Neuropsychiatric Presentation of Non-paraneoplastic Voltage-Gated Calcium Channel Autoimmune Encephalitis: A Case Report

TL;DR

A 39-year-old man with psychiatric symptoms was diagnosed with autoimmune encephalitis linked to voltage-gated calcium channel antibodies, showing the condition can present without cancer or typical neurological signs.

Contribution

This case expands the known clinical spectrum of non-paraneoplastic VGCC antibody-associated autoimmune encephalitis with psychiatric dominance.

Findings

VGCC antibodies were detected in a patient with psychiatric symptoms and no malignancy.

The patient partially responded to immunotherapy and showed sustained improvement with rituximab.

Atypical psychiatric presentations of autoimmune encephalitis can occur without classical neurological features.

Abstract

Autoimmune encephalitis is an immune-mediated inflammatory disorder of the brain with diverse neurological and psychiatric manifestations. Voltage-gated calcium channel (VGCC) antibody-associated autoimmune encephalitis is rare and has been predominantly described in paraneoplastic settings. Emerging reports suggest a broader range of central nervous system involvement, but presentations dominated by psychiatric symptoms remain uncommon and diagnostically challenging.

A 39-year-old man with no prior medical illness presented with subacute progressive cognitive decline, behavioral changes, and religious-themed complex auditory hallucinations over three to four months. Initial evaluation, including magnetic resonance imaging, electroencephalography, and standard autoimmune encephalitis antibody testing, was unrevealing. Extended cerebrospinal fluid and serum autoimmune testing were done, which demonstrated elevated VGCC antibody levels. Comprehensive malignancy screening, including whole-body positron emission tomography, showed no evidence of an underlying neoplasm. The patient showed partial improvement following intravenous methylprednisolone and intravenous immunoglobulin (IVIG). Symptom recurrence necessitated repeat IVIG and escalation to rituximab therapy, resulting in sustained clinical improvement.

This case broadens the recognized clinical spectrum of VGCC antibody-associated autoimmune encephalitis by highlighting a presentation dominated by psychiatric symptoms in the absence of malignancy or classical neurological features. Recognition of such atypical presentations is essential, as early diagnosis and appropriate immunotherapy can lead to favorable outcomes.

Figures