In status epilepticus, neuronal injury probably results primarily from an excitotoxic mechanism mediated by intrinsic neuronal seizure activity ⁽²²⁾. During status epilepticus, neuronal seizure activity increases release of glutamate from the pre-synaptic terminal of neuronal axons. Glutamate crosses the synaptic cleft to bind to NMDA receptors, which leads to prolonged depolarization resulting in apoptosis or necrotic cell death. Encephalopathy with status epilepticus often involves the hippocampus, other parts of the limbic system, thalamus, and cerebellum.

This distribution of the lesions on MRI/DWI seems to be related to the distribution of NMDA type glutamate receptors which are concentrated in the hippocampus and other parts of the limbic system (Figure 8). Increased glutamate/glutamine peaks are seen in patients with status epilepticus ⁽²⁰⁾.

Figure 8. A 2-year-old girl with status epilepticus

A. T2WI shows diffuse hyperintense lesions in the left thalamus and cerebral cortex.

B. FLAIR image shows hyperintense lesions in the left hippocampus, thalamus and temporo-fronto-parietal lobes.

C,D. DWI shows these lesions as hyperintense with decreased ADC that represents cytotoxic edema related to excitotoxic injury mediated by neuronal seizure activity.

E. MRS (TE 144 ms) shows increased glutamate/glutamine (Glx) peaks probably initiated by increased glutamate release into the extracellular space.