Temporal lobe epilepsy is a disease of faulty neuronal resonators rather than oscillators, and all seizures are provoked, usually by stress

Summary 

Temporal lobe epilepsy (TLE) is the most common cause of intractable adult epilepsy. It is proposed that different kinds of epilepsy be classified into one of two categories, which correspond to the two basic kinds of neurons in the brain, that is, as diseases of oscillators or as diseases of resonators. Oscillator (or pacemacker) neurons are endowed with intrinsic conductances that permit periodic spontaneous generation of action potentials; in contrast, resonators are neurons which process information coming from sensory stimuli or from other neurons. A literature review supports the idea that TLE is a disease of faulty resonators. This means that seizures do not arise de novo in the seizure focus. The seizure focus responds to normal input with an abnormally large discharge that causes seizures. The most frequent trigger for TLE is psychological stress.

A previously published theory of stress is reviewed. The stress circuit runs from the hippocampus to the amygdala to the dorsal raphe nucleus to the entorhinal cortex and back to the hippocampus. Cell loss in the dentate is central to the pathophysiology of both chronic stress and TLE, which establish a “vicious circle” relationship with one another. Once it is grasped that TLE is a disease of resonators and that all seizures in TLE are triggered, then it makes sense to address the major recognized trigger, which is stress. New therapeutic ideas for decreasing seizure frequency in TLE include the use of anti-depressants, ethosuximide (which blocks firing in the dorsal raphe nucleus), and mood-stabilizers (which block firing in the entorhinal cortex). The latter category includes several recognized anti-epileptic drugs. Drugs from all three categories should be used simultaneously and on an empirical basis in each patient.