Summary
The pathologic grasp reflex (“forced grasping”) was used to study restitution of function in monkeys conditioned to grasp and release a stick for food. Cortical lesions (area 6) made it impossible for the animals to relinquish the stick or to avoid grasping an unconditioned (tactile) stimulus. Normal tactile evasion was abolished but returned during recovery, i.e. as forced grasping waned. Pyramidal lesions alone provoked no forced grasping but abolished all tactile reflexes. Seriatim cortical and pyramidal (1 year later) lesions brought back pathological grasping after “total” restitution of normal grasping had occurred, whereas ventrolateral spinal lesions hastened restitution and enhanced tactile evasion. The possible mechanisms underlying restitution are discussed; it is suggested that the abnormal grasp is compensated by enhancement of its opposing reflex, tactile evasion, which is subserved by the pyramid. The fundamental physiological change due to area 6 lesion is a reflex imbalance which endures covertly in spite of behavioral restitution and is exposed once again when tactile evasion is abolished by pyramidotomy. Therefore, during “recovery”, pyramidal function vis a vis tactile evasion was enhanced in response to loss of inhibitory control over tactile and proprioceptive grasp reflex activity. This model is offered as an alternative to “functional reorganization” and “vicarious function”.
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Goldberger, M.E. Restitution of function in the CNS: The pathologic grasp in Macaca mulatta. Exp Brain Res 15, 79–96 (1972). https://doi.org/10.1007/BF00234959
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DOI: https://doi.org/10.1007/BF00234959