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At least 811 records · Page 45Linked to original sources
PubMed1992

'Socrates' symptom'.

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Auditory Perceptual Disorders↗
PubMed2004

In vivo evidence of neuronal loss in the hypothalamus of narcoleptic patients.

A dysfunction of the orexin (hypocretin) system in the hypothalamus has recently been linked to the pathogenesis of narcolepsy. The authors used in vivo proton MR spectroscopy to assess the N-acetylaspartate (NAA) content in the hypothalamus of narcoleptic patients. Hypothalamic NAA/creatine-phosphocreatine was reduced in narcoleptic patients compared with control subjects (p < 0.01). Hypothalamic neuronal loss/damage is a central pathogenetic feature in narcolepsy.

Adolescent↗
PubMed1980

Multiple sclerosis and narcolepsy/cataplexy in a monozygotic twin.

Symptoms of narcolepsy/cataplexy developed in a monozygotic twin at the age of 56 years, 25 years after the onset of multiple sclerosis. The diagnosis of narcolepsy/cataplexy was confirmed by polygraphic recordings demonstrating sleep-onset periods of rapid eye movements (REM), increase in REM time per 24 hours, and disturbed nocturnal sleep. Frequent catapletic attacks were almost completely controlled by clomipramine. These symptoms may constitute one of the paroxysmal syndromes in multiple sclerosis. The discordancy for multiple sclerosis is attributed to a submaximal risk factor in the HLA system and a strong environmental factor in only one of the twins.

Adult↗
PubMed2004

Behavioral state instability in orexin knock-out mice.

Narcolepsy is caused by a lack of orexin (hypocretin), but the physiologic process that underlies the sleepiness of narcolepsy is unknown. Using orexin knock-out (KO) mice as a model of narcolepsy, we critically tested the three leading hypotheses: poor circadian control of sleep and wakefulness, inadequate activation of arousal regions, or abnormal sleep homeostasis. Compared with wild-type (WT) littermates, orexin KO mice had essentially normal amounts of sleep and wake, but wake and non-rapid eye movement (NREM) bouts were very brief, with many more transitions between all behavioral states. In constant darkness, orexin KO mice had normal amplitude and timing of sleep-wake rhythms, providing no evidence for disordered circadian control. When placed in a new, clean cage, both groups of mice remained awake for approximately 45 min, demonstrating that, even in the absence of orexin, fundamental arousal regions can be engaged to produce sustained wakefulness. After depriving mice of sleep for 2-8 hr, orexin KO mice recovered their NREM and rapid eye movement sleep deficits at comparable rates and to the same extent as WT mice, with similar increases in EEG delta power, suggesting that their homeostatic control of sleep is normal. These experiments demonstrate that the fragmented wakefulness of orexin deficiency is not a consequence of abnormal sleep homeostasis, poor circadian control, or defective fundamental arousal systems. Instead, the fragmented behavior of orexin KO mice may be best described as behavioral state instability, with apparently low thresholds to transition between states.

Animals↗
PubMed1984

The neurobiology of the narcoleptic syndrome.

Relevant electroencephalographic, psychopharmacologic, and genetic research reports are described in support of a neurobiological explanation of the narcoleptic syndrome. Despite increased support in this realm, no single neurobiological theory has won unanimous approval among sleep researchers, which has led toward speculation that the condition may be heterogeneous in nature. A multifactorial perspective, including psychological as well as neurobiological influences, appears to be the most productive model for research. Future investigation of sleep disorders utilizing such a model may enhance the understanding of neurobiological correlates of behavioural disorders.

Amphetamines↗
PubMed2002

Hypersomnolence and narcolepsy; a pragmatic diagnostic neurophysiological approach.

Out of a group of 250 consecutive patients who were examined for various disorders of sleep and waking at Ghent University Hospital within a period of 24 months, 30 patients with hypersomnolence associated with a suspected underlying neurological etiology were selected. The population consisted of 15 males and 15 females with mean age of 36 years (range: 16-60 years). Twenty-one patients had had hypersomnolence for more than 2 years. All patients underwent a single night polysomnography (PSG) and a 4-nap multiple sleep latency test (MSLT). PSG was normal in 23 patients. Sleep onset REM period (SOREMP) was defined as the occurrence of REM sleep within 15 min. after initiation of sleep. PSG demonstrated SOREMP's in only 1 patient and showed evidence of obstructive sleep apnea in 4 patients. Two patients had a low sleep efficiency. MSLT demonstrated hypersomnolence in 17 patients of whom 6 showed SOREMP. Significant hypersomnolence was defined as a mean sleep latency < or = 5 min. 4 patients fulfilled the classical clinical and polygraphic criteria (> or = 2 SOREMP) of narcolepsy. In 8 patients the tentative diagnosis of idiopathic CNS hypersomnolence was made. 13 patients did not sleep during MSLT. These results emphasize the relative importance of MSLT. Our limited 4-nap MSLT protocol proved useful in distinguishing narcolepsy from idiopathic CNS hypersomnolence.

Adolescent↗
PubMedDate not supplied

[Narcolepsy and the psychiatric tableau. A specific form of narcolepsy?].

Narcolepsy is a well-known hypersomnia. Nevertheless narcolepsy in which the hallucinatory component is unusually prominent may lead to a false diagnosis of schizophrenia syndrome. This aspect is illustrated by the case of Miss B. who appears like a psychotic patient without dissociation syndrome and with a hysterical personality. Are the narcoleptics with psychiatric disorders a peculiar sub-type of narcolepsy? Fourty-five percent of our eleven narcoleptics patients have an associated psychiatric disorder. Most of them are depressive. Surprisingly fourty percent of our patients are non-DR2 at the Human Leucocyte Antigen typing. Furthermore seventy five percent of them have an associated psychiatric disorder. This would mean a peculiar sub-type of narcolepsy.

Adolescent↗
PubMed2003

[Hypocretins/orexins and narcolepsy: from molecules to disease].

In order to foresee a curative treatment for narcolepsy, it is crucial to determine whether or not human narcolepsy is a neurodegenerative disorder, as we suggested, and to understand the mechanisms involved. The current hypothesis regarding the etiology of human narcolepsy is that it is an autoimmune disorder, because of its strong association with the human leukocyte antigen (HLA DQB1*0602), with the Hcrt neurons as the target. This hypothesis is supported by our results (Peyron et al., 2000) and others (Thannickal et al., 2000) showing that Hcrt messengers RNA and mature peptides are absent or greatly reduced in the brain of HLA DQB1*0602 positive narcoleptic patients examined to date. It is of great importance to determine whether the absence of Hcrt is due to a neurodegenerative process or to a default in the transcription process. After a brief review on hypocretins and narcolepsy, we discuss on how to tackle the issue.

Adolescent↗