Status epilepticus is defined as continuous seizure activity that lasts longer than 30 minutes, or two or more sequential seizures that together last longer than 30 minutes and without full recovery of consciousness between the seizure attacks . This is a serious event and should be treated aggressively, as the mortality associated with status epilepticus is about 8% in children and 30% in adults [28,29].
In status epilepticus, neuronal injury is thought to result primarily from an excitotoxic mechanism mediated by intrinsic neuronal seizure activity. This is supported by the effect of kainic acid (an excitotoxic analog of glutamate), as shown in animal studies [30, 31].Neuronal seizure activity will increase the release of glutamate from the pre-synaptic terminal of neuronal axons. The released glutamate crosses the
Hippocampal lesion following status epilepticus in a 55-year-old male with prolonged seizures associated with tacrolimus toxicity. a FLAIR image at 2 days after seizure shows high signal areas in the bilateral frontal deep white matter and the left hippocampus (arrows). b DW image (y axis) shows high signal in the left hippocampus (arrow). c ADC (y axis) shows low signal intensity (arrow) consistent with cytotoxic edema. d 7 months follow-up coronal FLAIR image shows the resolution of white matter changes and residual high signal intensity with atrophy in the left hippocampus (arrow)
synaptic cleft to bind to NMDA receptors of the post-synaptic neurons, resulting in cytotoxic edema. Cyto-toxic edema is also seen in the astrocytes as an acute phase of reactive astrocytosis .
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