Delayed Sleep Phase Syndrome Clinical Trials, Diagnosis, and Treatment

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Delayed Sleep Phase Syndrome

Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or as delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of sleep timing. People with DSPS tend to fall asleep well after midnight and also have difficulty waking up in the morning.

Often, people with the disorder report that they cannot sleep until early morning, but they fall asleep at about the same time every "night", no matter what time they go to bed. Unless they have another sleep disorder such as sleep apnea in addition to DSPS, patients can sleep well, and have a normal need for sleep. Therefore, they find it very difficult to wake up in time for a typical school or work day if they have only slept for a few hours. However, they sleep soundly, wake up spontaneously, and do not feel sleepy again until their next "night" if they are allowed to follow their own late schedule, e.g. sleeping from 4 a.m. to noon.

The syndrome usually develops in early childhood or adolescence, and sometimes disappears in adolescence or early adulthood. It can be to a greater or lesser degree treatable, but cannot be cured.

DSPS was first formally described in 1981 by Dr. Elliot D. Weitzman and others at Montefiore Medical Center. It is responsible for 7 -10% of cases of chronic insomnia. However, as few doctors are aware of its existence, it often goes untreated or is treated inappropriately. DSPS is often frequently misdiagnosed as primary insomnia or as a psychiatric condition.

Current Research

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Definition

According to the International Classification of Sleep Disorders (ICSD), the key characteristics of DSPS are:

Sleep-onset and wake times that are intractably later than desired
Actual sleep-onset times at nearly the same daily clock hour
Little or no reported difficulty in maintaining sleep once sleep has begun
Extreme difficulty awakening at the desired time in the morning
A relatively severe to absolute inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake times.

The following features of DSPS distinguish it from other sleep disorders:

People with DSPS have at least a normal - and often much greater than normal - ability to sleep during the morning, and sometimes in the afternoon as well. In contrast, those with chronic insomnia do not find it much easier to sleep during the morning than at night.
People with DSPS fall asleep at more or less the same time every night, and sleep comes quite rapidly if the person goes to bed near the time he or she usually falls asleep. Young children with DSPS resist going to bed before they are sleepy, but the bedtime struggles disappear if they are allowed to stay up until the time they usually fall asleep.
DSPS patients can sleep well and regularly when they can follow their own sleep schedule, e.g. on weekends and during vacations.
DSPS is a chronic condition. A diagnosis of DSPS is generally not given unless symptoms have been present for at least a month.

Attempting to force oneself through 9–5 life with DSPS has been compared to constantly living with 6 hours of jet lag. Often, sufferers manage only a few hours sleep a night during the working week, then compensate by sleeping until the afternoon on weekends. Sleeping in on weekends, and/or taking long naps during the day, gives people with the disorder relief from daytime sleepiness but also perpetuates the late sleep phase.

People with DSPS tend to be extreme night owls. They feel most alert and say they function best and are most creative in the evening and at night. DSPS patients cannot simply force themselves to sleep early. They may toss and turn for hours in bed, and sometimes not sleep at all, before reporting to work or school.

By the time DSPS patients seek medical help, they usually have tried many times to change their sleeping schedule. Failed tactics to sleep at earlier times may include relaxation techniques, early bedtimes, hypnosis, alcohol, sleeping pills, dull reading, and home remedies. DSPS patients who have tried using sedatives at night often report that the medication makes them feel tired or relaxed, but that it fails to induce sleep. They often have asked family members to help wake them in the morning, or they have used several alarm clocks. As the syndrome is most common in adolescence, it is often the patient's parents who initiate seeking help, after great difficulty waking their child or teenager in time for school.

As of May 2007, the new International Classification of Sleep Disorders has changed the name from Delayed Sleep Phase Syndrome to Delayed Sleep Phase Disorder.

Prevalence

Using the strict ICSD diagnostic criteria, a random study in 1993 of 10,000 adults in Norway estimated the prevalence of DSPS at 0.17%. A similar study with 1525 adults in Japan estimated its prevalence at 0.13%. Other studies have indicated that the prevalence of DSPS among adolescents is as high as 7%.

Physiology

DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.

People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.

People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.

People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. Sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.

In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene. There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.

There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.

Diagnosis

DSPS is diagnosed by a clinical interview, actigraphic monitoring and/or a sleep log kept by the patient for at least three weeks.

DSPS is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPS is often confused with psychophysiological insomnia, depression, psychiatric disorders such as schizophrenia, ADHD or ADD, other sleep disorders, or willful behaviour such as school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders.

Impact on Patients

Lack of public awareness of the disorder contributes to the difficulties experienced by DSPS patients, who are commonly stereotyped as undisciplined or lazy. Parents may be chastised for not giving their children acceptable sleep patterns, and schools rarely tolerate chronically late, absent, or sleepy students and fail to see them as having a chronic illness.

By the time DSPS sufferers receive an accurate diagnosis, they often have been misdiagnosed or labelled as lazy and incompetent workers or students for years. Misdiagnosis of circadian rhythm sleep disorder as psychiatric conditions causes considerable distress to patients and their families, and leads to some patients being inappropriately prescribed psychoactive drugs. For many patients, diagnosis of DSPS is itself a life-changing breakthrough.

Treatment

Treatment for DSPS is specific. It is different from treatment of insomnia, and recognizes the patient's ability to sleep well while addressing the timing problem.

Before starting DSPS treatment, patients are often asked to spend a week sleeping regularly, without napping, at the times when the patient is most comfortable. It is important for patients to start treatment well-rested.

Treatments that have been reported in the medical literature include:

Light therapy (phototherapy) with a full spectrum lamp or portable visor, usually 10000 lux for 30-90 minutes in the morning. Sunlight can also be used. Light therapy generally requires adding some extra time to the patient's morning routine. It takes from a few days to two weeks to take effect, with occasional use thereafter to help maintain the schedule. Avoidance of bright light in the evening may also help.
Chronotherapy, which resets the circadian clock by manipulating bedtimes. It can be one of two types. The most common consists of going to bed two or more hours later each day for several days until the desired bedtime is reached. A modified chronotherapy (Thorpy, 1988) is called controlled sleep deprivation with phase advance, SDPA. One stays awake one whole night and day, then goes to bed 90 minutes earlier than usual and maintains the new bedtime for a week. This process is repeated weekly until the desired bedtime is reached.
A small (~1mg) melatonin supplement taken an hour or so before bedtime may be helpful in establishing an earlier pattern, especially in conjunction with bright light therapy at the time of spontaneous awakening. However, some suggest taking melatonin at sunset to mimic natural endogenous secretion of melatonin. Rather than taking melatonin as a sedative, it is used in this way as a natural way to reset the circadian clock. Side effects of melatonin may include disturbance of sleep, nightmares, daytime sleepiness and depression. The long-term effects of melatonin administration have not been examined and production is unregulated. In some countries the hormone is available only by prescription or not at all. In the United States and Canada, melatonin is freely available as a dietary supplement.
Cannabis has been successfully used as a sleeping aid to combat DSPS. Sleep onset is affected by the two primary cannabinoids, Δ9-Tetrahydrocannabinol (THC) dramatically increases melatonin production and Cannabidiol (CBD) has been shown to be effective in helping insomniacs sleep. Heavy cannabis use can lead to decreased levels of REM sleep and increased levels of slow-wave sleep along with reduced mental function the next morning however this is heavily dependent on dose, 5mg doses of THC and CBD have been shown not to have these effects. Anecdotal evidence suggests that the Indica strain is particularly effective.
Some claim that large doses of vitamin B12 help normalize the onset of sleepiness, but little is known of the effectiveness of the treatment.
A treatment option which shows promise is Ramelteon, a recently-approved drug which in some ways acts as melatonin does. Production of ramelteon is as regulated as any other prescription medicine, so it avoids any possible problem of variable purity with melatonin supplements.
Modafinil is approved in the USA for treatment of Shift-work sleep disorder, which shares some characteristics with DSPS, and a number of clinicians are prescribing it for DSPS patients. However, modafinil does not deal with underlying causes of DSPS, it merely improves sleep deprived patient's quality of life. Taking modafinil less than 12 hours before the desired sleep onset time will actually exacerbate the symptoms by pushing back the sleep/wake cycle.
There has been one documented case in which a person with DSPS was successfully treated with trazodone.

Once the patient has established an earlier sleep schedule, following highly regular sleep/wake times and practicing good sleep hygiene are essential. DSPS patients are counselled to not go to bed if they are not sleepy, as doing so generally does not result in earlier sleep times. They are also advised to avoid alcohol and caffeine before bedtime.

With treatment, some people with DSPS can sleep and function well with the early sleep schedule. Stimulant drugs (including caffeine) to keep the person awake during the day may not be necessary. A chief difficulty of treating DSPS is in maintaining an earlier schedule after it has been established. Inevitable events of normal life, such as staying up late for a celebration or having to stay in bed with an illness, tend to reset the person's sleeping schedule to late times again.

Adaptation to Late Sleeping Times

Long-term success rates of treatment have not been evaluated. However, experienced clinicians acknowledge that DSPS is extremely difficult to treat.

Working the evening or night shift, or working at home, make DSPS less of an obstacle for some. Many of these people do not think of describing their pattern as a "disorder." Some DSPS individuals nap, even taking four hours of sleep a day and four at night. Some DSPS-friendly careers include security work, work in theater, the entertainment industry, the media, work in hospitality such as restaurants, hotels, bars, freelance writing, call center work, nursing, and taxi or truck driving.

Some people with the disorder are unable to adapt to earlier sleeping times, even after many years of treatment. Sleep researchers have proposed that the existence of untreatable cases of DSPS be formally recognized as a "sleep-wake schedule disorder disability".

"Patients suffering from SWSD disability should be encouraged to accept the fact that they suffer from a permanent disability, and that their quality of life can only be improved if they are willing to undergo rehabilitation. It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation"

Rehabilitation for DSPS patients includes acceptance of the condition, and choosing a career that allows late sleeping times. In a few schools and universities, students with DSPS have been able to arrange to take exams at times when their concentration is good.

DSPS and Depression

In the DSPS cases reported in the literature, about half of the patients have suffered from clinical depression or other psychological problems. The relationship between DSPS and depression is unclear. The fact that half of DSPS patients are not depressed indicates that DSPS is not merely a symptom of depression. Even in depressed patients, treatment methods such as chronotherapy can be effective without directly treating the depression.

According to the ICSD, "Although some degree of psychopathology is present in about half of adult patients with DSPS, there appears to be no particular psychiatric diagnostic category into which these patients fall. Psychopathology is not particularly more common in DSPS patients" compared with others complaining of "insomnia".

It is conceivable that DSPS often has a major role in causing depression, because it can be such a stressful and misunderstood disorder. A direct neurochemical relationship between sleep mechanisms and depression is another possibility.

DSPS patients who also suffer from depression should seek treatment for both problems. There is some evidence that effectively treating DSPS can improve the patient's mood and make antidepressants more effective. In addition, treatment for depression can make patients more able to successfully follow DSPS treatments.

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Delayed_Sleep_Phase_Syndrome)

Findings From Current Research

A Prospective Study of Delayed Sleep Phase Syndrome in Patients with Severe Resistant Obsessive-Compulsive Disorder

Authors: Turner J, Drummond LM, Mukhopadhyay S, Ghodse H, White S, Pillay A, Fineberg NA.

Behavioural Cognitive Psychotherapy Unit, Springfield Hospital, London SW17 7DJ, UK.

There have been relatively few studies examining sleep in patients with obsessive-compulsive disorder (OCD) and these have produced contradictory findings. A recent retrospective study identified a possible association between OCD and a circadian rhythm sleep disorders known as delayed sleep phase syndrome (DSPS). Patients with this pattern of sleeping go to bed and get up much later than normal. They are unable to shift their sleep to an earlier time and, as a result, suffer considerable disruption to social and occupational functioning. In this study, we examined the sleep of patients with OCD prospectively. We aimed to establish the frequency of DSPS in this population and any associated clinical or demographic factors which might be implicated in its aetiology.

Journal: World Psychiatry. 2007 Jun;6(2):44-7.
Adapted from PubMed; click here to access full journal article.

Practice Parameters for the Use of Actigraphy in the Assessment of Sleep and Sleep Disorders: An Update for 2007

Authors: Morgenthaler T, Alessi C, Friedman L, Owens J, Kapur V, Boehlecke B, Brown T, Chesson A Jr, Coleman J, Lee-Chiong T, Pancer J, Swick TJ; Standards of Practice Committee; American Academy of Sleep Medicine.

Mayo Clinic, Rochester MN, USA.

BACKGROUND: Actigraphy is increasingly used in sleep research and the clinical care of patients with sleep and circadian rhythm abnormalities. The following practice parameters update the previous practice parameters published in 2003 for the use of actigraphy in the study of sleep and circadian rhythms. METHODS: Based upon a systematic grading of evidence, members of the Standards of Practice Committee, including those with expertise in the use of actigraphy, developed these practice parameters as a guide to the appropriate use of actigraphy, both as a diagnostic tool in the evaluation of sleep disorders and as an outcome measure of treatment efficacy in clinical settings with appropriate patient populations. RECOMMENDATIONS: Actigraphy provides an acceptably accurate estimate of sleep patterns in normal, healthy adult populations and inpatients suspected of certain sleep disorders. More specifically, actigraphy is indicated to assist in the evaluation of patients with advanced sleep phase syndrome (ASPS), delayed sleep phase syndrome (DSPS), and shift work disorder. Additionally, there is some evidence to support the use of actigraphy in the evaluation of patients suspected of jet lag disorder and non-24hr sleep/wake syndrome (including that associated with blindness). When polysomnography is not available, actigraphy is indicated to estimate total sleep time in patients with obstructive sleep apnea. In patients with insomnia and hypersomnia, there is evidence to support the use of actigraphy in the characterization of circadian rhythms and sleep patterns/disturbances. In assessing response to therapy, actigraphy has proven useful as an outcome measure in patients with circadian rhythm sleep disorders and insomnia. In older adults (including older nursing home residents), in whom traditional sleep monitoring can be difficult, actigraphy is indicated for characterizing sleep and circadian patterns and to document treatment responses. Similarly, in normal infants and children, as well as special pediatric populations, actigraphy has proven useful for delineating sleep patterns and documenting treatment responses. CONCLUSIONS: Recent research utilizing actigraphy in the assessment and management of sleep disorders has allowed the development of evidence-based recommendations for the use of actigraphy in the clinical setting. Additional research is warranted to further refine and broaden its clinical value.

Journal: Sleep. 2007 Apr 1;30(4):519-29.
Adapted from PubMed; click here to access full journal article.

A Clinical Approach to Circadian Rhythm Sleep Disorders

Authors: Barion A, Zee PC.

Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

Circadian rhythm sleep disorders are characterized by complaints of insomnia and excessive sleepiness that are primarily due to alterations in the internal circadian timing system or a misalignment between the timing of sleep and the 24-h social and physical environment. In addition to physiological and environmental factors, maladaptive behaviors often play an important role in the development of many of the circadian rhythm sleep disorders. This review will focus on the clinical approach to the diagnosis and management of the various circadian rhythm sleep disorders, including delayed sleep phase disorder, advanced sleep phase disorder, non-entrained type, irregular sleep-wake rhythm, shift work sleep disorder and jet lag disorder. Diagnostic tools such as sleep diaries and wrist activity monitoring are often useful in confirming the diagnosis. Because behavioral and environmental factors often are involved in the development of these conditions, a multimodal approach is usually necessary. Interventions include sleep hygiene education, timed exposure to bright light as well as avoidance of bright light at the wrong time of the day and pharmacologic approaches, such as melatonin. However, it should be noted that the use of melatonin is not an FDA-approved indication for the treatment of circadian rhythm sleep disorders.

Journal: Sleep Med. 2007 Sep;8(6):566-77. Epub 2007 Mar 28.
Adapted from PubMed; click here to access full journal article.

Attention Bias for Sleep-Related Stimuli in Primary Insomnia and Delayed Sleep Phase Syndrome Using the Dot-Probe Task

Authors: MacMahon KM, Broomfield NM, Espie CA.

University of Glasgow Sleep Research Laboratory, Section of Psychological Medicine, Sackler Institute of Psychobiological Research, Southern General Hospital, Glasgow, Scotland, UK.

STUDY OBJECTIVES: Cognitive models of primary insomnia (PI) suggest attention bias as a maintaining process. This study used a hallmark measure of attention bias, the dot-probe task, to determine whether attention bias to sleep-related stimuli is present in individuals with PI. Control groups of good sleepers (GS) and individuals with delayed sleep phase syndrome (DSPS), a sleep disorder with no presumed cognitive pathway and, hence, no predicted association with attention bias, were included. DESIGN: A between-groups (PI, DSPS, GS) design was employed. Participants completed a dot-probe task with stimuli comprising sleep-related and neutral words, balanced for length and frequency of usage. It was predicted a priori that PI would show greater attention bias to sleep stimuli compared with GS and DSPS groups. No difference between GS and DSPS was predicted. PARTICIPANTS: Sixty-three individuals completed the study (PI = 21; DSPS = 22; GS = 20), with those in PI and DSPS classified by International Classification of Sleep Disorders criteria according to self-report sleep diaries and actigraphy. GS scored < 5 on the Pittsburgh Sleep Quality Index, reported being good sleepers, and met no criteria for a current or previous sleep disorders. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: As predicted, PI showed increased vigilance for sleep-related stimuli relative to GS and DSPS. No differences between GS and those with DSPS were found. The PI group showed shorter response latencies relative to the GS and DSPS groups. CONCLUSIONS: Results support an association between attention bias and PI. Further work must determine whether or not attention bias is a causal factor. Speeded responses in the PI group suggest heightened arousal, indicating that physiologic factors may play a related role.

Journal: Sleep. 2006 Nov 1;29(11):1420-7.
Adapted from PubMed; click here to access full journal article.

Circadian Phase in Delayed Sleep Phase Syndrome: Predictors and Temporal Stability Across Multiple Assessments

Authors: Wyatt JK, Stepanski EJ, Kirkby J.

Sleep Disorders Center, Rush University Medical Center, 1653 West Congress Parkway, Chicago, IL 60612-3833, USA. jwyatt@rush.edu

STUDY OBJECTIVES: To assess temporal stability across multiple assessments and predictors of circadian phase in participants with delayed sleep phase syndrome (DSPS), relative to normal-sleeping matched controls. DESIGN: Circadian phase was assessed by salivary dim light melatonin onset (DLMO) during 3 laboratory visits, separated by at least 5 days--2 scheduled at the end of the week (Friday) and 1 scheduled at the end of the weekend (Sunday). PATIENTS: Eight young volunteers who met International Classification of Sleep Disorders-Revised criteria for DSPS, and 8 age- and sex-matched controls (age range 19-27 years old). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: As expected, salivary DLMO occurred significantly later in patients with DSPS than in controls (F 10.561, p = .006). However, circadian phase did not change significantly across the 3 DLMO assessments in either group. Estimations of circadian phase were not significantly different in the assessments conducted on weekdays versus weekends. Predictors of circadian phase included time of morning light exposure (R2 = 0.777; p < .001), recent wake time (R2 = 0.701, p < .001), and self-reported chronotype (R2 = 0.320, p = .016). DLMO preceded wake time in both groups by approximately 10.75 hours. CONCLUSIONS: Across serial laboratory assessments on an ad lib sleep schedule, patients with DSPS appeared more similar to than different from normal-sleeping control subjects, except for a stable delay in circadian phase.

Journal: Sleep. 2006 Aug 1;29(8):1075-80.
Adapted from PubMed; click here to access full journal article.

Phase-Dependent Treatment of Delayed Sleep Phase Syndrome with Melatonin

Authors: Mundey K, Benloucif S, Harsanyi K, Dubocovich ML, Zee PC.

Department of Neurology, Northwestern University Feinberg School of Medicine, Evanston, IL, USA.

STUDY OBJECTIVE: Delayed sleep phase syndrome (DSPS) is a circadian-rhythm sleep disorder characterized by abnormally late sleep and wake times. Melatonin, taken in the evening, advances sleep and circadian phase in patients with DSPS. However, little is known about the most effective dose or time of administration. In the present study, we tested the effectiveness of melatonin to advance the timing of sleep and circadian phase in individuals with DSPS. DESIGN: Following baseline assessment of sleep and circadian phase, subjects were randomly assigned to 1 of 3 treatment groups. The administration of melatonin (0.3 or 3.0 mg) or placebo was double-blinded. SETTING: All procedures were conducted on an outpatient basis. PARTICIPANTS: Thirteen subjects with DSPS, recruited via flyers, advertisements, and referrals from the Sleep Clinic, completed this study. INTERVENTIONS: Melatonin (0.3 or 3.0 mg) or placebo was administered between 1.5 and 6.5 hours prior to dim light melatonin onset for a 4-week period. MEASUREMENTS AND RESULTS: Both doses of melatonin advanced the circadian phase of endogenous melatonin. The magnitude of phase advance in dim-light melatonin onset correlated strongly with the time of melatonin administration, with earlier times being more effective (r2 = 0.94, P < .0001). Similar, though weaker, relationships were obtained between the timing of melatonin administration and changes in sleep time. CONCLUSIONS: These results indicate that melatonin advances the circadian clock and sleep in patients with DSPS in a phase-dependent manner. This is the first study that reports a relationship between timing of melatonin administration and phase changes in patients with DSPS.

Journal: Sleep. 2005 Oct 1;28(10):1271-8.
Adapted from PubMed; click here to access full journal article.

Reevaluating Spells Initially Identified as Cataplexy

Authors: Krahn LE.

Mayo Clinic in Scottsdale AZ, Mayo Clinic College of Medicine, 13400 East Shea Boulevard, Scottsdale, AZ 85234, USA. krahn.lois@mayo.edu

BACKGROUND AND PURPOSE: Cataplexy, transient episodes of bilateral muscle weakness with areflexia provoked by emotions, is a state highly specific to narcolepsy. Cataplexy is diagnosed based on clinical interview. Two screening tools have been developed recently but their usefulness has been limited because of length or current lack of psychometric data. Used effectively even these screening tests require the interpreting physician to have an understanding of the typical features of cataplexy. Most physicians encounter patients with cataplexy fairly infrequently, making it difficult to gain proficiency in detecting cataplexy based on clinical interview alone. Relatively little attention has been given to the differential diagnosis of cataplexy, which increases the likelihood of unnecessary sleep testing or false positive diagnosis. PATIENTS AND METHODS: This case series describes six cases where cataplexy was initially diagnosed. In all cases the weakness spells were eventually not attributed to cataplexy. The presentation and characteristics of these cases will be presented as a means to discuss the differential diagnosis of cataplexy. RESULTS: These cases represent a diverse set of medical disorders including bradycardia, migraine, delayed sleep phase syndrome, conversion disorder, malingering and a chronic psychotic disorder. CONCLUSIONS: A more in-depth understanding of the classic features of cataplexy should improve recognition of this fascinating state. Improved cataplexy recognition will enhance the appropriate usage of sleep tests and eventually increase the timeliness and accuracy of the diagnosis of narcolepsy with cataplexy.

Journal: Sleep Med. 2005 Nov;6(6):537-42. Epub 2005 Jul 5.
Adapted from PubMed; click here to access full journal article.

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