Answer for BIR CoW 21 Jul 2024
CHRONIC METHANOL POISONING
Clinical History
45 years old male presents with Dystonic posturing involving left lower and upper limb, slurring of speech for 1 ½ years and diminished vision in bilateral eyes for 3 years
Additional History
Patient is chronic alcoholic for 20 years.
Findings
Volume loss with encephalomalacic changes noted in bilateral putamen with areas of patchy FLAIR hyperintensities and gradient blooming.
Discussion
Methanol is a clear and colorless chemical that can usually be seen in household cleaning products, antifreeze, varnishes, and fuel Methanol exerts its toxicity on the human body through 2 mechanisms. First, methanol can cause death through the central nervous system depression mechanism (similar to ethanol). Second, the metabolic product of methanol, formic acid, leads to metabolic acidosis and severe neurological consequences, including visual disturbances (optic nerve necrosis or demyelination), headache, dizziness, nausea-vomiting, weakness, and discomfort. In severe cases, it can lead to seizures, coma, and death. Acute methanol toxicity may present with mild symptoms such as headache, altered mentation, blurring of vision, abdominal pain, and vomiting. However, in more severe cases, patients may develop blindness, severe metabolic acidosis, and coma Chronic methanol toxicity can have neurologic sequelae such as vision loss that can potentially be irreversible.
IMAGING FEATURES
The most characteristic MR findings in methanol toxicity are bilateral putaminal necroses, which may have varying degrees of hemorrhage. This finding is by no means specific to methanol toxicity but is seen also in a variety of conditions, including Wilson disease and Leigh disease. Putaminal necrosis and hemorrhage probably result from the direct toxic effects of methanol metabolites and metabolic acidosis in the basal ganglia. The lesions typically show restricted diffusion on DWI and decreased ADC values during the acute phase Cerebral and intraventricular hemorrhage, cerebellar necrosis, diffuse cerebral edema, bilateral subcortical white matter necrosis or edema, and optic nerve necrosis all have been described in severe methanol intoxication. Differential diagnosis of Bilateral putaminal lesions with optic neuropathy, Hydrogen sulfide toxicity, Leigh’s disease and other mitochondrial diseases, Differential diagnosis of bilateral putamen necrosis included more conditions such as Wilson’s disease, Hypoxic-ischemic insults Encephalitis Kearns-Sayre syndrome Striatal degeneration associated with Leber’s optic atrophy, carbon monoxide inhalation and hypoxic-anoxic injuries such as near-drowning . Predilection to putamen not caudate helps to differentiate methanol poisoning from other ischemic conditions (CO poisoning) that tends to involve mainly the caudate nucleus. Also the combination of optic nerve atrophy eliminates other differentials
Reference:
Sahar M. Elkhamary, Dalia M. Fahmy, Alberto Galvez-Ruiz, Nasira Asghar, Thomas M. Bosley, Spectrum of MRI findings in 58 patients with methanol intoxication: Long-term visual and neurological correlation, The Egyptian Journal of Radiology and Nuclear Medicine, Mojica CV, Pasol EA, Dizon ML, Kiat WA Jr, Lim TRU, Dominguez JC, Valencia VV, Tuaño BJP. Chronic methanol toxicity through topical and inhalational routes presenting as vision loss and restricted diffusion of the optic nerves on MRI: A case report and literature review. eNeurologicalSci. 2020 Jul 21;20:100258. doi: 10.1016/j.ensci.2020.100258. PMID: 32775706; PMCID: PMC7394764.
Clinical History
45 years old male presents with Dystonic posturing involving left lower and upper limb, slurring of speech for 1 ½ years and diminished vision in bilateral eyes for 3 years
Additional History
Patient is chronic alcoholic for 20 years.
Findings
Volume loss with encephalomalacic changes noted in bilateral putamen with areas of patchy FLAIR hyperintensities and gradient blooming.
Discussion
Methanol is a clear and colorless chemical that can usually be seen in household cleaning products, antifreeze, varnishes, and fuel Methanol exerts its toxicity on the human body through 2 mechanisms. First, methanol can cause death through the central nervous system depression mechanism (similar to ethanol). Second, the metabolic product of methanol, formic acid, leads to metabolic acidosis and severe neurological consequences, including visual disturbances (optic nerve necrosis or demyelination), headache, dizziness, nausea-vomiting, weakness, and discomfort. In severe cases, it can lead to seizures, coma, and death. Acute methanol toxicity may present with mild symptoms such as headache, altered mentation, blurring of vision, abdominal pain, and vomiting. However, in more severe cases, patients may develop blindness, severe metabolic acidosis, and coma Chronic methanol toxicity can have neurologic sequelae such as vision loss that can potentially be irreversible.
IMAGING FEATURES
The most characteristic MR findings in methanol toxicity are bilateral putaminal necroses, which may have varying degrees of hemorrhage. This finding is by no means specific to methanol toxicity but is seen also in a variety of conditions, including Wilson disease and Leigh disease. Putaminal necrosis and hemorrhage probably result from the direct toxic effects of methanol metabolites and metabolic acidosis in the basal ganglia. The lesions typically show restricted diffusion on DWI and decreased ADC values during the acute phase Cerebral and intraventricular hemorrhage, cerebellar necrosis, diffuse cerebral edema, bilateral subcortical white matter necrosis or edema, and optic nerve necrosis all have been described in severe methanol intoxication. Differential diagnosis of Bilateral putaminal lesions with optic neuropathy, Hydrogen sulfide toxicity, Leigh’s disease and other mitochondrial diseases, Differential diagnosis of bilateral putamen necrosis included more conditions such as Wilson’s disease, Hypoxic-ischemic insults Encephalitis Kearns-Sayre syndrome Striatal degeneration associated with Leber’s optic atrophy, carbon monoxide inhalation and hypoxic-anoxic injuries such as near-drowning . Predilection to putamen not caudate helps to differentiate methanol poisoning from other ischemic conditions (CO poisoning) that tends to involve mainly the caudate nucleus. Also the combination of optic nerve atrophy eliminates other differentials
Reference:
Sahar M. Elkhamary, Dalia M. Fahmy, Alberto Galvez-Ruiz, Nasira Asghar, Thomas M. Bosley, Spectrum of MRI findings in 58 patients with methanol intoxication: Long-term visual and neurological correlation, The Egyptian Journal of Radiology and Nuclear Medicine, Mojica CV, Pasol EA, Dizon ML, Kiat WA Jr, Lim TRU, Dominguez JC, Valencia VV, Tuaño BJP. Chronic methanol toxicity through topical and inhalational routes presenting as vision loss and restricted diffusion of the optic nerves on MRI: A case report and literature review. eNeurologicalSci. 2020 Jul 21;20:100258. doi: 10.1016/j.ensci.2020.100258. PMID: 32775706; PMCID: PMC7394764.
Note:
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
If you feel you have answered rightly but cannot find your name in the above list, please call 09551942599.
Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
If you feel you have answered rightly but cannot find your name in the above list, please call 09551942599.
Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!