LOCALIZED CEREBELLAR HYPOMETABOLISM IN PATIENTS WITH COMPLEX PARTIAL SEIZURES

Purpose: We sought to determine the cause of cerebellar dysfunction in epilepsy and whether this dysfunction was directly related to seizure s. Methods: Cerebellar metabolism was evaluated in 48 patients with a well-defined region of seizure onset and with corresponding hypometabo lism. Regions of interest (ROI) were drawn according to a standardized template. If the ROI/nonepileptogenic cortex count rate ratio was out side 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 co ntrols (n = 8); patients who had seizure onsets and corresponding hypo metabolism mesially in a temporal lobe (patient group 1, n = 19); pati ents whose seizures had onset mesially in a temporal lobe but spread r apidly 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 hypometabol ism in the frontal lobe (patient group 3, n = 6). Results: Significant hypometabolism was noted in the contralateral cerebellum of patients in groups 2 and 3 [p = 0.007 and p = 0.008, respectively; two-way anal ysis of variance (ANOVA)]. In contrast, patients in group 1 tended to have lower values in the ipsilateral cerebellum (p = 0.057). Conclusio ns: The observed cerebellar changes are consistent with animal data sh owing that cerebellar connections to frontal lobes are numerous and cr ossed, whereas the connections to mesial temporal lobes are less abund ant, bilateral, with an ipsilateral predominance. The difference betwe en the two groups of patients with mesial temporal seizures suggests t hat cerebellar dysfunction in partial epilepsy, at least to a certain extent, is related to mechanisms involved in seizure generation and sp read.