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From the Department of Neurology (Drs. Schlaug, Antke, Arnold, Witte, and Seitz), Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; the Department of Neurology (Dr. Schlaug), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; the Epilepsy Center Bethel (Drs. Holthausen, Arnold, Ebner, Tuxhorn, and Lüders), Bielefeld, Germany; the Institute of Medicine (Dr. Jäncke), Research Center Jülich, Jülich, Germany; and the Department of Neurology (Dr. Lüders), Cleveland Clinic Foundation, Cleveland, OH, USA.
Address correspondence and reprint requests to Dr Seitz, Dept. of Neurology, Heinrich-Heine-University Düsseldorf, POB 101007, D-40001 Düsseldorf, Germany, or Dr. Gottfried Schlaug, Department of Neurology, Dana 779, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA.
Early motor manifestations are the main components of focal seizures involving the frontal lobe. We examined the relationship between the initial ictal motor manifestations and interictal abnormalities of cerebral glucose consumption (rCMRGlc) as assessed by PET in 48 consecutive patients with focal seizures of neocortical origin. Group data analysis revealed that patients with predominantly unilateral clonic seizures had a significant contralateral perirolandic hypometabolism and to a lesser degree a contralateral frontomesial hypometabolism. Patients with predominantly focal tonic manifestations showed a hypometabolism within the frontomesial and perirolandic regions that was unilateral in all patients with lateralized tonic seizures. Patients with versive seizures had mainly contralateral metabolic depressions without a consistent regional pattern. Patients with hypermotor seizures had metabolic depressions involving frontomesial, anterior cingulate, perirolandic, and anterior insular/frontal operculum areas. In all patient groups, bilateral and symmetric hypometabolism of the thalamus and cerebellum was observed. We propose that this pattern of distinctly abnormal metabolic brain regions demonstrates not only possible epileptogenic zones but also symptomatogenic brain regions as shown by the associations between clinical manifestations and sets of abnormal brain regions, particularly if epileptogenic zones are in a clinically silent neocortical brain region. The detection and possible differentiation of symptomatogenic and epileptogenic zones might improve the effectiveness of presurgical noninvasive studies.
Presented in part at the 47th annual meeting of the American Academy of Neurology, Seattle, WA, May 1995.
Received July 17, 1996. Accepted in final form January 17, 1997.
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