Teaching Case

A 35-year-old man was brought to the Emergency Department with a history of unconsciousness. He had a history of acute wild alcohol (made out of fox meat) intake 24 hours prior to the presentation.  Examination revealed the Glasgow Coma Scale to be 6. An arterial blood gas analysis showed a high anion gap metabolic acidosis.

Magnetic Resonance Imaging (MRI) showed symmetrical well defined T2 and FLAIR hyperintensity and T1 hypointensity noted in bilateral lentiform nucleus (predominantly involving the putamen) (Figure 1), subcortical white matter of both frontal, temporal and occipital lobes(Figure 1), insular cortex, body of corpus callosum (Figure 3), infundibulum. These areas show marked diffusion restriction which appears hyperintense in DWI and suppressed in ADC (Figure 4). There is no mass effect. T2 and FLAIR hyperintensity noted in bilateral optic nerves (intraocular, intraorbital and intracanalicular parts) which showed diffusion restriction (High signal on DWI and low signal on ADC sequence) (Figure 5). No evidence of blooming noted in SWI sequences (No haemorrhage noted within the lesions). Few Similar discrete areas also noted in subcortical white matter of bilateral high parietal lobes without hemorrhagic component within.  The ventricles and sulcal spaces are within normal limits. There are no abnormal signal intensity within the midbrain, pons and medulla oblongata. There are no abnormal signal intensity within the cerebellar hemispheres.

Usually considered to be accidental or suicidal intoxication, acute methanol poisoning results from adulteration of alcoholic drinks.[1] Clinical presentation is varied with a latent period of 12- 24 hours.[2] Methyl alcohol is metabolized to toxic components formaldehyde and formic acid resulting in varied clinical symptoms.[3]

Acute intoxication results in severe metabolic acidosis resulting in severe neurological features and sequelae as seen in our case. Visual symptoms like blindness due to optic nerve necrosis and demyelination is seen in most of the patients and persists even after recovery. [4]  Neurological symptoms like nausea, vomiting, dizziness, headache, altered sensorium are common in the acute phase. [5]

Hemorrhagic putaminal necrosis is the most common and characteristic MRI finding in methanol poisoning. Subcortical, deep white matter, caudate nuclei, cerebral and cerebellar cortical and mid-brain lesions are other common findings. [1, 2, 6] Bilateral necrosis of pontine tegmentum and optic nerves indicate poor prognosis. [7] The vulnerability of basal ganglia to toxic and ischemic damage may be the reason behind involvement of basal ganglia in methanol poisoning. Basal ganglia is also affected because of severe metabolic acidosis due to toxins like formic acid.

Classically Computed Tomography [CT] shows hypodensity in the bilateral putamen, cerebral white matter and shows haemorrhages within. [6]

MRI shows variable signal (due to aging of haemorrhage) on T1 sequence and demonstrates high signal on T2, FLAIR with variable enhancement pattern on affected areas.[8] Acute phase shows increased diffusion restriction (high signal on DWI and low signal on ADC sequences) as seen in our case. [8] Similar signal changes might also be seen in bilateral optic nerves, cerebellum. There is diffusion restriction in bilateral putamen, subcortical white matter, corpus callosum and bilateral optic nerves visualized in our case. Chronic phase might show cystic patterns around the putamen. Our case showed almost all the common area affected by methanol poisoning without any hemorrhagic component.

Various metabolic diseases such as Wilson’s disease, Leigh’s disease, Kearns- Sayre syndrome and Leber’ s optic atrophy are other diseases characterized by bilateral putaminal necrosis. [9] Carbon monoxide inhalation and hypoxic injury are other differential diagnoses. Carbon monoxide inhalation has affinity towards globus pallidus and hypoxic injury typically involves caudate nucleus and central grey nuclei. [10]

MRI can also narrows down the differential diagnosis in patients with alcohol intoxication and help rule out metabolic hypoglycemic brain damage and other traumatic head injuries.

Acute methanol poisoning is treated with administration of intravenous ethanol that reduces the production of formate which is further enhanced by administration of fomepizole and folinic acid.  [6] Intravenous sodium bicarbonate, gastric lavage and hemodialysis are some other treatment modalities. [6, 7]

Written informed patient consent for publication has been obtained from patient party (relative).