# Diagnostic Detour: A Case of Opsoclonus-Myoclonus-Ataxia Syndrome Initially Misdiagnosed As Tricyclic Antidepressant Toxicity in a Child

## TL;DR

A child was initially thought to have TCA poisoning but was later diagnosed with OMAS, a rare neuroinflammatory disorder, highlighting the importance of accurate diagnosis and timely treatment.

## Contribution

This case report highlights the diagnostic challenges of OMAS and the risk of anchoring bias in pediatric emergency settings.

## Key findings

- Initial symptoms of TCA toxicity led to misdiagnosis of a child with OMAS.
- Neurological symptoms and cerebrospinal fluid analysis confirmed the diagnosis of OMAS.
- Immunotherapy with IV immunoglobulin and corticosteroids led to rapid improvement and full recovery.

## Abstract

Opsoclonus-Myoclonus-Ataxia Syndrome (OMAS) is a rare pediatric neuroinflammatory disorder. Its recognition is challenging, as early manifestations may resemble toxic, infectious, or metabolic processes. Misdiagnosis and diagnostic delay remain important contributors to poor outcomes. The aim of this report is to describe an unusual case of OMAS initially mistaken for tricyclic antidepressant (TCA) ingestion and to underscore the diagnostic lessons relevant to pediatric emergency, neurology, and toxicology practice. We present a previously healthy four-year-11-month-old boy who was brought to the emergency department following the discovery of missing TCA tablets and three days of vomiting and fever. Initial findings included dehydration, confusion, urinary retention, and dilated pupils, suggesting TCA toxicity. He was treated empirically for possible meningitis while a toxicological evaluation was pursued. Over the next 48 hours, opsoclonus, hyperreflexia with myoclonus, and a wide-based gait emerged, redirecting the differential diagnosis toward OMAS. Neuroimaging and malignancy screening were unremarkable. Cerebrospinal fluid analysis showed lymphocytic pleocytosis, elevated protein (1189 mg/L), positive oligoclonal bands, reduced glucose (2.0 mmol/L), elevated lactate (2.8 mmol/L), increased lactate dehydrogenase (291 IU/L), and negative neuronal antibody testing. Immunotherapy with intravenous immunoglobulin and corticosteroids produced rapid improvement, with complete recovery by six months of follow-up. This case highlights the risk of anchoring bias in acute pediatrics, the necessity of malignancy surveillance, and the favorable impact of timely immunotherapy in OMAS.