Clinical presentation: Frequent seizures, altered sensorium.
MRI brain shows marked left hemi Atrophy, ex vacuo
dilatation of left lateral ventricle owing to volume loss. Left cerebral hemisphere show multifocal
patchy areas of cortical T2 hyper intensities without diffusion restriction. Associated Atrophy of left deep grey
nuclei, changes of distal Wallerian degeneration involving left cerebral
peduncle of mid brain, Pons.
Imaging diagnosis: Sequel of encephalitis / rasmussen
encephalitis.
Right cerebellar hemisphere show
marked atrophy can attributed to associated contralateral cerebellar diaschisis.
Crossed cerebellar diaschisis
Refers to supra tentorial lesion leading to depressed function, metabolism and perfusion of contra lateral cerebellar hemisphere which is connected via white matter tracts.
Interruption of this cortico-ponto-cerebellar white matter tracts which then results in deafferentation and hypometabolism of the contralateral cerebellar hemisphere.
Classically seen following cerebral infarction, although it can be a sequel of any significant supratentorial lesion like bleed, encephalitis as in our case. The same phenomenon can also occur in thalamus called ipsilateral thalamic diaschisis, occurring after an ipsilateral middle cerebral artery territory infarction.
CT or MRI perfusion performed during an acute stroke may show a contralateral cerebellar hypo perfusion. In chronic stages volume loss involving contralateral cerebellar hemisphere.
Clinically other than the neurological deficits associated with the contra lateral supra tentorial lesion, the condition is generally asymptomatic. No treatment apart from management of the supratentorial insult.
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