Epilepsy: Clinical Background and Basic Mechanisms
 

The clinical and laboratory study of epilepsy has contributed significantly to our understanding of the neurobiology of normal brain. Epilepsy is a symptom of disordered brain function, rather than a disease per se. The clinical aspects of classification will be reviewed along with examples from taped seizures. Diverse symptomatology results from involvement of different brain areas and circuits, and different underlying pathophysiologies. Three factors contributing to epileptogenesis after focal brain injury, including alterations in intrinsic membrane properties, enhanced excitatory synaptic connectivity, and abnormalities in GABAergic inhibition will be discussed. Gene mutations that give rise to epileptic syndromes can involve both agonist-activated and voltage-dependent ion channels.  Although an increasing number of such genetic epilepsies have been reported, the mechanisms leading from the defective gene to the epilepsy phenotype are not known in any disorder.  Absence epilepsy is an example of thalamocortical circuit dysfunction that is a distortion of normal brain rhythm generation. Abnormalities of intrinsic voltage-dependent and transmitter-activated ion channels in neurons of the thalamus may be the basis for generation of th diffuse 3 Hz spike-wave EEG activity that characterizes absence epilepsy. Differences in the pathophysiology of the focal cortical epilepsies and absence epilepsy underlie differences in the efficacy of anti-epileptic drugs in the two conditions.

Papers for student presentation:

Brusa et al, Higuchi et al RNA Editing and epilepsy

Eid et al Transmitter transporters and epilepsy

Yamamato et al Electrical stimulation in human epilepsy