Epilepsylearning and memory

Patients with temporal lobe epilepsy can have problems with learning and memory. Antiepileptic drugs can have marked side-effects, but the observation that chronic animal models of temporal lobe epilepsy also have impairments in learning and memory suggests that this is not the only cause. Memory impairments could result from gross damage, such as hippocampal sclerosis. Gross hippocampal pathology will have effects similar to experimental lesions of the hippocampus, but the observation that at least some of the chronic animal models lack gross hippocampal pathology does not support neuronal death as being the sole cause of impaired learning and memory.

At least two chronic experimental epilepsies have either limited or no cell loss during their induction. These are kindling and stereotaxic injection of a minute dose of tetanus toxin. The tetanus toxin model results in a well-characterized and enduring impairment of learning and memory, which outlasts the active epileptic syndrome in all but a few rats that show relapse. The absence of medication and of cell loss suggest that the psychological impairments in this model have some functional cause. Long-term potentiation remains intact, at least over a period of up to an hour. There is an association of learning impairment with the size of population spikes recorded from the same rats in vivo and under anaesthesia. Inhibition remains impaired in rats at a stage (>3 months after injection) when they had recovered from the active epileptic stage, but retained learning impairments. Abnormalities of the cellular electrophysiology of the postepileptic phase can lead to disruption of network properties, including gamma rhythms, which may, in time, provide a link to the behavioural problem.

Humans with limbic epilepsy often do have substantial hippocampal damage, and this will contribute to learning impairments. The experimental evidence suggests that even in the absence of gross hippocampal damage learning impairments can arise as a result of functional disruption of the hippocampal network.

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