Non-positional severe obstructive sleep apnea on polysomnogram became positional OSA with CPAP therapy.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Sudhansu Chokroverty.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Sleep disturbances are common in neurodegenerative diseases. Disturbed sleep can result in fatigue, irritability, morning headaches, impaired motor and cognitive skills, depression, and daytime somnolence. The major sleep complaints include: insomnia, hypersomnia, parasomnia, excessive nocturnal motor activity, circadian sleep-wake rhythm disturbance, and respiratory dysrhythmia. The pathogenetic mechanisms of sleep disturbances may be secondary to direct structural alteration of the sleep-wake generating neurons or from several other indirect mechanisms. At the biochemical level, neurodegenerative diseases may be largely classified as tauopathies, alpha-synucleinopathies, and other diseases. Overnight polysomnography (PSG) and multiple sleep latency test are the two most important diagnostic laboratory tests in the evaluation of sleep disturbances. Management of sleep disturbances is complex and is based primarily on the nature of the sleep disturbance. The clinical profiles, pathogenetic mechanisms, PSG findings, and management issues are discussed here with reference to some common neurodegenerative diseases.
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.