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From the Departments of Neuroradiology (Drs. Krainik, Marsault, Chiras, and Lehéricy) and Neurosurgery (Drs. Duffau, Capelle, Cornu, and Boch), INSERM EMI 007 (Drs. Krainik, Duffau, and Lehéricy), Hôpital de la Pitié-Salpêtrière, Paris; and Service Hospitalier Frédéric Joliot (Drs. Mangin, Le Bihan, and Lehéricy), CEA, Orsay, France.
Address correspondence and reprint requests to Dr. Stéphane Lehéricy, Service de Neuroradiologie Fishgold, Hôpital de la Pitié-Salpêtrière, 47 bd de lHôpital, 75013 Paris, France; e-mail: stephane.lehericy{at}psl.ap-hop-paris.fr
Objective: To determine the compensatory mechanisms involved in the recovery of motor function following surgical lesions of the supplementary motor area (SMA) and their relation to the clinical characteristics of recovery.
Subjects and Methods: Twelve patients were referred for surgery of low-grade gliomas located in the SMA, and compared to eight healthy controls using fMRI before and after surgery during self-paced movements of both hands, successively. Magnitude and volume of activation within regions of interest (primary sensorimotor cortex, premotor cortex, SMA, preSMA, and parietal lobes) were compared and tested for correlation with anatomic characteristics of the tumor and resection, and clinical data.
Results: Tumor growth induced preoperative underactivity in the adjacent SMA and overactivity in the opposite SMA. Postoperative recovery was associated with recruitment of a premotor network located in the healthy hemisphere including the SMA and the lateral premotor cortex. Postoperative premotor recruitment in the healthy hemisphere increased with the percentage of resection of preoperative SMA activation. Shortened onset and duration of recovery was associated with increased preoperative changes in activation levels.
Conclusions: These findings suggest a dysfunction of the SMA ipsilateral to the tumor, partially compensated by a recruitment of the contralesional SMA which correlated with shortened postoperative recovery. SMA resection was compensated by the recruitment of a medial and lateral premotor circuitry in the healthy hemisphere.
Received July 30, 2003. Accepted in final form December 23, 2003.
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