Pediatric Miller Fisher syndrome mimicking anti-histaminic drug toxicity

Abstract

Background: Miller Fisher syndrome (MFS) is a rare condition in childhood, characterized by acute-onset ataxia, ophthalmoplegia, and areflexia. It is mostly preceded by viral and bacterial infections, and the pathogenesis is speculated to be an immune response to cross-reacting antigens. We describe a case of acute ataxia which was initially misdiagnosed as antihistaminic toxicity and later emerged to be MFS. Clinical Description: A 4.5-year-old girl presented with acute-onset ataxia, giddiness, and limb pain, following toxic ingestion of an antihistaminic drug (chlorpheniramine) that had been prescribed for an upper respiratory infection. The absence of waning symptoms, new manifestations, and undetectable drug levels prompted us to consider an alternate diagnosis. Management: Magnetic resonance imaging of the cranium and spine was unremarkable. Hence, a central nervous system infection was considered. Cerebrospinal fluid (CSF) analysis revealed albumin-cytologic dissociation, a negative viral panel, and sterile culture. Serum anti-GQ1b antibody of immunoglobulin G type was positive. A nerve conduction study revealed absent H-reflexes in both gastrocnemius muscles. A diagnosis of MFS was made based on clinical features, CSF albumin-cytologic dissociation, positive anti-GQ 1b antibody, and absent H reflexes. She was treated with intravenous immunoglobulin therapy, following which there was an improvement in 1 week and complete recovery within 3 months. Conclusion: Although a rare entity, we need to consider MFS in the differential diagnosis of ataxia when the neurological signs persist beyond the expected time duration so that investigations can be planned accordingly and timely immunotherapy initiated.