Acute ataxic neuropathy as an incomplete Miller Fisher syndrome triggered by hepatitis B virus reactivation: a case report with negative GQ1b antibody

Background Miller Fisher syndrome (MFS) is a variant of Guillain-Barré syndrome (GBS) classically presenting with ophthalmoplegia, ataxia, and areflexia. Incomplete forms without ophthalmoplegia, such as acute ataxic neuropathy, are rare. Hepatitis B virus (HBV) infection has been occasionally associated with GBS, but never with incomplete MFS. Case presentation A 31-year-old woman with chronic hepatitis B (antiviral therapy discontinued without medical advice) presented with progressive sensory ataxia, limb numbness, and areflexia, but without ophthalmoplegia or muscle weakness. Electrophysiology showed severe demyelinating sensorimotor polyneuropathy. Cerebrospinal fluid (CSF) revealed albuminocytologic dissociation with elevated protein and positive oligoclonal bands. Serum and CSF anti-GQ1b antibodies were negative. HBV DNA was markedly elevated (5.13 × 10⁶ IU/mL) with active hepatitis. After two courses of intravenous immunoglobulin (IVIG) and entecavir, neurological function gradually improved, and gait recovered completely by two months post-discharge. Conclusion This is the first reported case of acute ataxic neuropathy as an incomplete MFS variant triggered by hepatitis B reactivation. The absence of ophthalmoplegia and negative GQ1b antibody does not exclude the diagnosis. Clinicians should consider MFS spectrum disorders in patients with post-hepatitic acute ataxia and areflexia, even without typical oculomotor involvement.