title: Localized cerebellar hypometabolism in patients with complex partial seizures.
abstract: OBJECTIVE
  We sought to determine the cause of cerebellar dysfunction in epilepsy and whether this dysfunction was directly related to seizures.
  
  
  METHODS
  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).
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurology, UCLA School of Medicine, USA.
authors.forename: I
authors.initials: I
authors.lastname: Savic
authors.forename: L
authors.initials: L
authors.lastname: Altshuler
authors.forename: E
authors.initials: E
authors.lastname: Passaro
authors.forename: L
authors.initials: L
authors.lastname: Baxter
authors.forename: J
authors.initials: J
authors.lastname: Engel
mesh_terms: D002531:Cerebellum / Q000000981:diagnostic imaging / Q000378:metabolism*; D003847:Deoxyglucose / Q000031:analogs & derivatives; D017029:Epilepsy, Complex Partial / Q000000981:diagnostic imaging / Q000378:metabolism*; D017034:Epilepsy, Frontal Lobe / Q000000981:diagnostic imaging / Q000378:metabolism; D004833:Epilepsy, Temporal Lobe / Q000000981:diagnostic imaging / Q000378:metabolism; D005260:Female; D019788:Fluorodeoxyglucose F18; D005625:Frontal Lobe / Q000000981:diagnostic imaging / Q000378:metabolism; D007839:Functional Laterality / Q000502:physiology; D005682:Gadolinium; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009434:Neural Pathways / Q000000981:diagnostic imaging / Q000378:metabolism; D013702:Temporal Lobe / Q000000981:diagnostic imaging / Q000378:metabolism; D014055:Tomography, Emission-Computed
chemical_list: D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005682:Gadolinium; D005947:Glucose