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PubMed2002

Narcolepsy.

Narcolepsy is a chronic disorder of EDS. All patients experience EDS. Other symptoms include cataplexy, sleep paralysis, hypnagogic hallucinations, and disrupted nocturnal sleep. Treatment, usually with stimulants and low-doses of antidepressant medications, can dramatically improve the patient's quality of life. Although only advanced practice nurses may be actively involved in the diagnosis and treatment of this disorder, all nurses can encourage their patients who complain of EDS to consult a specialist in sleep disorders medicine, provide emotional support after diagnosis, and educate patients and their families about narcolepsy and its treatment.

Behavior Therapy↗

PubMed1998

Narcolepsy and idiopathic hypersomnolence.

Narcolepsy is among the leading causes of excessive daytime sleepiness. Its classic form associates daytime sleepiness with cataplexy, sleep paralysis, hypnopompic hallucinations, and nocturnal disrupted sleep. This form is associated with HLA DQ betal-0602 in about 85% to 90% of affected subjects, independently of their ethnicity. But the definition of the variants of narcolepsy remains controversial, despite the fact that, in some cases, narcolepsy may be limited to daytime sleepiness. In its classic form, it is associated with two or more sleep onset rapid eye movement periods at the Multiple Sleep Latency Test. This test, performed after nocturnal polysomnography, can be helpful in diagnosing narcolepsy, in the absence of a convincing history of partial or complete attacks of cataplexy--a pathognomonic symptom. Investigation of narcoleptic Dobermans has indicated that a muscarinic cholinergic hypersensitivity exists in the brain of affected animals and abnormalities involve also the dopaminergic system. Despite its prevalence of 0.03% to 0.05%, it is still a neurologic entity often missed. Investigations of families of narcoleptics, including monozygotic twins, indicate that this syndrome is polygenic in nature with association of environmental factors. As the peak of onset of disabling symptoms occurs between 15 and 25 years of age, it is important to improve the treatment of this lifelong, disabling illness. Stimulants medications, independently of their mode of action, are prescribed to help daytime sleepiness, and tricyclic antidepressant drugs or serotonergic reuptake blockers are used on the other symptoms. But these medications have a limited efficacy. Short naps at regular intervals during the day are a strong therapeutic adjuvent.

Animals↗

PubMed2001

MAO-A and COMT polymorphisms and gene effects in narcolepsy.

Narcolepsy presents one of the tightest associations with a specific HLA antigen (DQB1*0602) but there is strong evidence that non-HLA genes also confer susceptibility. Recent observations have implicated the hypocretin/orexin system in narcolepsy in both humans and animals. In addition, the implication of monoaminergic systems in the pathophysiology of narcolepsy is well established and a significant association between the monoamine oxydase-A (MAO-A) gene and human narcolepsy has recently provided a possible genetic link. We investigated polymorphisms of MAO-A and catechol-O-methyltransferase (COMT) in 97 Caucasians with well-defined narcolepsy-cataplexy and sought for genotypic effects on disease symptoms. No evidence of association between genotype or allele frequencies of both MAO-A or COMT gene and narcolepsy was found. However, a sexual dimorphism and a strong effect of COMT genotype on disease severity were found. Women narcoleptics with high COMT activity fell asleep twice as fast as those with low COMT activity during the multiple sleep latency test (MSLT) while the opposite was true for men. COMT genotype also strongly affected the presence of sleep paralysis and the number of REM sleep onsets during the MSLT. In agreement with well-documented pharmacological results in canine narcolepsy, this study reports the first genetic evidence for the critical involvement of the dopaminergic and/or noradrenergic systems in human narcolepsy.

Cataplexy↗

PubMed1990

Narcolepsy.

Narcolepsy is a neurological condition with a prevalence of up to 1 per 1,000 that is characterized by irresistible bouts of sleep. Associated features include the pathological manifestations of rapid-eye-movement (REM) sleep: cataplexy, sleep paralysis, hypnagogic hallucinations, and abnormal sleep-onset REM periods and disturbed nocturnal sleep. The condition is strongly associated with the HLA-DR2 and DQw1 phenotype. The phenomenology of narcolepsy is discussed, and diagnostic procedures are reviewed. Treatment modalities involving central nervous system stimulants for somnolence and tricyclic drugs for REM-sleep abnormalities are discussed. Sleep laboratory studies on the treatment efficacy of methylphenidate, pemoline, dextroamphetamine, protriptyline, and viloxazine are presented. Data suggest that: (1) methylphenidate and dextroamphetamine objectively improve somnolence; (2) pemoline, at doses up to 112.5 mg, is less effective in controlling somnolence but may improve certain aspects of performance; and (3) protriptyline and viloxazine are effective anticataplectic agents that produce little improvement in somnolence.

Adult↗

PubMed2005

[Clinical features of early-onset narcolepsy].

OBJECTIVE: To investigate the clinical features of early onset narcolepsy. METHODS: The clinical data of 105 consecutive patients with narcolepsy, 63 of which with an onset age of 9.7 +/- 3.1 on average and 42 with an onset age of 22.8 +/- 9.3 on average. Interrogation, physical examination, CT, and MRI were carried out. Polysomnography was conducted. Then the data were compared between these 2 groups. RESULTS: All 105 patients showed daytime sleepiness. The incidence rate of cataplexy was 92% in the early onset group, significantly higher than that of the late onset group (P = 0.023). There were no significant differences in the rates of sleep paralysis, hypnagogic hallucination, and disturbed nocturnal sleep. Multiple sleep latency test showed that the mean sleep latency of the early-onset group was 4.5 +/- 4.0 min, significantly shorter than that of the late onset group (7.0 +/- 5.7 min, P = 0.018); the REM sleep latency of the early onset group was 3.4 +/- 3.2 min, significantly shorter than that of the late onset group (4.8 +/- 2.2 min, P = 0.02). The number of REM sleep of the early onset group was 3.4 +/- 2.0, significantly more than that of the late onset group (2.5 +/- 1.9, P = 0.09). The apnea and hypopnea index of the late onset group was 9.2 +/- 16.5, significantly higher than that of the early onset group (1.9 +/- 6.3, P = 0.009). The 3 cases of narcolepsy with family history were all cases of early onset narcolepsy. CONCLUSION: Early onset narcolepsy patients have more severe daytime sleepiness and higher rate of cataplexy. The pathogenesis of early onset narcolepsy may be more closely associated with genetic factors.

Adolescent↗

PubMed1985

The effects and effectiveness of gamma-hydroxybutyrate in patients with narcolepsy.

Thirty patients with polysomnographically confirmed narcolepsy were treated with GHB (gamma-hydroxybutyrate) for up to 30 weeks. The number of nightly awakenings significantly decreased, while Stages 3 and 4 sleep substantially increased. The clinical symptoms of cataplexy, sleep paralysis, hypnogogic hallucinations, daily naps, and sleep attacks all showed significant improvements. Daytime sleepiness, while not completely eliminated, was controlled with lower doses of stimulant medication than patients were taking before the study. No patient developed tolerance to the drug, and no serious side effects were noted.

Adult↗

PubMed1995

[Use of antidepressants in sleep disorders: practical considerations].

There is a general tendency to restrict the notion of sleep disorders to insomnia and consequently to limit treatment to the prescription of hypnotics. However, it is very often of benefit to prescribe psychotropic agents, in particular antidepressants, not only in insomnia but also in certain cases of hypersomnia, parasomnia and dysomnia associated with organic diseases. In some conditions, however, antidepressants may either induce or aggravate sleep disorders. This is the case with a number of psychostimulants that occasionally induce insomnia. It is also true of the tricyclic antidepressants, which may worsen or even induce a restlessleg syndrome that is often associated with periodic movement syndrome. On the other hand, the antidepressants may play a therapeutic role in certain sleep disorders : - depression-related insomnia is of course the << primary >> indication for antidepressants. Furthermore, certain antidepressants exhibit a sedative action resulting in a hypnogenic-type effect which appears well before the antidepressant effect; - the other types of insomnia may also often be treated with antidepressants : not acute reactional insomnia, against which hypnotics are remarkably effective, but chronic insomnia. In addition, all antidepressants may eventually correct depressive hypersomnia, but in these cases, it is evidently preferable to prescribe non-sedative drugs. Although some tricyclic antidepressants have been proposed for use in hypersomnia due to sleep apnea, their therapeutic interest is minor compared with mechanical and surgical treatment. In contrast, antidepressants play an important role in the treatment of narcolepsy, particularly for the correction of attacks of cataplexy. Antidepressants have also been used for some time in the treatment of parasomnia related to slow deep sleep (night terrors and sleepwalking), but the antidepressants may also be used in enuresis and in parasomnia related to REM sleep : nightmares, sleep paralysis, behavioral problems associated with REM sleep. Antidepressant (mainly serotoninergic drugs) are often used in the treatment of fibrolitis syndrome. Finally, antidepressants (particularly the serotoninergic antidepressants) play an important role in the drug treatment of fibromyalgia.

Antidepressive Agents↗

PubMed1998

[A case of multiple sclerosis with initial symptoms of narcolepsy].

We reported a 13-year-old boy diagnosed as multiple sclerosis associated with narcolepsy. He had suffered from retrobulbar optic neuritis at the age of 11 years which was improved gradually by prednisolone. Four months later he was admitted because of excessive somnolence. The diagnosis of narcolepsy was made based on hypnagogic hallucination, sleep paralysis, changes of personality and the sleep onset sREM (SOREM). The elevation of anti-measles antibody and a positive oligoclonal band in CSF, low density areas in the bilateral internal capsule on CT scan, and high signal areas in the same region on T2-weighted MRI confirmed the diagnosis of multiple sclerosis. An abnormal arousal response occurred occasionally in sleep stage 2 and 4, which started with electrical silence followed by a period with irregular high voltage slow waves and repetitive focal spike train. Those clinical symptoms and abnormalities of biochemical and electrophysiological studies normalized after treatment with prednisolone. However, abnormalities on MRI showed no improvement even after long term administration of prednisolone (2.5 mg/day).

Adolescent↗

PubMed2006

The protean manifestations of childhood narcolepsy and their misinterpretation.

Narcolepsy often begins in childhood but is infrequently recognized, partly because of its many manifestations that can be confused with other conditions. The clinical presentations of excessive sleepiness, cataplexy, hallucinatory phenomena, and sleep paralysis (not always occurring together) are very varied. The picture may be further complicated by the occurrence of automatic behaviour, memory and visual problems, and associated sleep disorders, as well as the psychological and social consequences of having narcolepsy. Not surprisingly, therefore, misinterpretation of the symptoms as primarily psychological, or otherwise physical, may well occur leading to inappropriate management including initial referral to psychiatric or educational rather than neurological or sleep disorder services. The wide-ranging and special features of childhood narcolepsy need to be appreciated by health care and other professionals as well as by parents.

Child↗

PubMedDate not supplied

The function of 'brain waves': a cybernetic model of electroencephalography.

Electroencephalograms recorded from sleeping subjects are reinterpreted, from first principles, to explain the relationship between the observed wave-forms and cerebral processes. The manifestations of narcolepsy, namely, sleep paralysis, hypnopompic hallucinations and cataplexy are consistent with a hypothesis that the disorder is the result of entrainment of cerebral waves, causing almost instantaneous descent into a REM sleep state.

Cataplexy↗

PubMed2000

[Narcolepsy. An illness in transition].

The signs of narcolepsy have been known since the last century and the tetrad of symptoms was described 50 years ago: excessive sleepiness, cataplexy, sleep paralysis, and hallucinations. Polysomnography typically shows decreased sleep and REM sleep latency, and laboratory testing reveals a high association with the human leucocyte antigens (HLA) DQB1*0602 and DQA1*102. Actual studies suggest disturbances in the orexin (hypocretin) neurotransmitter system. However, the exact pathophysiology is still unclear. In Germany, about 1500 patients diagnosed with narcolepsy are known. The prevalence in Caucasian populations is estimated at 50/100,000. Thus, the number of undiagnosed patients is likely to be high.

Cross-Sectional Studies↗

PubMed1987

Disorders of excessive sleepiness: narcolepsy and hypersomnia.

Besides sleep apnea, the main disorders of excessive daytime sleepiness include narcolepsy and hypersomnia. Narcolepsy is characterized by periods of irresistible sleepiness and sleep attacks of brief duration and, most often, by one or more of the auxiliary symptoms: cataplexy, sleep paralysis, and hypnogogic hallucinations. Generally, sleepiness and sleep attacks in hypersomnia are of longer duration and are more resistible than in narcolepsy; also, the auxiliary symptoms are absent. There are three types of hypersomnia: idiopathic, secondary, and periodic. Nocturnal sleep is typically disrupted in narcolepsy, whereas in idiopathic hypersomnia it is prolonged and in secondary hypersomnia it is variable. The exact causes of narcolepsy and idiopathic hypersomnia are unknown; however, there is evidence for genetic predisposition for either disorder. In secondary hypersomnia causative factors include: neurologic, such as head injuries, cerebrovascular insufficiency, and brain tumors; general medical, such as metabolic disorders, various intoxications, and conditions leading to brain hypoxia; and psychiatric, most notably depression. Although the cause of periodic hypersomnia is unclear, most research supports the notion of underlying organic disease. Often, the evaluation of patients with excessive daytime sleepiness can be completed in the office setting, based on the sleep history and a thorough neurologic, general medical, and psychiatric assessment. Whenever indicated, ancillary laboratory studies, such as computed tomography and magnetic resonance scans, should be performed. Sleep laboratory recordings generally are not necessary unless there is suspicion of sleep apnea or narcolepsy in the absence of auxiliary symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Sleep patterning and behaviour in cats with pontine lesions creating REM without atonia.

Lesions of the dorsal pontine tegmentum release muscle tone and motor behaviour, much of it similar to orienting during wakefulness, into rapid eye movement sleep (REM), a state normally characterized by paralysis. Sleep after pontine lesions may be altered, with more REM-A episodes of shorter duration compared to normal REM. We examined behaviour, ponto-geniculo-occipital (PGO) waves (which may be central markers of orienting) and sleep in lesioned cats: (i) to characterize the relationship of PGO waves to behaviour in REM-A; (ii) to determine whether post-lesion changes in the timing and duration of REM-A episodes were due to activity-related awakenings: and (iii) to determine whether alterations in sleep changed the circadian sleep/wake cycle in cats. Behavioural release in REM-A was generally related to episode length, but episode length was not necessarily shorter than normal REM in cats capable of full locomotion in REM-A. PGO wave frequency was reduced overall during REM-A, but was higher during REM-A with behaviour than during quiet REM-A without overt behaviour. Pontine lesions did not significantly alter the circadian sleep/wake cycle: REM-A had approximately the same Light/Dark distribution as normal REM. Differences in the patterning of normal REM and REM-A within sleep involve more than mere movement-induced awakenings. Brainstem lesions that eliminate the atonia of REM may damage neural circuitry involved in REM initiation and maintenance; this circuitry is separate from circadian control mechanisms.

Journal Article↗

PubMed2001

[Narcolepsy in a prepubertal boy].

We reported a 10-year-old boy with narcolepsy, the onset of which was at the age of 8 years and 6 months. The initial symptom was excessive daytime sleepiness, followed by cataplexy and disrupted nocturnal sleep. There was neither hallucination nor sleep paralysis. A daytime polysomnogram showed a sleep-onset rapid eye movement period (SOREMP), and human leukocyte antigen (HLA) analysis revealed HLA-DR2/DQB1 * 0602. Treatment with methylphenidate and clomipramine was effective; methylphenidate (30 mg/day) improved his wakefulness and alertness throughout the day, and clomipramine (20 mg/day) reduced the number of cataplexic episodes. Because of their abnormal behavior, prepubertal narcoleptic children may often be misdiagnosed as having epilepsy or an attention deficit hyperactivity disorder. Therefore, they need early diagnosis and treatment. Assistance should be provided to protect them from being labeled as lazy by their parents and school teachers.

Child↗

PubMed1985

Narcolepsy. Clinical features and aetiology.

Narcolepsy is not a rare disease. Age of onset varies from childhood to the 5th decade. Evidence for a genetic basis stems from the overall rate of narcolepsy and/or disorder of excessive somnolence among first degree relatives. The clinical features include overwhelming episodes of sleep, excessive daytime somnolence, hypnagogic hallucinations, disturbed nocturnal sleep; manifestations of dissociated REM sleep inhibitory process, cataplexy and sleep paralysis; and a special polygraphic pattern: the sleep onset REM episode. Not all symptoms are necessarily present at the onset or even during the course of narcolepsy. Excessive daytime somnolence never disappears completely while other symptoms may. Narcolepsy is a disabling condition. Its aetiology is still poorly understood but the use of natural animal models, namely dogs and horses, has been an important contribution in the areas of genetic, pharmacological and direct neurochemical analysis. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants while treatment of cataplexy and other related symptoms rests on chlorimipramine. However, new treatments are being tested, which could be of significant value.

Adolescent↗

PubMed2006

Mental representation of space: insights from an oblique distribution of hallucinations.

Three-dimensional spatial distributions of hypnagogic and hypnopompic hallucinations associated with sleep paralysis were used to investigate the internal representation of space. Left-right asymmetries in human preferences and abilities are well established. Parallel effects are also observed as lower-upper asymmetries. These parallels could reflect common underlying mechanisms or additive effects of independently evolved horizontal and vertical asymmetries. This study adds to the growing literature on multidimensional spatial biases in a context free from the influence of task-related factors. We present evidence of an oblique bias in the projection of both sensory and motor hallucinations toward lower-left and especially upper-right external space exceeding that accounted for by an additive model of separate horizontal and vertical biases. These observations are consistent with theories regarding a systematic functional relation of hemispheric with ventral and dorsal cerebral organization.

Adult↗

PubMed1989

Mechanisms of seizure suppression during rapid-eye-movement (REM) sleep in cats.

REM sleep is the most antiepileptic state in the sleep-wake cycle for human generalized epilepsy, yet the neural mechanism is unknown. This study verified the antiepileptic properties of REM sleep in feline generalized epilepsy and also isolated the responsible factors. Conclusions are based on 20 cats evaluated for generalized EEG and motor seizure susceptibility before and after dissociation of specific REM sleep components. Bilateral electrolytic lesions of the medial-lateral pontine tegmentum created a syndrome of REM sleep without atonia. Systemic atropine created a syndrome of REM sleep without thalamocortical EEG desynchronization. Identical results were obtained in two seizure models, systemic penicillin epilepsy and electroconvulsive shock. (1) Normal REM sleep retarded the spread of EEG seizure discharges and had even more potent anticonvulsant effects. (2) Selective loss of 'sleep paralysis' (skeletal muscle atonia) during REM abolished REM sleep protection against myoclonus and convulsions without affecting generalized EEG paroxysms. (3) Conversely, selective loss of thalamocortical EEG desychronization abolished REM sleep protection against generalized EEG seizures without affecting clinical motor accompaniment. These results suggest that the descending brainstem pathways which mediate lower motor neuron inhibition also protect against generalized motor seizures during REM sleep. Protection against spread of EEG paroxysms is governed by a separate mechanism, presumably the ascending brainstem pathways mediating intense thalamocortical EEG desynchronization during REM sleep.

Animals↗

PubMed1998

The clinical diagnosis of the narcoleptic syndrome.

Sleep-wake habits and control of postural muscle tone were investigated by self-report questionnaire in 183 subjects considered to have the narcoleptic syndrome, 62 subjects with hypersomnia and 10 with obstructive sleep apnoea. Results were compared with those in a group of 188 control subjects with normal sleep wake habits. Excessive daytime sleepiness, determined by the Epworth Sleepiness Scale (ESS), was five times greater in the narcoleptic syndrome than in control subjects (score range 0-24, mean scores +/-SD 19.6+/-3.0; and 4.5+/-3.3 respectively; P<0.001). The propensity to cataplexy, as determined by a rating scale developed to estimate the likelihood of loss of postural tone in response to sudden emotional stimuli, including laughter, was 10 times greater in narcoleptic syndrome than in control subjects (postural atonia total score range 0-600; mean + SD 334+/-122 and 28+/-45, respectively; P<0.001). Narcoleptics had more disturbances of night sleep than controls with episodes of muscle jerking, sleep walking, sleep talking and sleep terrors, as well as sleep paralysis, and higher insomnia self-rating scores. Sleep latency from bedtime to sleep-onset time was shorter in narcoleptics than controls. The hypersomniac group of 62 subjects was heterogeneous. Subsequent investigation showed that 18 subjects (29%) had idiopathic hypersomnia, four (6%) 'incomplete' narcolepsy without cataplexy and 10 (16%) hypersomnia accompanying a mood disorder. The mean ESS scores in this group and in subjects with obstructive sleep apnoea were comparable to those of the narcoleptic syndrome subject group. Mean postural atonia scores were similar to those of control subjects.

Adult↗