Abstract
The symptoms of Miller-Fisher syndrome (MFS) are a triad of areflexia, ataxia, and ophthalmoplegia. The condition is a rare variant of Guillain-Barré syndrome (GBS), an acute immune-mediated nerve disorder. Both conditions involve abnormal autoimmune responses that may often be triggered by infections such as Campylobacter jejuni, human immunodeficiency virus, Epstein-Barr virus, and Zika virus, among others. As a result, the immune system mistakenly attacks the body's own nerve tissues. MFS is characterised by ophthalmoparesis, which can progress to complete external ophthalmoplegia and may include ptosis, facial nerve paralysis, sensory impairments, and muscle weakness. Diagnosis is supported by lumbar puncture, revealing albumin-cytologic dissociation, although initial tests may not always be indicative. A diagnostic marker for MFS is the presence of anti-GQ1b antibodies, which target the GQ1b ganglioside in nerves and affect oculomotor function in particular. Electrodiagnostic studies often show absent or reduced sensory responses without reduced conduction velocity. Treatment options include intravenous immunoglobulin therapy and plasmapheresis, which are both equally effective. This case study demonstrated significant clinical improvement in a patient undergoing plasmapheresis due to financial constraints, highlighting the efficacy of this treatment approach. A 50-year-old female presented with limb paraesthesia, progressive ptosis, imbalance, and transient diplopia following a recent fever. Examination revealed stable vitals, decreased deep tendon reflexes, reduced vibratory sensation, cerebellar ataxia, and cranial nerve abnormalities. Cerebrospinal fluid analysis showed elevated protein, suggesting MFS. Normal magnetic resonance imaging and nerve conduction studies indicated GBS, with positive anti-GQ1b antibodies. After five plasma exchange cycles, the patient improved substantially and was discharged with no residual symptoms after one month.