Objective: The purpose of this study was to illustrate the electrophysiological features of sleep disturbances in patients with anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis in both active and recovery stages.
Methods: Retrospectively filed video electroencephalogram (VEEG) and polysomnography (PSG) data in 24 patients with anti-LGI1 encephalitis were analyzed in comparison with that in 20 individuals without sleep disorders as control group.
Results: Sleep efficiency (SE) and total sleep time involving REM and NREM sleep were significantly decreased in patients with anti-LGI1 encephalitis during the active stage compared to that during the recovery stage and in the control group. Imbalanced sleep structure was found, demonstrated by elevated N1, decreased N3 and REM components, as well as abnormal N2 structure characterized with significantly lower spindle duration and density during the active stage. These findings were independent of the presence of nocturnal episodic events or sleep hyperkinetic movements (HMs). HMs were present in 11/23 patients throughout NREM and REM sleep (nonspecific in sleep stages) during the active stage. During the recovery stage, SE and sleep structures were dramatically improved, including the percentage of N3 and REM sleep, spindle duration and density. Ten of 11 patients with HMs were followed up. HMs were totally remitted in 3 patients and still persistent in 1, while evolved into REM sleep behavior disorder (RBD) in 4 with comorbid periodic limb movement syndrome (PLMS) in 3/4, and only PLMS in 2.
Conclusion: Sleep disturbances were remarkable and intrinsic features in active anti-LGI1 encephalitis, marked by overall disruptions of both NREM and REM sleep, as well as the presence of HMs, which tend to evolve into RBD or PLMS during the recovery stage. Long-term follow-up with PSG is needed, especially for those patients with severe sleep disturbances during the active phase.
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http://dx.doi.org/10.2147/NSS.S299467 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
March 2025
Department of Neurology and Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt- Universität zu Berlin.
Background And Objectives: Cognitive deficits represent a major long-term complication of anti-leucine-rich, glioma-inactivated 1 encephalitis (LGI1-E). Although severely affecting patient outcomes, the structural brain changes underlying these deficits remain poorly understood. In this study, we hypothesized a link between white matter (WM) networks and cognitive outcomes in LGI1-E.
View Article and Find Full Text PDFWorld J Radiol
January 2025
Laboratory of Functional Chemistry and Nutrition of Food, Northwest A&F University, Yangling 712100, Shanxi Province, China.
Background: Autoimmune encephalitis (AE) is a rare and recently described neuroinflammatory disease associated with specific autoantibodies. Anti-leucine-rich glioma inactivated 1 (anti-LGI1) encephalitis is a rare but treatable type of AE discovered in recent years. Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia.
View Article and Find Full Text PDFNeurol Sci
January 2025
Department of Neurology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan, China.
The Fc receptor (FcRn) inhibitors can ameliorate autoimmune conditions such as myasthenia gravis through a rapid and specific clearance of serum IgG levels, and they also have potential for future use in a wider variety of antibody-mediated autoimmune diseases. Some patients with therapy-refractory autoimmune encephalitis (AE) continue to be unresponsive to initial and secondary treatment regimens. A 32-year-old male presented with predominant psychiatric symptoms and seizures, along with imaging evidence indicating multifocal cerebral cortical involvement.
View Article and Find Full Text PDFNeuropsychiatr Dis Treat
December 2024
Department of Neurology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangdong, 510180, People's Republic of China.
Background: Mitochondrial damage is significant in autoimmune diseases, with mitochondrial N-formyl methionine peptide (fMet) being released from damaged mitochondria. However, its potential as a marker for assessing the severity of two kinds of encephalitis - anti-N-methyl-D-aspartate receptor (anti-NMDAR) and anti-leucine-rich glioma-inactivated 1 (LGI1) - remains uncertain. We measured CSF fMet levels in anti-NMDAR encephalitis and anti-LG1 encephalitis patients, assessing its diagnostic and therapeutic potential.
View Article and Find Full Text PDFOxf Med Case Reports
December 2024
Department of Neurology, New Cross Hospital, Royal Wolverhampton NHS Trust, Wolverhampton Road, Heath Town, West Midlands, WV10 0QP, United Kingdom.
The leucine-rich glioma-inactivated protein 1 (LGI1) antibody-related autoimmune encephalitis can occur alone or in the setting of a malignancy and manifest with faciobrachial dystonic seizures (FBDS), cognitive decline, hyponatremia, and neuropsychiatric disorders. The importance of differentiating this entity from acute delirium cannot be overemphasized. This review provides a detailed account of a 71-year-old man with previous diagnosis of lung cancer who presented with subacute onset behavioural changes, urinary retention, and FBDS.
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