Abstracts

Rationale: Although transient post-ictal MRI brain changes are well described in the literature, abnormal MRI brain findings with limited pathologic correlation in the acute setting can cause significant uncertainty in diagnosis and management. We present a patient with focal status epilepticus who underwent a brain biopsy. Methods: Case study Results: 52 year old male with past medical history of HCV, type II diabetes mellitus, seizure disorder was transferred for focal status epilepticus and altered mental status. On admission, he was confused, head and eyes deviated to left with subtle jerking movements of the right upper and lower extremity. With ativan 2 mg IV and Fosphenytoin 20mg/kg IV, right upper and lower extremity movements resolved. Due to focal neurological findings, stat CT head was done, and showed new hypodensities in the left subinsular region extending to left temporal lobe, and in left anterior parafalcine frontal region likely representing subacute infarcts. EEG showed mild to moderate diffuse slowing, focal slowing in left hemisphere, and abundance of epileptiform spikes/sharp waves in the left frontotemporal region. MRI brain (day 3) showed abnormal T2/FLAIR signal, and subtle restricted diffusion in the left hippocampus, left inferior frontal lobe, left cingulate gyrus and basal forebrain, which were suggestive of limbic versus herpes encephalitis, glioma of the left temporal lobe, and post-seizure related excitotoxic edema. CT angiogram head and neck, and MRV brain were normal. CSF was normal except for elevated protein (WBC 1, RBC 56, proteins 68, glucose 57, cytology negative for malignant cells). HSV 1/2, CMV, WNV, VZV by PCR were negative. NMDA receptor antibodies and paraneoplastic panel were negative. Due to uncertainty of diagnosis, left temporal lobe biopsy was done (day 13), revealing hypercellular white matter without inflammation, consistent with reactive gliosis. Repeat MRI brain (day 20) showed resolution of previous areas of restricted diffusion and decreased T2/FLAIR abnormalities. However, signal abnormality in the left hippocampus persisted with questionable new enhancement. The left hippocampus was minimally larger than the right. In sum, artifact versus a glioma were still a concern. After antiepileptic therapy, patient clinically returned to baseline with no focal deficits. A follow-up MRI brain was scheduled in 4-6 weeks. Conclusions: Our case demonstrates the complexity in the clinical management of patients with focal status epilepticus. Despite the initial suspicion for encephalitis versus glioma, early improvement clinically and on neuroimaging were more suggestive of post-ictal changes as described in the literature. However, repeat neuroimaging at three weeks was still concerning due to left hippocampal signal and size abnormality and new focus of enhancement. This requires follow-up MRI brain in 4-6 weeks. Therefore, neuroimaging shortly after an ictal event can potentially be misleading. Early recognition that these changes can occur as the consequence of seizure activity could avoid unnecessary intervention in these patients. Follow-up imaging several weeks after seizure control might be the best strategy moving forward to distinguish these clinical entities. Funding: No funding obtained