What's wrong with the amygdala in temporal lobe epilepsy?

Abstract

The amygdala has long been implicated in the semiology of temporal lobe epilepsy. John Hughlings Jackson's (1880) earliest description of the ‘dreamy state’ published in Brain stresses the sensations of terror and anger, as well as the premonitory and epigastric sensations, olfactory hallucinations and automatic behaviours that we recognize as features of complex partial seizures arising in the temporal lobe. It is tempting to think of affective symptoms as separate from the déjà vu and premonitions that imply involvement of the hippocampal formation. However, Gloor et al. (1982) showed that stimulation in the amygdala could elicit a full spectrum of experiential symptoms in patients with intractable temporal lobe epilepsy, even when after-discharges implying stimulus spread were not seen. More recently the term ‘dysphoric disorder of epilepsy’ has been proposed to describe a combination of emotional instability, dysphoria, irritability and aggression, and associated decreases in amygdalar volume suggest a causal link to abnormalities of this nucleus (van Elst et al., 2009). But what are these abnormalities? How do they relate to either ictal or interictal affective symptoms? And what is the role of the amygdala in the initiation, spread and termination of seizures in temporal lobe epilepsy? Answers to these questions are still far off, but the study reported by Graebenitz and colleagues in this issue of Brain (page 2929) provides a glimpse into possible links among these phenomena.