Abstracts

Rationale: Whenever status epilepticus is suspected, neuroimaging studies are needed to rule out associated conditions. Imaging findings in complex partial status epilepticus (CPSE) include focal hipodensity on CTscan, effacement of sulci, loss of grey–white matter differentiation, cortical hypersignal on T2-weighted and diffusion-weighted (DWI) MR images, hyposignal on ADC maps and cortex widening. Although anecdotally correlated with selective neuronal necrosis these changes have been referred for the most as transient. Methods: Clinical and imaging data of two patients with CPSE were reviewed. CT and MRI were performed in acute phase. MRI of patient 2 included DWI and ADC maps. Patients were followed-up for 6 years (patient 1) and 5 months (patient 2) and both underwent control MRI scans. Case 1: 31-y-old Caucasian male was admitted, suspected of having CPSE. Known left mesial sclerosis and 5-6 seizures/year. CPSE lasted for 8 hours, was confirmed through EEG, reverted with phenytoin. Other causes of SE were ruled out. Right hemiplegia and global aphasia persisted after control of CPSE. No further seizures and no new neurologic signs on follow-up. Persistent right brachial paresis, anomia, alexia, agrafia and acalculia. Case 2: 45-year-old Caucasian male, heavy drinker, was admitted due to strange behaviour lasting for 6 hours. Global aphasia and right hemiplegia was detected. EEG supported the clinical suspicion of CPSE, reverted with phenytoin. One week later only Wernicke aphasia persisted. Readmitted 5 months later because of tonic-clonic seizures. No new neurological sign detected. Results: CT scan of patient 1 on day 1 showed confluent hypodense areas on left cerebral hemisphere, loss of grey-white matter differentiation and collapse of regional sulci, later confirmed on MRI scan (day 5). Cerebellum was normal. Control MRI scan 6 years later depicted left cerebral and right cerebellar atrophy. CT scan of patient 2 on day 1 showed an area of insular left oedema. Brain MRI at day 5 showed multiple hyperintense areas on left cerebral hemisphere with restricted diffusion on ADC maps, consistent with cytotoxic oedema. MRI at five months revealed left central and cortical cerebral atrophy. Conclusions: Our report strongly evidences that MRI signal changes after prolonged CPSE can be irreversible, remaining focal even after generalization of SE, probably reflecting selective neuronal necrosis of the most vulnerable regions of the brain after acute cytotoxic and vasogenic oedema. Crossed cerebellar atrophy (CCA) may coexist and might be explained either by increased demand on Purkinge cells for inhibition during SE resulting in final neuronal toxicity or by damage to the corticopontocerebellar pathway due to focal excitotoxic cell injury in cerebral cortex during seizures. Surprisingly, signs of cerebellar dysfunction caused by CCA have not been observed and partial cerebral recovery is possible.