title: Primate models of postural disorders.
abstract: Dorsal column lesions in the high cervical region of the monkey result in severe defects of movements projected into space and contactual orienting reactions of the forelimbs. The hindlimbs are less affected provided a pathway through the lateral columns, Morin's tract, remains intact. Interruption of this pathway results in a defect of hindlimb function similar to that of the forelimbs. Cerebellar ablations in monkeys result in postural and movement disorders, including hypotonia of limb extensor muscles. An important mechanism underlying the hypotonia is a depression of the responses to muscle extension of spindle primary afferents owing to a decrease of fusimotor activity. In the decerebellate animal abnormalities of limb trajectory during active movements projected into space (cerebellar "dysmetria") appear to result principally from dysfunction of systems separate from the peripheral fusimotor efferent-spindle afferent reflex arc. Precentral cortical ablation results initially in a contralateral hypotonic hemiparesis, later in a hypertonic hemiparesis. A depression of the responses of muscle spindle afferents occurs during the hypotonic phase, but during the hypertonic phase spindle function returns to normal levels. Accordingly a depression of fusimotor function appears to be important in the hypotonic phase of hemiplegia; however, there is no evidence that an enhancement of fusimotor function underlies the hypertonic phase. Bilateral section of the medullary pyramids results in an enduring hypotonic paresis. Abnormalities of contactual orienting responses of limbs are similar to those following dorsal column lesions. Responses of spindle primary afferents are depressed during the initial stages after acute pyramidotomy, then approach but do not reach normal levels. It is concluded that the dorsal columns constitute an afferent, and the pyramidal tracts an efferent, pathway important in oriented contactual reactions of the limbs. The hypotonia resulting from cerebellar lesions, precentral ablation, and pyramidal tract section stems, at least in part, from a depression of the fusimotor innervation of muscle spindle afferent activity.
mesh_terms: D000818:Animals; D002531:Cerebellum / Q000502:physiology; D002540:Cerebral Cortex / Q000502:physiology; D002818:Cordotomy; D004195:Disease Models, Animal; D004576:Electromyography; D007866:Leg / Q000502:physiology; D009069:Movement Disorders; D009132:Muscles / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*; D009476:Neurons, Efferent / Q000502:physiology; D011187:Posture; D011323:Primates; D011712:Pyramidal Tracts / Q000473:pathology / Q000502:physiology; D013116:Spinal Cord / Q000473:pathology; D013119:Spinal Cord Injuries