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

Abstract

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.