The association between posterior fossa malformations and epilepsy is rarely reported in the literature. We describe 54 cases with posterior fossa malformations, according to embryogenesis classification, divided into two groups on the basis of presence or absence of epilepsy. Epilepsy occurred in 22 cases (40.7%) and was not related to the type of posterior fossa malformation or to supratentorial cerebral lesions associated with the malformation. Familial antecedents for epilepsy and/or febrile convulsions influenced the presence of epilepsy in patients with posterior fossa malformations (P < .01). Epilepsy was mainly partial (77.3%); benign partial/generalized epilepsies and febrile convulsions occurred in 27.3% of cases. Seizures disappeared for 2 or more years at the end of follow-up in 36.4% of patients. Good epilepsy prognosis was not related to the age at onset of seizures, familial antecedents for epilepsy and/or febrile convulsions, supratentorial associated lesions, or age of patients at the last observation. Profound mental retardation prevailed in patients with epilepsy (P < .01), as did pathologic electroencephalograms (EEG) (P < .0001), with paroxysmal abnormalities (P < .001) and asymmetry (P < .01). In our 54 cases of posterior fossa malformation, we identified two risk factors for epilepsy: familial antecedents for epilepsy and/or febrile convulsions and the involvement of the cerebellum in the malformation.
The cerebellum is involved in motor and cognitive functions and behavior. Its role in controlling epileptic seizures has been demonstrated in the literature. Genetic factors can enhance epilepsy susceptibility when the cerebellum is damaged. We examined the occurrence and features of epilepsy, intelligence, and psychiatric disorders in 28 patients with cerebellar hypoplasia. We compared patients with (10; 35.7%) and without (18; 64.3%) epilepsy. The statistical evaluation showed a significant prevalence of familial antecedents for seizures in patients with epilepsy (P < .01); cerebral associated lesions and type of cerebellar hypoplasia did not influence the occurrence of epilepsy, which was partial in 80% of cases. Profound mental retardation prevailed in patients with epilepsy (P < .05). Both mental retardation (75%) and pervasive developmental disorders (17.8%) prevailed in our cases with respect to the general population (P < .000). Cerebellar hypoplasia in our sample seems to be an important risk factor for the occurrence of epilepsy, mental retardation, and psychiatric disorders.
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