Sleep and the temporal lobe.

The main interest in the association between sleep and temporal lobe dysfunction is based on the activation of ictal and interictal epileptic phenomena. The clinical semiology of NREM and REM parasomnias may resemble complex partial seizures. The differentiation between epilepsy and dissociated states of wakefulness and sleep is of high diagnostic and therapeutic importance. Systems within temporal lobe structures are also responsible for disturbed sleep or dyssomnia. The limbic brain is connected with different nodal points in the network underlying sleep organisation and participates in both sleepinducing and arousal mechanisms. Experimental amygdala kindling, an animal epilepsy model involving temporal structures, induces disturbed sleep patterns favouring waking and light sleep. In epilepsy unstable disrupted and superficial sleep patterns prevail without overt seizures. Sleep-fragmentation and deprivation may impair daytime functioning and cognitive performance by lowering the seizure-threshold. The recognition of dyssomnia and of excessive sleepfragmentation and sleepiness has obvious implications for behavioural and drug treatment.