Intracranial and optic nerve MRI findings from methanol toxicity in a young adult male patient presenting with blurring of vision

A 21-year-old male patient was brought to the emergency room due to nausea, vomiting, and blurring of vision. A day prior, the patient had a drinking spree consuming locally-made alcohol, lambanog. Physical examination revealed only light perception on both eyes. The rest of the findings were unremarkable.

On cranial MRI, fairly-defined, symmetric, T1WI-hypointense, T2W-/FLAIR-hyperintense signals with punctate magnetic susceptibility artefacts were observed in the bilateral putamen (Fig. 1A-D). No restricted diffusion was appreciated. There was also irregular and wavy contour of the intra-orbital segments of bilateral optic nerves. Post-contrast studies showed subtle enhancement of the optic nerves. Minimal surrounding fat stranding was evident (Fig. 2A-B).

Methanol intoxication is usually secondary to oral ingestion of industrial solvents. Rarely, it is caused by the consumption of alcoholic beverages containing methanol. Its metabolic by-product, formic acid, causes a direct neurotoxic effect with putaminal predilection. The intrinsic putaminal microvascular anatomy, direct toxic effects of metabolites, higher metabolite concentrations, and higher sensitivity of putaminal neurons are suggested reasons for its susceptibility. Other neurotoxic effects may include intracerebral haemorrhage, cerebral oedema, cerebellar and white matter necrosis, and optic nerve necrosis.  A direct myelinoclastic effect of formic acid on the optic nerves is the explanation for its usual involvement in methanol toxicity.  [1][2][3][4]

The clinical presentation of patients varies but the onset of symptoms occurs after 12 to 24 hours of ingestion. This time interval relates to the period of methanol conversion into its toxic metabolites. Usual manifestations include dizziness, headache, gastrointestinal symptoms, and blurring of vision, some of which were present in our case. Severe symptoms include dyspnea, convulsions, or even death. Due to its high mortality and morbidity, early diagnosis and management are therefore necessary. Diagnostic methods include blood methanol level measurement and arterial blood gas analysis. Due to the neurotoxic effect of methanol, radiologic imaging is essential to diagnose possible neurologic sequelae. [1][2][5]

The bilateral putaminal necroses with varying degrees of haemorrhage are the most typical findings of methanol toxicity. Both CT and MRI may reveal similar results but the latter provides higher sensitivity and anatomic detail. [3][4] In severe intoxication, a combination with optic nerve neuropathy is generally observed. Bilateral optic nerve enhancement, with or without atrophy, is a classic finding. However, these findings are not pathognomonic. Other conditions such as Wilson disease and some mitochondrial disorders may present similarly. [2][3][5] The main diagnostic clue is still the history of recent alcohol consumption. [3] Other findings may include subcortical and deep white matter necrosis, cerebellar lesions, cerebral oedema or haemorrhages, and midbrain involvement. [4][6]

Gastric lavage, ethanol therapy, fomepizole therapy, and hemodialysis comprise the usual therapeutic regimen for methanol toxicity. Prognosis depends on the dose of methanol exposure and the timing of treatment. Despite the current medical management, high mortality remains due to delayed diagnosis. The presence of ocular toxicity also pertains to a poor long-term visual outcome. Hence, early detection and management are necessary to prevent permanent optic nerve damage. [1][4][5]

In cases wherein neurologic symptoms are present, radiologic imaging may support the clinical parameters to confirm the diagnosis, facilitate early treatment, and prevent long-term neurologic outcomes.