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Summary   Objective  In vivo studies of epilepsy typically use prolonged status epilepticus to generate recurrent seizures. However, reports on variable status duration have found discrete differences in injury after 40–50 min of seizures, suggesting a pathophysiologic sensitivity to seizure duration. In this report we take a multivariate cluster analysis to study a short duration status epilepticus model using in vivo 7T magnetic resonance spectroscopy ( MRS ) and histologic evaluation.    Methods  The Hellier Dudek model was applied with 45 min of status epilepticus after which the animals were imaged twice, at 3 days and 3 weeks post–status epilepticus. Single voxel point resolved spectroscopy (PRESS)  MRS  was used to acquire data from the dentate gyrus and  CA 3 region of the hippocampus, assessing metabolite ratios to total creatine (t C r). In a subset of animals after the second imaging study, brains were analyzed histologically by Nissl staining.    Results  A hierarchical cluster analysis performed on the 3‐day data from 21 kainate‐treated animals (dentate gyrus voxel) segregated into two clusters, denoted by  KM  (more injured, n = 6) and  KL  (less injured, n = 15). Although there was no difference in kainate dosing or seizure count between them, the metabolic pattern of injury was different. The  KM  group displayed the largest significant changes in neuronal and glial parameters; the  KL  group displayed milder but significant changes. At 3 weeks, the  KL  group returned to normal compared to controls, whereas the  KM  group persisted with depressed  N ‐acetyl aspartate (NAA)/t C r, glutamate/t C r, and increased inositol/t C r and glutamine/t C r. The classification was also consistent with subsequent histologic patterns at 3 weeks.    Significance  Although a short status period might be expected to generate a continuous distribution of metabolic injury, these data show that the short Hellier Dudek model appears to generate two levels of injury. The changes seen in segregated groups persisted into 3 weeks, and can be interpreted according to neuronal and glial biomarkers consistent with histology results.

Metabolic injury in a variable rat model of post–status epilepticus