Objective: To report a case of methanol-induced mixed cerebellar and parkinsonian sequelae, emphasizing the pathophysiological mechanisms underlying the neuroimaging findings and the paradoxical response to levodopa.

Background: Methanol poisoning causes severe neurological damage through its toxic metabolite, formic acid. Formic acid inhibits mitochondrial cytochrome c oxidase, leading to cellular hypoxia and ATP depletion. This mechanism selectively affects regions with high metabolic demands: the putamen, optic nerve, and cerebellar pathways. Putaminal necrosis typically manifests as parkinsonism, while cerebellar involvement produces ataxia. The response to dopaminergic therapy depends on whether the damage is presynaptic or postsynaptic.

Method: We present a longitudinal case of a previously healthy [age]-year-old male followed for two years after severe methanol intoxication requiring ICU admission and mechanical ventilation. Serial neurological examinations, therapeutic trials, and brain imaging were analyzed with focus on pathophysiological correlations.

Results: Following acute intoxication in late 2023, the patient developed right eye posterior capsule opacification. Over subsequent months, a cerebellar syndrome emerged: gait ataxia, dysarthria, dysmetria, and wide-based gait. By late 2025, superimposed parkinsonian features appeared: bradykinesia, rigidity, freezing, short-stepped gait, and apraxia. A contrasted brain CT performed in January 2026 revealed bilateral hypodense lesions in the putamen and external capsule, pathognomonic for methanol-induced necrotizing encephalopathy. A levodopa/carbidopa trial paradoxically worsened bradykinesia and coordination with associated nausea, indicating predominantly postsynaptic putaminal neuronal damage. Physical and hydrotherapy provided only mild, temporary benefit.

Conclusion: This case illustrates that methanol toxicity produces a mixed movement disorder through dual pathophysiological mechanisms: cerebellar Purkinje cell damage causing ataxia, and putaminal neuronal necrosis causing parkinsonism. The paradoxical levodopa response confirms postsynaptic striatal damage, which carries poor prognosis for dopaminergic therapy. Neuroimaging is essential for identifying characteristic putaminal lesions. Rehabilitation remains the cornerstone of management.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/methanol-intoxication-presenting-as-a-mixed-ataxic-parkinsonian-syndrome-with-a-paradoxical-response-to-levodopa-a-case-report/