Sleep Disorders in Neurologic Practice: A Case-based Approach.

Sleep disorders are common in neurology practice, but are often undiagnosed and untreated. Specific patient cohorts, such as older adults, patients residing in nursing homes, and patients with underlying chronic neurologic and psychiatric disorders, are at particular risk. If these sleep problems are not properly evaluated and managed the patient may experience exacerbation of the underlying neurologic disorder.

Extended wakefulness: compromised metabolics in and degeneration of locus ceruleus neurons.

Modern society enables a shortening of sleep times, yet long-term consequences of extended wakefulness on the brain are largely unknown. Essential for optimal alertness, locus ceruleus neurons (LCns) are metabolically active neurons that fire at increased rates across sustained wakefulness. We hypothesized that wakefulness is a metabolic stressor to LCns and that, with extended wakefulness, adaptive mitochondrial metabolic responses fail and injury ensues.

Effects of chronic sleep fragmentation on wake-active neurons and the hypercapnic arousal response.

Study Objectives: Delayed hypercapnic arousals may occur in obstructive sleep apnea. The impaired arousal response is expected to promote more pronounced oxyhemoglobin desaturations. We hypothesized that long-term sleep fragmentation (SF) results in injury to or dysfunction of wake-active neurons that manifests, in part, as a delayed hypercapnic arousal response.

C/EBP homologous binding protein (CHOP) underlies neural injury in sleep apnea model.

Study Objectives: Obstructive sleep apnea (OSA) is associated with cognitive impairment and neuronal injury. Long-term exposure to intermittent hypoxia (LTIH) in rodents, modeling the oxygenation patterns in sleep apnea, results in NADPH oxidase 2 (Nox2) oxidative injury to many neuronal populations. Brainstem motoneurons susceptible to LTIH injury show uncompensated endoplasmic reticulum stress responses with increased (CCAAT/enhancer binding protein homologous protein (CHOP).

Sleep-disordered breathing.

Purpose Of Review: This article introduces readers to the clinical presentation, diagnosis, and treatment of sleep-disordered breathing and reviews the associated risk factors and health consequences.

Recent Findings: Sleep-disordered breathing is associated with significant impairments in daytime alertness and cognitive function as well as adverse health outcomes. The initial treatment of choice is positive airway pressure.

Daytime sleepiness in obesity: mechanisms beyond obstructive sleep apnea--a review.

Increasing numbers of overweight children and adults are presenting to sleep medicine clinics for evaluation and treatment of sleepiness. Sleepiness negatively affects quality of life, mental health, productivity, and safety. Thus, it is essential to comprehensively address all potential causes of sleepiness.

SIRT1 regulation of wakefulness and senescence-like phenotype in wake neurons.

Wake neurons in the basal forebrain and brainstem provide critical inputs to optimize alertness and attention. These neurons, however, evidence heightened vulnerability to a diverse array of metabolic challenges, including aging. SIRT1 is an nicotinamide adenine dinucleotide responsive deacetylase serving diverse adaptive responses to metabolic challenges, yet this metabolic rheostat may be downregulated under conditions of significant oxidative stress.

Review of sleep disorders.

Sleep disorders are common and may result in significant morbidity. Examples of the major sleep disturbances in primary care practice include insomnia; sleep-disordered breathing, such as obstructive sleep apnea; central nervous system hypersomnias, including narcolepsy; circadian rhythm sleep disturbances; parasomnias, such as REM sleep behavior disorder; and sleep-related movement disorders, including restless legs syndrome. Diagnosis is based on meticulous inventory of the clinical history and careful physical examination.