Sleep Manifestations of Voltage-Gated Potassium Channel Complex Autoimmunity

Cornelius, Jason R.; Pittock, Sean J.; McKeon, Andrew; Lennon, Vanda A.; Aston, Paula A.; Josephs, Keith A.; Tippmann‐Peikert, Maja; Silber, Michael H.

doi:10.1001/archneurol.2011.106

Cited by 108 publications

(64 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Disorders of sleep, especially insomnia, as also occurred in our case, are cardinal manifestations in MoS and other disorders of VGKC-complex autoimmunity [16]. Insomnia was in fact the earliest manifestation in our patient and started months before the full clinical presentation of the syndrome.…”

Section: Discussionsupporting

confidence: 72%

See 1 more Smart Citation

Morvan's syndrome associated with antibodies to multiple components of the voltage-gated potassium channel complex

Loukaides

Schiza

Pettingill

et al. 2012

Journal of the Neurological Sciences

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 72%

“…Insomnia was in fact the earliest manifestation in our patient and started months before the full clinical presentation of the syndrome. Other sleep disturbances in MoS include rapid eye movement sleep behavioral disorder with dream enactment and hypersomnia, or even complete absence of sleep [16].…”

Section: Discussionmentioning

confidence: 99%

Morvan's syndrome associated with antibodies to multiple components of the voltage-gated potassium channel complex

Loukaides

Schiza

Pettingill

et al. 2012

Journal of the Neurological Sciences

View full text Add to dashboard Cite

“…The most common association is with voltage-gated potassium antibody encephalopathies such as limbic encephalitis and Morvan's syndrome [59]. It has also been reported in other encephalitides like Ma-2 enchephalitis and paraneoplastic cerebellar degeneration [6,7].…”

Section: Inflammatory/autoimmune Rapid Eye Movement Sleep Behavior DImentioning

confidence: 95%

Rapid Eye Movement Sleep Behavior Disorder: Overview and Current Perspective

Irfan

Howell

2016

Curr Sleep Medicine Rep

View full text Add to dashboard Cite

Rapid eye movement (REM) stage of sleep in normal circumstances is composed of vivid dream mentation associated with physiological skeletal muscle paralysis and thus, quiescence of motor activity. REM sleep behavior disorder (RBD) is a parasomnia characterized by disinhibition of motor control facilitating dream enactment behaviors. These nocturnal motoric behaviors due to lack of REM atonia range from benign limb movements to complex aggressive actions but are often manifested by violent, aggressive flailing, punching and kicking with vocalizations enacting action-filled hostile dreams. Polysomnographic evidence of increased electromyographic tone during REM with or without capturing clinical dream enactment together with careful history helps diagnose RBD. It is considered a prodromal feature of neurodegenerative alpha-synucleinopathies with high rate of eventual phenoconversion. The mainstay of treatment is to first ensure physical safety. When medications are necessary, options include either low-dose clonazepam, high-dose melatonin or both. Yearly surveillance with detailed neurological evaluation is vital for early detection and eventual management of neurodegenerative disorder.

show abstract

“…Sleep disorders were noted in a group of patients with antibodies to VGKCs, without further specification of the target antigen [130]. Affected patients with LE may develop myoclonic movements resembling Creutzfeldt-Jakob disease [113] [131].…”

Section: Anti-vgkc-complex Encephalitismentioning

confidence: 99%

Autoimmune Encephalitides

Younger¹

2017

WJNS

View full text Add to dashboard Cite

Autoimmune encephalitis is a potentially severe disorder of the brain of diverse causes with a complex differential diagnosis. Recent advances in the past decade have led to the elucidation of new syndromes and biological markers transforming the approach to diagnosis and management of autoimmune encephalitis. Limbic encephalitis, the commonest form of autoimmune encephalitis, combines common presentations of cognitive, psychiatric, and epileptic disorders and has until recently been considered paraneoplastic or postinfectious in origin. The autoimmune encephalitides are clinically and histopathologically associated with serum and intrathecal antibodies to intracellular and surface neuronal antigens, and constituents of the limbic system neuropil. This has led to a reconsideration of a number of neuropsychiatric and neurocognitive disorders as having shared mechanisms of origin. This chapter reviews their historical background, clinical presentation, laboratory evaluation, histopathology, diagnosis and management. KeywordsAutoimmune, Encephalitis, Hashimoto, Encephalopathy Historical PerspectiveCorsellis and colleagues [1] coined the term limbic encephalitis (LE) in 1968, noting a relation to bronchial cancer in three patients in the sixth to eighth decade of life, and showing close clinicopathologic similarity to cases described by Brierley and colleagues [2] six years earlier. All three cases had subacute temporal lobe seizures, neuropsychiatric, and memory disturbances for two years before death. Postmortem examination showed inflammatory lesions in limbic grey matter sections of the brain, especially in medial temporal lobe structures of the uncus and amygdala nuclei, and hippocampal, cingulum and dentate gyri. Case 2 had an undifferentiated non-metastatic lung carcinoma removed six months after onset of neurological symptoms, while two others had a clinically unsus- The formulation of the relation of GAD antibodies to SPS has been especially instructive in understanding how far the science of autoimmune neurologic disorder has advanced. In 1988, Solimena and colleagues [28] investigated the existence of non-paraneoplastic CNS autoimmunity in a patient with SPS, epilepsy and type-1 diabetes (T1D), and increased titers of oligoclonal CSF IgG. Both the serum and CSF produced identical intense staining of all gray-matter regions. GAD65 was thence an important autoantigen in T1D, being highly expressed in the cytoplasm of pancreatic β cells. GAD-derived peptides were presentable by main histocompatibility complex (MHC) class I molecules and recognized by CD8+ cells on the surface of β cells [29]. Activation of CD8+ GAD-specific T-cells further differentiated into memory cells suggesting a pathogenic role in T1D [30]. However, only patients with very high titers of GAD were associated with LE [31], and they typically presented with recent-onset temporal lobe epilepsy (TLE) and intrathecal secretion, defining a form of non-paraneoplastic LE. Other patients within the SPS spectrum harbored antibodies agains...

show abstract

Sleep Manifestations of Voltage-Gated Potassium Channel Complex Autoimmunity

Cited by 108 publications

References 30 publications

Morvan's syndrome associated with antibodies to multiple components of the voltage-gated potassium channel complex

Morvan's syndrome associated with antibodies to multiple components of the voltage-gated potassium channel complex

Rapid Eye Movement Sleep Behavior Disorder: Overview and Current Perspective

Autoimmune Encephalitides

Contact Info

Product

Resources

About