Unilateral Status Epilepticus Research Articles

Chronic epilepsy with damage restricted to the hippocampus: possible mechanisms.

We studied the time course and possible mechanisms of the development of chronic epilepsy following unilateral stimulation of the perforant path. After 24 h of perforant path stimulation by a modified Sloviter method, lesions were restricted to the hippocampus, except for 2 of 24 rats with minimal entorhinal neuronal injury in layer 3. Lesions were exclusively ipsilateral in the polymorph layer of the hilus and in CA4-CA3C, predominantly ipsilateral in CA3, in CA1 and in the granule cell layer. Feedforward and feedback inhibition were studied by paired pulse stimulation. In the week following inhibition, there was complete loss of GABAA-mediated, short interstimulus interval (ISI)-dependent inhibition and frequency-dependent inhibition, and also of GABAB-mediated long ISI-dependent inhibition. Yet no spontaneous seizures were observed at that time. In the next four weeks, we saw no evidence of increasing excitatory drive such as would be expected from recurrent mossy fiber sprouting. On the contrary, there was progressive return of inhibition. By four weeks post-lesion, the majority of animals had developed spontaneous recurrent seizures, and/or seizures on 2 Hz stimulation (never seen in controls), in spite of complete or near-complete recovery of short ISI-dependent, GABAA-mediated inhibition. A small but significant loss of frequency-dependent inhibition persisted, but individual animals with complete recovery of frequency-dependent inhibition showed spontaneous seizures, suggesting that loss of GABAA-mediated inhibition was not the direct cause of chronic epilepsy. GABAB-mediated, long ISI-dependent inhibition continued to show a significant loss. The ratio of the population spike amplitude at 250 microA to the maximal population spike amplitude, a measure of granule cell excitability, was unchanged immediately after stimulation, but increased in the next few weeks in a manner identical to that seen in kindling, suggesting the possibility that during the transient loss of inhibition, spontaneous kindling had occurred. Intracellular recordings from granule cells in hippocampal slices prepared from these animals showed a significant loss of GABAB-mediated slow inhibitory postsynaptic potentials (IPSPs). These data show that the sequellae of unilateral status epilepticus with damage restricted to the hippocampus are sufficient to cause chronic recurrent seizures. There is a possibility that chronic epilepsy is not the direct result of the loss of inhibitory drive or of a sprouting-induced increase in excitatory drive, but represents plastic changes akin to spontaneous kindling, possibly facilitated by loss of GABAB-mediated inhibition.

Neuropathologic asymmetries in the brain of a patient with a unilateral status epilepticus

Autopsy study of a patient who died after an episode of prolonged unilateral status epilepticus revealed neuronal loss in the hippocampus on the epileptic side, with gliosis confined to the CA1 and CA3 fields. There was loss of the parvalbumin-immunoreactive γ-aminobutyric acid (GABA)-ergic interneurons in the hippocampus on that side. There was also loss of the normal laminar pattern of substance P staining with increased substance P immunoreactivity in the supragranular plexus on that side. Met-enkephalin immunoreactivity was also increased in the outer molecular layer of the dentate gyrus on the epileptic side. Mossy fibers on the epileptic side stained more strongly with the Hicks' silver stain and with antibodies against glutamate and taurine, but less intensely with antibodies against calbindin. In the contralateral cerebellum, there was Purkinje cell loss, injury to the remaining Purkinje cells, and increased prominence of the Bergmann glia. Our observations show that prolonged unilateral seizure activity can be associated with specific histochemical changes in the human hippocampus.

Les etats de mal unilateraux au cours de la periode neonatale

Twenty-one newborns displaying a strictly unilateral status epilepticus were studied. Three groups have been isolated according to the aetiology: neonatal anoxia (n = 5), postcardiac surgery (n = 8), cerebral hemispheric lesions confirmed by CT scan (n = 7). The authors relate in detail the clinical features and the EEG abnormalities, ictal and interictal in each group, and comment on their results. They show the importance of EEG in establishing or detecting a unilateral status epilepticus and in helping the aetiologic diagnosis.

MYOGLOBINURIA FOLLOWING UNILATERAL STATUS EPILEPTICUS AND IPSILATERAL RHABDOMYOLYSIS: A CLINICOPATHOLOGICAL REPORT.

MYOGLOBINURIA following convulsive seizures is a rare occurrence.1 2 3 4 This report describes a patient in whom myoglobinuria developed after unilateral status epilepticus. Although rhabdomyolysis was widespread on the side affected by epileptic seizures, the uninvolved side was normal and served as a control. Case Report A 37-year-old Negro was admitted to the University of Chicago Hospitals because of status epilepticus. This involved the entire left side and lasted for 2 hours. He was unconscious on admission. After the convulsions had been brought under control with an intramuscular injection of 240 mg. of sodium phenobarbital physical examination revealed a robust man who . . .