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Results for “CATAPLEXY”

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PubMed1993

Heterozygosity at the canarc-1 locus can confer susceptibility for narcolepsy: induction of cataplexy in heterozygous asymptomatic dogs after administration of a combination of drugs acting on monoaminergic and cholinergic systems.

Narcolepsy is a genetically determined disorder of sleep characterized by excessive daytime sleepiness and abnormal manifestations of REM sleep that affects both humans and animals. Although its exact pathophysiologic mechanisms remain undetermined, recent experiments have demonstrated that in both humans and canines, susceptibility genes are linked with immune-related genes. A striking difference, however, is that the genes thought to be involved in the human pathology are autosomal dominant, whereas canine narcolepsy in Dobermans is transmitted as a single autosomal recessive gene with full penetrance (canarc-1). In this study, we have examined the development of narcoleptic symptoms in homozygous narcoleptic, heterozygous, and control Dobermans. Animals were behaviorally observed until 5 months of age and then treated at weekly intervals with cataplexy-inducing compounds that act on cholinergic or monoaminergic systems (alone and in combination). Our data indicate that cataplexy can be induced in 6-month-old asymptomatic heterozygous animals, but not in control canines, with a combination of drugs that act on the monoaminergic and cholinergic systems. This demonstrates that disease susceptibility may be carried by heterozygosity at the canarc-1 locus. Our data further suggest that cataplexy, a model of REM sleep atonia, is centrally regulated by a balance of activity between cholinergic and monoaminergic neurons.

Aging↗

PubMed2004

Monozygotic twins concordant for narcolepsy-cataplexy without any detectable abnormality in the hypocretin (orexin) pathway.

Narcolepsy with cataplexy is thought to be a hypocretin ligand or hypocretin receptor deficiency syndrome caused by genetic and environmental factors. We looked for an abnormality of the hypocretin pathway in HLA-DQB1*0602-positive monozygotic twins who were concordant for narcolepsy-cataplexy. They had normal cerebrospinal fluid concentrations of hypocretin-1, and we found no mutation in the prepro-hypocretin gene or either hypocretin receptor gene. Our finding points to the existence of presumably genetic forms of narcolepsy with cataplexy without any demonstrable defect in the hypocretin pathway.

Adult↗

PubMed2004

Effect of age on MSLT results in patients with narcolepsy-cataplexy.

OBJECTIVE: To measure the effect of age on Multiple Sleep Latency Test (MSLT)characteristics, sleep latency, and number of sleep-onset REM periods (SOREMP) in two large populations of narcoleptic patients with similar genetic backgrounds. METHODS: Clinical and polygraphic information on the severity of the condition was obtained on 236 well-defined narcolepsy-cataplexy-human leukocyte antigen DR2-positive patients from Montpellier (France) and on 147 similar patients from Montreal (Canada). RESULTS: The results show a progressive decrease in the number of SOREMP with age and a progressive increase in the mean sleep latency on the MSLT as a function of age. This finding is also related to the severity of cataplexy as assessed from the clinical history with a progressive decrease in the frequency of cataplexy attacks with age. These results may reflect the progressive increase in sleep latency seen in normal aging and suggest that clinical improvement might be due to changes in the neural mechanisms responsible for SOREMP, which may weaken with age. CONCLUSIONS: The progressive decrease in the number of SOREMP and increase in the mean sleep latency on the MSLT as a function of age suggest that the current criteria used for diagnosis may be too stringent in older patients. The major influence of age on MSLT results should therefore be taken into account when diagnosing a narcoleptic patient.

Adolescent↗

PubMed2002

[Narcolepsy-cataplexy].

The diagnosis of narcolepsy-cataplexy is based on three axes: 1) the medical history is strongly suggestive when diurnal sleep attacks (narcolepsy) and drop attacks (cataplexy) are reported or observed; 2) the polysomnography is mandatory and shows nocturnal and diurnal (multiple sleep latency test) REM sleep onsets; 3) HLA typing, practically helps to exclude the diagnosis when HLA DR15-DQB1*0602 is not present. New pathogenetic hypotheses have been proposed, mostly based the absence of hypocretin in narcoleptic cerebrospinal fluid. This neurotransmitter was previously known exclusively by its involvement in alimentary behaviours. The new therapies remain symptomatic, but they are powerful to prevent somnolence, daytime sleepiness, cataplexy and insomnia associated with this syndrome.

Carrier Proteins↗

PubMed1996

Diagnosing narcolepsy through the simultaneous clinical and electrophysiologic analysis of cataplexy.

OBJECTIVE: To demonstrate the utility of accurate clinical and electroencephalographic characterization of provoked cataplexy spells in the diagnosis of narcolepsy. METHODS: Four individuals, three with suspected and one with known narcolepsy, were clinically assessed during split-screen, video polysomnographic monitoring sessions after cataplectic events were induced by emotional provocation. RESULTS: The subjects experienced a total of nine cataplectic-like events, one occurring spontaneously (sleep paralysis) in association with a hypnagogic hallucination. During all events, the patients appeared to be sleeping with polysomnographic rapid eye movement sleep patterns, but when questioned they were able to give appropriate verbal responses. The diagnosis of narcolepsy was substantiated in all cases using standard overnight polysomnograms and multiple sleep latency tests. CONCLUSION: The diagnosis of narcolepsy can be greatly enhanced by documenting cataplexy with thorough clinical assessment and demonstration of typical rapid eye movement sleep patterns during provoked spells in the course of polysomnographic monitoring sessions.

Adolescent↗

PubMed1977

Anorgasmia and cataplexy.

Ten married women with cataplexy were found to be rarely orgasmic. Cataplexy is characterized by recurrent episodes of short-lived generalized muscle paralysis. It is precipitated by arousing emotional precipitants such as laughter, fear, and anger. Patients learn to avoid situations exposing them to these precipitants. It is suggested that anorgasmia is a consequence of this general tendency to avoid arousal.

Adult↗

PubMed1982

Auditory evoked potentials compared to performance measures and EEG in assessing excessive daytime sleepiness in narcolepsy-cataplexy.

The AEP to the repetitive stimuli of the Wilkinson auditory vigilance task was compared between untreated patients with narcolepsy-cataplexy and matched controls for periods during which the tones were preceded by 13 sec or more of wakefulness (defined by EEG-polygraphic criteria). During these periods it had been found previously that narcoleptics did not perform worse than did controls. The AEP, nevertheless, showed significant differences for narcoleptics. These were similar to changes described for drowsiness in normals. The AEP, therefore, showed changes related to excessive day time drowsines in narcolepsy-cataplexy when a sensitive performane measure and visual analysis of EEG-polygraphic recordings did not.

Adult↗

PubMed1991

Sleep and EEG disturbances in a rat neurological mutant (taiep) with immobility episodes: a model of narcolepsy-cataplexy.

The electroencephalographic sleep patterns recorded during short periods of time (3 h) of a neurological mutant rat (taiep) were studied. This rat exhibits, among other signs, immobility episodes that are similar to those observed in narcolepsy-cataplexy. We describe findings of long term (6 months) electroencephalographic studies done in 9 mutant and 5 control rats. The mutant rats present electroencephalographic and behavioral disorders consisting of: (a) bursts of cortical waxing and waning waves occurring during the drowsy state; in some animals this activity represents up to 25% of the total drowsiness time; (b) shortened sleep time; (c) fragmented paradoxical sleep; (d) immobility episodes when the animals are subjected to an emotional excitement; and (e) electrographic activity of paradoxical sleep without atonia during the immobility episodes. These findings show that the taiep mutant shows several aspects of narcolepsy-cataplexy and it may represent an experimental model for the study of this pathology.

Animals↗

PubMed1991

Effects of SDZ NVI-085, a putative subtype-selective alpha 1-agonist, on canine cataplexy, a disorder of rapid eye movement sleep.

Canine narcolepsy is an animal model of the human rapid eye movement sleep disorder. Dogs exhibit bouts of sleep attacks and muscle atonia (cataplexy) that are induced by emotions and thought to be abnormal rapid eye movement sleep episodes. We have previously demonstrated that cataplexy is strongly inhibited by increases in noradrenergic activity. This effect is mediated through central alpha 1-adrenoceptors, presumably of the alpha 1B subtype. In this study, we demonstrate with the canine model that SDZ NVI-085, a new compound with alerting effects, is a potent anticataplectic agent that may act through stimulation of an alpha 1-adrenoceptor subtype.

Adrenergic alpha-Agonists↗

PubMed1996

Cataplexy and the switch process of multiple personality disorder.

A case history is presented of an 18-year-old male with dissociative disorder and polysubstance abuse. The patient was observed to switch between three personalities, and the personality changes were often associated with symptoms of cataplexy. Both dissociative episodes and cataplexy are associated with strong affective stimuli. Similar reports in the literature are briefly reviewed.

Adolescent↗

PubMed2004

Pharmacotherapy for cataplexy.

A variety of medications representing several major drug classes improve cataplexy in patients with narcolepsy. These include aminergic reuptake inhibitors such as venlafaxine and clomipramine as well as sodium oxybate. This review is intended to familiarize readers with the safety and efficacy of these medications, thus enabling clinicians to optimize their management of cataplexy.

Antidepressive Agents↗

PubMed1979

The treatment of narcolepsy-cataplexy with nocturnal gamma-hydroxybutyrate.

Sixteen patients with narcolepsy and cataplexy were treated with gamma-hydroxybutyrate (GHB) given at night and tailored to achieve as continuous a night's sleep as possible. The dosage usually consisted of 1.5-2.25 gm orally at bedtime and then one or two further 1.0-1.5 gm doses with awakenings during the night, and totaled about 50 mg/kg. Apart from one patient who took only the bedtime dose, the subjective quality of night sleep improved in all patients and the number of irresistible daytime attacks of sleep and cataplexy substantially diminished. Some residual daytime drowsiness remained and this usually responded well to low doses of methylphenidate. Improvement has been maintained for up to 20 months without the development of tolerance. Two patients experienced adverse side effects necessitating withdrawal of GHB treatment, but no serious toxic effects have occurred.

Adult↗

PubMed1989

Prostaglandin E2 and its methyl ester reduce cataplexy in canine narcolepsy.

The effects of intravenous administration of prostaglandins (PGs) were investigated in genetically narcoleptic Doberman pinschers. The treatment of narcoleptic dogs with PGE2 and PGE2 methyl ester, but not PGD2 and PGD2 methyl ester, induced a dose-dependent reduction of canine cataplexy, a dissociated manifestation of rapid-eye-movement sleep. The effect was specific and not associated with any change in other behavior. Furthermore, the effect was long-lasting (up to 2 hr) and could not be explained by the acute cardiovascular changes seen after intravenous PG administration. PGE2 methyl ester, a lipophilic derivative of PGE2 with more central penetration than PGE2, was 4 times more potent than PGE2. These results indicate that PGE2 modifies cataplexy through a central effect and suggest that this prostaglandin may play a role in rapid-eye-movement sleep regulation.

Animals↗

PubMed1991

Pupillometric assessment of excessive daytime sleepiness in narcolepsy-cataplexy.

Ten untreated patients with narcolepsy-cataplexy and age- and sex-matched normals between the ages of 20 and 71 years underwent pupillometric analyses immediately prior to each of five multiple sleep latency test sessions. Although narcoleptics were sleepier as indicated both by their Stanford Sleepiness Scale ratings and by their latencies to sleep onset, the baseline pupil diameter, pupillary light reflex, and pupillary orienting response did not differentiate between groups. Narcoleptics did, however, exhibit a significantly greater frequency of spontaneous oscillations in the dark-adapted state than did controls. These findings indicate that pupillary stability may serve as a supplementary diagnostic tool for narcolepsy-cataplexy. The results are discussed with the view that psychosensory restoration of alertness, among other extraneous variables, must be controlled when utilizing pupillometric techniques. A review of the literature indicates a variety of methodological and statistical shortcomings that must be amended. Suggestions are made for improving the reliability and validity of the pupillometric approach.

Adult↗

PubMed1983

Cataplexy brought on by playing checkers.

A 55-year-old man had experienced spells of weakness and trembling daily for 24 years before the correct diagnosis of cataplexy was reached. While the patient played checkers, the degree of cataplexy worsened when it was the patient's move and improved when it was his opponent's. Response to therapy was excellent.

Cataplexy↗

PubMed2005

Brainstem hyperexcitability during cataplexy.

The exact cause of narcolepsy-cataplexy syndrome remains unclear; however, the recent discovery of hypocretin deficiency in the lateral hypothalamus of narcoleptic patients has increased our understanding of its etiology. The authors performed masseter reflex, tibial F response, and blink reflex excitability studies during and between attacks in a 66-year-old man with status cataplecticus. Masseter reflex and F responses were inhibited while the blink reflex R2 component was enhanced during attacks, suggesting either hyperexcitability or disinhibition of pontine and/or medullary interneurons but hypoexcitability of pontine and spinal motor neurons during cataplexy.

Aged↗

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↗

PubMed1991

Isolated cataplexy of more than 40 years' duration.

For over 40 years, a 55-year-old woman had suffered from cataplexy, which had been mistakenly identified as hysteria. Sleepiness, hypnagogic hallucinations and sleep-onset paralysis were not present. This is the longest duration of isolated cataplexy reported so far.

Cataplexy↗