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J Neurophysiol 94: 1312-1324, 2005. First published May 4, 2005; doi:10.1152/jn.01251.2004
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Dissociation of Sensorimotor Deficits After Rostral Versus Caudal Lesions in the Primary Motor Cortex Hand Representation

Kathleen M. Friel, Scott Barbay, Shawn B. Frost, Erik J. Plautz, Douglas M. Hutchinson, Ann M. Stowe, Numa Dancause, Elena V. Zoubina, Barbara M. Quaney and Randolph J. Nudo

Department of Molecular and Integrative Physiology, Landon Center on Aging, and Smith Mental Retardation Research Center, University of Kansas Medical Center, Kansas City, Kansas

Submitted 7 December 2004; accepted in final form 25 April 2005

Primary motor cortex (M1) has traditionally been considered a motor structure. Although neurophysiologic studies have demonstrated that M1 is also influenced by somatosensory inputs (cutaneous and proprioceptive), the behavioral significance of these inputs has yet to be fully defined in primates. The present study describes differential sensory-related deficits after small ischemic lesions in either the rostral or caudal subregion of the M1 hand area in a nonhuman primate. Squirrel monkeys retrieved food pellets out of different sized wells drilled into a Plexiglas board. Before the lesion, monkeys retrieved pellets by directing the hand to the well, inserting fingers directly into it, and extracting the pellet. After a lesion to the rostral portion of M1, monkeys frequently failed to direct the hand accurately to the well. Instead, fingers contacted the surface of the board outside the well before entering the well. These aiming errors are consistent with both the large amount of proximal motor outputs and the predominant proprioceptive inputs of rostral M1. Overall, these aiming errors are suggestive of dysfunctional processing of proprioceptive information or the failure to integrate proprioceptive information with motor commands. In contrast, after a lesion to the caudal portion of M1, monkeys frequently examined their palm visually for the presence of the pellet after an attempted retrieval. These errors are consistent with both the large amount of distal motor outputs and the predominant cutaneous inputs of caudal M1. Thus these errors are suggestive of a deficit in processing of cutaneous information or the failure to integrate cutaneous information with motor commands. Rostral and caudal M1 lesions result in different deficits in sensory-dependent motor control that appear to correlate with broad segregation of motor outputs and previously described sensory inputs of M1.


Address for reprint requests and other correspondence: K. M. Friel, Center for Neurobiology, and Behavior, Columbia University, 1051 Riverside Drive, New York, NY 10032 (E-mail: kf2105{at}columbia.edu)




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