Status Epilepticus–Induced Neuronal Loss in Humans Without Systemic Complications or Epilepsy
Article first published online: 2 AUG 2005
Volume 41, Issue 8, pages 981–991, August 2000
How to Cite
Fujikawa, D. G., Itabashi, H. H., Wu, A. and Shinmei, S. S. (2000), Status Epilepticus–Induced Neuronal Loss in Humans Without Systemic Complications or Epilepsy. Epilepsia, 41: 981–991. doi: 10.1111/j.1528-1157.2000.tb00283.x
- Issue published online: 2 AUG 2005
- Article first published online: 2 AUG 2005
- Accepted March 27, 2000
- Status epilepticus;
- Cell death;
- Neuronal necrosis;
Summary: Purpose: To determine the regional distribution of neuronal damage caused strictly by status epilepticus (SE) without systemic complications, underlying brain pathology, or a history of preexisting epilepsy.
Methods: The medical records and electroencephalograms (EEGs) of three deceased patients who developed SE in the hospital were reviewed. Their brains were formalin-fixed, and 17 brain regions were selected, embedded in paraffin, and sectioned. Alternate sections were stained with either hematoxylin and eosin and cresyl violet to determine the extent of neuronal loss and gliosis or glial fibrillary astrocytic protein to confirm the extent of astrocytic proliferation.
Results: The three patients died 11 to 27 days after the onset of focal motor SE; none had hypotension, hypoxemia, hypoglycemia, or significant hyperthermia. Two patients had no prior seizures and no underlying brain pathology. The third patient, who had leptomeningeal carcinomatosis, had one seizure 2 months before the onset of SE. The duration of SE was 8.8 hours to 3 days. EEGs showed unilateral temporal lobe sharp-wave discharges in one patient and independent temporal lobe sharp-wave discharges bilaterally in the other two patients. In addition to widespread neuronal loss and reactive gliosis in the hippocampus, amygdala, dorsomedial thalamic nucleus, and Purkinje cell layer of the cerebellum, we report for the first time periamygdaloid (piriform) and entorhinal cortical damage occurring acutely after SE in humans.
Conclusions: In the absence of systemic complications or preexisting epilepsy, SE produces neuronal loss in a distribution similar to that from domoic acid-induced SE in humans and from kainic acid- and pilocarpine-induced SE in rats.