RESUMEN
SUMMARY: Sleep/wake disorders are common in patients with autoimmune encephalitis, sometimes the most prominent or sole initial symptom, then delaying diagnosis. Sleep/wake disorders in autoimmune encephalitis vary and include severe sleeplessness, hypersomnia, central and/or obstructive sleep apnea, rapid eye movement sleep behavior disorder, indeterminate sleep/wake states, and loss of circadian sleep/wake rhythms. N-methyl- d aspartate receptor encephalitis (NMDAR) is often associated with insomnia, then hypersomnia and sleep-related central hypoventilation. Profound sleeplessness and rapid eye movement sleep behavior disorder are seen in patients with voltage-gated potassium channel-complex antibodies. Fragmented sleep and hypersomnia are common in paraneoplastic syndromes associated with anti-MA protein encephalitis; rapid eye movement sleep behavior disorder in those with antibodies against leucine-rich glioma inactivated protein (LGI1) or contactin-associated protein 2 (CASPR2) antibodies. Antibodies against a cell adhesion protein IGLON5 may result in obstructive sleep apnea, inspiratory stridor, disorganized nonrapid eye movement sleep, and excessive movements and parasomnias fragmenting nonrapid and rapid eye movement sleep. Recognizing a particular sleep/wake disorder is often a presenting or prominent feature in certain autoimmune encephalitis permit for earlier diagnosis. This is important because reduced morbidity and better short- and long-term outcomes are associated with earlier diagnosis and immunotherapies.
Asunto(s)
Trastornos de Somnolencia Excesiva , Encefalitis , Trastorno de la Conducta del Sueño REM , Apnea Obstructiva del Sueño , Trastornos del Inicio y del Mantenimiento del Sueño , Trastornos del Sueño-Vigilia , Anticuerpos , Autoanticuerpos , Moléculas de Adhesión Celular Neuronal , Encefalitis/complicaciones , Encefalitis/diagnóstico , Enfermedad de Hashimoto , Humanos , Trastornos del Sueño-Vigilia/diagnóstico , Trastornos del Sueño-Vigilia/etiologíaRESUMEN
SUMMARY: Freud said we are lucky to be paralyzed during sleep, so we cannot act out our dreams. Atonia of skeletal muscles normally present during rapid eye movement sleep prevents us from acting out our dreams. Observing rapid eye movement sleep without atonia in a polysomnogram in older adults first and foremost warrants consideration of rapid eye movement behavior disorder. Seventy-five to 90% of older adults with isolated rapid eye movement behavior disorder will develop a neurodegenerative disease within 15 years, most often a synucleinopathy. Rapid eye movement sleep without atonia in those younger than 50 years is commonly found in individuals with narcolepsy and those taking antidepressant medications.
Asunto(s)
Enfermedades Neurodegenerativas , Trastorno de la Conducta del Sueño REM , Anciano , Humanos , Hipotonía Muscular , Pronóstico , Trastorno de la Conducta del Sueño REM/diagnóstico , Trastorno de la Conducta del Sueño REM/tratamiento farmacológico , Sueño/fisiología , Sueño REM/fisiologíaRESUMEN
PURPOSE OF REVIEW: The purpose of this article is to provide a contemporary review of sleep issues affecting patients with multiple system atrophy (MSA). RECENT FINDINGS: Prodromal symptoms of MSA may occur years prior to diagnosis, including autonomic dysfunction such as orthostatic hypotension, urogenital dysfunction, rapid eye movement (REM) sleep behavior disorder (RBD), and stridor. Patients may also develop sleep-related respiratory disorders such as obstructive sleep apnea (OSA), central sleep apnea (CSA), and stridor. The development of stridor is associated with a shortened lifespan and sudden death, which may be further accelerated by autonomic instability. MSA appears to follow a 'prion-like' disease progression. SUMMARY: MSA is a rapidly progressive neurodegenerative disease characterized by a combination of autonomic failure and motor symptoms. MSA is often misdiagnosed as the initial presentation mimics other neurodegenerative disorders. There are diagnostic criteria to identify possible, probable, and definite MSA. Prodromal symptoms may occur years prior to diagnosis, including autonomic dysfunction such as orthostatic hypotension, urogenital dysfunction, REM RBD, and stridor. In previous years, treatment consisted of tracheostomy but did not address the component of CSA, which commonly coexisted or developed later because of destruction of medullary chemoreceptors. Positive airway pressure may be as effective as tracheostomy alone in ameliorating obstruction at the vocal cord level.
Asunto(s)
Atrofia de Múltiples Sistemas/complicaciones , Atrofia de Múltiples Sistemas/diagnóstico , Trastornos del Sueño-Vigilia/etiología , Progresión de la Enfermedad , Humanos , Atrofia de Múltiples Sistemas/terapia , Respiración con Presión Positiva , Ruidos Respiratorios/etiología , Apnea Central del Sueño/etiología , Apnea Obstructiva del Sueño/etiología , TraqueostomíaRESUMEN
PURPOSE OF REVIEW: This review provides a contemporary review of sleep apnea with emphasis on definitions, epidemiology, and consequences. RECENT FINDINGS: Amyloid ß-42 is one of the main peptides forming amyloid plaques in the brains of Alzheimer patients. Poorer sleep quality and shorter sleep duration have been associated with a higher amyloid burden. Decreased sleep time in the elderly is a precipitating factor in amyloid retention. Studies have shown that the dysregulation of the homeostatic balance of the major inhibitory and excitatory amino acid neurotransmitter systems of gamma-aminobutyric acid (GABA) and glutamate play a role in sleep disordered breathing (SDB). SUMMARY: Untreated sleep disordered breathing (obstructive sleep apnea and/or central sleep apnea) are an important cause of medical mortality and morbidity. OSA is characterized by recurrent episodes of partial or complete collapse of the upper airway during sleep followed by hypoxia and sympathetic activation. Apneic events are terminated by arousal, followed by increases in pulse and blood pressure, and re-oxygenation and the release of inflammatory factors. Individuals with OSA have an increased risk of developing atrial fibrillation. Hypoxemia and poor sleep quality because of OSA increase the risk of cognitive decline in the elderly.