Neurophysiological and neuroimaging changes (crossed cerebrocerebellar atrophy) after prolonged non-convulsive status epilepticus

Neuroimaging alterations related to status epilepticus in an adult population: Definition of MRI findings and clinical‐EEG correlation

“…9,13,14 PMAs have been observed in different cortical areas, 9,[15][16][17] as well as involving subcortical structures. Previous studies also highlighted some preferential susceptibility regions or networks: the mesolimbic structures, 9,10,15,18 the pulvinar nucleus of thalamus, 13,18,19 the splenium of corpus callosum, 18,20 the contralateral cerebellum (a sign known as crossed cerebellar diaschisis), 13,18,21,22 the insular cortex and basal ganglia, 9,13 and the claustrum. 10,23 The majority of these cases had focal SE 18,24 and showed PMAs both locally, in the cortical area of the ictal activity, as well as in remote cortical or subcortical areas generally believed to represent regions involved by ictal activity at the network level (eg, the thalamus and ipsilateral pulvinar).…”

“…Variable periictal MRI alterations 9,10 (PMAs) have been reported in patients with SE, in either the ictal or the postictal period. Previous studies also highlighted some preferential susceptibility regions or networks: the mesolimbic structures, 9,10,15,18 the pulvinar nucleus of thalamus, 13,18,19 the splenium of corpus callosum, 18,20 the contralateral cerebellum (a sign known as crossed cerebellar diaschisis), 13,18,21,22 the insular cortex and basal ganglia, 9,13 and the claustrum. These changes represent a continuum of cytotoxic (increased DWI and decreased ADC signal) and vasogenic edema (increased DWI and increased T2 without decreased ADC signal) mostly depending on the timing of MRI performance.…”