ABSTRACT
Previous studies have shown that after injury to the hand representation in primary motor cortex (M1), size of the spared hand representation decreased dramatically unless the unimpaired hand was restrained and monkeys received daily rehabilitative training using the impaired fingers. The goal of this study was to determine if restriction of the unimpaired hand was sufficient to retain spared hand area after injury or if retention of the spared area required repetitive use of the impaired limb. After infarct to the hand area of M1 in adult squirrel monkeys, the unimpaired hand was restrained by a mesh sleeve over the unimpaired arm. Monkeys did not receive rehabilitative training. Electrophysiologic maps of M1 were derived in anesthetized monkeys before infarct and 1 month after infarct by using intracortical microstimulation. One month after the lesion, the size of the hand representation had decreased. Areal changes were significantly smaller than those in animals in a previous study that had received daily repetitive training after infarct (p < 0.05). Areal changes were not different from those in a group of animals that received neither rehabilitative intervention nor hand restraint after injury. These results suggest that retention of hand area in M1 after a lesion requires repetitive use of the impaired hand.
Subject(s)
Brain Injuries/rehabilitation , Motor Cortex/injuries , Movement Disorders/rehabilitation , Neural Pathways/injuries , Neuronal Plasticity/physiology , Recovery of Function/physiology , Animals , Brain Injuries/pathology , Brain Injuries/physiopathology , Brain Mapping , Female , Functional Laterality/physiology , Male , Motor Cortex/pathology , Motor Cortex/physiopathology , Movement Disorders/pathology , Movement Disorders/physiopathology , Neural Pathways/pathology , Neural Pathways/physiopathology , Physical Conditioning, Animal , Restraint, Physical/adverse effects , Saimiri , Treatment OutcomeABSTRACT
The goal of the present study was to examine factors affecting motor impairment and recovery in a primate model of cortical infarction. Microelectrode stimulation techniques were used to delineate the hand representation in the primary motor cortex (M1). Microinfarcts affecting approximately 30% of the hand representation were made by electrocoagulation of surface vessels. Electrophysiologic procedures were repeated at 1 month after the infarct to examine changes in motor map topography. Before the infarct, and at approximately 1 week (early period) and 1 month (late period) after the infarct, manual performance was assessed on a reach-and-retrieval task that required skilled use of the digits. Contrary to the expected outcome, early impairment was inversely related to the amount of digit representation destroyed by the infarct. That is, animals with less involvement of the M1 digit area demonstrated the greatest motor deficit in the early postinfarct period. In addition, improvement in motor performance between early and late postinfarct periods was directly related to a decrease in the extent of the digit + wrist/forearm area in the final postinfarct map. These results suggest that specific aspects of motor-map remodeling are expressions of adaptive mechanisms that underlie functional recovery after stroke. Further, they suggest that the adaptive mechanisms underlying postinjury recovery differ in detail from those that operate in normal motor learning. The potential role of compensatory mechanisms in these phenomena is discussed.
