Abstract

Voltage gated potassium channel (VGKC) autoimmune encephalitis is caused by antibodies against cell surface proteins that are part of the voltage-gated potassium complex in neurons. We hereby present a case of a 46-year-old female who manifested with subacute onset of memory loss, behavioral changes, hyponatremia, and focal motor seizures. She was diagnosed with anti-VGKC encephalitis (LGI1 variant), treated with pulse steroid therapy with marked improvement of symptoms. Case report On initial admission, patient underwent plain cranial MRI which showed hyperintense signals on the right amygdala and hippocampus. Electroencephalography revealed epileptiform discharges on the right temporal lobe with focal slowing over the same region. She was managed as a case of focal motor seizure secondary to right mesial temporal sclerosis and was given levetiracetam. Interim, there was persistence of memory loss until one day, she experienced focal motor seizures. Repeat cranial MRI showed increased signal intensities on bilateral medial temporal lobes. Electroencephalography showed focal slowing on the right frontotemporal and left frontal regions while serum tests revealed euovolemic hyponatremia. Patient underwent lumbar puncture and cerebrospinal fluid analysis revealed high titers for antibodies against voltage-gated potassium channel complex. Patient underwent pulse steroid therapy with tapering doses of oral steroids. The patient showed marked improvement of symptoms without recurrence of motor seizures. This case highlights VGKC autoimmune encephalitis as an important diagnostic consideration in patients presenting with subacute onset of memory loss, behavioral changes, hyponatremia, and focal seizures. Prompt initiation of immunotherapy results to improvement with excellent prognosis.

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