When should we test for voltage-gated potassium channel complex antibodies? A retrospective case control study

O’Sullivan, B.; Steele, Tyler; Ellul, Mark; Kirby, Eimear; Duale, A.; Kier, Gregory; Crooks, Daniel; Jacob, Anu; Solomon, Tom; Michael, Benedict

doi:10.1016/j.jocn.2016.04.021

Cited by 9 publications

(6 citation statements)

References 32 publications

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“…These earlier mechanistic investigations thus demonstrate that autoantibodies can cause pain either indirectly, by stimulating release of proalgesic mediators from other cells [11], or by directly affecting the activity of sensory neurons [16]. Importantly, VGKCC autoantibodies have not been observed in CRPS patients [4,33,42], and we did not detect functional abnormalities in D-hair fibers in tCRPS mice, highlighting that VGKCC autoantibodies generate pain by mechanisms that are distinct from those that are engaged by CRPS IgG.…”

Section: A C C E P T E Dsupporting

confidence: 55%

Autoantibodies produce pain in complex regional pain syndrome by sensitizing nociceptors

Cuhadar

Gentry

Vastani

et al. 2019

PAIN

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Section: A C C E P T E Dsupporting

confidence: 55%

Autoantibodies produce pain in complex regional pain syndrome by sensitizing nociceptors

Cuhadar

Gentry

Vastani

et al. 2019

PAIN

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“…Autoimmune encephalitis is an increasingly recognised cause of encephalitis and over the last 10 years there has been a marked expansion in the range of antibodies identified [13]. Some specific clinical phenotypes are reported to correspond with specific antibodies, such as orofacial dyskinesia with N-methyl-D-aspartate receptor antibodies [14]. However, in the majority there is significant clinical overlap with the most common features reflecting a limbic encephalitis, behavioural change or psychosis and seizures, which may be refractory [15].…”

Section: Discussionmentioning

confidence: 99%

Autoimmune encephalitis as an increasingly recognised cause of non-convulsive status epilepticus: A retrospective, multicentre evaluation of patient characteristics and electroencephalography (EEG) results

Mitchell

Valdoleiros

Jefferson

et al. 2020

Seizure

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Status epilepticus (SE) is a severe condition of unrelenting seizures requiring urgent identification and treatment. SE may be unprovoked, occurring in someone with epilepsy, or may be provoked by acute intracranial disease or metabolic derangement. Increasingly encephalitis, particularly autoimmune types, is reported to cause refractory seizures. Whilst convulsive SE is readily identified, non-convulsive SE (NCSE) can be difficult to identify clinically, and electroencephalography (EEG) is required. Therefore, it is critical to identify the key clinical features associated with NCSE on EEG to inform future use of EEG. Methods: We conducted a multicentre, retrospective analysis of EEG requests from four general and one specialist neurology hospital in the Northwest of England (2015England ( -2018. Cases were identified from EEG requests for patients with suspected NCSE or other indications such as encephalopathy. We compared demographic and clinical characteristics between EEG-confirmed cases of NCSE and a randomly selected sample of negative controls. Results: 358 EEGs were reviewed, and 8 positive cases of NCSE were identified. Epilepsy was identified as the aetiology in 2 of these cases, and autoimmune encephalitis another 2 cases (one patient with N-methyl-D-aspartate receptor antibodies and another with voltage gated potassium channel antibodies). Previous alcohol excess (p = 0.005) and subtle motor signs (p = 0.047) on examination were observed more frequently in patients with NCSE compared to controls. Conclusion: Physicians should have a low threshold for urgent EEG in patients with suspected or previous encephalitis, especially if autoimmunity is suspected or subtle motor signs are present.

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“…These are not associated with the typical neurological findings as described above. Hyponatremia is commonly seen in anti-VGKC limbic encephalitis, more specifically the anti-LGl1 subtype, and has been postulated as a marker to prompt testing for anti-VGKC antibodies in patients with seizures and faciobrachial movements [10]. The exact cause of hyponatremia is unknown, but the expression of LGl1 in both the brain and kidneys has been cited as a possible mechanism [11].…”

Section: Discussionmentioning

confidence: 99%

Autoimmune Limbic Encephalitis in a Patient with Acute Encephalopathy and Hyponatremia

Agarwal

Albertolle

Tiru

2019

Case Reports in Medicine

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Acute encephalopathy is a common clinical presentation for hospital admissions. Autoimmune encephalitis is a rare cause of encephalopathy which has increasingly been recognized over the last decade. The detection of various neuronal antibodies has helped diagnose these syndromes, but they have limited availability, mostly in the developed countries. We present a case of a middle-aged female presenting with memory impairment, gait disturbances, and hyponatremia. A clinical diagnosis of autoimmune limbic encephalitis was made based on faciobrachial dystonic seizures, SIADH, and MRI changes 10 days prior to autoantibody titer returned. Prompt treatment with steroids and intravenous immunoglobulin was started with improvement in her neurological symptoms. This case highlights the importance of considering autoimmune encephalitis syndromes in the differential diagnosis of patients with classical neurological presentations and prompt diagnosis and immunotherapy to improve neurological outcomes.

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When should we test for voltage-gated potassium channel complex antibodies? A retrospective case control study

Cited by 9 publications

References 32 publications

Autoantibodies produce pain in complex regional pain syndrome by sensitizing nociceptors

Autoantibodies produce pain in complex regional pain syndrome by sensitizing nociceptors

Autoimmune encephalitis as an increasingly recognised cause of non-convulsive status epilepticus: A retrospective, multicentre evaluation of patient characteristics and electroencephalography (EEG) results

Autoimmune Limbic Encephalitis in a Patient with Acute Encephalopathy and Hyponatremia

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