Objective:

To describe a bimodal presentation of autoimmune GFAP Astrocytopathy following aseptic meningitis, complicated by early post-discharge status epilepticus, and to highlight diagnostic challenges in recognizing post-infectious autoimmune CNS conversion.

Background:

GFAP astrocytopathy is a rare autoimmune inflammatory CNS disorder characterized by glial fibrillary acidic protein antibodies and typically presents sub acutely with meningoencephalitis, movement disorders, or optic neuritis. A biphasic course following viral or aseptic meningitis is recognized, usually emerging over weeks after apparent clinical improvement. However, rapid post-infectious autoimmune conversion with severe neurological deterioration is less well characterized and may be under-recognized, particularly when initial infectious evaluations are negative and early symptoms are nonspecific..

Design/Methods:

Case Report

Results:

A 23-year-old man presented with fever, headache, neck stiffness, and vomiting, with CSF showing lymphocytic pleocytosis (116 WBCs) consistent with aseptic meningitis; infectious studies including viral PCRs were negative. He improved clinically with supportive care and was discharged. Shortly after discharge, he re-presented with severe hyponatremia, intractable hiccups, and new-onset status epilepticus requiring intubation and anesthetic coma. MRI brain demonstrated new bilateral T2/FLAIR hyperintensities involving the basal ganglia, insular cortex, hippocampi, and brainstem, with leptomeningeal enhancement. CSF GFAP-IgG was positive (1:16), confirming autoimmune GFAP astrocytopathy. Extensive infectious, autoimmune, and malignancy workup was negative. High-dose corticosteroids resulted in neurological stabilization, though residual deficits persisted.

Conclusions:

This case illustrates a bimodal encephalitic process in which apparent recovery from aseptic meningitis was followed by rapid autoimmune CNS conversion. Hyponatremia and intractable hiccups emerged as early clinical warning signs preceding severe neurological decline. Recognition of this pattern may improve early identification of autoimmune GFAP astrocytopathy and support timely initiation of immunotherapy in patients with relapsing or atypical post-meningitic presentations.