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Neurology 2002;58:381-390
© 2002 American Academy of Neurology

Activation in primary and secondary motor areas in patients with CNS neoplasms and weakness

T. Krings, MD, R. Töpper, MD, K. Willmes, PhD, M. H.T. Reinges, MD, J. M. Gilsbach, MD and A. Thron, MD

From the Department of Neuroradiology (Drs. Krings and Thron), Clinic for Neurosurgery (Drs. Krings, Reinges, and Gilsbach), Clinic for Neurology (Dr. Töpper), Subdepartment of Neuropsychology of the Clinic for Neurology (Dr. Willmes), and the Interdisciplinary Center for Clinical Research–Central Nervous System, University Hospital of the University of Technology, Aachen, Germany.

Address correspondence and reprint requests to Dr. T. Krings, Department of Neuroradiology, University Hospital of the University of Technology, Aachen Pauwelsstr. 30, 52057 Aachen, Germany; e-mail: tkrings{at}izkf.rwth-aachen.de

Objective: To demonstrate whether cortical activation within different cortical motor regions in neurosurgical patients varies with the degree of paresis induced by mass lesions near the central region.

Methods: A total of 110 patients with brain tumors infiltrating the central region and with varying degrees of paresis were investigated employing fMRI during the performance of hand motor tasks. The percent signal change between rest and activation was calculated for four cortical regions: primary motor cortex (M1), supplementary motor area, premotor area, and superior parietal lobule.

Results: Significant decreases in activation with increasing degrees of paresis were found in M1, whereas significant increases in activation were noted in secondary motor areas that were not affected by the tumor.

Conclusions: The signal loss in areas adjacent to tumor tissue may relate either to tumor-induced changes in cerebral hemodynamics or to a direct loss of cortical neurons resulting in a lesser degree of hemodynamic changes after motor activation. The increase in activation within secondary motor areas with increasing degrees of paresis supports the growing evidence of a practice- and lesion-dependent reorganization of the cortical motor system and the ability of the brain to modulate its excitatory output according to external demands.




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