Localized cerebellar hypometabolism in patients with complex partial seizures

We sought to determine the cause of cerebellar dysfunction in epilepsy and whether this dysfunction was directly related to seizures.

Cerebellar metabolism was evaluated in 48 patients with a well-defined region of seizure onset and with corresponding hypometabolism. Regions of interest (ROI) were drawn according to a standardized template. If the ROI/nonepileptogenic cortex count rate ratio was outside the 95% confidence interval (CI) of controls, the ROI was defined as abnormal. The ratios from cerebellar hemispheres (defined as ipsi- or contralateral to the seizure onset region), were compared among controls (n = 8); patients who had seizure onsets and corresponding hypometabolism mesially in a temporal lobe (patient group 1, n = 19); patients whose seizures had onset mesially in a temporal lobe but spread rapidly to the ipsilateral frontal lobe and who had hypometabolism both in the affected temporal lobe and frontal lobe (patient group 2, n = 23); and patients who had seizure onsets and corresponding hypometabolism in the frontal lobe (patient group 3, n = 6).

Significant hypometabolism was noted in the contralateral cerebellum of patients in group 2 and 3 [p = 0.007 and p = 0.008, respectively; two-way analysis of variance (ANOVA)]. In contrast, patients in group 1 tended to have lower values in the ipsilateral cerebellum (p = 0.057).

The observed cerebellar changes are consistent with animal data showing that cerebellar connections to frontal lobes are numerous and crossed, whereas the connections to mesial temporal lobes are less abundant, bilateral, with an ipsilateral predominance. The difference between the two groups of patients with mesial temporal seizures suggests that cerebellar dysfunction in partial epilepsy, at least to a certain extent, is related to mechanisms involved in seizure generation and spread.