Katherine H Noe | PubMed Health

PubMed2005

Cardiac pathology in status epilepticus.

Massive catecholamine release resulting in the formation of cardiac contraction bands may represent the cause of death in status epilepticus (SE). We reviewed the cardiac pathology of patients who died during SE to asses for contraction bands. Eight of 11 patients who died during SE had identifiable myocardial contraction bands compared with 5 of 22 control patients (p < 0.05, Fisher's exact t test). These findings delineate a pathological substrate and provide compelling evidence that excessive catecholamine release is the mechanism responsible for death in SE.

Adolescent↗

PubMed2005

Mechanisms underlying status epilepticus.

Status epilepticus is a state of prolonged or recurrent seizure activity that is associated with significant mortality and morbidity. At a cellular level, status epilepticus results from a failure of normal inhibitory pathways, primarily mediated by gamma-n-aminobutyric acid (GABA) acting via GABA(A) receptors. This loss of inhibitory drive allows the activation of excitatory feedback loops, leading to repetitive, synchronous firing of large groups of neurons. As seizure activity continues, there is further decline in GABAergic function. Continued excitatory input mediated primarily by glutamate leads to neuronal cell death. These alterations in inhibitory and excitatory pathways have important implications for the pharmacologic management of status epilepticus. Currently recommended agents act primarily through the GABA(A) receptor and have been shown to become less effective in status epilepticus of longer duration. Agents designed to inhibit glutamate activity show promise both in the treatment of status epilepticus and in the prevention of associated neuronal injury.

Animals↗