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PubMed1988

Narcolepsy: a review of a common, life-long sleep disorder.

Narcolepsy is a severe debilitating chronic life-long sleep disorder that can be ameliorated but not cured. In the United States, its prevalence is at least 1 in 1000 making it more common than multiple sclerosis or Parkinson's disease. Its symptoms lead to severe lifestyle consequences, with profound impact on the affected persons, their interpersonal relationships, job, school experiences, and family life. Despite this, little has appeared in the nursing literature about the disorder. The most characteristic symptoms include uncontrollable excess daytime sleepiness, cataplexy (bilateral voluntary muscle weakness), sleep paralysis, hypnagogic hallucinations and disturbed night-time sleep. Characteristics of normal sleep are reviewed and compared with disturbances seen in narcolepsy. The aetiology, assessment, diagnosis, pharmacologic therapy, non-pharmacologic therapy and psychosocial issues are discussed along with needed research directions.

Achievement↗
PubMed2002

Benefits and risks of pharmacotherapy for narcolepsy.

Narcolepsy is a life-long central nervous system (CNS) syndrome characterised by excessive sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations and disturbed night-time sleep. Unsuccessfully treated narcolepsy confers increased risks on patients and on society due to the patient's increased chance of becoming involved in vehicle crashes and workplace mishaps. The syndrome may be diagnosed by a clinical history positive for cataplexy and excessive daytime sleepiness and negative for other more common sleep disorders such as sleep apnoea and sleep deprivation. Night-time polysomnography and multiple sleep latency testing are helpful in differentiating narcolepsy from other sleep problems. Recent data from canine, murine, and human forms of narcolepsy indicate that genetically or developmentally mediated deficits in the hypocretin neurotransmitter system may cause some, but not all, forms of narcolepsy. Pharmacotherapy for narcolepsy is required to control symptoms and involves the use of CNS stimulants or modafinil to control sleepiness and antidepressant medications or sodium oxybate to control cataplexy. Modafinil and sodium oxybate have been developed and approved specifically for the indication of narcolepsy based on large, double-blind, placebo-controlled, parallel group efficacy and safety studies. The efficacy of drugs in the treatment of narcolepsy is variable from patient to patient and usually associated with adverse effects that can limit patient compliance and, therefore, symptom control. Nevertheless, the benefits of pharmacotherapy are judged to outweigh the risks to the patient. The favourable benefit-risk ratio of pharmacotherapy is greater if one considers the reduced risk to society of vehicle crashes and workplace mishaps that might be precipitated by attentional lapses or sleep attacks in the untreated or under-treated patient with narcolepsy.

Animals↗
PubMed1976

Narcolepsy. Diagnosis and treatment.

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.

Adolescent↗
PubMed2005

Sleep and psychiatry.

Psychiatric disorders constitute 15.4% of the disease burden in established market economies. Many psychiatric disorders are associated with sleep disturbances, and the relationship is often bidirectional. This paper reviews the prevalence of various psychiatric disorders, their clinical presentation, and their association with sleep disorders. Among the psychiatric disorders reviewed are affective disorders, psychosis, anxiety disorders (including posttraumatic stress disorder), substance abuse disorders, eating disorders, and attention deficit/hyperactivity disorders. The spectrum of associated sleep disorders includes insomnia, hypersomnia, nocturnal panic, sleep paralysis, hypnagogic hallucinations, restless legs/periodic limb movements of sleep, obstructive sleep apnea, and parasomnias. The effects on sleep of various psychotropic medications utilized to treat the above psychiatric disorders are summarized.

Humans↗
PubMed1977

The effects of gamma-hydroxybutyrate on sleep.

Sodium gamma-hydroxybutyrate (GHB) is a remarkably safe and nontoxic hypnotic agent which is reported to be free of addicting properties. It is also a normal metabolite of the mammalian nervous system. We examined its effects on the sleep-EEG of eight patients with histories of impaired sleep, as a prelude to a more detailed study of its clinical potential. Sleep induced with GHB was indistinguishable subjectively from natural sleep as well as by behavioral and electroencephalographic criteria. Unlike most synthetic hypnotics, GHB increased delta sleep and did not suppress REM sleep. It shortened the REM sleep latency and shifted REM sleep into the first third of the night. On one occasion it induced a sleep onset REM period which was experienced as an attack of sleep paralysis. Withdrawal was simple; there was no REM sleep rebound and sleep patterns immediately returned to their pre-drug form. Its major clinical drawback was its short duration of action: its hypnotic effect lasting only 2 to 3 hr. We suggest that GHB may serve as the prototype for a new class of hypnotic compounds derived from natural sources and capable of activating the neurological mechanisms of normal human sleep.

Adult↗
PubMed1998

Narcolepsy in prepubertal children.

Narcolepsy was diagnosed in 51 children (29 boys). The age range was 2.1 to 11.8 years (mean, 7.9 +/- 3.1 years). A mean of three referrals was made before narcolepsy was considered. In 10 children, cataplexy was the presenting symptom. Thirty-eight children acknowledged sleep paralysis and 30 acknowledged hypnagogic hallucinations. All children had sleep studies; 31 exhibited rapid eye movement at sleep onset. The mean sleep latency was 1.5 minutes +/- 39 seconds on the Multiple Sleep Latency Test. All children had at least two sleep-onset rapid eye movement sleep episodes in this test. Forty-six children were HLA class II-positive for DQw6, and 45 were also positive for DRw15. Thirty (65%) families refused referrals to support and counseling groups. Teachers often refused to acknowledge a medical problem. During follow-up, all children presented at least once with depressive symptoms in reaction to their syndrome. Narcolepsy should be considered when evaluating children with behavioral and depressive symptoms.

Attitude to Health↗
PubMed1998

Novel chromosomal abberation in a patient with a unique sleep disorder.

A 45 year old woman presenting with periodic hypersomnia for 17 years is reported on. She would sleep for three weeks followed by the same period awake. Polysomnography in the somnolent period disclosed an excess of total sleeping time with remarkably increased stage 1, 3/4, and REM sleep, without cataplexy or sleep paralysis. HLA typing was incompatible with narcolepsy or REM sleep behavioural disorder. Her chromosomes showed premature centromere division with chromatid puffing in areas of constitutive heterochromatin, which is exclusively found in the syndrome of infants termed Roberts' syndrome/SC phocomelia. Other laboratory findings were not normal. It is suggested that the present case is a novel sleep disorder related to a unique chromosomal aberration.

Centromere↗
PubMed1981

The treatment of narcolepsy and cataplexy.

Narcolepsy may affect as many as 250,000 Americans. It involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, and automatic behavior, as well as disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Satisfactory treatment is not available at the present time. The current treatments of choice include general measures (such as patient and family counseling and frequent napping) and drug treatments, including methylphenidate for sleepiness and sleep episodes and imipramine for cataplexy. Medication dosages mut be adjusted for individual patients. Pharmacists have a special responsibility to monitor narcoleptic patients by becoming familiar with the disease and its symptoms and by encouraging patients to follow their drug regimens and to take drug holidays under the supervision of the physician when the drug dose becomes excessive.

Cataplexy↗
PubMed1980

The use of clomipramine as an REM sleep suppressant in narcolepsy.

Clomipramine is known to suppress REM sleep, and this property may be of value in treating certain features of narcolepsy. In a case reported here, clomipramine produced relief of cataplexy, sleep paralysis and hallucinations with considerable subjective improvement. Although the sleep attacks were little changed, the time spent asleep increased, leaving clearer intervals of wakefulness.

Clomipramine↗
PubMed1998

[Sleep-arousal dissociation in a case of hypersomnia].

INTRODUCTION: Dissociated sleep-arousal states are clinical and experimental phenomena which represent mixed forms of the three stages of this cycle (arousal, NREM sleep and REM sleep). CLINICAL CASE: We describe the case of a man who presented with a history of excessive diurnal somnolence for the previous 5 years. He also had symptoms of sleep paralysis, hypnagogic hallucinations, automatic behavior and excessive movements during sleep. He had had no episodes of loss of muscle tone; MR was normal; HL DR2 and DQwl antigens were negative; two polisomnographic and a Multiple Latency Sleep test showed: 1. Absence of respiratory disorders. 2. Normal latency of REM sleep. 3. Periods of dissociated sleep (REM without atonia and arousal with atonia), and 4. An average sleep latency of 3.2 minutes and absence of REM periods. CONCLUSION: This case adds a new type of dissociated sleep state which may accompany the disorder known as hypersomnia without REM periods.

Adult↗
PubMed1988

Narcolepsy in a pediatric population.

Narcolepsy, a sleep-wake disorder of unknown cause, has been reported as occurring in the pediatric population, but only two reports of cases in the literature have included polysomnographic data on children with narcolepsy. We compared the clinical and polysomnographic data on a series of eight patients 15 years of age or younger and an adult comparison group with narcolepsy. All patients presented with excessive daytime sleepiness, and no significant difference was found between groups for the incidence of cataplexy, hypnagogic hallucinations, and sleep paralysis. On polysomnographic evaluation the pediatric group had increased total sleep time, percent-stage 3/4 sleep, percent rapid eye movement sleep, and decreased stage 1 sleep, which all are expected age-related differences. The pediatric group also showed a greater degree of daytime sleepiness and an increased frequency of sleep-onset rapid eye movement periods. While pediatric patients with narcolepsy resemble adults in their mode of presentation and the incidence of accessory symptoms, the increase in severity of sleepiness highlights the importance of diagnosing narcolepsy in children as early as possible so that treatment can be initiated.

Adult↗
PubMedDate not supplied

Successful treatment of post-traumatic narcolepsy with methylphenidate: a case report.

Narcolepsy is a rare sequela of brain injury. We report the case of a 27-yr-old male with post-traumatic narcolepsy who was successfully treated with methylphenidate. This patient sustained moderate brain injury from a motorcycle accident. Subsequently, he manifested the classic tetrad of narcolepsy: cataplexy, excessive daytime sleepiness, sleep paralysis, and hypnogogic hallucinations. There was no premorbid seizure or sleep disorder. There was no family history of sleep disorders. Polysomnography and Multiple Sleep Latency Test confirmed the diagnosis of narcolepsy. Sleep latency (time to sleep onset), rapid eye movement sleep latency (time from sleep onset to rapid eye movement sleep onset), and mean multiple sleep latency were all pathologically shortened (2.5, 66, and 1.2 min, respectively). Twenty-four hour electroencephalographic monitoring and magnetic resonance imaging of the brain were normal, as were serum chemistries. Treatment with caffeine was unsuccessful. He was then started on methylphenidate, 10 mg twice daily, which was increased to 30 mg twice daily over a 4-mo period. Cataplexy and excessive daytime sleepiness started to improve 1 mo after adjustments in methylphenidate dosing. Six months after the initiation of methylphenidate therapy, the patient is completely asymptomatic.

Adult↗
PubMed2003

[HLA-DRB and -DQB allele contribution to narcolepsy susceptibility in Chinese patients with narcolepsy].

OBJECTIVES: To study the association of narcolepsy with HLA class II alleles in Chinese narcoleptic patients. METHODS: 31 patients with narcolepsy underwent brain computed tomography (CT) scan and magnetic resonance imaging (MRI) testing. All patients received a MSLT test following a routine night's sleep, and serological HLA typing for HLA DR(2). 21 patients received PCR-SSP HLA DR and DQ typing. RESULTS: All patients had sleepiness and cataplexy. There was no evidence for other functional or structural diseases. Sleep paralysis was elicited in 45%; hypnagogic hallucinations, in 61%. Mean sleep latency on MSLT was 2.1 min +/- 1.3 min; sleep-onset rapid eye movement (SOREM) occurred during 2/5 naps in 30 of 31 patients. The average number and latency of SOREM episodes were 4.2 +/- 1.0 episodes and 4.0 min +/- 1.8 min, respectively. All patients but one were HLA DR(2) positive and 86% were HLADRB(1) * 1501-HLADQB(1)*0602 positive. CONCLUSIONS: HLA DR(2) and HLADQw6 are markers for narcolepsy-cataplexy in Chinese.

Adolescent↗
PubMed1996

Perspectives in narcolepsy research and therapy.

Narcolepsy with associated cataplexy is a disabling sleep disorder that affects 0.05% of the general population. Whereas narcolepsy-cataplexy is largely considered as etiologically homogeneous, hypersomnias without cataplexy represent a very heterogeneous group of clinical entities that must be thoroughly explored before final diagnosis of narcolepsy is given. A typical treatment for narcolepsy-cataplexy associates amphetamine-like stimulants for sleepiness and antidepressant therapy for abnormal rapid eye movement sleep (cataplexy, sleep paralysis, and hypnagogic hallucinations). This treatment is purely symptomatic and involves activation of central dopaminergic and adrenergic activity respectively. Genetic research indicates a role for the immune system rather than abnormalities in monoaminergic or cholinergic systems as the primary cause for narcolepsy. Human narcolepsy is tightly associated with HLA-DQB1*0602; canine narcolepsy is linked with a DNA segment with high homology with the human immunoglobulin mu-switch segment, and the onset of canine narcolepsy is associated with increased microglial expression of major histocompatibility complex DQ and DR molecules. Taken together with the lack of direct evidence for an autoimmune process in narcolepsy, these results may suggest the existence of novel neuroimmune interactions in narcolepsy and open new perspectives in the treatment of this disabling disorder.

Adrenergic Agonists↗
PubMed1988

Current pharmacologic management of narcolepsy.

Narcolepsy is an incurable sleep disorder characterized by attacks of sleepiness and a series of auxiliary symptoms: cataplexy, sleep paralysis and hypnagogic hallucinations. Classic treatment has included stimulants to control sleepiness and tricyclic antidepressants to control the auxiliary symptoms. Polysomnography is necessary to confirm the diagnosis and to detect other sleep disorders. Recent developments in treatment include the use of codeine for sleepiness and gamma-hydroxybutyrate for auxiliary symptoms.

Amphetamines↗
PubMed1990

Narcolepsy update.

Narcolepsy, a disorder of excessive daytime sleepiness that affects more than 125,000 people in the United States, is technically defined as a daytime mean sleep latency (time elapsed before falling asleep) of less than 5 minutes in conjunction with verification of rapid eye movement sleep in at least two of five daytime nap periods. Cataplexy, hypnagogic hallucinations, and sleep paralysis are frequently associated with narcolepsy. Currently, overnight polysomnography and multiple sleep latency testing in a sleep disorders laboratory are used to diagnose narcolepsy. Standard pharmacologic therapy consists of the judicious use of stimulants to improve alertness and the administration of tricyclic and other antidepressant drugs to suppress cataplexy. In addition, good sleep hygiene (a regular sleep-wake schedule, an adequate amount of sleep at night, and scheduled daytime naps) is essential for optimal management of this disorder. Patient and family education about narcolepsy and its treatment is also important. Even with use of the best available treatment regimens, many patients with narcolepsy have substantial vocational and social impairments.

Animals↗
PubMed2003

Clinical aspects and pathophysiology of narcolepsy.

UNLABELLED: Narcolepsy is a chronic debilitating sleep disorder first described in the late 19th century. It is characterized by two major symptoms, excessive daytime sleepiness and cataplexy, and two so-called auxiliary symptoms, hypnagogic hallucinations and sleep paralysis. The final diagnosis relies on polysomnography showing the presence of sleep onset rapid eye movement periods (SOREMPs) during the multiple sleep latency test. The presence of HLA DQA1*0102-DQB1*0602 is supportive of the diagnosis. The pathophysiology of the disorder is still unknown but an imbalance between monoamines and acetylcholine is generally accepted. Recent findings in narcoleptic dogs, a natural model of narcolepsy, and in knockout mice revealed that a mutation of type 2 hypocretin receptor plays a major role in the etiology of narcolepsy. Up to now, no mutation has been found in humans except a case of early onset and atypical narcolepsy. However, a marked reduction of hypocretin type 1 has been found in the cerebrospinal fluid (CSF) of a majority of patients and a global loss of hypocretins was noted in post-mortem brain tissue of narcoleptic subjects. Conversely, no hypocretin neuron degeneration has been observed in the genetic form of narcolepsy in dogs but no trace of hypocretin was seen in the brain or the CSF in cases of sporadic canine narcolepsy. This suggests that different hypocretinergic mechanisms are involved in sporadic and genetic forms of canine narcolepsy. Treatment has not evolved significantly over the last few years. However, new drugs, such as hypocretin agonists, are currently being developed. SIGNIFICANCE: After the discovery of the type 2 hypocretin receptor mutation in canine narcolepsy and the finding of a CSF hypocretin-1 deficiency in human narcolepsy, the major stream of research has involved the hypocretinergic system. However, other lines of research deserve to be pursued simultaneously, in view of comprehensive advancements in the understanding of narcolepsy.

Animals↗
PubMed2002

Hypocretin (orexin) and melatonin values in a narcoleptic-like sleep disorder after pinealectomy.

Narcolepsy secondary to other neurologic processes has been recently associated with hypocretin (orexin) deficiency. We present a patient who developed a narcoleptic-like sleep disorder after receiving treatment for a choroid plexus carcinoma of the pineal gland. She underwent a pinealectomy, chemotherapy, and radiation treatment. The primary features of this condition were excessive daytime sleepiness, sleep paralysis and hypnagogic hallucinations. Increased percentage of rapid eye movement (REM) sleep and sleep onset REM periods were seen during the multiple sleep latency test. Circadian rhythmicity was preserved for melatonin and cortisol. She was negative for human leukocyte antigen DQB1*0602 and had a detectable cerebrospinal fluid hypocretin level (518 pg/ml). We emphasize that the narcoleptic-like disorder likely resulted from the surgical intervention or radiation therapy. Her symptoms are caused by an unknown mechanism unrelated to hypocretin depletion which merits more research.

Journal Article↗