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PubMed1973

Levo(-) amphetamine and dextro(+) amphetamine in the treatment of narcolepsy.

The narcoleptic syndrome is a life-long and sometimes familial disorder in which there is a disturbance of the rapid eye movement phase of sleep. Patients with periodic sleep in the daytime but no other symptoms seldom develop the narcoleptic syndrome and have a separate unrelated disorder. Twelve patients with the narcoleptic syndrome were treated separately with l(-) amphetamine and d(+) amphetamine. Both drugs abolished narcolepsy, d(+) amphetamine being slightly more potent than l(-) amphetamine. In equipotent doses, unwanted effects of nervousness and insomnia were equal in frequency. No tolerance to either preparation developed during a six month period. Cataplexy was not affected by amphetamine treatment, but was abolished in two patients when clomipramine was given together with either amphetamine.

Adult↗
PubMed1983

Daytime polysomnogram diagnosis of sleep disorders.

The daytime polysomnogram was used to evaluate 310 consecutive patients with suspected sleep disorders, referred mainly because of excessive daytime sleepiness. Abnormalities consistent with pathologic sleep apnoea were present in 102 cases, and with narcolepsy-cataplexy in 49 cases. The daytime polysomnogram is a readily accessible, accurate, and cost-effective method for diagnosing many sleep disorders.

Adult↗
PubMed1985

Psychopathology and narcolepsy.

Twenty-eight patients with narcolepsy are compared to a sex- and age-matched control population with regard to the frequency of psychiatric symptoms. The occurrence of psychiatric syndromes in narcolepsy patients is also examined. The frequency of psychiatric illness in patients with cataplexy or hypnagogic/hypnopompic hallucinations is evaluated as well. Analysis with the Mann-Whitney test found a significant association between narcolepsy and the symptoms of schizophrenia. Premorbid history of organic brain disease was associated with mental illness, but was nonspecific for psychopathology.

Adolescent↗
PubMed1976

Problems in the differential diagnosis of narcolepsy versus schizophrenia.

The authors discuss the problems of accurately diagnosing narcolepsy when patients manifest the auxiliary symptoms of this disorder, i.e., cataplexy, hypnagogic hallucinations, and sleep paralysis, which conclude that misdiagnosis of narcolepsy can be avoided if clinicians are aware that this illness can simulate a psychiatric disorder and if they give careful attention to the histroy of the patient's illness.

Adult↗
PubMed1984

Pseudocataplexy: gelastic-atonic seizures.

Gelastic-atonic seizures are characterized by laughing and then loss of muscle tone. They are difficult to differentiate from laughter-induced cataplexy and may be indicative of Niemann-Pick disease Type C or variants. We studied an 11-year-old girl who had gelastic-atonic seizures that were triggered by laughing. The nature of her attacks was established by ictal EEG ambulatory recordings at home. There was no evidence of Niemann-Pick disease.

Cataplexy↗
PubMed2002

Prevalence of narcolepsy symptomatology and diagnosis in the European general population.

OBJECTIVE: To determine the prevalence of narcolepsy in the general population of five European countries (target population 205,890,882 inhabitants). METHODS: Overall, 18,980 randomly selected subjects were interviewed (participation rate 80.4%). These subjects were representative of the general population of the UK, Germany, Italy, Portugal, and Spain. They were interviewed by telephone using the Sleep-EVAL expert system, which provided narcolepsy diagnosis according to the International Classification of Sleep Disorders (ICSD). RESULTS: Excessive daytime sleepiness was reported by 15% of the sample, with a higher prevalence in the UK and Germany. Napping two times or more in the same day was reported by 1.6% of the sample, with a significantly higher rate in Germany. Cataplexy (episodes of loss of muscle function related to a strong emotion), a cardinal symptom of narcolepsy, was found in 1.6% of the sample. An ICSD narcolepsy diagnosis was found in 0.047% of the sample: The narcolepsy was severe for 0.026% of the sample and moderate in 0.021%. CONCLUSION: This is the first epidemiologic study that estimates the prevalence of narcolepsy in the general population of these five European countries. The disorder affects 47 individuals/100,000 inhabitants.

Adolescent↗
PubMed2002

Novel therapies for narcolepsy.

Narcolepsy is a primary neurological disorder, which often produces disabling symptoms, including excessive daytime sleepiness and cataplexy. Although the precise aetiology of narcolepsy has not been determined, our understanding of the pathophysiology of this complex disorder has grown dramatically during the past several years, especially as it relates to the newly discovered hypocretin system. While symptomatic treatment of narcolepsy is available, the commonly used pharmacological agents are often not completely effective and may be poorly tolerated. The need for new therapeutic tools is, therefore, apparent. This paper explores some exciting new approaches to the treatment of narcolepsy. It is important to emphasise that, although narcolepsy is not a common disorder, new agents for its treatment will undoubtedly find more extensive use in other conditions.

Adrenergic Agents↗
PubMed2004

Hypocretinergic control of spinal cord motoneurons.

Hypocretinergic (orexinergic) neurons in the lateral hypothalamus project to motor columns in the lumbar spinal cord. Consequently, we sought to determine whether the hypocretinergic system modulates the electrical activity of motoneurons. Using in vivo intracellular recording techniques, we examined the response of spinal motoneurons in the cat to electrical stimulation of the lateral hypothalamus. In addition, we examined the membrane potential response to orthodromic stimulation and intracellular current injection before and after both hypothalamic stimulation and the juxtacellular application of hypocretin-1. It was found that (1) hypothalamic stimulation produced a complex sequence of depolarizing- hyperpolarizing potentials in spinal motoneurons; (2) the depolarizing potentials decreased in amplitude after the application of SB-334867, a hypocretin type 1 receptor antagonist; (3) the EPSP induced by dorsal root stimulation was not affected by the application of SB-334867; (4) subthreshold stimulation of dorsal roots and intracellular depolarizing current steps produced spike potentials when applied in concert to stimulation of the hypothalamus or after the local application of hypocretin-1; (5) the juxtacellular application of hypocretin-1 induced motoneuron depolarization and, frequently, high-frequency discharge; (6) hypocretin-1 produced a significant decrease in rheobase (36%), membrane time constant (16.4%), and the equalizing time constant (23.3%); (7) in a small number of motoneurons, hypocretin-1 produced an increase in the synaptic noise; and (8) the input resistance was not affected after hypocretin-1. The juxtacellular application of vehicle (saline) and denatured hypocretin-1 did not produce changes in the preceding electrophysiological properties. We conclude that hypothalamic hypocretinergic neurons are capable of modulating the activity of lumbar motoneurons through presynaptic and postsynaptic mechanisms. The lack of hypocretin-induced facilitation of motoneurons may be a critical component of the pathophysiology of cataplexy.

Animals↗
PubMed2006

Sodium oxybate for narcolepsy.

Sodium oxybate (Xyrem), also known as gamma-hydroxybutyric acid, is the only therapeutic specifically approved in the USA for the treatment of cataplexy in narcolepsy. The US FDA has recently expanded its indication to include excessive daytime sleepiness associated with narcolepsy. In contrast to the antidepressants and stimulants commonly used to treat the disorder, sodium oxybate is the only compound that addresses both sets of symptoms and, when used properly, is less likely to lead to the development of tolerance and other undesirable side effects. In this review, the results of clinical trials and the place of sodium oxybate in narcolepsy treatment are discussed.

Anesthetics, Intravenous↗
PubMed1986

Narcolepsy/cataplexy. III: Nocturnal sleep and wakefulness patterns.

Nocturnal sleep and wakefulness patterns of 50 patients with narcolepsy and cataplexy were compared to those of 50 control subjects. A sleep onset REM period (SOREM) occurred in 22 (44%) of the patients but in none of the controls. Comparisons among patients showing a SOREM, patients without this abnormality, and controls demonstrated that the timing, number and duration of the remaining REM periods did not differ across the three groups. Thus, the basic REM sleep disturbance in narcolepsy appears to relate to the timing of onset of the initial REM period. This finding lends further support to the theory of dual control of REM-NREM cycling. While narcoleptics took significantly less time to fall asleep, they had significantly more awakenings, wake time after sleep onset and total wake time. The disturbed sleep experienced by patients could not be accounted for by the presence of a sleep onset REM period or the use of medication. Nocturnal wakefulness appeared to be distributed in a regular oscillating manner throughout the recording period similar to the pattern of daytime vigilance previously reported in normal subjects. Thus, typical nocturnal dampening of daytime ultradian vigilance rhythms may be lost in the narcoleptic patient.

Adult↗
PubMed2001

[Treatment of the neurological sleep disorders restless legs syndrome and narcolepsy].

Pharmacological therapies are presented for two typical neurological sleep-wake disorders, restless legs syndrome (RLS) and narcolepsy. The individual discomfort caused by RLS and the accompanying problems with initiating and maintaining sleep often require a therapy with L-dopa and dopamine agonists. Positive treatment effects on sensory and motor symptoms have been shown in open trials and controlled studies. Development of time shift and/or augmentation of symptoms is a problem of L-dopa therapy. Further efficient drugs are opioids and benzodiazepines. The therapy of narcolepsy depends on its severity and the pattern of the symptoms. Excessive daytime sleepiness and sleep attacks are the most impairing symptoms, which are difficult to treat. These symptoms require an optimal combination of CNS stimulants with regular napping. Cataplexy and other REM sleep associated symptoms are effectively treated with REM sleep suppressing antidepressants.

Anti-Anxiety Agents↗
PubMed2001

Electromagnetic field of mobile phones affects visual event related potential in patients with narcolepsy.

The effects of the mobile phone (MP) electromagnetic fields on electroencephalography (EEG) and event-related potentials (ERP) were examined. With regard to the reported effects of MP on sleep, 22 patients with narcolepsy-cataplexy were exposed or sham exposed for 45 min to the MP (900 MHz, specific absorption rate 0.06 W/kg) placed close to the right ear in a double blind study. There were no changes of the EEG recorded after the MP exposure. A subgroup of 17 patients was studied on visual ERP recorded during the MP exposure. Using an adapted "odd-ball" paradigm, each patient was instructed to strike a key whenever rare target stimuli were presented. There were three variants of target stimuli (horizontal stripes in (i) left, (ii) right hemifields or (iii) whole field of the screen). The exposure enhanced the positivity of the ERP endogenous complex solely in response to target stimuli in the right hemifield of the screen (P < 0.01). The reaction time was shortened by 20 ms in response to all target stimuli (P < 0.05). In conclusion, the electromagnetic field of MP may suppress the excessive sleepiness and improve performance while solving a monotonous cognitive task requiring sustained attention and vigilance.

Brain Mapping↗
PubMed1979

[Connections between respiratory regulation and paradoxical sleep in a patient with Joubert's syndrome (author's transl)].

This study reports on eight patients whose cases have been described in literature, and two patients treated by the author, showing the typical signs of Joubert's syndrome. This disease pattern is characterised by episodic hyperpnoeas and apnoeas, retardation, muscular hypotension, opsoclonia, complete or partial agenesis of the vermiform process of cerebellum, as well as a dilated fourth ventricle. The clinical symptoms are compared with the characteristic signs of REM sleep and of cataplexy.

Abnormalities, Multiple↗
PubMed1990

[A case of narcolepsy with increased cataplectic attacks after suffering from cerebrovascular disease].

It is well known that narcoleptic patients have DR2 and DQw-1 on HLA typing. The development of narcolepsy is considered to depend on the two factors; genetic predispositions and exogenous factors such as head trauma, encephalitis, etc., mainly affecting the brainstem or diencephalon. We reported a 46-year-old man who had occasional sleep attacks after suffering from left thalamic hemorrhage and pontine vascular disorders. Rehabilitation was markedly disturbed due to frequent episodes of cataplectic attacks which was triggered by emotional lability such as laughing, anxiety, and excitement. HLA type examination showed both DR-2 and DQw-1 loci in the proband and his four other siblings. His elder brother also suffered from mild excessive daytime sleepiness during his younger age, but it subsided gradually. Analysis of overnight polysomnography in the patient revealed remarkable paradoxical alpha-blocking and frequent sleep onset REM stages as typically observed in narcoleptic patients. MRI examination showed multiple small hemorrhages and infarctions in the pontine tegmentum, in addition to the left thalamic hemorrhage and multiple subcortical ischemic lesions. Concerning the mechanism of frequent cataplexy in this patient, it is postulated that increased emotional incontinence might have stimulated the descending reticular system in the brainstem which in turn may inhibit anterior horn motor cell activities. Methylphenidate was initially given to the patient, resulting in some relief of attacks, and addition of imipramine dramatically suppressed cataplectic attacks. Imipramine is considered to inhibit the excitatory afferent pathway to the brainstem suppressing the hyperactivity of descending motor inhibitory system due to its anti-muscarinergic action.

Cataplexy↗
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↗
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↗
PubMed1979

Narcolepsy and automatic behavior: a case report.

Narcolepsy is characterized by excessive daytime sleepiness and cataplexy, which may be accompanied by hypnogogic or hypnopompic hallucinations and sleep paralysis. Automatic behavior is a relatively newly recognized symptom of the narcolepsy syndrome. This case report describes a particularly troublesome sort of automatic behavior--shoplifting--in a narcoleptic patient. It illustrates how a sleep-laboratory evaluation was used to confirm the diagnosis of narcolepsy and considers aspects of the treatment of the problem.

Automatism↗
PubMed1974

Narcolepsy.

NARCOLEPSY IS A DISORDER OF SLEEP CONTROL CHARACTERIZED BY A TETRAD OF SYMPTOMS: sleep attacks, cataplexy, sleep paralysis and hypnagogic hallucinations. A diagnosis is made from a careful history. The incidence is estimated as high as 0.3% of the population. Unfortunately patients go for many years before the diagnosis is made and often have experienced disruption of their employment, social and family life, and may have experienced a number of car accidents because of falling asleep at the wheel. An unknown number of narcoleptics kill themselves on the highways before the diagnosis is ever made. Sleep attacks can usually be controlled by methylphenidate, and if the other symptoms persist they can often be effectively managed by imipramine.

Accidents, Traffic↗