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Sleep Disorder
A
sleep disorder (somnipathy) is a disorder in the sleep patterns of a person or animal. Some sleep disorders can interfere with mental and emotional function. A test
commonly ordered for some sleep disorders is the polysomnogram.
Current Research
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Common Sleep Disorders
The most common sleep disorders include:
- Bruxism: The sufferer involuntarily grinds his or her teeth while sleeping.
- Delayed sleep phase syndrome (DSPS): A sleep disorder of circadian rhythm, characterized by the inability to wake up and fall asleep at the desired times, but not
by inability to stay asleep.
- Hypopnea syndrome: Abnormally shallow breathing or slow respiratory rate while sleeping.
- Narcolepsy: The condition of falling asleep spontaneously and unwillingly.
- Night terror or Pavor nocturnus or sleep terror disorder: abrupt awakening from sleep with behavior consistent with terror.
- Parasomnias: Include a variety of disruptive sleep-related events.
- Periodic limb movement disorder (PLMD): Involuntary movement of arms and/or legs during sleep. See also Hypnic jerk, which is not a disorder.
- Rapid eye movement behavior disorder (RBD): Acting out violent or dramatic dreams while in REM sleep.
- Restless legs syndrome (RLS): An irresistible urge to move legs while sleeping. Often accompanies PLMD.
- Shift work sleep disorder (SWSD).
- Sleep apnea: The obstruction of the airway during sleep.
- Sleepwalking or somnambulism: Engaging in activities that are normally associated with wakefulness (such as eating or dressing), which may include walking,
without the conscious knowledge of the subject.
- Snoring: Loud breathing patterns while sleeping, sometimes accompanying sleep apnea.
Broad Classifications of Sleep Disorders
- Dysomnias - A broad category of sleep disorders characterized by either hypersomnolence or insomnia. The three major subcategories include intrinsic (i.e., arising
from within the body), extrinsic (secondary to environmental conditions or various pathologic conditions), and disturbances of circadian rhythm.
- Insomnia
- Narcolepsy
- Obstructive sleep apnea
- Restless leg syndrome
- Periodic limb movement disorder
- Hypersomnia
- Recurrent hypersomnia - including Kleine-Levin syndrome
- Posttraumatic hypersomnia
- "Healthy" hypersomnia
- Circadian rhythm sleep disorder
- Parasomnias
- REM sleep behaviour disorder
- Sleep terror
- Sleepwalking (or somnambulism)
- Tooth-grinding
- Bedwetting or sleep enuresis.
- Sudden infant death syndrome (or SIDS)
- Sleep talking (or somniloquy)
- Sleep sex (or sexsomnia)
- Medical or Psychiatric Conditions that may produce sleep disorders
- Sleeping sickness - can be carried by the Tsetse fly
- Snoring - Not a disorder in and of itself, but it can be a symptom of deeper problems.
Common Causes of Sleep Disorders
Changes in life style, such as shift work change (SWC), can contribute to sleep disorders.
Other problems that can affect sleep:
- Back pain
- Chronic osteoarthritis
- Sciatica
- Neck problems
- Environmental noise
- Incontinence
- Babies that wake frequently
- Various drugs - Many drugs can affect the ratio of the various stages of sleep, thus affecting the overall quality of sleep. Poor sleep can lead to accumulation of Sleep
debt.
A sleep diary can be used to help diagnose, and measure improvements in sleep disorders. The Epworth Sleepiness Scale is another useful diagnostic
According to Dr. William Dement, of the Stanford Sleep Center, anyone who snores and has daytime drowsiness should be evaluated for sleep disorders.
Any time back pain or another form of chronic osteoarthritis is present, both the osteoarthritis and the sleep problems should be treated simultaneously, as osteoarthritis can lead to sleep problems and vice
versa.
General Principles of Treatment
Treatments for sleep disorders generally can be grouped into three categories: 1) behavioral/ psychotherapeutic treatments, 2) medications, and 3) other somatic treatments.
None of these general approaches is sufficient for all patients with sleep disorders. Rather, the choice of a specific treatment depends on the patient's diagnosis, medical and
psychiatric history, and preferences, as well as the expertise of the treating clinician. In general, medications and somatic treatments provide more rapid symptomatic relief
from sleep disturbances. On the other hand, some emerging evidence suggests that treatment gains with behavioral treatment of insomnia may be more durable than those
obtained with medications.
Some sleep disorders, such as narcolepsy, are best treated pharmacologically, whereas others, such as chronic and primary insomnia, are more amenable to behavioral
interventions. The management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.
For most sleep disorders, behavioral/psychotherapeutic and pharmacological approaches are not incompatible and can be effectively combined to maximize therapeutic benefits.
(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Sleep_disorders)
Nonarteritic Anterior Ischemic Optic Neuropathy and Presumed Sleep Apnea Syndrome Screened by the Sleep Apnea Scale of the Sleep Disorders
Questionnaire (SA-SDQ)
Authors: Li J, McGwin G Jr, Vaphiades MS, Owsley C
University of Alabama at Birmingham, United States
BACKGROUND: Two recent studies reported over 70% of the patients with nonarteritic anterior ischemic optic
neuropathy (NAION) had sleep apnea syndrome (SAS) diagnosed by
overnight polysomnography. The current study used the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) to evaluate this association. METHODS: A matched
case-control study was conducted among 73 cases of NAION matched on age and gender to 73 controls without a history of NAION. Information regarding demographics, medical
conditions, health behaviors, and SAS was obtained via a telephone questionnaire that included the SA-SDQ. Conditional logistic regression was used to calculate odds ratios (OR)
and the 95% confidence intervals (CI) for the association between NAION and the SA-SDQ. RESULTS: Cases were significantly more likely to report symptoms and characteristics
consistent with SAS than controls (OR 2.62; 95% CI 1.03-6.60) when adjusted for medical and health behavior characteristics. CONCLUSIONS: The results of this study suggest
that patients with SAS are at increased risk of NAION. Additional research in a larger population is needed to confirm the observed results and validate the use of the SA-SDQ in
patients with NAION.
Journal: Br J Ophthalmol. 2007 May 15
Adapted from PubMed; click here to access full journal article.
Sleep and Aging: 2. Management of Sleep Disorders in Older People
Authors: Wolkove N, Elkholy O, Baltzan M, Palayew M
Sleep Clinic, Mount Sinai Hospital Center, Montreal, Que. norluco@yahoo.com
The treatment of sleep-related illness in older patients must be undertaken with an appreciation of the physiologic changes associated with aging.
Insomnia is common among
older people. When it occurs secondary to another medical condition, treatment of the underlying disorder is imperative. Benzodiazepines, although potentially effective, must be
used with care and in conservative doses. Daytime sedation, a common side effect, may limit use of benzodiazepines. Newer non-benzodiazepine drugs appear to be promising.
Rapid eye movement (REM) sleep behavior disorder can be treated with clonazepam, levodopa-carbidopa or newer dopaminergic agents such as pramipexole. Sleep hygiene is
important to patients with
narcolepsy. Excessive daytime sleepiness can be treated with central stimulants; cataplexy may be improved with an antidepressant. Restless legs
syndrome and periodic leg-movement disorder are treated with benzodiazepines or dopaminergic agents such as levodopa-carbidopa and, more recently, newer dopamine
agonists. Treatment of obstructive sleep apnea includes weight reduction and proper sleep positioning (on one's side), but may frequently necessitate the use of a continuous
positive air-pressure (CPAP) device. When used regularly, CPAP machines are very effective in reducing daytime fatigue and the sequel of untreated obstructive sleep apnea.
Journal: CMAJ. 2007 May 8;176(10):1449-54
Adapted from PubMed; click here to access full journal article.
Therapeutic Advances in Narcolepsy
Authors: Thorpy M
Sleep-Wake Disorders Center, Montefiore Medical Center and Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY 10467, USA
Narcolepsy treatment has changed dramatically over the last century. For the treatment of sleepiness in
narcolepsy, we have progressed from the early use of caffeine. We have
available a variety of different stimulants, and a wake-promoting agent, modafinil, which is widely regarded as the first-line medication for
narcolepsy. Cataplexy is managed by
medications whereas behavioral treatment, such as avoidance of emotion, was the only treatment available in the past. Following the widespread use of antidepressant medications
for cataplexy, we now have sodium oxybate, which works by an unknown mechanism but is the only Food and Drug Administration (FDA)-approved medication for cataplexy. We also
recognize that other sleep disorders can occur in
narcolepsy, such as obstructive sleep apnea syndrome or rapid eye movement sleep behavior disorder, and new treatments allow
these comorbid conditions to be effectively treated. However, although we cannot cure narcolepsy, the current treatments for excessive sleepiness and cataplexy can be effective for
many patients. We are improving the quality of life for our patients without producing clinically significant adverse effects. We need new therapeutic advances and several medications
that work, though different mechanisms are likely to be available in the near future.
Journal: Sleep Med. 2007 Jun;8(4):427-40. Epub 2007 May 1
Adapted from PubMed; click here to access full journal article.
Neuroimaging in Sleep Medicine
Authors: Dang-Vu TT, Desseilles M, Petit D, Mazza S, Montplaisir J, Maquet P
Cyclotron Research Centre B30, University of Liege - Sart Tilman, 4000 Liege, Belgium; Neurology Department, Centre Hospitalier Universitaire (CHU), Liege, Belgium.
The development of neuroimaging techniques has made possible the characterization of cerebral function throughout the sleep-wake cycle in normal human subjects. Indeed,
human brain activity during sleep is segregated within specific cortical and subcortical areas in relation to the sleep stage, sleep physiological events and previous waking activity.
This approach has allowed sleep physiological theories developed from animal data to be confirmed, but has also introduced original concepts about the neurobiological
mechanisms of sleep, dreams and memory in humans. In contrast, at present, few neuroimaging studies have been dedicated to human sleep disorders. The available work has
brought interesting data that describe some aspects of the pathophysiology and neural consequences of disorders such as
insomnia, sleep apnea and
narcolepsy. However, the
interpretation of many of these results is restricted by limited sample size and spatial/temporal resolution of the employed technique. The use of neuroimaging in sleep medicine is
actually restrained by concerns resulting from the technical experimental settings and the characteristics of the diseases. Nevertheless, we predict that future studies, conducted with
state of the art techniques on larger numbers of patients, will be able to address these issues and contribute significantly to the understanding of the neural basis of sleep
pathologies. This may finally offer the opportunity to use neuroimaging, in addition to the clinical and electrophysiological assessments, as a helpful tool in the diagnosis,
classification, treatment and monitoring of sleep disorders in humans.
Journal: Sleep Med. 2007 Jun;8(4):349-72. Epub 2007 Apr 30
Adapted from PubMed; click here to access full journal article.
The Impact of Continuous Positive Airway Pressure on Blood Pressure in Patients with Obstructive Sleep Apnea Syndrome: Evidence from a Meta-Analysis of
Placebo-Controlled Randomized Trials
Authors: Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, Velkeniers B
Center for Outcomes Research and Laboratory for Experimental Surgery, Endocrinology, Pharmacology, and General Internal Medicine, Universitair Ziekenhuis Brussel, Vrije
Universiteit Brussel, Brussels, Belgium. patrick.haentjens@uzbrussel.be
BACKGROUND: Continuous positive airway pressure (CPAP) in patients with obstructive sleep apnea syndrome (OSAS) might lower blood pressure, but evidence from clinical
studies is inconsistent, perhaps as a result of small sample size or heterogeneity in study design. This study aimed to assess whether CPAP reduces ambulatory blood pressure
in patients with OSAS, to quantify the effect size with precision, and to identify trial characteristics associated with the greatest blood pressure reductions. METHODS: We identified
randomized controlled trials of CPAP vs. placebo in patients with OSAS specifically reporting 24-hour ambulatory mean blood pressure (MBP). RESULTS: We included a total of 572
patients from 12 randomized controlled trials. According to a random-effects model, the pooled estimate of the effect of the CPAP intervention was a net decrease of 1.69 mm Hg in
24-hour MBP (95% confidence interval, -2.69 to -0.69). Statistical heterogeneity was moderate (I(2) = 41%). Predefined metaregression analyses estimated that 24-hour MBP would
decrease by 0.89 mm Hg per 10-point increase in apnea-hypopnea index at entry (P = .006), by 0.74 mm Hg for each increase of 10 arousal events per hour slept (P = .008), and by
1.39 mm Hg for each 1-hour increase in effective nightly use of the CPAP device (P = .01). CONCLUSIONS: Among patients with OSAS, CPAP reduces 24-hour ambulatory MBP, with
greater treatment-related reductions in ambulatory MBP among patients with a more severe degree of OSAS and a better effective nightly use of the CPAP device. These reductions
in blood pressure are likely to contribute to a better prognosis in terms of adverse cardiovascular events.
Journal: Arch Intern Med. 2007 Apr 23;167(8):757-64
Adapted from PubMed; click here to access full journal article.
Inflammation, Sleep, Obesity and Cardiovascular Disease
Authors: Miller MA, Cappuccio FP
Clinical Sciences Research Institute, Warwick Medical School, University of Warwick, Coventry, CV2 2DX, UK. Michelle.Miller@warwick.ac.uk
Evidence is emerging that disturbances in sleep and sleep disorders play a role in the morbidity of chronic conditions. However, the relationship between sleep processes, disease
development, disease progression and disease management is often unclear or understudied. Numerous common medical conditions can have an affect on sleep. For example,
diabetes or inflammatory conditions such as arthritis can lead to poor sleep quality and induce symptoms of excessive daytime sleepiness and fatigue. It has also been suggested
that poor sleep may lead to the development of cardiovascular disease for which an underlying inflammatory component has been proposed. It is therefore important that the
development and progression of such disease states are studied to determine whether the sleep effect merely reflects disease progression or whether it may be in some way
causally related. Sleep loss can also have consequences on safety related behaviors both for the individuals and for the society, for example the increased risk of accidents when
driving while drowsy. Sleep is a complex phenotype and as such it is possible that there are numerous genes which may each have a number of effects that control an individual's
sleep pattern. This review examines the interaction between sleep (both quantity and quality) and parameters of cardiovascular risk. We also explore the hypothesis that inflammation
plays an essential role in cardiovascular disease and that a lack of sleep may play a key role in this inflammatory process. AIM: To review current evidence regarding the endocrine,
metabolic, cardiovascular and immune functions and their interactions with regard to sleep, given the current evidence that sleep disturbances may affect each of these areas.
Journal: Curr Vasc Pharmacol. 2007 Apr;5(2):93-102
Adapted from PubMed; click here to access full journal article.
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