Neuropsychological Outcome Following Prolonged Febrile Seizures Associated with Hippocampal Sclerosis and Temporal Lobe Epilepsy in Children

Conclusion

The evidence presented in this chapter demonstrates that hippocampal sclerosis is a substrate for TLE also in children.

The pathophysiological mechanisms responsible for hippocampal sclerosis are not completely understood. Given the high correlation between early PFCs and hippocampal sclerosis, there is a strong suggestion that the two may be causally related, although the basis for this relationship is not clear.

Hippocampal damage has been shown to produce long-term memory deficits of different severity; however, since most of the evidence relating memory impairment to hippocampal lesions has been derived from patients referred to neurosurgery centers for temporal lobectomy as relief of severe epilepsy, it is difficult to disentangle the effects of severe and recurrent seizures on memory from that of structural damage to the hippocampus.

We report evidence of mild memory deficits in a group of young patients with unilateral hippocampal sclerosis and normal intelligence who had either mild TLE or were seizure free.

Right hippocampal lesions were associated with reduced potential for learning spatial material. Our data support the idea that hippocampal sclerosis per se is sufficient to interfere with normal memory development.

Furthermore, early prolonged febrile convulsions may be considered a risk factor for neuropsychological outcome, as well as for subsequent epilepsy.

Further studies should be directed at corroborating our results with larger samples and at analyzing if and to what extent recurrent seizures specifically aggravate memory dysfunction.