The main interest in the association between sleep and temporal lobe d
ysfunction is based on the activation of ictal and interictal epilepti
c phenomena. The clinical semiology of NREM and REM parasomnias may re
semble 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 ar
e also responsible for disturbed sleep or dyssomnia. The limbic brain
is connected with different nodal points in the network underlying sle
ep organisation and participates in both sleepinducing and arousal mec
hanisms. Experimental amygdala kindling, an animal epilepsy model invo
lving temporal structures, induces disturbed sleep patterns favouring
waking and light sleep. In epilepsy unstable disrupted and superficial
sleep patterns prevail without overt seizures. Sleepfragmentation and
deprivation may impair daytime functioning and cognitive performance
by lowering the seizure-treshold. The recognition of dyssomnia and of
excessive sleepfragmentation and sleepiness has obvious implications f
or behavioural and drug treatment.