Recognizing New-Onset Sleep Disorders in Autoimmune Encephalitis Often Prompt Earlier Diagnosis.

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.

What Is the Prognostic Significance of Rapid Eye Movement Sleep Without Atonia in a Polysomnogram?

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.

Respiratory and sleep-related complications of multiple system atrophy.

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.

A contemporary review of obstructive sleep apnea.

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.

Rapid eye movement sleep and neuronal development.

PURPOSE OF REVIEW: To understand the importance of rapid eye movement (REM) sleep in the cognitive and sensorimotor development via neural plasticity during embryonic development and infants. RECENT FINDINGS: REM sleep has remained a mystery as many of the underlying mechanisms of REM sleep remain unclear. Recent findings have demonstrated that REM sleep selectively prunes newly formed dendritic spines in the developing brain as well as strengthening new synapses in the developing brain. This process is critical for normal neuronal circuit development and behavioral improvement after learning. SUMMARY: Although many mechanisms of REM sleep remain unclear, recent findings strongly suggest that REM sleep is vitally important in pruning synapses as well as maintaining new synapses for the development of a healthy brain. Developmental neuroplasticity refers to the continuous change of the developing brain during fetal development. Lack of plasticity may result in reduced intellectual ability, reduced learning and memory consolidation, and mental illness.

Sleep disorders in adults with epilepsy: past, present, and future directions.

PURPOSE OF REVIEW: To summarize recent studies on the complex relationships between sleep disorders, sleep, and epilepsy. RECENT FINDINGS: Insomnia in adults with epilepsy (AWE) warrants consideration of depression, anxiety, and suicidal ideation. Daytime sleepiness in AWE is more often due to undiagnosed sleep disorders. Sleep deprivation is an important provoker of seizures in juvenile myoclonic epilepsy. Abnormalities in frontal lobe executive function with difficulties making advantageous decisions may explain failure of juvenile myoclonic epilepsy patients to adhere to treatment recommendations and regulate their sleep habits. Sleep architecture in AWE is more likely to be abnormal if seizures are poorly controlled or occur during sleep. Obstructive sleep apnea is much more common in AWE who are man, older, heavier, or whose seizures are poorly controlled. Chronobiology and chronopharmacology of epilepsy is an emerging field worthy of future research and clinical applications. SUMMARY: Identifying and treating unrecognized sleep disorders and understanding the impact of circadian rhythms on epilepsy can improve quality of life and seizure control in AWE.

Treatment strategies for complex behavioral insomnia in children with neurodevelopmental disorders.

PURPOSE OF REVIEW: This review describes recent research in pediatric behavioral insomnias in neurodevelopmental disorders and their treatment. RECENT FINDINGS: Insomnia in children with autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDDs) is typically complex, chronic, and difficult to adequately control. Abnormalities in genetic and/or epigenetic regulation of sleep/wakefulness and its timing predispose patients with NDD to insomnia, although poor sleep hygiene, maladaptive associations, and limit-setting are likely to contribute. Parents are agents for change in problematic sleep behaviors in patients with NDD. We review the benefits of behavioral therapies and melatonin to treat sleep problems in children with NDD. Problematic sleep is so prevalent in some neurodevelopmental syndromes (Rett, Angelman, Williams, and Smith-Magenis) that it is part of their diagnostic criteria. SUMMARY: Children and adolescents with neurological disorders frequently have complex sleep disorders that require treatment. Understanding the basic pathology and treatment strategies provides an opportunity to improve well being and quality of life in those affected by NDD and their families.

Roles of gender, age, race/ethnicity, and residential socioeconomics in obstructive sleep apnea syndromes.

PURPOSE OF REVIEW: Review recent research on the roles of gender, race/ethnicity, residential socioeconomics and age in obstructive sleep apnea syndromes (OSA) and their treatment. RECENT FINDINGS: Men have a higher prevalence of OSA than women and require higher continuous positive airway pressure (CPAP) pressures for treatment, given similar severity of OSA. When comparing age, women have less severe apnea at all ages. Menopause, pregnancy and polycystic ovarian syndrome increase the risk for OSA in women. Neck fat and BMI influence apnea-hypopnea index (AHI) severity in women; abdominal fat and neck-to-waist ratio do so in men. Obesity, craniofacial structure, lower socioeconomic status and neighborhood disadvantage may better explain ethnic/racial differences in the prevalence and severity of OSA. Ethnicity was no longer significantly associated with OSA severity when WHO criteria for obesity were used. SUMMARY: OSA has a male predominance; women have a lower AHI than men during certain stages of sleep; women require less CPAP pressure for treatment of similar severity of OSA, and there are ethnic/racial differences in the prevalence and severity of OSA but these may be due to environmental factors, such as living in disadvantaged neighborhoods.

Cognitive dysfunction and obstructive sleep apnea: from cradle to tomb.

PURPOSE OF REVIEW: To understand clinical characteristics and risk factors for cognitive impairment in patients with obstructive sleep apnea (OSA) syndromes. RECENT FINDINGS: Primary snoring increases the risk of neurocognitive impairment and lower intelligence quotients in infants and children. Middle-aged adults with severe OSA are at greater risk for cognitive impairment than young adults with apnea of equal severity. Older women with OSA are at increased risk for minimal cognitive impairment or dementia, 5 years later. SUMMARY: Certain age groups (younger and older) are particularly susceptible to the negative effects of OSA on cognition. Other influences that increase the risk for cognitive dysfunction in OSA include premature birth, apolipoprotein e4 allele status and other genetic polymorphisms, lower socioeconomic status, fewer years of education, and ethnicity.

Primary sleep disorders and paroxysmal nocturnal nonepileptic events in adults with epilepsy from the perspective of sleep specialists.

Sleep specialists are frequently referred adults with epilepsy to evaluate their sleep/wake complaints, sometimes to determine whether their paroxysmal nocturnal behaviors are epileptic or not. Many patients with epilepsy have at least one parasomnia (some more than one), and the sleep specialists are often asked to differentiate and treat these. Sleep specialists review which primary sleep disorders are more common in adults with epilepsy and how to evaluate and best treat these. The authors summarize (1) how to evaluate and differentiate parasomnias using video-polysomnography; (2) the value of sleep deprivation and loud auditory stimuli to increase the likelihood of provoking a non-rapid eye movement arousal parasomnia with a single night of video-polysomnography; and (3) how to score excessive muscle activity during rapid eye movement sleep to confirm a diagnosis of rapid eye movement sleep behavior disorder. The clinical semiology and video-polysomnography features of simple and complex sleep-related movement disorders and parasomnias are reviewed.