NEUROLOGICAL AND OCULAR MANIFESTATIONS IN ACUTE METHANOL POISONING: A SYSTEMATIC REVIEW OF CLINICAL AND RADIOLOGICAL OUTCOMES
DOI:
https://doi.org/10.56238/levv16n53-092Keywords:
Methanol Poisoning, Optic Neuropathy, Magnetic Resonance Imaging, Basal GangliaAbstract
Introduction: Methanol poisoning is a rare but life-threatening toxicological emergency characterized by severe neurological and ocular sequelae resulting from the metabolism of methanol to formic acid, which induces mitochondrial dysfunction and tissue hypoxia.
Objective: To systematically review the neurological and ophthalmological manifestations of acute methanol intoxication, with emphasis on neuroimaging findings, mechanisms of injury, and clinical outcomes. Secondary objectives included evaluation of diagnostic markers, prognostic predictors, and therapeutic approaches related to visual and neurological recovery.
Methods: A comprehensive literature search was performed in PubMed, Scopus, Web of Science, Cochrane Library, LILACS, ClinicalTrials.gov, and the World Health Organization International Clinical Trials Registry Platform (ICTRP). Studies published between January 2015 and March 2025 were included without language restriction. Eligible studies comprised clinical trials, observational studies, case series, and radiological analyses addressing neurological or ocular outcomes in human methanol poisoning.
Results and Discussion: A total of 41 studies met the inclusion criteria, including prospective and retrospective cohorts, radiological reviews, and case series. Magnetic resonance imaging (MRI) revealed characteristic bilateral putaminal necrosis and optic nerve hyperintensity, while optical coherence tomography (OCT) demonstrated irreversible loss of retinal nerve fiber layer. Clinically, visual loss and parkinsonian syndromes were the most common sequelae. Early diagnosis and combined therapy with fomepizole, ethanol, and hemodialysis were associated with better outcomes.
Conclusion: Methanol poisoning causes complex neurological and ocular damage through metabolic acidosis and formate-induced cellular hypoxia. Neuroimaging and ophthalmologic assessment are essential for prognosis and management. Multidisciplinary care integrating neurology, ophthalmology, and critical care remains vital for minimizing long-term morbidity.
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