The role of the monkey sensory cortex in the recovery from cerebellar injury

Summary

The aim of the study was to investigate the contribution of the primary sensory cortex in the compensation of cerebellar deficits during self-paced movements. For this purpose, monkeys were trained on motor tasks which required goal-reaching and independent finger movements. The intermediate and lateral deep cerebellar nuclei and the sensory cortex were lesioned in isolation and in sequence and the course of motor recovery was studied on the test performances. The deep nuclei were lesioned by kainic acid injections, the sensory cortex was removed by ablation. Cerebellar lesions in isolation produced obvious deficits at proximal and distal joints, affecting both slow and fast motor adjustments. Only lesions of the anterior portions of the intermediate and lateral deep nuclear complexes produced deficiencies in voluntary movements. Lesions of the posterior portions produced postural disturbances. The process of recovery following cerebellar lesions was slow and, depending on the nature of the task, was found to be differentially disruptive for motor performances requiring fast and slow motor adjustments. The deficits at distal joints appeared to be more enduring than those at proximal joints. Sensory cortical lesions in isolation produced much less severe and more transient motor deficits. They consisted of hand clumsiness and their recovery was fast and reached higher levels of performance than following cerebellar lesions. When the sensory cortex was removed secondarily to a cerebellar lesion and after recovery from the cerebellar deficits, the initially recovered motor performance became much worse again (decompensation). Removal of the sensory cortex prior to a cerebellar lesion exaggerated the cerebellar deficits and severely limited their recovery. Slow and fast motor performances were completely abolished for three weeks following sequential lesions. Signs of recovery subsequently appeared and stabilized at low levels of performance by five to seven weeks. The effects of combined, sequential cerebellar and sensory cortical lesions were much worse than expected if the effects from the two lesions were merely additive. This indicates that there is some functional interrelationship between the sensory cortex and the cerebellum, which promotes compensation. The somatosensory cortex appears to play a crucial role in the process of recovery from cerebellar motor deficits and it is likely that sensation is an important component in the process of recovery. It is suggested that the sensory cortex exerts its compensatory actions via a structure or structures which receives convergent cerebellar and sensory cortical inputs.