Cases reported "Narcolepsy"

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1/5. Sudden daytime sleep onset in Parkinson's disease: polysomnographic recordings.

    sleep attacks in Parkinson's disease are controversially discussed. This paper describes a patient with Parkinson's disease suffering from sudden, irresistible onset of sleep during daytime. Medication included levodopa, entacapone, budipine, and cabergoline. Introduction of entacapone was the last therapeutic action preceding onset of sleep events, suggesting increased bioavailabilty of levodopa to be provocative in this case. In contrast to previous cases, the sudden sleep events were witnessed by clinical staff members and documented by polysomnographic and video recordings. polysomnography during these sleep events remarkably showed abrupt slowing of EEG-background activity and occurrence of slow eye movements and K-complexes within 10 seconds after stable wakefulness. Within 60 seconds, the polysomnographic pattern proceeded to stable sleep stage 2.
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2/5. kleine-levin syndrome with periodic apnea during hypersomnic stages--E.E.G. study.

    A 33 year old male, suffering from Kleine-Levine syndrome associated with periods of apnea during the hypersomnic attacks, is reported. Ventilatory studies negate the Pickwickian syndrome. The E.E.G.'s recorded during the hypersomnic attacks and the apneic periods showed a direct correlation between high-voltage delta waves paroxysmal E.E.G. activity, and apneic period. Medications known to improve kleine-levin syndrome, in our case, had no effect upon the clinical hypersomnic and apnea periods, nor on the correlatives E.E.G.'s pattern and spirometric studies. Theoretical considerations let us assume that these paroxysmal E.E.G. patterns associated with apnea are NRem-sleep serotonin dependent, and have an inhibitory influence on the respiratory centers, by alternating the equilibrium between the catecholamines and acetylcholine activities.
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3/5. Efficacy of trazodone in narcolepsy.

    A 25-year-old man with narcolepsy and cataplexy experienced partial relief of symptomatology following administration of methylphenidate. Moreover, the latter caused extreme agitation and aggression. However, administration of the antidepressant agent trazodone resulted in almost complete alleviation of the narcoleptic and cataplectic attacks within 48 h after initiation of therapy. trazodone, a novel antidepressant agent may be useful in the long-term management of individuals suffering from narcolepsy.
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4/5. A method for provoking EEG abnormalities by administration of nialamide.

    nialamide, a kind of monoamine oxydase inhibitor, was used for provoking centrencephalic EEG abnormalities and 6-14 Hz positive spikes. It was assumed that these EEG abnormalities have close relationship with dysfunctions of the brainstem which is rich in monoamines and monoamine oxydase. The nialamide provocation was carried out on 49 inpatients who had centrencephalic discharges in their EEG reports. These patients consisted of four cases of epilepsy, one case of anorexia nervosa, two cases of narcolepsy and 42 cases of diencephalosis. Another series of 22 patients suffering from other diseases, in whome EEG no centrencephalic EEG abnormallities were detected, were examined with nialamide. Out of the 49 patients, 35 cases (71.4 ) showed increased EEG abnormalities following the administration of nialamide. It was noteworthy that this drug had provocative effect not only for EEG abnormalities, but also for the symptoms from which patients were suffering. In 26 out of 49 patients, both EEG abnormalities and clinical symptoms were provoked by nialamide. And the nialamide administration resulted in negative on all 22 patients who did not register centrencephalic EEG abnormalities. The mechanism and characteristics of this provocative procedure by the use of nialamide were evaluated.
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5/5. Reversal of atypical depression, sleepiness, and REM-sleep propensity in narcolepsy with bupropion.

    We successfully treated a 46-year-old narcoleptic woman suffering from atypical depression with bupropion hydrochloride. Diagnostic evaluation revealed a Beck depression Inventory (BDI) score of 24, a short nocturnal REM-sleep latency, subjective and objective sleepiness (mean sleep latency (MSL) = 1.8 minutes), and three sleep onset REM-sleep periods during the five nap multiple sleep latency test. bupropion (100 mg t.i.d.) normalized her mood (BDI = 6), sleepiness (MSL = 9.1 minutes), and REM-sleep propensity. Upon discontinuation of bupropion, these parameters reverted to pretreatment levels. This "activating" antidepressant's reversal of the sleepiness and REM-sleep propensity in narcolepsy may be due to blockade of dopamine or norepinephrine reuptake. Clinicians need to be alert to the fact that depression can mask the diagnosis of narcolepsy. bupropion warrants further investigation as a treatment for narcolepsy in an open-label, double-blind, placebo-controlled paradigm.
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