Pathophysiology and consequences
Dr. Martin Holtkamp
58 slide(s) – 00:32:50– English –2010-09-28
Pathophysiological considerations on non-convulsive status epilepticus (NCSE) have to reflect that neuronal networks generating generalised absence SE are completely different from those underlying simple- or complex-partial SE. Whereas thalamocortical neuronal populations are crucial in absence SE, neuronal networks within the hippocampal formation and adjacent limbic structures are relevant in complex-partial SE.Marked differences are also seen on the level of neurotransmitter changes. The synchronisation of thalamocortical discharges occurring during absence SE depends on GABAergic processes. In contrast, the generation of partial SE relies on activation of NMDA and other glutamate receptors. Continuing partial epileptic activity itself induces a cascade of pathological alterations in the brain including decrease of inhibitory GABAA receptors and increase of excitatory NMDA receptors at the postsynaptic membrane that contribute to maintenance of SE. Such pathophysiological differences as seen in absence and partial SE may also explain possible consequences of either form. The development of excitotoxicity may be seen during partial SE but not in absence SE. Experimental models of partial SE suggest that the severity of neuronal injury strongly correlates with the extent of motor seizure activity, but non-convulsive epileptic activity damages neurons as well. Translation of these experimental findings to human NCSE should be made cautiously, as SE in animal models is often associated with extensive continuous excitatory seizure activity while NCSE in humans generally is interrupted by periods of less severe activity. Controlling for the underlying aetiology, human studies on consequences of complex-partial SE did not demonstrate clinically relevant findings in neuroimaging and neuropsychology.