment of sleep disorders in children and adolescents. J Child Psychol Psychiatry. 1996 Nov;37(8):907–925.

Palm L, Persson E, Elmqvist D, Blennow G. Sleep and wakefulness in normal preadolescent children. Sleep. 1989 Aug;12(4):299–308.

Schlieper A, Alcock D, Beaudry P, Feldman W, Leikin L. Effect of therapeutic plasma concentrations of theophylline on behavior, cognitive processing, and affect in children with asthma. J Pediatr. 1991 Mar;118(3):449–455.

Bender BG, Lerner JA, Kollasch E. Mood and memory changes in asthmatic children receiving corticosteroids. J Am Acad Child Adolesc Psychiatry. 1988 Nov;27(6):720–725.

Celano MP, Geller RJ. Learning, school performance, and children with asthma: how much at risk? J Learn Disabil. 1993 Jan;26(1):23–32.

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Judith A Owens

Department of Pediatrics Brown University School of Medicine Providence, RI02903

Correspondence to : Dr OwensJOwens/at/Lifespan.org

See the article “A systematic review of treatment of settling problems and night waking in young children” on page 33. 

Ramchandani and colleagues have systematically reviewed trials of interventions for the 2 most common sleep concerns in children younger than 5years : delayed sleep onset and problematic night waking. As the authors note, there is a relative paucity of well-controlled and methodologically sound studies of these interventions. This paucity reflects the difficulties in conducting this type of research, and it leads to difficulty in translating study results to the clinical setting.

Methodologic weaknesses in many of these studies include small sample size, the failure to include a control group, and reliance on subjective parental reporting to assess efficacy. In addition to these flaws in study design, a variety of other factors could have influenced treatment outcome, including individual differences in child temperament, educational level of the parent, and the presence or absence of marital difficulties. It is therefore not surprising that the more “generic” approaches, which failed to include a behavioral program tailored to the individual family or to address potential barriers to compliance with the treatment plan, were generally associated with worse clinical outcomes. In weighing the likelihood of success of any of the treatment methods discussed for an individual patient, the clinician must take these variables into account. In complex cases, referral to a sleep disorders center or a mental health professional is entirely justified.

The use of medication to treat childhood behavioral problems is highly controversial. This review addresses the use of sedative medication to treat sleep problems in young children, either alone or in combination with behavioral management. There is widespread concern that medication is being used inappropriately for treating a wide range of behavioral difficulties in young children. Anecdotal evidence suggests that both over-the-counter and prescription sedatives are commonly used for pediatric sleep problems in theUnited States, even in infants. For example, in a recent survey of pediatric practitioners in the northeastern United States, we found that over 20% of the practitioners were at least occasionally recommending diphenhydramine(Benadryl) at bedtime as a treatment for night terrors, a practice not based on empirical evidence.1 Clonidine, analpha agonist with sedative properties, is used by child psychiatrists for treating delayed sleep onset in children, despite reports of potentially serious and even fatal cardiovascular side effects.2

Although the study by Ramchandani and colleagues suggests that the addition of sedative medication at the initiation of a behavioral treatment program might improve outcome, perhaps through improving parental compliance, they found little evidence supporting the use of medication as an isolated method of treatment, especially on a long-term basis. In addition, such treatment practices may implicitly encourage parents to seek out pharmacologic solutions for their child’s behavioral problems, instead of instituting a more labor-intensive but ultimately more successful behavior management program.

Finally, it is worth emphasizing that the definitions of sleep onset and night waking problems in young children are, to a certain extent, culturally determined. Our society places a high value on early acquisition of independent skills by children. This promotes the belief that“self-soothing” in infants is an important developmental milestone and that co-sleeping, or sleeping with a parent or sibling, is not an acceptable practice because it prevents the infant from becoming independent.Health care practitioners should be sensitive to potential cultural and individual family differences in the perception of sleep behaviors in children and take these into account in preventive and management strategies.

Notes

Competing interests : None declared

West J Med 2000 ; 173 : 38

References

1. Owens J, McGuinn M. The practice of pediatric sleep medicine :preliminary results of a regional community survey. J Dev BehavPediatr 1999. ; 20 :403.

2. Prince JB, Wilens TE, Biederman J, Spencer TJ, Wozniak JR.Clonidine for sleep disturbances associated with attention-deficit hyperactivity disorder : a systematic chart review of 62 cases. JAm Acad Child Adolesc Psychiatry 1996. ;35 : 599-605. [PubMed]

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Studies conducted in the past have shown that sleep apnoea increases the risk of high blood pressure, heart attack and stroke.

The latest study, presented at European Sleep Research Society”s conference in Glasgow last month, suggests that some sufferers live longer than those who do not have the condition.

The new finding also indicates that doctors may be causing more harm to some patients than good by treating them for the disorder.

The study followed 611 patients aged 65 and over for more than four years.

According to the researchers, patients with moderate sleep apnoea were less likely to die over the course of the study than those who did not have the condition.

By the end of the four years, three times as many people without sleep apnoea died as had the condition.

Mortality rates among patients with light and severe sleep apnoea were the same as the general population, the study showed.

Peretz Lavie, who carried out the research at the Lloyd Rigler Sleep Apnoea Research Laboratory in Haifa, Israel, called the findings “astonishing”.

“We know that sleep apnoea does reduce life expectancy for people under the age of 50, so to find that it could actually prolong life for elderly patients was quite a shock,” the Telegraph quoted him as saying.

He now wants to identify the exact mechanism behind the syndrome, and discover whether there is a way to determine which patients are experiencing the benefits of sleep apnoea.

He said that the findings should change the way that doctors treat some patients with sleep apnoea.

At the moment we are treating people indiscriminately, but this study suggests that if elderly patients are not suffering any of the symptoms of sleep apnoea, then they should probably not be treated at all.”

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PMH:
Obesity, OSA (a sleep study was ordered), DJD, psoriasis

SH:
Denies any history of alcohol, tobacco or illicit drugs.

FH:
Father has OSA.

Medications:
Motrin PRN, HCTZ

Physical examination:
VS 36.8-16-84-133/85
Morbidly obese, in NAD
The rest of the examination is unremarkable.

EKG: NSR, HR 79, left axis.

What happened?
He had a sleep study which conformed the clinical suspicion of OSA. The recommended setting was CPAP 10 cm H2O QHS. The first step in treating OSA is to find the right CPAP setting. The second is to find the device that fits the patient and is tolerated. Nasal trumpets are tolerated best but they cannot deliver pressure higher than 10 cm H2O. The full face mask is the most effective device, delivering pressure up to 20 cm H20, but many patients experience claustrophobia, find it very uncomfortable, and for these reasons, do not use it.

Sleep Study Report
 
Weight (lbs) = 406
Height = 70

Study type: SPLIT NIGHT PSG

Indications: Loud snoring, excessive daytime sleepiness.
ESS = 6

PMH: morbid obesity

Medications: Ambien given for the test

He is undergoing preop evaluation for bariatric surgery

PROCEDURE
An overnight/daytime full montage split night polysomnography was performed, recording EEG, EOG, chin and leg EMG, EKG airflow, thoracic and abdominal effort, snoring via a microphone, pulse oximetry, body positioning and CPAP pressure.

SLEEP ARCHITECTURE=
Total recording time=395
sleep efficiency was=increased
Sleep efficiency (normal about 85%)=96
Sleep latency was=reduced
Sleep Latency in minutes (normal 15-20 min)=3
Sleep architecture revealed=reduced amounts of REM sleep
REM % of TST (normal=20% of TST)=0.5
REM latency was=REM was absent
(Normal REM latency 70-120 min)=66
REM rebound was seen on CPAP

RESPIRATORY SUMMARY:
At (cmH20) =0
L/min O2 =0
Baseline SpO2 %=97
Min SpO2 %=87
NREM AHI=109
REM AHI=240
Overall RDI=112

Overall AHI=110

Respiratory Index=2
Obstructive apneas=38
Central Apneas=0
Hypopneas=158
Respiratory Effort Related Arousals (RERAS)=4

SNORING DATA:
Snoring without CPAP (% of sleep time)=49
Snoring was reported as=loud

CPAP ANALYSIS:
CPAP titration was started at=5
CPAP/BiPAP final pressure=13
In this study the most adequate pressure was=10
Higher pressures =no significant benefit

IMPRESSION:
Obstructive Sleep Apnea with hypersomnia
OSA=severe

RECOMMENDATIONS:
Avoid sedatives, hypnotics and narcotics=unless sleep apnea treated.
CPAP/BIPAP cm H20=10.
Do not operate heavy machinery or drive=unless OSA/other sleep disorder treated
Weight reduction=to IBW
Heated humidifier=with CPAP

What happened next?
He has been on CPAP for 2 weeks and today he had a Roux-en-Y gastric bypass surgery 2 hours ago.

He has been on CPAP for more than one week, VS are stable and he can be transferred to RMF.

What did we learn from this case?
The most important parameter for diagnosing OSA is AHI (Apnea-Hypopnea Index). In healthy people AHI is less than 10.

If you have to choose just one number to diagnose OSA, choose AHI. As a single measurement AHI is comparable to the importance of RSBI in weaning and extubation. RSBI of less than 100 predicts the successful extubation of a ventilated patient in 85 percent of the cases.

This is a simple bedside evaluation for OSA:
Physical exam – just check two things:

-Neck size
The risk size for OSA is 17′ for men, and 16′ for women

-Look inside the patient’s mouth: “Open your mouth please” and check the the Mallampati Score (MS)

Mallampati Score (source: med.univ-rennes1.fr)

History:
-Epworth Sleepiness Scale (ESS), if more than 12, the patient is at high risk for OSA

References:
Obstructive Sleep Apnea-Hypopnea Syndrome – eMedicine
Snoring and Obstructive Sleep Apnea, Upper Airway Evaluation – eMedicine
Epworth Sleepiness Scale – University of Maryland, SMMC.com,

Treatment of Obstructive Sleep Apnea in Primary Care – AFP 02/04
Obstructive Sleep Apnea – AFP 11/99
Dr. Magboul Anesthesia page – MSN
Obstructive Sleep Apnea as a Risk Factor for Stroke and Death – NEJM 11/05
Continuous Positive Airway Pressure for Central Sleep Apnea and Heart Failure – NEJM 11/05
Sleep — A New Cardiovascular Frontier – NEJM Editorial 11/05

Design  Longitudinal survey.

Setting  Multisite group practice in Massachusetts.

Participants  Nine hundred fifteen children in Project Viva, a prospective cohort.

Main Exposure  At children’s ages 6 months, 1 year, and 2 years, mothers reported the number of hours their children slept in a 24-hour period, from which we calculated a weighted average of daily sleep.
Main Outcome Measures  We used multivariate regression analyses to predict the independent effects of sleep duration (< 12 h/d vs  12 h/d) on body mass index (BMI) (calculated as the weight in kilograms divided by the height in meters squared) z score, the sum of subscapular and triceps skinfold thicknesses, and overweight (BMI for age and sex  95th percentile) at age 3 years.
Results  The children’s mean (SD) duration of daily sleep was 12.3 (1.1) hours. At age 3 years, 83 children (9%) were overweight; the mean (SD) BMI z score and sum of subscapular and triceps skinfold thicknesses were 0.44 (1.03) and 16.66 (4.06) mm, respectively. After adjusting for maternal education, income, prepregnancy BMI, marital status, smoking history, and breastfeeding duration and child’s race/ethnicity, birth weight, 6-month weight-for-length z score, daily television viewing, and daily participation in active play, we found that infant sleep of less than 12 h/d was associated with a higher BMI z score (β, 0.16; 95% confidence interval, 0.02-0.29), higher sum of subscapular and triceps skinfold thicknesses (β, 0.79 mm; 95% confidence interval, 0.18-1.40), and increased odds of overweight (odds ratio, 2.04; 95% confidence interval, 1.07-3.91).
Conclusion  Daily sleep duration of less than 12 hours during infancy appears to be a risk factor for overweight and adiposity in preschool-aged children.
 

 
 
 
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Data from the Wisconsin sleep cohort study of patients without obvious barriers to health care access estimate that 93% of women and 82% of men with moderate-to-severe sleep apnea were undiagnosed.  Significant cardiovascular morbidity (including systemic hypertension and congestive heart failure) as well as increased mortality rates have been associated with both OSA and OHS. While large-scale studies of the prevalence of sleep-disordered breathing in children are lacking, Guilleminault et al report estimates of 5-6% and raise concerns about the impact of the obesity epidemic on sleep in children.

Obstructive sleep apnea (OSA) is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. OSA is a sleep disorder characterized by recurrent episodes of upper airway (UA) collapse during sleep. By definition, apnea episodes last 10 seconds or longer and commonly last 30 seconds or longer. Apnea may occur hundreds of times nightly, 1-2 times per minute in severe OSA patients, and is often accompanied by wide swings in heart rate, precipitous decrease in oxygen saturation, and brief electroencephalogram (EEG) arousals concomitant with stertorous breathing sounds as a bolus of air is exhaled when the airway reopens. This may occur hundreds of times nightly. Obstructive apnea events are most often associated with recurrent sleep arousals and recurrent oxygen desaturation.

Three cardinal symptoms of sleep apnea include snoring, sleepiness, and significant-other report of sleep apnea episodes. This 3 S alliteration is a helpful mnemonic to busy clinicians in assessing patients for OSA. It has proven to be valuable in teaching residents to be sensitive in the identification and appropriate referral of these patients for further study Also helpful is if the patient’s spouse or someone close to him or her can attend the visit because often the sleeper is unaware he or she  has OSA, and, in fact, he or she may regard themselves as “a good sleeper” because they “can sleep anytime, anywhere” (eg, waiting in the physician’s, in traffic, in class, at his or her office) Sleepiness is one of the potentially most morbid symptoms of sleep apnea, owing to the accidents that can occur as a result of it.

OSA is a very important diagnosis for physicians to consider because of its strong association with and potential cause of the most debilitating medical conditions, including hypertension, cardiovascular disease, coronary artery disease, insulin-resistance diabetes, depression, and, as mentioned, sleepiness-related accidents, which are discussed in greater detail in Mortality/Morbidity and Medicolegal Pitfalls.

OSA is an increasingly prevalent condition, in both adults and children, in modern society.  Approximately 24% of men and 9% of women have OSA, with and without excessive daytime sleepiness. The prevalence in children is less certain, but an increasingly large segment of the adolescent population is seen in the author’s sleep center who are often obese and present similar to many of their adult counterparts, with one important exception: they may be sleepy and/or hyperactive. A 2007 study has suggested that approximately 6% of adolescents have weekly sleep-related disordered breathing. Also see Obstructive Sleep Apnea Syndrome in eMedicine’s Pediatrics section.

OSA should be diagnosed and treated promptly. OSA can be reversed quickly with the appropriate titration of continuous positive airway pressure (CPAP) devices. CPAP is the standard treatment option for OSA.
 
A sleep-related disordered breathing (SRDB) continuum has been described and is supported by research. The SRDB continuum suggests that snoring is the initial presenting symptom, and it increases in severity over time and it increases in association with medical disorders that may serve to exacerbate the disorder, such as obesity. Snoring has a constellation of pathophysiological effects ; as the disease progresses SRBD patients begin to develop increased UA resistance that results in a new hallmark symptom: sleepiness. Sleepiness is caused by increased arousals from sleep. This syndrome has been described as the UA resistance syndrome (UARS).

Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.

[ CLOSE WINDOW ]

Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.

UARS patients are not hypoxic, and hypoxia does not explain why they are sleepy, nor can sleep stage percentages or other polysomnography (PSG) variables. The SRDB continuum predicts that over time, a UARS patient develops OSA, if untreated.

OSA has as its hallmark symptoms snoring, sleepiness, spouse apnea report, and hypoxia. The SRDB continuum suggests that over time, untreated OSA may hasten death through heart disease, hypertension, stroke, myocardial infarction, heart failure, cardiac arrhythmia, diabetes, metabolic syndrome, or vehicular or other accident due to sleepiness or other behavioral affects noted.

The SRDB continuum suggests that optimal OSA treatment must correct OSA, UARS, and snoring. If it does not eliminate all 3 problems, the symptoms and the pathophysiological process that was evident at the start of disease will recur. Therefore, in the treatment of SRDB, CPAP corrects OSA first, UARS next, and snoring last.

An unlikely occurrence is snoring being corrected before OSA and/or UARS; if this is thought to have occurred, then consideration should be given to the integrity of the snoring microphone.

Consider whether snoring has been correctly interpreted on the PSG during a CPAP titration. When a mask leak occurs, the noise may be transferred by the microphone to the PSG snore channel and appear as snoring. One can determine the difference between snoring and a CPAP mask leak because snoring occurs at the point of peak inspiration and the beginning of expiration; mask leak occurs during expiration.

Consider whether the patient has had UA corrective surgery. If pharyngeal tissue has been eliminated, snoring may not occur, but OSA can occur (so-called silent apnea).

OSA patients with sleepiness despite apparent effective treatment of OSA with CPAP

One patient group remains sleepy despite correction of SRDB. This subset of patients has excessive daytime sleepiness (EDS) that largely responds to modafinil treatment, usually at the higher doses of the medication (200-400 mg/d), whereas fatigue seems to be better treated with lower doses of the medication (100-200 mg/d). Active research has thus far demonstrated that these patients may have intermittent hypoxia that may have changed the brain’s ability to overcome EDS without modafinil and SRDB corrective treatment together.

Before OSA with residual daytime sleepiness is considered and treated, it is important to know if the pressure is indeed ideal. The author’s approach is to be able to conclusively demonstrate that CPAP has effectively eliminate snoring, UARS, and OSA in the supine position and in rapid eye movement (REM) sleep, 2 sleep states during which SRDB is worsened. Sometimes, a single-night CPAP titration study is not sufficient to make this conclusion. Data suggest that the author’s sleep center titration under titrates  an average of 2 cm water.¹ Based on these data, some may increase the CPAP pressure by 2 cm water. If the empirical increase does not effectively treat the EDS, then a PSG with a CPAP titration in the sleep disorders center is warranted to adjust the pressure while the patient is in the supine position and in REM sleep so that snoring, UARS, and OSA are eliminated.
 
If these steps have been taken, then performing a multiple sleep latency test (MSLT) is reasonable in order to (1) verify objective daytime sleepiness compared with the subjective sleepiness of the Epworth Sleepiness Scale (ESS), because the correlation is low (r = 0.34) and(2) exclude other sleep disorders known to have hypersomnia as a major presenting symptom (eg, insufficient sleep syndrome, narcolepsy), because insufficient sleep syndrome is the most common cause of hypersomnia and OSA is more common among patients who have narcolepsy (a 30% incidence rate vs 1-4% in the population).

The description of a continuum may have first been described by Elio Lugaresi, an Italian Sleep Specialist, during a 1987 Association for the Psychophysiological Study of Sleep presentation in Copenhagen, Denmark). Dr Lugaresi used the term “heavy snorers disease” to articulate the SRDB continuum. He made the argument that snoring is the beginning of the so-called heavy snorers disease. He presented data showing that the earlier snoring occurred in adult life, the more severe the obstructive apnea would be later, and OSA presented earlier in life.

Historical perspectives

The history of the discovery of sleep apnea is interesting and is the topic of a paper published in 2008.⁷

In literature, Charles Dickens has been credited with one of the first descriptions in print regarding sleep apnea when he wrote of “Sleepy Joe,” an obese man who sat in the corner of an English pub asleep. The archetype of a rotund, sleepy man became eponymous with “pickwickian syndrome” by Burwell in 1956.⁸ The prevailing belief at the time was that “pickwickians” had breathing disorders and drowsiness due to “carbon dioxide poisoning.”

A number of individuals have played important roles in advancing sleep science to the point that we have come to understand OSA. Detailing the history of OSA is beyond the scope of this article; however, a few highlights are mentioned.

Gestaut, Tassinari, and Duron⁹ in France and Jung and Kuhlo¹⁰ in Germany provided perhaps the most accurate descriptions of OSA at about the same time, in 1965.

The first known successful treatment for OSA was tracheostomy in 1970 by Elio Lugaresi and colleagues at the University of Bologna in Italy. A primary reason a tracheostomy was important to the understanding of OSA is that performing the tracheostomy left little doubt that OSA was due to an obstructed UA, and not due to a dysfunction of the brain’s respiratory centers. The elevated blood pressure in these patients was of grave concern to Dr Lugaresi, and post-tracheostomy the blood pressure dropped substantially. For the next 11-16 years, tracheostomy and weight loss were the only established beneficial remedies for OSA

In 1981, Sullivan et al introduced CPAP as a treatment for OSA.¹¹ It quickly gained worldwide acceptance by 1986, and it replaced tracheostomy as the most useful and desirable treatment. As is often the case in history, it is perplexing how such a simple device introduced so long ago can transform modern medicine in ways not sooner foreseen. CPAP was a tremendous advance for thousands of OSA patients who needed care and for clinicians who would soon solely specialize in sleep medicine.

Around the time when CPAP was introduced, corrective surgery was introduced and would become the forerunner of further developments in the field of sleep medicine. In 1981, Fugita and colleagues introduced uvulopalatopharyngoplasty (UPPP).¹²

Other treatments, including oral appliance (OA) therapy, are also now treatment alternatives for OSA. Future advances in these and other therapies (eg, stimulation of the genioglossus muscle) are exciting. As was the case with CPAP, the simplest procedure, mechanical device, or drug may astound the medical community by providing the next revolution in the treatment of OSA. For a complete and elegant description of the history of sleep medicine, see Principles and Practice of Sleep Medicine.¹³

Definition

According to the American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,¹⁴ OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) UA obstruction occurring during sleep. By definition, apneic and hypopneic events last a minimum of 10 seconds. At least 5 apnea events must occur per hour of sleep time in association with clinical symptoms, or at least 15 apnea events must occur per hour of sleep time with or without clinical symptoms.

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• Adenotonsillar hypertrophy: This is most common cause of obstructive sleep apnea in children. The size of the tonsils and adenoids alone does not predict the presence or severity of obstructive sleep apnea.
• Chronic nasal obstruction, including choanal stenosis, severe septal deviation, allergic rhinitis, nasal polyps, and rare nasal and/or pharyngeal tumors
• Down syndrome
• Pierre Robin anomaly
• Crouzon syndrome
• Treacher Collins syndrome
• Klippel-Feil syndrome
• Beckwith-Wiedemann syndrome
• Apert syndrome
• Prader Willi syndrome
• Morbid obesity
• Marfan syndrome
• Achondroplasia
• Laryngomalacia
• Mucopolysaccharidoses
• Conditions involving neuromuscular weakness, including Duchenne muscular dystrophy, Werdnig-Hoffman disease, late onset spinal muscular atrophy, Guillain Barré syndrome, myotonic dystrophy, and myotubular myopathy
• Chiari malformation

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Obstructive sleep apnea in pediatric patients generally responds to adenotonsillectomy. However, not all children with obstructive sleep apnea (OSA) are surgical candidates.

Adenotonsillectomy, along with weight normalization, is considered the first line of therapy in children and adolescents with obstructive sleep apnea. Surgically removing the tonsils and adenoids increases cross-sectional airway caliber in patients, although it does not directly affect the fatty infiltration of the soft tissues of the velopharynx and hypopharynx that occurs in children who are obese. Children with obstructive sleep apnea who are obese generally require follow-up polysomnography 8-12 weeks following adenotonsillectomy to assess for residual sleep apnea and determine whether other interventions (eg, continuous positive airway pressure [CPAP]) are needed.

Some children have profound craniofacial deformities that are not easily remedied. Occasionally, surgical procedures undertaken to remedy obstructive sleep apnea only help the problem but do not completely eliminate it. In these situations, therapy is usually best accomplished with devices that deliver CPAP.

• CPAP is the mainstay of therapy for most adults with obstructive sleep apnea, as well as a large number of children and adolescents. Continuous distending airway pressure is applied during sleep using a nasal mask and small compressor. CPAP acts as a pneumatic splint to maintain airway patency. By simultaneously increasing the functional residual capacity, this pressure also helps prevent oxygen desaturation even if airway obstruction breaks through.
• Various patient interfaces are available, including nasal masks, facemasks, gel masks, and nasal pillows to help facilitate a comfortable fit and adherence to therapy. The amount of CPAP pressure must be individualized for each patient and is determined during a CPAP titration study in the sleep laboratory. The goal is to find an optimal pressure that eliminates apnea and minimizes snoring but is still comfortable and does not lead to excessive air swallowing, gastric distention, and air leak around the mask or through the mouth. Long-term effects of nasal CPAP therapy on maxillofacial structure development in children are unknown.
• Numerous commercially available oral (PO) appliances assist in bringing the lower jaw and tongue forward during sleep, thus improving obstructive sleep apnea. These devices are expensive, require special dental expertise, and are associated with frequent adverse effects such as jaw pain and temporal mandibular joint dysfunction. Small growing children are likely to outgrow appliances, necessitating refitting and replacement. In general, PO appliances have extremely limited usefulness, if any, in pediatric patients.
• Over-the-counter, disposable, adhesive covered nasal strips purported to decrease nasal airflow resistance have been promoted as a treatment for snoring and obstructive apnea. These have not been proven to be effective in pediatric sleep apnea, and their use should be discouraged.
• Obstructive apnea is generally worse in supine sleeping than in prone sleeping. Measures to encourage patients to sleep prone, such as sewing a pocket to the back of the pajama shirt and putting a tennis ball into it, have some minimal success among adults who snore or have very mild obstructive apnea. This strategy is generally not helpful in managing significant childhood sleep apnea.
• Nasal fluticasone administered daily for 6 weeks is shown to ameliorate the frequency of obstructive events in children with mild-to-moderate obstructive sleep apnea due to tonsil or adenoid hypertrophy by about one half.
• Nasal steroids offer an opportunity to reduce obstructive events pending surgery or can be an alternative remedy for children with mild disease whose parents are reluctant to pursue surgical treatment.³
  • Steroids are not shown to decrease obstructive symptoms, eliminate the need for surgery, prevent oxygen desaturation, or shrink tonsil or adenoid tissue.
  • No long-term studies are available to assess the duration of steroid effect, and whether beneficial aspects persist even if therapy is continued is unknown.
  • A trial of topical steroid therapy should not delay surgical treatment of obstructive apnea in children with severe tonsillar hypertrophy or moderate-to-severe obstructive sleep apnea.
  • No studies have assessed the efficacy of topical steroid therapy in children with craniofacial abnormalities and obstructive sleep apnea.
  • Short courses of systemic steroids (prednisone, 1 mg/kg/d PO for 5 d) have been shown to be ineffective in the treatment of childhood obstructive sleep apnea due to tonsil or adenoid hypertrophy.

Surgical Care

• In the pediatric population, most obstructive sleep apnea is related to tonsillar hypertrophy or adenoid hypertrophy. Adenotonsillectomy is curative in most instances. Children with obstructive sleep apnea who undergo adenotonsillectomy demonstrate improvement in measures of neurocognitive function.
• Certain children who are known to have a high risk of postoperative complications should only undergo surgery at institutions that possess pediatric intensive care facilities (PICUs). This high-risk group includes children younger than 3 years and those with craniofacial abnormalities, failure to thrive, hypotonia, morbid obesity, a history of previous airway trauma, and severe abnormalities on polysomnography (respiratory disturbance index [RDI] >40 or oxygen desaturations <70%).
• Uvulopalatopharyngoplasty (UPPP [ie, UP3]) is not commonly performed in children. During the procedure, the uvula, posterior margins of the soft palate, and lateral pharyngeal wall mucosa are removed via scalpel or laser ablation. UPPP surgery is likely to be successful in relieving obstructive sleep apnea only if the major site of obstruction is localized to the soft palate. This surgery carries a risk of velopharyngeal insufficiency, which may be increased among pediatric patients. Although UPPP may effectively eliminate most snoring, the procedure does not always cure obstructive sleep apnea. Follow-up polysomnography 2-3 months after surgery is warranted to reassess for residual apnea.
• Tongue reduction procedures (midline partial glossectomy) may have some use in a small number of carefully selected pediatric patients (eg, Beckwith-Wiedeman syndrome).
• Tracheotomy remains an effective surgical option for life-threatening obstructive apnea that is not amenable to other therapies.

Consultations

Teams of pediatric specialists often collaborate in the care of infants and children with sleep apnea. Members of the following specialty groups have specific expertise that may help the primary care physician coordinate the care of their patient with sleep apnea:

• Pediatric sleep medicine
• Pediatric otolaryngology
• Pediatric plastic surgery
• Orthognathic surgery
• Pediatric neurosurgery
• Pediatric anesthesia
• PICU
• Pediatric endocrinology
• Pediatric pulmonology
• Pediatric cardiology

Diet

• Obstructive sleep apnea may aggravate gastroesophageal reflux. Children and adolescents with significant sleep apnea should avoid eating large amounts just before bedtime. This is especially the case if children are being treated with CPAP, which can lead to air swallowing and gastric distention.
• Caloric intake limitation and dietary counseling are necessary if obesity complicates obstructive apnea.

Activity

• Many individuals with obstructive sleep apnea have daytime sleepiness with reduced attention span and difficulty focusing their concentration. Warn teenagers who drive about the potential danger of falling asleep at the wheel; advise them to avoid driving long distances without a break or driving when they are unusually tired. Numerous epidemiologic studies link obstructive sleep apnea to motor vehicle accidents.⁴

Medication

No effective pharmacologic therapy for childhood obstructive sleep apnea (OSA) is recognized. Individuals with obstructive sleep apnea and hypersomnolence should have the underlying cause of their obstructive apnea addressed, rather than use stimulant medication during the day in an attempt to help stay alert.

Nocturnal supplemental oxygen is generally not advised as a primary treatment for obstructive sleep apnea. Although oxygen may blunt the degree of hemoglobin desaturation during sleep, it does not prevent sleep fragmentation, sleep deprivation, or associated autonomic stimulation during the obstructive episodes. Preoperative supplemental oxygen treatment has been reported to worsen obstructive hypoventilation in some children. Therefore, if oxygen is used as a bridge to more definitive therapy, the effect of supplemental oxygen should be documented during nocturnal polysomnography.

Intranasal fluticasone propionate (Flonase) administered daily for 6 weeks has been shown to ameliorate the frequency of obstructive events in children with documented mild-to-moderate obstructive sleep apnea caused by tonsil and/or adenoid hypertrophy by about one half. Intranasal corticosteroids have not been shown to decrease obstructive symptoms, eliminate the need for surgery, prevent oxygen desaturation, or shrink tonsil or adenoid tissue; therefore, if intranasal corticosteroids are used, the treatment is only temporary pending a more permanent solution. Systemic corticosteroids have not been shown effective and have no role in treatment.

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• Polysomnography remains the criterion standard for establishing the diagnosis of obstructive sleep apnea (OSA) in infants, children, and adults. Ideally, polysomnography should be performed overnight and during the patient’s usual bedtime.
  • Multiple physiologic parameters are monitored during polysomnography, although the specific montage may vary slightly between sleep laboratories. Generally, electrooculography, chin and leg surface electromyography (EMG), and at least 2 EEG channels are included to confirm sleep and assess sleep architecture. Breathing is assessed using nasal/oral airflow sensors, pulse oximetry, and end-tidal (ET) CO₂ measurements monitoring and by placing piezo crystal belts across the chest and abdomen to detect respiratory efforts. At least one ECG channel is necessary to determine heart rate and rhythm. Occasionally, other channels are incorporated into the study as needed. These might include additional EEG leads to better detect seizure activity, esophageal pH measurements, or transcutaneous carbon dioxide monitoring.
  • Polysomnographic normal standards differ between children and adults. In the pediatric age range abnormalities include oxygen desaturation under 92%, more than one obstructive apnea per hour, and elevations of ET CO₂ measurements of more than 50 mm Hg for more than 9% of sleep time or a peak level of greater than 53 mm Hg.
• Daytime nap studies are specific, but not sensitive, in detecting sleep apnea. This is because obstructive events are more likely to occur during rapid eye movement (REM) sleep than during other sleep stages, and very little (if any) REM sleep occurs during daytime naps in noninfants. Therefore, children with symptoms of obstructive sleep apnea who have normal nap study findings must undergo nocturnal polysomnography to exclude the diagnosis. Sleep studies should be performed without sedation.
• Unattended home overnight oximetry has been proposed as a screening study. However, it may miss the child with significant obstructive sleep apnea who does not have marked episodes of oxygen desaturation.
• Multichannel studies lack reliable assessment of sleep disruption.

Imaging Studies

• Anteroposterior and lateral neck radiography: Neck radiography for soft tissue detail help define upper airway anatomy and adenoid size and exclude the possibility of rare nasal pharyngeal neoplasms.
• Cephalometric radiography and 3-dimensional CT reconstruction imaging are rarely, if ever, necessary in the pediatric age group.
• Cine MRI during sleep may be helpful in identifying specific sites of airway obstruction in the complicated patient being evaluated for surgical interventions. This technique is currently only available at a handful of specialized tertiary care facilities.

Other Tests

• Highly sensitive thyroid-stimulating hormone and thyroxine: Thyroid function studies are useful to exclude hypothyroidism, which is associated with tongue enlargement, weight gain, and obstructive sleep apnea .
• CBC count: Chronic hypoxia related to recurrent airway obstruction may lead to polycythemia.
• Electrocardiography and echocardiography: These studies are not necessary in all children with suspected sleep apnea. However if very severe long-standing obstruction is suspected, an ECG and echocardiography are helpful in assessing ventricular thickness and function and to check for evidence of pulmonary hypertension.
• Multiple sleep latency test (MSLT): If the clinical history suggests the possibility of narcolepsy, the MSLT should be ordered in conjunction with overnight polysomnography.
• MRI of the brain and brainstem: A history of severe snoring, headaches, neck pain, urinary frequency, or swallowing problems raises the suspicion of Chiari malformation. Chiari malformations may occur in otherwise normal children and in association with congenital myelomeningocele. If brainstem dysfunction is suspected, MRI is necessary. Cranial CT imaging is not adequate to assess for brainstem and upper cervical cord lesions.

Procedures

• Polysomnography is necessary to document obstructive sleep apnea and gauge its severity. A history of snoring alone is not adequate for making a diagnosis of obstructive sleep apnea or for determining its seriousness.
• Some children with obstructive sleep apnea have primarily obstructive hypoventilation in which repetitive partial obstructions occur with some degree of relative oxygen desaturation and hypercarbia. Because of this, pediatric polysomnographic testing should include some means of determining CO₂ levels, such as end-tidal (ET) CO₂ monitoring or transcutaneous CO₂ monitoring.
• Overnight pulse oximetry by itself is not adequate for establishing the diagnosis or excluding obstructive sleep apnea in children because it provides no information concerning sleep staging/sleep fragmentation or carbon dioxide.

Histologic Findings

• Little consistent difference in tonsil and adenoid weights and volumes is seen in individuals with obstructive sleep apnea compared with patients whose tonsils and adenoids were removed for other reasons.
• No distinct histologic findings separate adenoid and/or tonsillar hypertrophy from hypertrophy associated with obstructive sleep apnea.

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curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Disordered breathing during sleep is a hallmark of obstructive sleep apnea syndrome. Breathing abnormalities include apnea (cessation of air flow) and hypopnea (decreased air flow). In addition, in contrast to adults, some children exhibit a variation of obstructive sleep apnea termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercarbia that occur in the absence of discrete respiratory events that fulfill criteria for apnea or hypopnea.

Physiologic recording methods can differentiate the types of apnea. During obstructive apnea, an individual makes respiratory efforts, but no airflow occurs because of upper airway obstruction. Central apnea is an interruption in both airflow and breathing effort. Mixed apneas have both central and obstructive components to them. A typical mixed event begins with a central apnea, which is followed immediately by one or more obstructed breaths.

Hypopneas are episodes of shallow breathing during which airflow is decreased by at least 50%. They are usually accompanied by some degree of oxygen desaturation, which can be minor and transient. Like apnea, hypopnea is subdivided as being obstructive, central, or mixed. Obstructive hypopneas are episodes of partial upper airway obstruction. Respiratory efforts occur, but airflow is reduced. In central hypopnea, breathing effort and airflow are both decreased. Mixed hypopneas have both central and obstructive components.

In adults, episodes of disordered breathing must last 10 seconds or more before being considered an apnea or hypopnea. Normal resting respiratory rates in children are faster than those in adults. The child has a smaller functional residual capacity and a more compliant chest wall. As a result, children undergo oxygen desaturation more rapidly than adults whenever airflow is interrupted. A definition of apnea or hypopnea requiring that an event last 10 seconds or more before it is considered significant is somewhat arbitrary and does not take into account the physiologic differences between adults and children. Consequently, pediatric sleep centers use different duration criteria for labeling events such as apnea or hypopnea. In children, if obstruction occurs with 2 or more consecutive breaths, the event can be called an apnea or hypopnea, even if it lasts less than 10 seconds.

Individuals with obstructive sleep apnea syndrome have pathologic degrees of obstructive apnea, obstructive hypopnea, or both. Severity is quantified using a polysomnographic-derived index known as the apnea hypopnea index (AHI). The AHI is the total number of apneas and hypopneas that occur divided by the total duration of sleep in hours. An AHI of less than or equal to 1 is considered to be normal by pediatric standards. An AHI of 1-5 is very mildly increased, 5-10 is mildly increased, 10-20 is moderately increased, and greater than 20 is severely abnormal.

OH in children is a sleep-related breathing disorder that is considered a variation of obstructive sleep apnea. Children with OH may have a normal ranged AHI, but they have episodic periods of hypercarbia, as identified based on end-tidal (ET) CO₂ monitors. Peak ET CO₂ measurements of greater than 53 mm Hg are considered abnormal. The percentage of sleep time spent with ET CO₂ measurements greater than 50 mm Hg should not be more than 9%.

Most physicians who treat children with sleep apnea generally recommend specific interventions when the AHI is greater than 5 or respiratory events are associated with oxygen desaturations of less than 85%. When the AHI falls between 1 and 5, other clinical factors must be taken into account to determine whether to pursue adenotonsillectomy or other therapy.

Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including nasopharynx (area from the nose to the hard palate), mouth, velopharynx (space behind the palate), retroglossal region (area behind the tongue), hypopharynx (region between the tongue base and larynx), and larynx.

The upper airway is a pliant tube whose sidewalls consist of muscle and other soft tissues. During wakefulness, neural input to a number of small muscle groups in the pharynx maintains muscle tone and airway patency. With sleep, an increased resistance to airflow normally accompanies muscular relaxation of these muscle groups. Although most people compensate for these changes, individuals with certain anatomic problems have repeated episodes of partial or complete upper airway obstruction when they sleep.

Childhood differs from adult obstructive sleep apnea. Adults with sleep apnea frequently present with hypersomnia, whereas children often demonstrate short attention spans, emotional lability, and behavior problems. Among adults, obesity is a major risk factor for obstructive sleep apnea. Fatty infiltration of the pharyngeal soft tissues narrows the caliber of the upper airway and contributes to airway resistance. Although obesity plays a role in some cases of childhood sleep apnea, the airway obstruction is usually related to tonsillar hypertrophy, adenoid hypertrophy, or craniofacial abnormalities. Children with some types of neuromuscular disease (eg, Duchenne muscular dystrophy, spinal muscular atrophy, cerebral palsy) may also have a higher risk of developing sleep apnea.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

The common classes of drugs used for the treatment of parasomnias are benzodiazepines and anticonvulsants. The general aim of drug treatment is to prevent arousal out of sleep or to suppress REM sleep.

Benzodiazepines 

Benzodiazepines help suppress REM sleep and limit arousal. They include the following drugs:

• Diazepam (Valium) is most frequently used in children, especially children with night terrors.
• Alprazolam (Xanax) is the second choice in this category for parasomnias. It has a brief duration of action; therefore, the likelihood of morning effects, such as grogginess, is decreased. However, it has a potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
• Clonazepam (Klonopin) is similar to alprazolam; it is a good alternative option to diazepam.

Anticonvulsants 

Anticonvulsants inhibit arousal. They include the following drugs:

• Carbamazepine (Tegretol, Carbatrol) is the most commonly used drug for parasomnias.
• Valproate (Depakene, Depakote) has been reported to be effective in treating parasomnias, in both a once nightly dosage schedule and a standard dosage schedule.
• Gabapentin (Neurontin) has not been used as frequently as the other 2 anticonvulsants. As with carbamazepine and valproate, no information is available and no consensus has been reached regarding the use of a once nightly dosage versus a standard antiepileptic dosage.

Antiparkinsonian 

Antiparkinsonian drugs are very effective for the treatment of persons with restless legs syndrome and periodic limb movement disorder.

• Levodopa is the most commonly used drug for the treatment of restless legs syndrome and periodic limb movement disorder. An oral dose of 50-100 mg, controlled-release formulation, is prescribed as initial therapy for restless legs syndrome.
• For periodic limb movement disorder, a controlled-release preparation of levodopa combined with a decarboxylase inhibitor (carbidopa) at a dose of 50-100 mg is started.
• A dose increase not to exceed 200 mg may be required to completely suppress restless legs syndrome and periodic limb movement disorder.
• The major adverse effects of levodopa therapy are (1) rebound of symptoms during the daytime and (2) tardive dyskinesia (difficulty in performing voluntary movements), which is extremely uncommon.
• Ropinirole (Requip), pergolide (Permax), and pramipexole (Mirapex) cause fewer side effects compared with levodopa and have become first-line drugs in the treatment of restless legs syndrome and periodic limb movement disorder. Pramipexole is started at a lowest dose of one half tablet of 0.25 mg once a day for 5 days and then increased to 0.25 mg per day. The dose may be increased to a maximum of 0.5 mg per day. Ropinirole is started at 0.25 mg at bedtime for individuals with primarily nighttime symptoms. For those with symptoms throughout the day, it may be given 2 times per day. The dose may be gradually increased each week. Average doses are 2.5 mg per day.

Opiates
 
Opiates, such as codeine, propoxyphene, and dihydromorphone, have been used in persons who have severe restless legs syndrome and who do not benefit from other therapy. One should be closely observed for development of tolerance and dependency 

Medications

The common classes of drugs used for the treatment of parasomnias are benzodiazepines and anticonvulsants. The general aim of drug treatment is to prevent arousal out of sleep or to suppress REM sleep.

Benzodiazepines 

Benzodiazepines help suppress REM sleep and limit arousal. They include the following drugs:

• Diazepam (Valium) is most frequently used in children, especially children with night terrors.
• Alprazolam (Xanax) is the second choice in this category for parasomnias. It has a brief duration of action; therefore, the likelihood of morning effects, such as grogginess, is decreased. However, it has a potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
• Clonazepam (Klonopin) is similar to alprazolam; it is a good alternative option to diazepam.

Anticonvulsants 

Anticonvulsants inhibit arousal. They include the following drugs:

• Carbamazepine (Tegretol, Carbatrol) is the most commonly used drug for parasomnias.
• Valproate (Depakene, Depakote) has been reported to be effective in treating parasomnias, in both a once nightly dosage schedule and a standard dosage schedule.
• Gabapentin (Neurontin) has not been used as frequently as the other 2 anticonvulsants. As with carbamazepine and valproate, no information is available and no consensus has been reached regarding the use of a once nightly dosage versus a standard antiepileptic dosage.

Antiparkinsonian 

Antiparkinsonian drugs are very effective for the treatment of persons with restless legs syndrome and periodic limb movement disorder.

• Levodopa is the most commonly used drug for the treatment of restless legs syndrome and periodic limb movement disorder. An oral dose of 50-100 mg, controlled-release formulation, is prescribed as initial therapy for restless legs syndrome.
• For periodic limb movement disorder, a controlled-release preparation of levodopa combined with a decarboxylase inhibitor (carbidopa) at a dose of 50-100 mg is started.
• A dose increase not to exceed 200 mg may be required to completely suppress restless legs syndrome and periodic limb movement disorder.
• The major adverse effects of levodopa therapy are (1) rebound of symptoms during the daytime and (2) tardive dyskinesia (difficulty in performing voluntary movements), which is extremely uncommon.
• Ropinirole (Requip), pergolide (Permax), and pramipexole (Mirapex) cause fewer side effects compared with levodopa and have become first-line drugs in the treatment of restless legs syndrome and periodic limb movement disorder. Pramipexole is started at a lowest dose of one half tablet of 0.25 mg once a day for 5 days and then increased to 0.25 mg per day. The dose may be increased to a maximum of 0.5 mg per day. Ropinirole is started at 0.25 mg at bedtime for individuals with primarily nighttime symptoms. For those with symptoms throughout the day, it may be given 2 times per day. The dose may be gradually increased each week. Average doses are 2.5 mg per day.

Opiates
 
Opiates, such as codeine, propoxyphene, and dihydromorphone, have been used in persons who have severe restless legs syndrome and who do not benefit from other therapy. One should be closely observed for development of tolerance and dependency

Vasopressin analogs

Desmopressin is a synthetic antidiuretic hormone with actions mimicking vasopressin. It is used for treating enuresis.

Desmopressin (DDAVP)

For use in primary nocturnal enuresis in children > 6 y. Increases cellular permeability of collecting ducts, resulting in reabsorption of water by kidneys.

Dopamine agonists

Preliminary efficacious results for treatment using these agents have been noted in youths with RLS and PLMS. Findings are based on nonrandomized non – placebo-controlled study. Pergolide was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. Do not abruptly stop pergolide. Health care professionals should assess patients’ need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

Pergolide (Permax)

Pergolide withdrawn from US market. Not FDA-approved for RLS or PLMS. Potent and long-acting dopamine agonist. Reduces tonic stimulation of dopaminergic D-2 receptors located on intrastriatal cholinergic neurons.

Tricyclic antidepressants

These agents are used for treating narcolepsy and enuresis. Please note that scant data exist for use in childhood narcolepsy. Sudden death has been reported in 8 children, possibly related to use of imipramine and desipramine; findings have been inconclusive about the causes of these deaths. No FDA indication exists for use in children with narcolepsy and enuresis.

Imipramine (Tofranil)

Inhibits the reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neuron. May be useful in pediatric ADHD as well as enuresis and possibly pediatric-onset narcolepsy.

Anticonvulsants

Valproic acid was efficacious in small case series for adults with RLS and PLMS.

Valproic acid (Depakene, Depakote)

It is likely that all forms of valproic acid have similar efficacy. The following preparations can be used: 250-mg tab, 125-mg sprinkle caps, or 250 mg/5-mL liquid (US preparations).

Hormones

These agents are used for treating circadian rhythm disturbances.

Melatonin

Used to treat circadian rhythm disturbances in blind patients without light perception.

Sedative/hypnotic agents

Studies for these drugs are limited to adults, and no FDA indications are approved for children younger than 18 years.

Eszopiclone (Lunesta)

Nonbenzodiazepine hypnotic pyrrolopyrazine derivative of the cyclopyrrolone class. The precise mechanism of action is unknown, but believed to interact with GABA-receptor at binding domains close to, or allosterically coupled to, benzodiazepine receptors. Indicated for insomnia in adults to decrease sleep latency and improve sleep maintenance. Short half-life of 6 h. Higher doses (ie, 2 mg for elderly and 3 mg for nonelderly adults) are more effective for sleep maintenance, whereas lower doses are (ie, 1 mg for elderly and 2 mg for nonelderly adults) are suitable for difficulty in falling asleep.

Ramelteon (Rozerem)

Melatonin receptor agonist with high selectivity for human melatonin MT₁ and MT₂ receptors. MT₁ and MT₂ are thought to promote sleep and be involved in maintaining circadian rhythm and normal sleep-wake cycle. Indicated for insomnia in adults characterized by difficulty with sleep onset.

Nightmare disorder

• Person complains of a frightening dream.
• Arousal during the dream is common.
• The presence of a dream is the essential feature that differentiates nightmare disorder from sleep terror disorder.

Sleep terror disorder

• A sleep terror is characterized by a sudden arousal.
• Commonly, the person cries out or screams as he or she is aroused.
• The person has an increased heart rate, an increase in the respiratory rate, flushing, sweating, and increased muscle tone.  
• The person is routinely unresponsive to external stimuli and, when awakened, is confused, disoriented, and does not remember the event.  
• Incoherent speech or passing of urine has been reported to accompany the event.

Sleepwalking disorder

• Episodes of sleepwalking are associated with behaviors that range from simply sitting up in bed to walking, possibly with associated complex behaviors such as eating. Talking behavior has also been noted during episodes of sleepwalking.

• Upon awakening, the person most often is confused and does not remember the event.

• The event may spontaneously terminate, or the person may return to bed or lie down somewhere else and go off to sleep without waking up from sleep.

REM sleep behavior disorder

• The main feature of this disorder is the acting out of dreams. The behavior can include punching, kicking, leaping, and running from the bed. The most common reason for medical consultation is injury to the bed partner, although the effects of sleep disruption can also precipitate such consultation. The event occurs during REM sleep.  
• In persons with REM sleep behavior disorder, arousals from sleep to alertness and orientation occur rapidly, and they usually vividly recall their dreams.
• After awakening, the person’s behavior and interactions are normal.
• Acute (short-term) and chronic (long-term) forms exist. The acute form can emerge during withdrawal from ethanol or sedative-hypnotic abuse and with anticholinergic and other drug intoxication states. The chronic form presents for evaluation following observations of bed partners.  
• Despite nighttime behavior, few persons develop excessive daytime sleepiness or fatigue.

Restless legs syndrome and periodic limb movement disorder

• Persons with restless legs syndrome describe discomfort in the legs, using terms, such as “pulling, searing, crawling, creeping, and boring” to describe these sensations. The symptoms usually occur at bedtime or during other periods of inactivity. These distressing symptoms are relieved by moving the legs, walking about, rubbing the legs, squeezing or stroking the legs, and by taking hot showers or baths. The symptoms may wax and wane over the person’s lifetime.
• Persons with restless legs syndrome commonly present with complaints of insomnia (inability to sleep), and, in severe cases, the disorder may cause depression and suicidal thoughts.

• Periodic limb movement disorder primarily occurs during sleep. This disorder is described as rhythmic extension of the great toe, associated with dorsiflexion (upward movement) of the ankle and light flexion (bending) of the knee and hip. Because periodic limb movement disorder occurs during sleep, the symptoms are often not noticed by the person. Affected persons often complain of excessive daytime sleepiness, initially during passive activities, such as watching TV, being a passenger in a car, or reading. In later stages, one may have excessive daytime sleepiness during activities requiring alertness, such as driving, operating machinery, or talking with people.
• Restless legs syndrome and periodic limb movement disorder may occur even during childhood and present as attention deficit disorder with hyperactivity or as growing pains.
• Restless legs syndrome and periodic limb movement disorder are present in a significant percentage of pregnant women, and exacerbations are observed during menstruation and menopause.
• These disorders are associated with numerous neurological conditions, such as peripheral neuropathy, postpolio syndrome, and spinal cord pathology (disease).
• Restless legs syndrome and periodic limb movement disorder affect 20-40% of persons with chronic renal (kidney) failure who are on dialysis.
• A history of iron-deficiency anemia is also common in persons with restless legs syndrome and periodic limb movement disorder.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Nightmare disorder

• Personality disorders
• Relationship difficulties
• Other stressors
• Drugs, for example, levodopa, beta-adrenergic drugs, and withdrawal of REM-suppressing medications 

Sleep terror disorder

• Fever
• Sleep deprivation (lack of sleep)
• CNS depressant medications

Sleepwalking disorder

• Possible hereditary/familial trend
• Drugs, for example, thioridazine, fluphenazine, perphenazine, desipramine, chloral hydrate, and lithium
• Fever
• Sleep deprivation and obstructive sleep apnea (condition in which breathing stops temporarily while sleeping)
• Other disorders that disrupt slow-wave sleep
• Internal stimuli, such as a full urinary bladder
• External stimuli, such as noises

REM sleep behavior disorder

• Mostly no known cause
• Has been associated with dementia (progressive loss of intellectual functions), subarachnoid hemorrhage (leakage of blood into the space surrounding the brain), ischemic cerebrovascular disease (brain dysfunction due to reduced blood supply), olivopontocerebellar degeneration (brain disease), multiple sclerosis (disease of the central nervous system), and brain stem neoplasms (tumor)

Restless legs syndrome and periodic limb movement disorder

• Mostly no known cause
• Iron-deficiency anemia (amount of hemoglobin is less than normal)
• Pregnancy, menstruation, and menopause
• Chronic renal failure
• Osteoarthritis of the hips and knees
• Drugs, for example, caffeine, tricyclic antidepressants, selective serotonin reuptake inhibitors, and dopamine receptor-blocking drugs
• Neurological disorders
• Peripheral neuropathies (disorder affecting any segment of the nervous system)
• Various causes of myelitis
• Postpolio syndrome
• Diseases of the spinal cord
• Disorders of the lumbar/sacral region

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Historically, sleep was thought to be a passive state. However, sleep is now known to be a dynamic process, and our brains are active during sleep. Sleep affects our physical and mental health, and is essential for the normal functioning of all the systems of our body, including the immune system. The effect of sleep on the immune system affects one’s ability to fight disease and endure sickness.

States of brain activity during sleep and wakefulness result from different activating and inhibiting forces that are generated within the brain. Neurotransmitters (chemicals involved in nerve signaling) control whether one is asleep or awake by acting on nerve cells (neurons) in different parts of the brain. Neurons located in the brainstem actively cause sleep by inhibiting other parts of the brain that keep a person awake.  

Importance of Sleep

Animal studies have shown that sleep is necessary for survival. The normal life span of rats is 2-3 years. However, rats deprived of sleep live for only about 3 weeks. They also develop abnormally low body temperatures and sores on their tails and paws. The sores probably develop because of impairment of the rats’ immune systems.

In humans, it has been demonstrated that the metabolic activity of the brain decreases significantly after 24 hours of sustained wakefulness. Sleep deprivation results in a decrease in body temperature, a decrease in immune system function as measured by white blood cell count (the soldiers of the body), and a decrease in the release of growth hormone. Sleep deprivation can also cause increased heart rate variability.

For our nervous systems to work properly, sleep is needed. Sleep deprivation makes a person drowsy and unable to concentrate the next day. It also leads to impairment of memory and physical performance and reduced ability to carry out mathematical calculations. If sleep deprivation continues, hallucinations and mood swings may develop.

Release of growth hormone in children and young adults takes place during deep sleep. Most cells of the body show increased production and reduced breakdown of proteins during deep sleep. Sleep helps humans maintain optimal emotional and social functioning while we are awake by giving rest during sleep to the parts of the brain that control emotions and social interactions.

Rhythms That Influence Sleep

Biological variations that occur in the course of 24 hours are called circadian rhythms. Circadian rhythms are controlled by the body’s biological clock. Many bodily functions follow the biologic clock, but sleep and wakefulness comprise the most important circadian rhythm. Circadian sleep rhythm is one of the several body rhythms modulated by the hypothalamus (a part of the brain).

Light directly affects the circadian sleep rhythm. Light is called a zeitgeber, a German word meaning time-giver, because it sets the biological clock. A practical purpose has been proposed for the circadian rhythm, using the analogy of the brain being somewhat like a battery charging during sleep and discharging during wakefulness.

Body temperature cycles are also under control of the hypothalamus. An increase in body temperature is seen during the course of the day and a decrease is observed during the night. The temperature peaks and troughs are thought to mirror the sleep rhythm. People who are alert late in the evening (ie, evening types) have body temperature peaks late in the evening, while those who find themselves most alert early in the morning (ie, morning types) have body temperature peaks early in the evening.

Melatonin (a chemical produced by the pineal gland in the brain) has been implicated as a modulator of light entrainment. It is secreted maximally during the night. Prolactin, testosterone, and growth hormone also demonstrate circadian rhythms, with maximal secretion during the night.

Circadian rhythms can be affected to a certain degree by almost any kind of external stimulus, for example, the beeping of the alarm clock or the timing of meals. When we cross time zones, our circadian rhythms get disrupted leading to jet lag. It usually takes several days for our body rhythms to adjust to the new time.

Symptoms similar to those seen in people with jet lag are common in people who work during nights or work in shifts. Because these people’s wake time conflicts with powerful sleep-regulating cues like sunlight, they often become uncontrollably drowsy during work or may have difficulty falling asleep during their off time. Their biological clock wants to do one thing, while they are doing something entirely different. People working in shifts have an increased risk of heart, gastrointestinal, emotional, and mental problems. All these problems may be related to the disruption of the circadian sleep rhythm.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

These sleep hygiene measures are important for all parasomnias:

• Go to bed at the same time each night.
• Use the bed only for sleeping and intimacy.
• Avoid napping.
• Avoid stress, fatigue, and sleep deprivation.
• Avoid vigorous activity prior to bedtime, though a brief period of aerobic activity 4 hours before bedtime may be helpful.
• Avoid cigarettes, alcohol, and excessive caffeine.

In general, when a person has been diagnosed with sleepwalking, the following precautions need to be taken:

• Remove potentially dangerous items.

• Have the person sleep in a bedroom on the ground floor if possible.

• Lock the doors and windows.

• Cover glass windows with heavy drapes.

• Place an alarm or bell on the bedroom door.

Medical Care

This section primarily reviews cognitive-behavioral treatments (CBT) effective in treating a broad range of childhood behavioral sleep problems. Treatment modalities can be adapted easily to the youth’s developmental level. Furthermore, consider the role of sleep hygiene in all sleep problems. The effectiveness of CBT for childhood sleep disorders has been well demonstrated in controlled studies and clinical case reports. Specific interventions for sleep problems have gained the status of established evidence-based interventions. The issues that received the most attention pertain to settling problems and night awakenings in infants and toddlers. These topics have been extensively studied, with an impressive volume of well-controlled and informative clinical studies. Clinical research of all other sleep problems and in other age ranges is still very limited.

Pharmacologic treatments of sleep disorders lack adequate and significant empirical data. Given the lack of data supporting pharmacological treatment, initially use behavioral and cognitive strategies in most cases. Because of the paucity of adequate empirical studies, pharmacotherapy data are limited to treatment in select sleep disorders.

• Limit-setting problems, bedtime resistance, and frequent nightly awakenings represent common problems encountered in pediatric practice. Cognitive-behavioral techniques use relatively straightforward and safe strategies for enhancing overall parenting effectiveness as well as ameliorating the aforementioned problems.
  • Extinction technique: This technique involves the parents putting their child to bed at a designated time and ignoring the child’s or infant’s protests until an established time the next morning.
  • Graduated extinction: Many parents may experience or perceive pure extinction as overly taxing or cruel; therefore, a graduated extinction technique may be used. This may include progressive time delays in responding to bedtime protests or refusals (ie, a checking technique), or it may include comforting the child for increasingly shorter intervals when checking on the child.
  • Positive routine-stimulus control techniques: This technique involves developing a consistent, pleasurable, and calming nighttime routine, with pleasurable activities being halted if the child protests or throws a tantrum. The child is then put to bed.
  • Scheduled awakenings: Parents awaken the child approximately 15 minutes prior to the child’s typical nightly awakening times. The scheduled awakenings gradually are stopped or weaned.
     
• Nocturnal enuresis: History and physical examination usually are sufficient to rule out urological abnormality. Routine dipstick urinalysis, growth/height trajectory, and blood pressure are used to exclude other medical causes of enuresis. Children younger than 6 years should be managed with child and family reassurance that the enuresis is developmentally normal.
  • Alarm clock method: An alarm is set before the most probable time of the event based on the trend of enuretic episodes. The alarm may be set for a predetermined time, such as 2-3 hours after usual onset of enuresis. Children eventually avoid wetting themselves before the alarm is triggered, unlike the bell and pad method. Longer treatment duration results in a higher success rate.
  • Parent education: Parents need to know that sleep hygiene practices serve as prevention of enuresis. Fluid restriction, bedtime voiding, and parent awakening later are components of sleep hygiene (see Patient Education). The earlier the child begins practicing sleep hygiene, the better. Individual families may require creative combinations of the aforementioned interventions.
  • Desmopressin and nocturnal enuresis: Desmopressin reduces nocturnal urine production, has better short-term results than the alarm method, is effective in 50-85% of individuals, and generally is well tolerated. Recidivism after discontinuation can present a problem.
  • Imipramine and nocturnal enuresis: Imipramine is effective, but concern exists for potentially serious adverse effects. Imipramine dosing is 25-100 mg depending on the age and size of the patient. Risks involved in imipramine use often outweigh the benefits for the relatively benign problem. The use of imipramine requires ECG at baseline, with titration and dose increases and periodic monitoring. The clinician should monitor blood pressure and pulse rate and review cardiovascular system issues at each visit.
     
• Sleep-related fears and anxiety: Treatment for sleep-related fears and anxiety include relaxation training, guided imagery, positive self-talk, positive reinforcement for increasingly successful efforts, systematic desensitization, and gradual exposure to child-determined hierarchy of sleep-related fears or anxiety. The child progresses from envisioning less threatening fears to conquering in vivo actual feared objects or situations. Exposure-response prevention is combined with relaxation techniques and positive reinforcement for treatment gains.
• OSAS: Adenotonsillectomy is the primary treatment modality in children with OSAS. Positive airway pressure is needed in cases of continued postsurgical symptomatology. Continuous positive airway pressure (CPAP), variable pressure devices (eg, bilevel positive airway pressure [BiPAP]), and on-demand pressure when airflow is impeded (D-PAP) may be needed. Weight loss can be helpful for obese patients.
• PLMS: Focus cognitive and behavioral therapy on alleviating stress and promoting relaxation. Dopaminergic therapy may be necessary; however, only limited data on dopaminergic therapy in youths are available. Pergolide (withdrawn from US market March 29, 2007) is effective in treating ADHD or Tourette syndrome and comorbid sleep disorder. Caffeine restriction can be helpful. Low-dose Depakote has been shown to be effective in a small case series of adults.
• RLS: Focus cognitive and behavioral therapy on alleviating stress and promoting relaxation. Dopaminergic therapy may be necessary; however, limited data exist for treatment in youths. Pergolide (withdrawn from US market March 29, 2007) has been found to be effective in treating ADHD or Tourette syndrome and comorbid sleep disorder. Caffeine restriction may be helpful. Low-dose Depakote has been shown to be effective in small case series of adults.
• Circadian rhythm disorders
  • Light therapy resets suprachiasmatic nuclei.
  • Melatonin acts directly upon suprachiasmatic nuclei. The effect of light on phase shifts is opposite. Phase delay requires morning dosing of melatonin. Advanced sleep phase syndrome requires evening dosing.
  • In manipulating the internal sleep-wake clock, gradually delaying sleep onset resynchronizes the internal clock. Delay sleep onset by 15-minute increments each night until desired sleep time is established.

Surgical Care

Adenotonsillectomy may be indicated for OSAS.

Medical Treatment

The treatment of parasomnias is aimed at lessening the frequency and/or intensity of the events.

Sleepwalking and sleep terror disorder 

In children, sleepwalking and sleep terrors usually do not need to be treated. However, risk factors should be identified and minimized. 

In adults, especially in cases involving sleep-related injury, drugs may be required and can be lifesaving. Benzodiazepines, which are used for insomnia situations where an individual awakens after falling asleep, such as estazolam (ProSom), have been found to be safe and remarkably effective in adults with sleepwalking and sleep terrors.

REM sleep behavior disorder 

Treatment for REM sleep behavior disorder is initiated with clonazepam (Klonopin) at 0.5-1.5 mg taken at bedtime. Clonazepam is remarkably effective in controlling both the behavioral and the dream-disordered components of REM sleep behavior disorder. This drug has been shown to be beneficial in the long term. Drug discontinuation often results in prompt relapse.

Tricyclic antidepressants are occasionally used in the treatment of REM sleep behavior disorder. Imipramine has been used, but the effects are unpredictable. 

Several reports of levodopa/carbidopa, gabapentin, pramipexole, and clonidine have been published, but the benefit of these drugs has not been systemically evaluated.

Restless legs syndrome and periodic limb movement disorder 

Restless legs syndrome and periodic limb movement disorder are treated with 3 classes of medications. Treatment guidelines are as follows:

• Anti-parkinsonian drugs, such as levodopa/carbidopa, bromocriptine, ropinirole (Requip), pergolide (Permax), and pramipexole (Mirapex), have been used.
• Benzodiazepines, especially clonazepam have been effective. Other benzodiazepines used have included diazepam, temazepam, and lorazepam.
• Opiates, such as codeine, oxycodone, methadone, and propoxyphene, are other drugs that have been used.
• Dopamine agonists, such as levodopa or pergolide, may be effective, but the effectiveness may not last, and some individuals are unable to tolerate side effects. 
• Other drugs that have shown effectiveness include clonidine or anticonvulsants, such as carbamazepine, valproate, and gabapentin. 
• Several studies have reported efficacy of different medications belonging to the aforementioned groups, but comparative studies between various classes of drugs or even individual drugs do not exist. Therefore, persons should receive one drug, and, if no response is noted, they should be placed on another drug of the same class or a different class.
• A combination of drugs may be required in more severe cases. Some persons who do not respond to benzodiazepines alone, levodopa alone, or a combination of both may be treated with opiates.
• One should receive the smallest possible dose and should be closely observed for the development of dependency. Experience reveals that the incidence of abuse, tolerance, or addiction to opiates or benzodiazepines in persons with severe restless legs syndrome appears to be insignificant. The disabling condition of severe restless legs syndrome must be treated aggressively.
• Restless legs syndrome and periodic limb movement disorder are chronic conditions that require long-term drug therapy. Some persons may develop symptoms of restless legs during the daytime, and this may be treated with controlled release of levodopa/carbidopa administered in the evening and morning.
• Avoidance of certain drugs, such as tricyclic antidepressants, fluoxetine, or lithium, may be helpful because these drugs generally worsen the symptoms of restless legs syndrome and periodic limb movement disorder.
• A decrease in body iron stores, as indicated by serum ferritin (an iron-protein complex) levels less than 50 mcg/L, should be corrected with iron supplementation. Oral iron is preferred but takes a long time to provide improvement, because gastrointestinal absorption is low. However, replenishment is an effective treatment strategy for iron-deficiency anemia and may also relieve symptoms of restless legs syndrome and periodic limb movement disorder (if present).

Medications

The common classes of drugs used for the treatment of parasomnias are benzodiazepines and anticonvulsants. The general aim of drug treatment is to prevent arousal out of sleep or to suppress REM sleep.

Benzodiazepines 

Benzodiazepines help suppress REM sleep and limit arousal. They include the following drugs:

• Diazepam (Valium) is most frequently used in children, especially children with night terrors.
• Alprazolam (Xanax) is the second choice in this category for parasomnias. It has a brief duration of action; therefore, the likelihood of morning effects, such as grogginess, is decreased. However, it has a potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
• Clonazepam (Klonopin) is similar to alprazolam; it is a good alternative option to diazepam.

Anticonvulsants 

Anticonvulsants inhibit arousal. They include the following drugs:

• Carbamazepine (Tegretol, Carbatrol) is the most commonly used drug for parasomnias.
• Valproate (Depakene, Depakote) has been reported to be effective in treating parasomnias, in both a once nightly dosage schedule and a standard dosage schedule.
• Gabapentin (Neurontin) has not been used as frequently as the other 2 anticonvulsants. As with carbamazepine and valproate, no information is available and no consensus has been reached regarding the use of a once nightly dosage versus a standard antiepileptic dosage.

Antiparkinsonian 

Antiparkinsonian drugs are very effective for the treatment of persons with restless legs syndrome and periodic limb movement disorder.

• Levodopa is the most commonly used drug for the treatment of restless legs syndrome and periodic limb movement disorder. An oral dose of 50-100 mg, controlled-release formulation, is prescribed as initial therapy for restless legs syndrome.
• For periodic limb movement disorder, a controlled-release preparation of levodopa combined with a decarboxylase inhibitor (carbidopa) at a dose of 50-100 mg is started.
• A dose increase not to exceed 200 mg may be required to completely suppress restless legs syndrome and periodic limb movement disorder.
• The major adverse effects of levodopa therapy are (1) rebound of symptoms during the daytime and (2) tardive dyskinesia (difficulty in performing voluntary movements), which is extremely uncommon.
• Ropinirole (Requip), pergolide (Permax), and pramipexole (Mirapex) cause fewer side effects compared with levodopa and have become first-line drugs in the treatment of restless legs syndrome and periodic limb movement disorder. Pramipexole is started at a lowest dose of one half tablet of 0.25 mg once a day for 5 days and then increased to 0.25 mg per day. The dose may be increased to a maximum of 0.5 mg per day. Ropinirole is started at 0.25 mg at bedtime for individuals with primarily nighttime symptoms. For those with symptoms throughout the day, it may be given 2 times per day. The dose may be gradually increased each week. Average doses are 2.5 mg per day.

Opiates
 
Opiates, such as codeine, propoxyphene, and dihydromorphone, have been used in persons who have severe restless legs syndrome and who do not benefit from other therapy. One should be closely observed for development of tolerance and dependency 

Medications

The common classes of drugs used for the treatment of parasomnias are benzodiazepines and anticonvulsants. The general aim of drug treatment is to prevent arousal out of sleep or to suppress REM sleep.

Benzodiazepines 

Benzodiazepines help suppress REM sleep and limit arousal. They include the following drugs:

• Diazepam (Valium) is most frequently used in children, especially children with night terrors.
• Alprazolam (Xanax) is the second choice in this category for parasomnias. It has a brief duration of action; therefore, the likelihood of morning effects, such as grogginess, is decreased. However, it has a potential for exacerbating symptoms at lower doses when effects attenuate, owing to possible rebound.
• Clonazepam (Klonopin) is similar to alprazolam; it is a good alternative option to diazepam.

Anticonvulsants 

Anticonvulsants inhibit arousal. They include the following drugs:

• Carbamazepine (Tegretol, Carbatrol) is the most commonly used drug for parasomnias.
• Valproate (Depakene, Depakote) has been reported to be effective in treating parasomnias, in both a once nightly dosage schedule and a standard dosage schedule.
• Gabapentin (Neurontin) has not been used as frequently as the other 2 anticonvulsants. As with carbamazepine and valproate, no information is available and no consensus has been reached regarding the use of a once nightly dosage versus a standard antiepileptic dosage.

Antiparkinsonian 

Antiparkinsonian drugs are very effective for the treatment of persons with restless legs syndrome and periodic limb movement disorder.

• Levodopa is the most commonly used drug for the treatment of restless legs syndrome and periodic limb movement disorder. An oral dose of 50-100 mg, controlled-release formulation, is prescribed as initial therapy for restless legs syndrome.
• For periodic limb movement disorder, a controlled-release preparation of levodopa combined with a decarboxylase inhibitor (carbidopa) at a dose of 50-100 mg is started.
• A dose increase not to exceed 200 mg may be required to completely suppress restless legs syndrome and periodic limb movement disorder.
• The major adverse effects of levodopa therapy are (1) rebound of symptoms during the daytime and (2) tardive dyskinesia (difficulty in performing voluntary movements), which is extremely uncommon.
• Ropinirole (Requip), pergolide (Permax), and pramipexole (Mirapex) cause fewer side effects compared with levodopa and have become first-line drugs in the treatment of restless legs syndrome and periodic limb movement disorder. Pramipexole is started at a lowest dose of one half tablet of 0.25 mg once a day for 5 days and then increased to 0.25 mg per day. The dose may be increased to a maximum of 0.5 mg per day. Ropinirole is started at 0.25 mg at bedtime for individuals with primarily nighttime symptoms. For those with symptoms throughout the day, it may be given 2 times per day. The dose may be gradually increased each week. Average doses are 2.5 mg per day.

Opiates
 
Opiates, such as codeine, propoxyphene, and dihydromorphone, have been used in persons who have severe restless legs syndrome and who do not benefit from other therapy. One should be closely observed for development of tolerance and dependency

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• When evaluating a child or adolescent for a sleep disorder, obtaining a thorough sleep history cannot be overemphasized. A sleep diary usually kept for about 2 weeks provides information regarding night-to-night variability over time. Sleep diaries also are helpful in tracking patient compliance with behavioral interventions and response to treatment. Rating scales have been developed to quantify subjective sleepiness of patients. The Epstein Sleepiness Scale and Stanford Sleepiness Scale are examples.
  • Temporal history
  • When the problem began
  • Predisposing, precipitating, and perpetuating factors
  • Review of evening activities and bedtime rituals
  • Sleep environment
  • Latency to sleep onset
  • Arousals – When, duration, frequency, behavior during awakening, and ease with which child returns to sleep
  • History of snoring, breathing pauses, sleepwalking, talking, enuresis, and nocturia
  • Sleep position
  • Nightmares and sleep terrors
  • Seizure symptoms – Tongue biting, chewing, blood on bed clothes, and encopresis
  • Time of morning awakening, sleep paralysis, and early-morning headache
  • Total sleep time
  • Restorative sleep
  • Daytime sleepiness, fatigue, and school performance
  • Questions about depression, anxiety, worries or concerns, hyperactivity, and irritability
  • Frequency and duration of naps
  • Existing comorbid disorders
  • Substance use
  • Use of caffeine, alcohol, drugs, medications (prescription or over-the-counter [OTC]), and herbal preparations
  • Family history of sleep disorder or metabolic disorder
  • Parents’ sleep habits
  • Efforts made to control symptoms
  • Overall impact of sleep disturbance on family
     
• Dyssomnias
  • Primary insomnia: Insomnia is defined as the subjective symptom of inadequate sleep quantity and quality. Patients with primary insomnia report difficulty falling asleep or maintaining sleep. Chronic insomnia may produce poor concentration and a low level of energy. Other symptoms include a decreased sensation of well-being and poor productivity. Some patients with primary insomnia feel that the sleep was not restorative. Distress due to inability to sleep may lead to a vicious cycle of frustration and insomnia.
  • Primary hypersomnia: Patients with primary hypersomnia require more sleep despite long and good sleep (about 12 h), usually require naps in the daytime, and are not refreshed by short naps.
  • Narcolepsy: Patients with narcolepsy may experience (1) excessive daytime sleepiness with irresistible daytime sleep attacks; (2) sleep paralysis, in which the individual awakens unable to move; (3) cataplexy, which may be subtle initially (eg, wobbly knees, dizziness) but may progress to sudden falls following a strongly experienced emotion; (4) hypnagogic hallucinations; and (5) feeling of refreshment after a sleep attack.
  • OSAS: Children with OSAS have a history significant for loud snoring, breathing pauses, mouth breathing, restless sleep, and increased perspiration at night. Snoring is the most common presenting symptom. Hyperactivity and failure to thrive are more common symptoms of childhood obstructive apnea. Other symptoms in children with OSAS include excessive daytime sleepiness, morning headaches, and behavioral changes (paradoxical hyperactivity as children try to stay awake). These children also experience emotional lability, changes in school performance, and cardiac failure.
  • Delayed sleep phase syndrome (DSPS): Of the circadian rhythm sleep disorders, DSPS is the most common, with a prevalence of about 7% for adolescents. It is characterized by early insomnia, little or no difficulty maintaining sleep, and difficulty waking in the morning.
     
• Parasomnias
  • Nightmare disorder: Nightmares affect 10-50% of children aged 3-6 years. Nightmares occur during REM sleep usually in the second half of the night. After a nightmare, the child is alert and can clearly describe in detail scenes and frightening images. Nightmares are common during stressful times or after frightening events, such as frightening movies. Nightmares are well remembered in the morning. If nightmares are severe and frequent, they may affect daytime functioning. In posttraumatic stress disorder (PTSD), nightmares may be associated with flashbacks, numbing, reenacting the events, and avoidance.
  • Night terrors (pavor nocturnus): This form of sleep disturbance occurs in the first 3 hours of sleep. The child is not awake but appears agitated. Abrupt, usually agitated, arousal from slow-wave sleep takes place. Night terrors are associated with autonomic arousal (eg, tachypnea, tachycardia, diaphoresis) and screaming. The child is often inconsolable during the episode. The episode terminates spontaneously after about 3-5 minutes and the child quickly returns to sleep. Recall of the event in the morning is poor. This type of disturbance may be associated with an ongoing illness or fever.
  • Sleepwalking disorder (somnambulism): The sleepwalker is difficult to arouse and usually has no recollection of the event in the morning. Actions taking place during sleepwalking frequently vary.
  • Bed-wetting (enuresis): In primary enuresis, no period of nighttime dryness occurs for more than 6 months. In secondary enuresis, a relapse of bed-wetting occurs after a period of at least 6 months of dryness. This sleep disturbance may be associated with shame and low self-esteem.
     
• Sleep disorders related to medical and psychiatric conditions: A wide variety of medical and psychiatric disorders may result in sleep disruption. The clinician must first establish the presence of a general medical condition. Furthermore, the clinician must determine whether the sleep disturbance is causally related to the medical illness through a physiological mechanism. Cluster headaches occur more frequently during the night than in the daytime. Sleep-related headaches usually awaken the patient and fragment sleep.
  • Insomnia related to another mental disorder is characterized by reports of difficulty falling asleep, frequent awakenings during the night, or a marked feeling of nonrestorative sleep that has lasted for at least 1 month and is associated with daytime fatigue or impaired daytime functioning.
  • Hypersomnia related to another mental disorder is characterized by reports of either prolonged nighttime sleep or repeated daytime sleep episodes for at least 1 month. In both insomnia and hypersomnia related to another mental disorder, the sleep symptoms cause significant distress or impairment in social, occupational, or other important areas of functioning.
     
• Diagnostic criteria for sleep disorders caused by a general medical condition include the following:
  • A prominent disturbance in sleep that is sufficiently severe to warrant independent clinical attention
  • Evidence from the history, physical examination, or laboratory findings that the sleep disturbance is the direct physiological consequence of a general medical condition
  • Disturbance that is not better accounted for by another mental disorder (eg, an adjustment disorder in which the stressor is a serious medical illness)
  • Disturbance that does not occur exclusively during the course of a delirium
  • Disturbance that does not meet the criteria for breathing-related sleep disorder or narcolepsy
  • Sleep disturbance that causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
     
• The following medical conditions fragment sleep, lead to excessive sleepiness during the day, and affect the individual’s concentration and performance in the day to various degrees. In pediatric populations, epilepsies occurring during sleep account for 30% of seizure disorders. Epilepsy appears to fragment sleep and causes impairment in daytime functioning. The sleep disturbances associated with developmental CNS disorders generally reflect fragmentation with frequent awakenings, difficulty in initiating sleep, and early morning awakenings. The physical abnormalities associated with Down syndrome and Prader-Willi syndrome that occlude the upper airway often lead to OSAS. Blind individuals experience cyclic disorders because of the lack of cues that continually reset the internal clock to fit the 24-hour day/night cycle.
• Klein-Levin syndrome: Klein-Levin syndrome refers to a constellation of symptoms that include episodes of excessive somnolence, overeating, and sexual disinhibition. Behavioral disturbances, such as irritability and confusion, are associated with Klein-Levin syndrome. Occasional hallucinations have been reported. Klein-Levin syndrome is 3 times more frequent in boys than in girls. Symptoms typically begin during adolescence, either gradually or abruptly. Onset follows a flu-like illness or injury with loss of consciousness in half the cases. Klein-Levin syndrome has a course that remits and relapses, with relapses occurring at intervals of weeks to months. Symptoms may last from 12 hours to 3 weeks. Klein-Levin syndrome usually resolves spontaneously during late adolescence or early adulthood.
• Down syndrome: Airway hypotonia leads to obstructive apnea that is not associated with obesity, age, or congenital heart disease. Central apnea also is common and is associated with significant desaturation.
• ADHD: Paradoxical hyperactivity in children with ADHD encourages them to stay awake. Emotional lability may be observed. Children with ADHD tend to have fewer arousals and shorter arousals than adults. These children also tend to have obstructive hypopnea with relatively few complete apneic events. Children with ADHD have a strong tendency to fall asleep during the day. Children with ADHD have high rates of RLS and PLMS, and they have a higher prevalence rate for OSAS comorbidity.
• Tourette syndrome: Approximately 50% of children with Tourette syndrome have sleep disturbances. Nocturnal awakenings and movements increase when tics persist into sleep. Comorbidity exists with obsessive-compulsive signs, traits associated with increased sleep latency, decreased REM sleep, and deceased REM sleep latency. Children and adolescents with this movement disorder are at risk for parasomnias. Patients with Tourette syndrome have a higher incidence of enuresis.
• Rett syndrome: This is associated with prolonged sleep latency. Short and fragmented sleep results in low sleep efficiency.
• Prader-Willi syndrome: Obesity, hyperphagia, and developmental delay are the most common features. Obesity can cause obstructive sleep apnea. An increased frequency of apneas, decreased nadir of oxygen saturation, increased maximum heart rate, and blunted respiratory response to hypercapnia during NREM sleep all may occur in patients with Prader-Willi syndrome. Sleep time and slow-wave sleep increase during the day and at night.
• Upper airway resistance syndrome: This results in REM fragmentation and extra daytime sleep (EDS).
• Menstrual-associated periodic hypersomnia: This is another cyclic sleep disorder, noted during the first few years after menarche. Attacks generally last 1-2 weeks after ovulation, with sudden resolution occurring at the time of menses.
• Sleep-related GERD: This is characterized by regurgitation of stomach contents into the esophagus during sleep. It is very common in patients using theophylline as a respiratory stimulant for apnea of prematurity or asthma.
• Nighttime exacerbations of childhood asthma: These are common and may lead to significant sleep disruption.
• Atopic dermatitis: Children with atopic dermatitis tend to have increased sleep-onset difficulty, night awakenings, and decreased sleep duration due to pruritus and medications, such as antihistamines and corticosteroids.
• Chronic illness: Children with chronic illnesses, such as juvenile rheumatoid arthritis (JRA) or sickle cell disease, can experience sleep difficulties.

• Insomnia related to another mental disorder is the most frequent diagnosis (35-50%) among individuals who present to sleep disorder facilities for evaluation of chronic insomnia. In young children, separation anxiety, stress, and trauma may result in nighttime awakening, nightmares, or resistance to going to bed.
• Patients who have major depressive disorder or dysthymic disorder often report difficulty falling asleep or staying asleep or early morning awakening with inability to return to sleep. Hypersomnia can be a feature of depression, especially major depression with atypical features. Children and adolescents with major depressive disorder generally present with less subjective sleep disturbance and fewer polysomnographic changes than do older adults with a similar degree of depression.

• Prepubertal children with depression are more likely to experience insomnia (75%) than hypersomnia (25%); after puberty, hypersomnias predominate. Hypersomnia is a common feature of depressive disorders in adolescents and young adults, and insomnia is more common in older adults.

• Individuals with generalized anxiety disorder often report difficulty falling asleep and may awaken with anxious thoughts in the middle of the night. Panic attacks can arouse patients and cause insomnia. Significant insomnia is often observed during exacerbations of schizophrenia and other psychotic disorders but rarely is a predominant symptom. Other mental disorders that may be related to insomnia include adjustment disorders, somatoform disorders, and personality disorders.
• Substance-induced sleep disorder most commonly occurs during intoxication with substances, such as alcohol, amphetamine and related substances, caffeine, cocaine, opioids and sedatives, hypnotics, or anxiolytics. Substance-induced sleep disorder can also occur in association with withdrawal from these same classes of substances.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• Level of consciousness
• Physical features
• • Head circumference
  • Weight and indicators of failure to thrive
  • Features suggestive of congenital anomalies
  • Size of the posterior pharynx
• Physical causes of airway blockage such as enlarged tonsils or adenoids
• Obesity, neck circumference
• Systemic signs of heart failure such as clubbing or cyanosis
• Signs indicative of seizure activity
• Tooth injuries on tongue
• Incontinence
• Postictal changes in sensorium

Tests For Sleep Disorder

• Sleep laboratory studies are very helpful when indicated, but most common pediatric sleep problems do not require formal sleep laboratory testing. Most sleep problems resolve with behavioral treatments. A detailed sleep history, thorough physical examination, and sleep logs provide the foundation for accurate diagnosis, treatment, and possible referral for polysomnography. Atypical presentations, snoring associated with daytime somnolence, behavioral-emotional problems, apneic or hypopneic episodes, suspicion of narcolepsy, abnormal and disruptive movements in sleep, unexplained or recalcitrant sleep difficulties, or daytime sleepiness indicate a need for sleep studies.
• Overnight polysomnography and next-day multiple sleep latency testings represent the most commonly used sleep studies. Clinical suspicion of any of the following disorders should prompt referral for sleep studies:
• • Sleep-related seizurelike activity
  • Sleep-related gastroesophageal reflux
  • Nighttime asthma or persistent cough
  • ADHD or Tourette syndrome associated with restless sleep and disrupted daytime functioning
  • RLS and PLMS – Relatively common in these patients
  • Recurrent REM sleep behaviors
  • Severe bruxism
  • Snoring and hypopnea or apnea
  • Recalcitrant or unexplained and daytime somnolence
  • Suspected narcolepsy
• Multiple sleep latency tests aid in clarifying unexplained excessive daytime sleepiness and narcolepsy symptoms.

These are the most important items for parasomnia evaluation: 

• Interview the person and his or her bed partner
• Review of medical records
• Elicit details about sleep-wake patterns
• Medical history
• Psychiatric history
• Alcohol and drug-use history
• Family history
• Past or current history of physical, sexual, and emotional abuse 
• Psychiatric and neurologic interviews and examinations

Polysomnography (sleep test)

This test is usually conducted in a sleep study center. The patient sleeps at the center, and the following parameters are monitored:

• Electrical activity of the brain (electroencephalogram)
• Electrical activity of the heart (electrocardiogram)
• Movements of the muscles (electromyogram)
• Eye movements (electrooculogram)

These parameters are monitored as the person passes through the various sleep stages. Characteristic patterns from the electrodes are recorded while the person is awake with eyes closed and

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Primary hypersomnia: Youths with primary hypersomnia have normal sleep efficiency, sleep/wake cycles, and sleep architecture. Patients with primary hypersomnia present with a normal variant sleep pattern except for longer sleep needs. It may be a lifelong pattern. No other identifiable cause exists for the excessive somnolence that continues for at least 4 weeks.

Primary or idiopathic insomnia: The pathogenesis of primary hypersomnia is poorly defined. Patients with primary or idiopathic insomnia may have a lifelong inability to initiate and maintain sleep with associated sequelae.

Sleep-state misperception: Youths with sleep-state misperception may have normal polysomnography. The pathology of sleep-state misperception is associated with an underestimate or misperception of the child’s sleep duration, which results in the patient’s mistaken belief of having experienced inadequate sleep.

Psycho-physiological insomnia: This disorder is related to psychological stressors that interfere with sleep onset or maintenance.

Narcolepsy: Rapid eye movement (REM) sleep mechanisms are dysregulated in youths with narcolepsy, but evidence also exists of nonrapid eye movement (NREM) and circadian sleep-wake cycle abnormalities. REM-associated sleep phenomena intrude into the awakened state. Sleep attacks (sleep), cataplexy (abrupt atonia precipitated by strong emotions), hypnagogic and hypnopompic hallucinations (experienced as dreamlike events immediately before sleep onset or upon awakening) are characteristic of narcolepsy. Excessive daytime somnolence leading to irresistible/involuntary sleep (sleep attacks) may occur. The role of the neuropeptide hypocretin (Orexin) and human leukocyte antigen (HLA)–DR2/DBQ1 as a genetic-neuroimmune interaction is being considered in current research on this issue. Narcolepsy is consistent with the polygenic model of development in most human cases.

Obstructive sleep apnea syndrome (OSAS): The pathophysiology of OSAS is poorly understood. Alterations exist in alveolar ventilation and oxygenation. OSAS is associated with adenotonsillar hypertrophy; however, most youths with adenotonsillar hypertrophy do not experience OSAS. Upper airway neuromotor dysfunction is possible in the initiation of OSAS.

Periodic limb movements in sleep (PLMS): PLMS is more prominent in NREM stage 1 and 2 sleep. PLMS is strongly associated with ADHD and restless legs syndrome (RLS) in the pediatric population. The response to dopaminergic agents and the association with ADHD suggest that PLSM may be a dopaminergic dysfunction. Characteristic movements may aid in further understanding of the pathology of PLMS. Repetitive flexion of lower extremities (more common) or upper extremities occurs in youths with PLMS with a 0.5- to 5-second duration occurring 5-90 seconds apart. Repetitive jerks are associated with frequent awakenings and daytime somnolence or insomnia. The pediatric population with PLMS often experiences inattention, overactivity, and mood lability due to associated sleep disruption/fragmentation. PLMS can occur without RLS.

RLS: The response to dopaminergic agents and the association to ADHD implicate that RLS is a dopaminergic dysfunction. Leg discomfort in patients with RLS is associated with a strong urge to move legs, and the relief with movement may ultimately reveal a pathophysiology similar to that of akathisia. Most patients with RLS have PLMS. The pediatric population with RLS often experiences inattention, overactivity, and mood lability due to associated sleep disruption/fragmentation.

Limit-setting sleep disorder: This is a parent-child transactional model with potentially numerous biopsychosocial variables that influence interactions. It is not simply a failure to set limits but has a more complex pathogenesis and ultimately pathophysiology. Children with limit-setting sleep disorder resist or refuse to go to bed at an appropriate time. Limit-setting sleep disorder may be related to underlying pathophysiology as observed in ADHD and other neurodevelopmental disorders or may be a combined medical-behavioral issue.

Insufficient sleep syndrome: This is a condition of chronic sleep deprivation without an underlying disease process. Youths with insufficient sleep syndrome may experience an increased need for sleep during puberty and adolescence. Insufficient sleep syndrome may represent a poor compensatory ability for sleep loss and includes failure to adequately synchronize sleep-wake behaviors and adapt to environmental demands, such as school. The patient with insufficient sleep syndrome attempts to decrease sleep debt incurred during the week by sleeping later on the weekends. They are unable to obtain sufficient sleep because of school, extracurricular, occupational, and other societal demands.

Circadian sleep disorders: A circadian clock/oscillator located in the suprachiasmatic nuclei of the anterior hypothalamus influences the wakefulness or alertness phase. A circadian clock potentiates alternate or diurnal phases of the sleep-wake cycle. A free-running human sleep-wake cycle is 25 hours; however, the cycle entrained by the environment results in a 24-hour cycle. Sleep and associated processes are at opposite phases or periods in patients with circadian sleep disorders. Circadian sleep disorders may represent a poor compensatory ability for sleep loss and includes failure to adequately synchronize sleep-wake behaviors and adapt to environmental demands, such as school. This disorder is frequently observed in adolescents with delayed sleep phase.

Parasomnias

Parasomnias are sleep-related phenomena disrupting normal sleep. Events can take place during sleep-wake transitions, arousal, or REM sleep. Sleep stages and other variables are related to pathogenesis.

Sleepwalking: Sleepwalking is described as partial arousal from sleep during slow-wave stages 3 and 4. It is most common during the initial third stage of the sleep period.

Bruxism (persistent grinding of the teeth): Bruxism is considered as a stereotyped movement disorder or rhythmic disorder. It is more frequent during the early part of sleep and may be related to stress and/or anxiety or dentition abnormalities. Bruxism is not limited to sleep but may also occur while the child is awake. Basal ganglia dysfunction has been hypothesized.

Nightmares: Nightmares appear to be related to the same etiology as other anxiety-related experiences. They occur during REM sleep.

Sleep terrors: Sleep terrors are associated with autonomic arousal and screaming. They transpire during the first third of sleep in the slow-wave sleep cycle.

Primary nocturnal enuresis: Bladder instability, which is an uninhibited or reduced threshold for detrusor contraction during bladder filling, and urethral instability, which is a failure of urethral sphincter to adequately relax with bladder filling, are characteristic of youths with primary nocturnal enuresis. Youths with primary nocturnal enuresis may have a relative resistance to an antidiuretic hormone at night. Genetic factors contribute significantly in primary nocturnal enuresis with linkage studies positive on chromosome 8. No correlation exists with sleep stage.

Rhythmic movement disorders: These disorders are related to the developmental age of the child. Head banging and body rocking are the most common presentations of this disorder. Rhythmic movement disorder occurs during sleep onset and stages 1 and 2 sleep (light sleep).

Confusional arousals: In a confusional arousal, the child may awaken from stage 1 and 2 sleep frightened and crying. Only minimal autonomic arousal occurs opposed to the high degree observed in sleep terrors. The patient usually fully awakens before returning to sleep. Confusional arousals are associated with higher rates of delayed sleep onset, night awakening, decreased sleep duration, and bedtime resistance.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• Narcolepsy (0.01-0.20%) may be underestimated in children because a classic tetrad of symptoms is uncommon in this age group.
• Bedtime resistance in school-aged children has been reported at 15% and is often associated with limit-setting disorder.
• Nightmares (30%) are more common in younger youths.
• Sleepwalking with at least more than 1 episode occurs in 25-30% of youths and is most common in children aged 3-10 years.
• Insomnia occurs in 23% of youths.
• Enuresis occurs from 8% in children aged 4 years to 4% in children aged 10 years.
• Bruxism is reported in 10% of youths and may occur in people of any age.
• Grinding and clenching teeth at night is reported in 5-8% of adults.
• Sleep rocking or head banging is reported in 5% of youths, with head banging being common in infants and in children aged 9 months to 12 years.
• OSAS is the most common reason for sleep laboratory referral and affects an estimated 2% of children.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

Interference with the signals of interest is encountered through many mechanisms, including physiological attenuation of the cerebral electric potentials by scalp muscle and bone; intrusion into the signal by slow cyclic respiration, movement, ECG signal, or external electric fields; and impaired contacts between the recording electrodes and the skin surface. Discriminating true signal from artifact can be one of the most challenging aspects of scoring the stages of sleep.

At a paper speed of 10 mm/s, 1 page equates to 30 seconds and is defined as 1 epoch. Computerized polysomnography usually displays one video screen as one 30-second epoch.

Polysomnographic Interpretation

Cortical signals

The electroencephalography (EEG) signal is of primary importance in interpreting polysomnographic studies. It records electric potentials generated by the interaction between the cortex and the deeper brain structures, especially the thalamus. Two centrocephalic and 2 occipital cortical channels are recorded. Measurement of EEG signals is possible because of the relative difference in potential between the 2 recording electrodes; 1 electrode is considered negative with respect to the other. Negative discharges, by convention, are represented by an upwardly deflecting wave.

The polysomnograph references the left and right centrocephalic electrodes (C3, C4) or the left and right occipital electrodes (O1, O4) to electrodes on the opposite right and left ears (A2, A1). The general rule is to read only from the left cortical channel. However, when the left channel develops artifact or the validity of the signalissuspected, comparison is made with the right cortical channel. By convention in the United States, the left channels are odd numbers and the right channels are even numbers. By convention in the United Kingdom, the opposite is true, with the left channels described by even numbers.

Cortical signals are defined slightly differently according to the reference used. The following convention is used here:

• Delta is the slowest activity at less than 4 counts per second (cps).
• Theta is between 4 and 8 cps.
• Alpha is between 8 and 14 cps.
• Beta is greater than 14 cps.
• Another range occasionally mentioned is gamma, which is part of the high end of the beta frequency and has been described to range from 30-45 cps.

High frequency signals above 50 cps are finding increased mention in the literature. High frequency bands (HFB) are described in the ranges 51-100 Hz (HFB1), 101-200 Hz (HFB2), and 201-500 Hz (HFB3) for analysis purposes. Frequencies in these bandwidths are reported as being associated with cognitive processing and alertness.

Muscle signals

The EMG signals are muscle twitch potentials that are of secondary importance in polysomnography. Their utilization is based on the finding that, during sleep, muscle activity decreases. During rapid eye movement (REM) sleep, muscle activity is at its nadir. However, in many cases appreciating the decreasing tone is difficult. The relative silence during REM sleep may not be of help in distinguishing REM sleep from the preceding or subsequent sleep stages.

Compounding the problem of interpreting EMG channels is intrusion of artifact into the signal. This has many etiologies. Some examples include cyclic chewing movements, irregular teeth grinding, steady high-amplitude noise generated by increased pressure on the electrode (eg, as caused by lying on the chin). Additionally, muscle artifact may spill over into the cortical leads. ECG signal is a specific type of cardiac artifact that can appear in all or several channels; it can be recognized by the QRS complexes in the cortical or other channels.

Eye movements

The electro-oculographic (EOG) signals measure changes in the electric potential of the positive anterior aspect of the eye relative to the negative posterior aspect. Horizontal axis electrodes are placed near the outer canthi and vertical axis electrodes below and above the eye to measure transient changes in potential during the actual eye movement. During any eye movement, the cornea (positive) moves toward 1 electrode, while the fundus (negative) moves away. When the eye is not moving, the change in relative position is zero, and the eye leads do not record a signal.

Slow, rolling eye movements are recorded as long gentle waves, while rapid jerking movements are represented by sharply contoured fast waves. Blinking of the eyes produces rapid vertical movements. Eye movements during drowsiness and stage I sleep may be jerky, irregular, or gently rolling. In deeper stages of sleep, macro eye movements cease altogether. During REM sleep, eye movements again become active and jerky. The intensity of the bursts of activity is used to describe the density of REM sleep.

Sleep Stages

Initially, the clinician should scroll through the entire record quickly to evaluate the quality of the recording and the usefulness of specific channels. Observe sections that represent the major stages to learn the specific shape of the features that represent the stages in that particular individual and to gain an overall picture of the cycles for that record. Specifically observe for sleep spindles, K complexes, slow waves, and REMs.

Wake stage

The first several epochs of the record will be the wake stage. The EEG will show mixed beta and alpha activities as the eyes open and close and predominantly alpha activity when the eyes remain closed. The EMG will reflect the high-amplitude muscle contractions and movement artifacts. The EOG will show eye blinking and rapid movement. The record will slow in frequency and amplitude as the subject stops moving and becomes drowsy.

Drowsiness

This stage is defined as sleepy but awake with eyes closed. The EEG will show predominant alpha activity, while the EMG activity becomes less prominent. The EOG may show slow, rolling eye movements. If, at any point, the subject rolls over, the record will reflect this as paroxysmal sustained increased artifact and high-amplitude activity. The subject may enter stage I of sleep for 1 or 2 epochs and then reawaken. Transitions may be difficult to score. From wake, sleepers normally proceed to stage I, but infrequently they may enter REM sleep or stage II sleep directly.

Stage I

Stage I sleep is scored when the alpha activity in the EEG drops to less than 50%. A transition is observed from alpha activity to a lower frequency activity, such as theta, possibly intermixed with low-amplitude delta activity. Amplitudes are less than 50-75 µV. Paroxysms of 2-7 cps activity up to 75 µV may occu

Stage I is usually brief, lasting for 1-7 minutes. Vertex sharp waves may occur, but no sleep spindles or K complexes are recorded. The EOG may show slow, rolling eye movements, especially early in the stage. No REMs are observed. The EMG shows less activity than in wake stage, but the transition is gradual and of little assistance in scoring.

Arousals are paroxysms of activity lasting 3 seconds or longer. The minimum arousal is simply a paroxysmal burst in the EEG channel, usually to alpha or theta activity. Arousal from stage I is common and usually is represented by a burst of activity on the EEG, EOG, and EMG. If the burst results in alpha activity for greater than 50% of the record, then the epoch is scored as wake.

Stage II

The EEG shows predominant theta activity with minimal alpha activity. Delta is permitted for less than 20% of the record. Amplitude may increase from that seen in stage I.

Sleep stage II EEG sample.

K complexes appear for the first time. K complexes are sharply negative (ie, up-deflecting) monophasic or polyphasic waves followed by a slower, positive (ie, down-deflecting) wave. The complex must persist for at least 0.5 seconds. No minimum amplitude is defined, but characteristically the waves stand out clearly from the background. K complexes can occur in response to a sudden sound and were so named because they were appreciated as following the knocking sound produced by knuckle rapping. In this respect, they may represent a form of cortical evoked potential in a brain still minimally responsive to external stimuli.

Sleep spindles may appear. These are paroxysms of 12-14 cps activity persisting for at least 0.5 seconds (that is, 6-7 small waves in 0.5 seconds). Although classically described as spindle shaped, they vary in morphology and may attach as a tail to a K complex.

No specific criteria exist for EOG and EMG in this stage.

Arousal from stage II may be into stage I or into wakefulness. If the arousal is 3 seconds or longer in duration, and the resulting alpha activity persists for less than 50% of the record, the epoch is scored as stage I. If the alpha persists for greater than 50% of the record, the epoch is scored as stage wake. If the first half of the following epoch demonstrates stage II characteristics (ie, spindles, K complexes, high-amplitude theta/delta activity), that epoch is scored as stage II.

Once in stage II, that score is maintained unless a reason to exit presents. One such reason to exit is described as the 3-minute rule. If no specific stage II indicators appear, and in the absence of arousals and muscle tone changes that would alter the staging, continue to score all epochs as stage II for up to 3 minutes. At 3 minutes, if no specific indicators for stage II have occurred, scroll back 3 minutes and score those epochs as stage I.

Stage III

The EEG shows 4 cps or slower activity, with peak-to-peak amplitudes greater than 75 µV for between 20% and 50% of the epoch. Both K complexes and sleep spindles may be seen in stage III sleep. No specific criteria exist for EOG and EMG. The transition to stage III from stage II may be gradual, and stage III may alternate with stage I.

Sleep stage III EEG sample.

Stage IV

The EEG shows 4 cps or slower activity, with peak-to-peak amplitudes greater than 75 µV for at least 50% of the epoch. Both K complexes and sleep spindles may be seen in stage IV sleep. No specific criteria for EOG and EMG exist. In general, muscle tone decreases gradually from stage II to stage IV. The transition from stage III to stage IV may be gradual, and stage III may alternate with stage IV.

Stage REM

The EEG of REM sleep shows relatively low-voltage and mixed-frequency activities and may resemble the EEG of stage I. Sawtooth-shaped waves may occur before or with REM EOG bursts. Slow alpha activity may occur, resembling that of wake stage.

Rapid eye movement sleep EEG sample.

Sleep spindles and K complexes are not part of the REM EEG; when they occur, they are reason to consider moving from REM to stage II. If 2 K complexes or spindles occur without REM activity between them, the epochs between the complexes are scored as stage II. If REM activity occurs on both sides of the K complexes or spindles, then the epoch is scored as REM and the complex is considered to represent a momentary breakthrough into REM rather than a change of stage. No high-amplitude activity may be counted as REM. Bursts of delta activity are reason to change sleep stage.

The EOG of REM shows paroxysmal, relatively sharply contoured, high-amplitude activity occurring in all eye leads simultaneously. The EOG activity is not needed to mark the start of an REM period. REM epochs may be recognized by EEG activity before EOG movements start. Small REMs on EOG may serve as a harbinger of REM stage and can indicate the actual onset of REM in another area where interscorer concordance is lower.

The EMG of REM shows an appreciable decrease in tone but may differ little from the EMG of stages III or IV. The EMG should show the lowest tone in the record, but no specific amplitude or frequency criteria are in place.

For excellent patient education resources, visit eMedicine’s Procedures Center. Also, see eMedicine’s patient education articles Sleep: Understanding the Basicsand Electroencephalography (EEG).

References :

• Butkov N. Atlas of Clinical Polysomnography. Ashland, Ore: Synapse Media;1996.
• Marzec ML, Malow BA. Approaches to staging sleep in polysomnographic studies with epileptic activity. Sleep Med. Sep 2003;4(5):409-17. 

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• 1-4 Months Old: 14 ½ – 15 ½ hours per day
• 4-12 Months Old : 14 – 15 hours per day
• 1-3 Years Old : 12 – 14 hours per day
• 3-6 Years Old : 10 ¾ – 12 hours per day
• 7-12 Years Old : 10 – 11 hours per day
• 12-18 Years Old : 8 ¼ – 9 ½ hours per day

Newborns typically sleep about 15 to 18 hours a day, but only in short periods of two to four hours. Premature babies may sleep longer and colicky ones shorter.

Since newborns do not yet have an internal biological clock or circadian rhythm, their sleep patterns are not related to the daylight and nighttime cycles. In fact, they tend not to have much of a pattern at all — their needs are unpredictable at this age. And there is not much you can do about it. You have to go with the flow, do what works to soothe and comfort your baby, and be on “baby time.”

During transitions from wake to sleep and vice versa, you may see a sudden jerk or body twitch, as well as her eyes rolling upward as she falls asleep. As the brain develops, you may also see restless movements and agitation accompanied by crying for no apparent reason. This is all quite normal and no cause for alarm.

1-4 Months Old: 14 ½ – 15 ½ hours per day

5-8 Weeks Old

By 6 weeks old social smiling begins, your baby is beginning to settle down a bit, and you may notice more regular sleep patterns emerging. The longest periods of sleep run four to six hours and now tend to occur more regularly in the evening. Day-night confusion ends.

Two hours is about the longest time your baby can stay awake and remain happy and alert. So he needs to take a nap within that time frame. Waiting until your child is overtired or keeping him up past two hours often results in resistance to going to sleep, as well as fussiness and behavioral changes. Interestingly, if naps are deprived on a regular basis, his body produces stimulating hormones to fight fatigue that may actually cause night awakenings. So it is important to become sensitive to your baby’s sleep needs.

Learn to recognize early when your baby is becoming tired. Look for signs like rubbing eyes, pulling ears, getting circles under the eyes. Begin the wind-down routine right away; soothe him in a consistent manner that works for you, and then put him to sleep in his crib. He is now developing sensitivity to his surroundings, recognizing cues like light, noise, and vibration. So when sleeping, he should be motionless and in a quiet, darkened area. All this helps your baby become a more regular sleeper.

3-4 Months Old

Your baby is now getting about two-thirds of sleep at night with three daytime naps, and so is beginning to establish a more firm day-night cycle. She may still sleep irregularly, and at this stage it is OK to forego rigid scheduling, because it is her biology and not her sleep habits that is the predominant factor.

That said, it is important to develop and maintain consistent routines so she does not develop unhealthy sleep habits, which will soon play a major role in her ability to sleep soundly. She needs to begin to learn how to soothe herself and put herself to sleep unassisted. Also, now that she is more interested in the world around her, it becomes more important to place her in a quiet, darkened room, where she will be able sleep well.

Now that your baby has become more social (smiling, giggling, laughing) she may well prefer to be with you and play rather than go to sleep. So you may find some resistance to nap- and bedtime. Do not deny her the critical sleep she needs. Overtired babies quickly become miserable; many may cry with such duration and intensity that they even appear to be sick.

I like the surfing analogy Mark Weissbluth, MD, uses in his book Healthy Sleep Habits, Happy Child: “You want to catch the wave of drowsiness as it is rising to enable your baby to have a long smooth ride to deep slumber. If your timing is off and your wave crashes into an overtired state, then the ride is bumpy and brief….Crying is the consequence of being overtired.”

4-12 Months Old : 14 – 15 hours per day

4-8 Months Old

While up to 15 hours is ideal, most infants up to 11 months old get only about 12½ hours sleep. Establishing healthy sleep habits is a primary goal during this period, as your baby is now much more social, and his sleep patterns are more adult-like. The key is being sensitive to his sleep needs and adapting your lifestyle and scheduling your activities to be in sync with them. As Weissbluth notes, “You are harming your child when you allow unhealthy sleep patterns to evolve or persist — sleep deprivation is as unhealthy as feeding a nutritionally deficient diet.”

You should use the clock together with your child’s natural daily sleep/wake rhythms, his internal clock or circadian rhythm. By learning when your child is naturally sleepy and awake, you can properly and consistently apply healthy sleep routines.

Crying when being put to bed and after awakening at night will only be reinforced and “learned” if you respond to it. So, as a general principal, unless your baby is sick or hungry, do not go to him. Starting routines early and being consistent are keys for success. It typically takes only a few days for a baby to learn to fall asleep unassisted, but it is up to you to maintain the schedule and routines so habits are not lost. The sound sleep that follows is a gift to him and you as well.

Babies at this stage may wake up early (5 – 6 a.m.) and go right back to sleep or wake up a bit later (7 a.m.) and start the day. Whichever the case, there is nothing you can do to change this (like keeping him up later). It is just part of his biology.

Babies typically have three naps and drop to two at around 6 months old, at which time (or earlier) they are physically capable of sleeping through the night. Establishing regular naps generally happens at the latter part of this time frame, as his biological rhythms mature. The midmorning nap usually starts at 9 a.m. and lasts about an hour. The early afternoon nap starts from 12 – 2 p.m. and lasts an hour or two. And the late afternoon nap may start from 3 – 5 p.m. and is variable in duration.

Don’t let the early afternoon nap start beyond 3 p.m., or it may mess up the rest of his sleep schedule. If he misses a nap, keep him up until the next sleep period, though it may begin a bit earlier. Remember that an overtired baby will have difficulty falling asleep and staying asleep.

9-12 Months Old

Your baby now typically sleeps from 10-12 hours at night, takes two naps, and no longer needs to be fed at night.

With the absence of the third nap you may find that she needs an earlier bedtime. It may vary, however, depending on her nap schedule. Interestingly, changes as small as 20 minutes may have a large impact on behavior. Contrary to what you may think, earlier bedtimes allow your child to sleep later and more soundly. Keeping her up too late will increase, not decrease, night awakenings and other sleep-related problems.

With the emergence of her ability to engage more socially and express herself, your little angel may become less cooperative. She is probably much more interested in playing with you and exploring the world than going to a boring, quiet room to take a nap. Naps are essential, though. So do not let naptimes slip and slide. If you do, your child will become fatigued.

Fighting this fatigue results in a heightened state of wakefulness that makes it harder to fall asleep and stay asleep. Nighttime sleep problems often develop. If loss of naps is persistent, the fatigue accumulates and creates a vicious cycle that may lead to emotional and behavioral difficulties. Luckily, when you re-establish your sleep schedule, the problems typically disappear.

Allowing your child to soothe herself and put herself to sleep unassisted are critical to establishing good sleep habits, sleeping soundly, and preventing future sleep problems. As Mark Weissbluth, MD, says in his book Healthy Sleep Habits, Happy Child, “The failure of our children to fall asleep and stay asleep by themselves is the direct result of parents’ failure to give their child the opportunity to learn … self-soothing skills…. Some parents can’t leave their kids alone long enough for them to fall asleep by themselves…. The major sleep problems in babies 4-12 months old develop and persist because of the inability of parents to stop reinforcing bad sleep habits.”

1-3 Years Old : 12 – 14 hours per day

As your child moves past the first year toward 18-21 months old he will lose his morning nap and nap only once a day for an hour and a half to two hours. While toddlers need up to 14 hours a day of sleep, they typically get only about 10½.

The transition to one nap may be a bumpy one, though, where one nap is not enough and two are too many. If this is the case, you may try moving his bedtime earlier, so that he is more rested and better able to skip the morning nap. Another approach involves alternating one-nap and two-nap days, depending on his sleep the previous night.

Most children from about 21-36 months old still need one nap a day, which may range from one to three and a half hours long. They typically go to bed between 7 – 9 p.m. and wake up between 6 – 8 a.m. It is important to be regular (but not necessarily rigid) with bedtimes and naptimes and consistent with your routines or rituals.

If your child is sleeping well and is rested, occasional changes in his daily routine are generally well tolerated. However, if he is not sleeping well, changes may cause quite a few problems. Children at this age move to a bed from a crib and often develop sleep issues that include fears (monsters, the dark, separation), refusing to take naps, resisting going to sleep, night waking, getting out of bed, and getting up too early.

Though this may sound overwhelming, starting early and consistently maintaining healthy sleep habits prevents many problems and makes dealing with those that do occur much, much easier.

3-6 Years Old : 10 ¾ – 12 hours per day

Children at this age typically go to bed around 7 – 9 p.m. and wake up at about 6 – 8 a.m., just as they did when they were younger. At 3, most children are still napping, while at 5 most are not. Naps gradually become shorter as well. New sleep problems do not usually develop after 3 years of age.

You are impressed and exasperated at how well your child has developed bedtime stalling tactics, and at how easily you may be manipulated — “I need to go to the bathroom (again). I need a glass of water; I am so thirsty. Wait, I love you (for the fourth time).”

As always, you must be sensitive to your child’s sleep needs and aware of how well rested she is. Nursery school, preschool, playgroups and the like may wind up eliminating naptime. This may or may not be problematic. If, by altering her nighttime sleep schedule, by going to bed earlier and/or sleeping later, she is well rested, then you’re OK. But don’t eliminate naps if she is not ready. Both you and she will pay the price if you do; major problems can occur.

Sleep, among other factors, influences your child’s temperament. Poor sleep (too little and/or poor quality) is associated with behavior problems like aggression, defiance, non-compliance, oppositional behavior, acting out, and hyperactivity. The inability to put herself back to sleep unassisted and irregular bedtimes are also associated with behavior problems. It is clear, then, that the proper amount and quality of sleep are very important for your child’s development.

7-12 Years Old : 10 – 11 hours per day

At these ages, with social, school, and family activities, bedtimes gradually become later and later, with most 12-years-olds going to bed at about 9 p.m. There is still a wide range of bedtimes, from 7:30 – 10 p.m., as well as total sleep times, from 9 – 12 hours, although the average is only 9 ½ hours.

Sleep needs do not decrease and remain vitally important to your child’s health, development, and well-being. Without the proper amount of sleep, your child will become increasingly sleepy during the day. Those children with a history of sleep problems see them persist. They do not “outgrow them.”

In his book Healthy Sleep Habits, Happy Child, Marc Weissbluth, MD, sums up what you may find in children who routinely do not get the sleep they need, with a bit of a Catch 22: “School achievement difficulties were found more often among poor sleepers compared to good sleepers…. Young children who have difficulty sleeping become older children with more academic problems. But children who are academically successful risk not getting the sleep they need!”

12-18 Years Old : 8 ¼ – 9 ½ hours per day

Sleep needs remain just as vital to health and well-being for teenagers as when they were younger. It turns out that many teenagers over 15 actually need more sleep than in previous years. Now, however, social pressures conspire against getting the proper amount and quality of sleep.

Teens are not getting the sleep they once did, and many have difficulty falling asleep and frequently wake up at night. This is not normal, and all this is taking a toll. Sleep deprivation is associated with mood changes and behavioral problems, including conduct disorders and inattention.

One study of U.S. high school students found that 13% were chronically sleep-deprived. Other international studies confirm the global nature of this problem. Not getting enough sleep and not sleeping well is not OK.

SOURCES: Healthy Sleep Habits, Happy Child. A step-by-step program for a good night’s sleep, March Weissbluth, MD. 1999. Solve Your Child’s Sleep Problems, Richard Ferber, MD, 1985. Sleeping Through the Night, How Infants, Toddlers and Their Parents Can Get a Good Night’s Sleep, Jodi Mindell, PhD, 1997.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• “What’s Going on in there? How the Brain and Mind Develop in the First Five Years of Life” by Lise Eliot, Ph.D.
  Book explains how the brain develops and evolves. A  technical book but really explains how the brain develops and about setting age appropriate expectations for your child.

• Baby411
  Excellent book for overall general information on all aspects of your baby’s life. Written in a lively and fun manner with real world practical advice.

• Toddler411
  Excellent book for overall general information on all aspects of your toddler’s life. Written in a lively and fun manner with real world practical advice.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

curriculum vitae

Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

• Later to bed = Baby sleeps later in the morning. Sleeping in—it’s wishful thinking for many parents.  Actually, the thought that babies will sleep later if put to bed later is a common myth.  Babies sleep better, longer, and cry less if they are put to bed early in the evening. Babies who go to sleep late in the evening are often “over tired”, even though they seem to have energy. Look for your baby’s “sleep signals” that show when she is tired.  Seize the moment before the “sleepy window” has passed. The first signs of tiredness—eye rubbing, yawning, slowing down—should signal a transition to the bedtime routine. This may occur as early as 6:00 or 7:00 pm for babies. 

• Babies should sleep through the night. Many parents dream of nothing more than getting their baby to sleep through the night.  Most babies have the capacity to make it 8 hours or more without a feeding when they are about 4 months and at least 16 pounds.  If babies at this age and stage are still waking up in the middle of the night, the problem is usually not the waking up…it’s the getting back to sleep. Most babies (and adults) wake up one or more times during the night.  As adults, we usually just roll over and go back to sleep.  Babies typically wake 2 to 4 times a night.  But while some babies cry briefly and then soothe themselves back to sleep, others don’t.  They have not yet learned how to get themselves back to sleep, so they cry out for help. The key is helping your baby learn how to get herself to sleep.  Creating a soothing routine of lullabies, books, and rocking before bedtime is very important.  Then put your baby down in her crib while she’s still awake.  This gives her the chance to learn what it feels like to fall asleep on her own. Offering your baby a “lovey” (stuffed animal or special blanket) is a good trick.  Babies will often comfort themselves with these objects, which helps them fall asleep.  You may also hear your baby singing or talking to herself before drifting off to sleep.  These are all ways babies have of putting themselves to sleep. 

• “Crying It Out” is bad for baby. Crying is a common and (understandable!) response to saying good-bye to a loved parent at bedtime.  However, learning to fall asleep on one’s own is an important skill that you can help your baby learn when she is old enough—at about 4 months. Most experts and research agree that letting a baby or toddler cry as they go to sleep will not have any long-term damaging effects. A child who is well-loved, nurtured, and responded to during the day will not be hurt by fussing a bit before bed in the evening.  And the good news is that the crying at bedtime will probably only go on for a few days before your baby adapts and begins to learn how to put herself to sleep. But that doesn’t mean it’s an easy choice for parents.  Many parenting decisions, and especially this one, involve understanding temperament—not only your baby’s, but your own as well.  If letting your baby cry herself to sleep is too emotionally painful for you, there are other options.  For example, you can go back to check on her every 10 minutes (but without rocking or nursing her).  Or, you can decide on a certain length of crying that you are willing to put up with (say 15 minutes) and if the crying goes beyond that, you will go in to comfort the baby.  Another option, if your partner is able to endure more of the crying, is that he or she takes on the bedtime routine. In any case, it is important for the two of you to be in agreement about your bedtime plan. Finding an approach that works for both your baby and your family is important.

• Babies on solid foods sleep longer. Many parents have heard that starting solids early (before 4-6 months) or adding cereal to their baby’s bottle will help their child sleep through the night. This is a myth. There is no research to support it, and in fact, the American Academy of Pediatrics discourages feeding babies solid foods before four months of age. This is due to their immature digestive systems and their lack of oral-motor skills. Some studies even indicate that early introduction of solids can trigger food allergies. It is normal and expected that babies younger than 4 months will wake during the night.  Beginning at about 4 months, you can start helping your baby learn to sleep though the night.  (See above on how to teach your baby to fall asleep on his own.) Until then, your young infant will be plenty full on a liquid (breastmilk or formula) diet, without using solids.  Make the baby’s last feeding part of his bedtime routine.  And try to put your baby down while he is still awake, but drowsy.  If you have concerns about your child’s weight gain or sleep patterns, talk to your health care provider.

• Never wake a sleeping child.     TRUE or FALSE. Answer: FALSE: you should wake a child to preserve the next sleep time or bedtime. Letting a child sleep too late into the morning can interfere with their morning nap or letting a child sleep to late into the afternoon can impact their bedtime.

• Cutting out naps and/or putting them to bed very late will help them sleep later or better. TRUE OR FALSE. FALSE: Sleep begets sleep. A rested child sleep better and longer than an overtired or chronically sleep deprived child. Lack of sleep actually makes falling asleep more difficult and promotes more frequent night wakings

• My baby wakes up because he’s hungry. Like adults, babies eat for reasons other than hunger. A baby will nurse because it’s the only way he knows how to get back to sleep.

• My baby is a poor sleeper. We inadvertently train our babies to be poor sleepers by not equipping them with the skills they need to fall asleep.

• Rice cereal before bedtime will help my baby sleep longer. Hunger is typically not the cause of sleep problems after 3 to 4 months of age.

• Crying damages a baby’s psyche. I’ve known babies who were raised on attachment parenting principles and those allowed to cry it out. Can I tell them apart by their intellectual, psychological, or emotional states? Absolutely not!

• It’s easier to sleep-train an older baby. The longer a habit is reinforced, the harder it is to break.
• Teething disrupts sleep. This may be true at times, but teething is blamed for way too many sleep problems.
• Poor sleep habits improve eventually. Without their parents’ help, the vast majority of babies will sleep worse, not better, over time. Sleep problems don’t magically disappear. Consider the 2004 Sleep in America Poll, which found that two-thirds of children from infancy to age 10 experience frequent sleep problems.

• Babies will get the sleep they need. If only! Babies resist sleep like similarly charged magnets resist each other. Parents need to insure a baby gets enough sleep.

• There’s no harm in getting up with my baby as long as I’m willing to do it. If you enable unhealthy sleep habits, you run the risk of your child developing long-standing sleep problems that will persist into the preschool years.

• Feeding formula, solids or mixing formula into breast milk will help my young baby sleep through the night. TRUE OR FALSE. FALSE: Sleep has to do with brain maturity and NOT food or calories. Actually over feeding a baby or frequent night feeds can cause more wakings and lead to poorer overall sleep for the child.

• A dream feed at 11pm will help my child sleep through the night. TRUE OR FALSE. FALSE: Brain maturity is what determines when a child sleeps through the night not food. Once a child is over 4 months of age (adjusted for premature babies) they will sleep longer and have more consolidated sleep at night. It’s actually not good to wake or disturb your sleeping baby to feed if they are older than 6 months.

• Babies will learn how to fall asleep on their own, as it’s a natural process. TRUE OR FALSE. FALSE: Although some children do learn to self-sooth more easily and naturally than other babies, for most babies it is a skill that they need to learn.  If parents are taking steps to develop good sleep habits, they can avoid developing poor sleep habits.

• Sleep is Just Rest. Sleep is more than simply a period of rest; it is an essential time for your body to perform routine maintenance, creating long-term memories and repair damage from your day. Sleep brings many health benefits. Getting 7 to 9 hours of sleep each night assures that your body and mind will function well the next day. Make sleep a priority for your health and energy.

• Losing an Hour of Sleep is No Big Deal. If you get less sleep than you need, your ability to do certain cognitive and physical tasks is decreased. If that sleep loss builds over time, it can interfere with the hormones that monitor appetite, changing your mood and increasing your risk of some chronic illnesses. Get 7 to 9 hours every night for good health.

• You Adjust to Sleep Changes Easily. Your body gets on schedule based on your activity and exposure to daylight. When you travel across many time zones or work night shifts, you confuse body’s sense of time, making sleep difficult and inhibiting some necessary sleep functions. For every one- to two-hour time change, it takes your body 1 day to adjust. That means it could take your body 6 to 12 days to adjust to a trip from New York to China.

• Older People Need Less Sleep. Older people need the same amount of sleep as everyone else, 7 to 9 hours per night. There is a cultural belief that as you age, you need less sleep. Unfortunately, because of this myth, many older people do not seek help for their sleep problems. Often, older people sleep less than they need to because of illness. Many of the medications older people may be using interfere with sleep. Talk to your doctor to find out more.

•  Extra Sleep Helps Fatigue. Some people assume that if they feel tired during the day, then they should sleep longer at night. This is not necessarily true. If a person is getting 7 to 9 hours of sleep each night, then he or she should seek another source for their fatigue. Some sleep disorders decrease sleep quality, even though the person is getting enough sleep. Many medical conditions can cause fatigue. If you are sleeping long enough but are still tired, try some exercise and daylight exposure during the day. If that doesn’t help, see your doctor.

• Sleep is Just Rest. Sleep is more than simply a period of rest; it is an essential time for your body to perform routine maintenance, creating long-term memories and repair damage from your day. Sleep brings many health benefits. Getting 7 to 9 hours of sleep each night assures that your body and mind will function well the next day. Make sleep a priority for your health and energy.

• Children With a Sleep Deficit Will be Tired. Children are different from adults. When children are overtired, their adrenaline kicks in and they seem energetic, even hyper. Children with sleep deficits may have behavior and attention problems. So don’t use daytime energy levels to assess your child’s sleep; use the clock. Children need an incredible amount of sleep. Find out how much sleep your child needs and troubleshoot your family’s schedule to make sure this happens.

• Snoring is a normal part of sleep. Snoring during sleep is common, particularly as a person gets older. Evidence is growing that snoring on a regular basis can make you sleepy during the day and more susceptible to diabetes and heart disease. In addition, some studies link frequent snoring to problem behavior and poorer school achievement in children. Loud, frequent snoring can also be a sign of sleep apnea, a serious sleep disorder that should be treated.

• Children who don’t get enough sleep at night will show signs of sleepiness during the day. Unlike adults, children who don’t get enough sleep at night typically become more active than normal during the day. They also show difficulty paying attention and behaving properly. Consequently, they may be misdiagnosed as having attentiondeficit hyperactivity.

• Sleep is a time when your body and brain shut down for rest and relaxation. No evidence shows that any major organ (including the brain) or regulatory system in the body shuts down during sleep. Some physiological processes actually become more active while you sleep. For example, secretion of certain hormones is boosted, and activity of the pathways in the brain needed for learning and memory is heightened.

• Extra sleep at night can cure you of problems with excessive daytime fatigue. Not only is the quantity of sleep important but also the quality of sleep. Some people sleep 8 or 9 hours a night but don’t feel well rested when they wake up because the quality of their sleep is poor. A number of sleep disorders and other medical conditions affect the quality of sleep. Sleeping more won’t alleviate the daytime sleepiness these disorders or conditions cause. However, many of these disorders or conditions can be treated effectively with changes in behavior or with medical therapies.

• Naps are a waste of time. Although naps do not substitute for a good night’s sleep, they can be restorative and help counter some of the impaired performance that results from not getting enough sleep at night. Naps can actually help you learn how to do certain tasks quicker. But avoid taking naps later than 3 p.m., as late naps can interfere with your ability to fall asleep at night. Also, limit your naps to no longer than 1 hour because longer naps will make it harder to wake up and get back in the swing of things. If you take frequent naps during the day, you may have a sleep disorder that should be treated.

• A baby or toddler will sleep through the night when they are ready to. TRUE OR FALSE. FALSE: Some children seem to be naturally better sleepers than others and start sleep through the night on their own at about 12 weeks of age. This can be a result of the child’s personality and parent’s interaction with the child at bedtime. For other children, they need more structure to learn how to fall asleep.  The ability to learn how to fall asleep is a learn skill and is not something we are born knowing how to do.  

• You can sleep train a newborn baby. TRUE OR FALSE False. You cannot nor should you want your 0-4 month old child sleeping through the night. It is natural and normal to have the child waking and feeding frequently, especially during the first three months.  Newborn babies will feed frequently and often during the night. Babies can have 0-2 feed per night from 4 months of age to 9 months of age.

• It will be easy to transition from co-sleeping to having my child sleep in their bed. TRUE OR FALSE. FALSE: Co-sleeping is a successful sleep choice many parents choose. Co-Sleeping or having a family bed is usually a 5-year plan. For some families co-sleeping doesn’t workout or they decide they no longer want to continue it. If you decide to co-sleep and then realize it doesn’t work for you and your family you may have difficulty transition your child from your bed to their bed. Your child has come to learn how to sleep with you and removing that association will cause disruption for your child. So you need to plan how to transition out of co-sleeping if you want to end it before 5 years of age.

• Naps do not need to be managed a child will take one if they are tired. TRUE OR FALSE. FALSE: Naps like all other important aspects of your child’s life need to be managed by the parents. Sleep begets sleep and a well-rested child will sleep better overall. 

•  I don’t need to manage my child’s sleep. I believe in spontenity and letting them go to sleep when they are ready.  True or FALSE. FALSE As parents we need to manage our children’s sleep routine just as you manage when they eat, how much activity and stimulation they get and other vital areas of your child’s life. This doesn’t mean following a ridge schedule but rather making sure your child is getting enough sleep overall  and using bio times to help your child sleep more easily. A well rested children is ready to learn and absorb information about their new world. Sleep is also important to ensure they stay healthy and keep their immune system strong.

• I need to follow a very strict schedule to get my child to sleep. Popular in SE Asia and Australia are methods that follow extremely strict and militant sleep schedules. Often these schedule or so regimented that as the child gets older they become to difficult to follow and stop working. Sleep has natural bio patterns and by understanding how these processes work in your child, you can leverage these bio-times to encourage sleep. Routine is important and does help sleep, but you do not need a ridge strict schedule to achieve good sleep.

• I cannot breast feed my baby before bedtime. You can continue to breast feed or bottle feed your child before bed. The important point to remember is to not breast feed your child to sleep or nurse them to sleep.

Supported  by

CHILDREN SLEEP CLINIC

Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email : judarwanto@gmail.com,

http://sleepclinic.wordpress.com/

Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email : judarwanto@gmail.com

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Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved

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