idiopathic hypersomnia/ácido gama aminobutírico

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Absence of γ-aminobutyric acid-a receptor potentiation in central hypersomnolence disorders.

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The pathophysiology of idiopathic hypersomnia (IH) remains unclear. Recently, cerebrospinal fluid (CSF)-induced enhancement of γ-aminobutyric acid (GABA)-A receptor activity was found in patients with IH compared to controls. Fifteen unrelated patients (2 males and 13 females) affected with typical

Update on treatment for idiopathic hypersomnia.

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BACKGROUND Idiopathic hypersomnia (IH) is a poorly characterized orphan central disorder of hypersomnolence responsible for excessive daytime sleepiness (EDS), prolonged nighttime sleep and sleep inertia that often require long-term symptomatic stimulant medication. To date, no drug has currently

Idiopathic hypersomnia.

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Idiopathic hypersomnia continues to evolve from the concept of "sleep drunkenness" introduced by Bedrich Roth in Prague in 1956 and the description of idiopathic hypersomnia with two forms, polysymptomatic and monosymptomatic, by the same Bedrich Roth in 1976. The diagnostic criteria of idiopathic

Use of subcutaneous flumazenil preparations for the treatment of idiopathic hypersomnia: A case report.

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Idiopathic hypersomnia (IH) is a rare sleep disorder, recently hypothesized to be related to the production of a molecule that facilitates the binding of gamma-aminobutyric acid (GABA) to the GABA receptor. This paper reports on the treatment of a patient with IH who was treated with a 96-hour

Biochemistry, Gamma Aminobutyric Acid

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Gamma-aminobutyric acid (GABA) acts as the principal inhibitory neurotransmitter in the central nervous system (CNS). Although researchers discovered GABA in biological tissues in 1910, its neurological role in mammals remained unknown until the late 1950s.[1] Cortical neuron studies completed in

Central Disorders of Hypersomnolence: Focus on the Narcolepsies and Idiopathic Hypersomnia.

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The central disorders of hypersomnolence are characterized by severe daytime sleepiness, which is present despite normal quality and timing of nocturnal sleep. Recent reclassification distinguishes three main subtypes: narcolepsy type 1, narcolepsy type 2, and idiopathic hypersomnia (IH), which are

Modulation of vigilance in the primary hypersomnias by endogenous enhancement of GABAA receptors.

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The biology underlying excessive daytime sleepiness (hypersomnolence) is incompletely understood. After excluding known causes of sleepiness in 32 hypersomnolent patients, we showed that, in the presence of 10 μM γ-aminobutyric acid (GABA), cerebrospinal fluid (CSF) from these subjects stimulated

Update on hypersomnias of central origin.

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OBJECTIVE To describe the multiple clinical aspects of hypersomnias of central origin. Emphasis is given to the new pathophysiological pathways and treatment options described in the current literature. RESULTS Narcolepsy is the most recognized of the hypersomnias of central origin. Hypocretin

Novel Indications for Benzodiazepine Antagonist Flumazenil in GABA Mediated Pathological Conditions of the Central Nervous System.

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This review paper discusses the central role of gamma-aminobutyric acid (GABA) in diverse physiological systems and functions and the therapeutic potential of the benzodiazepine antagonist flumazenil (Ro 15- 1788) for a wide range of disorders of the central nervous system (CNS). Our group and

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