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This is an MRI brain study, showing confluent white matter T2 / FLAIR hyperintensities, mostly in the subcortical white matter yet sparing the sub-cortical U fibres – this is also seen in the basal ganglia bilaterally, and in the cerebellar hemispheres and superior cerebellar peduncles. The involved areas of the white matter show high DWI signal and corresponding low ADC values, indicating restricted diffusion.
I can appreciate a focus of high T1 signal in the left putamen, which corresponds to blooming artifact on the susceptibility weighted series, indicating haemorrhage.
These features, in correlation with the provided history, are characteristic of toxic brain injury. The likely toxic agent is methanol, yet heroin inhalation and carbon monoxide poisoning are also possible.
The differential diagnosis includes severe global brain anoxia.
I would review any prior imaging if available, and discuss the findings with the referring physician. I would also recommend discussing this case at neurology MDT.
Question:
Which condition would you suspect if the patient initially presents in a comatose state, recovers to baseline cognitive function for 7 – 21 days, then develops sudden severe cognitive decline?
This clinical course would be characteristic of delayed post hypoxic leuko-encephalopathy.
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