Severe akinesia can be observed in macaques following MPTP injections destroying dopaminergic nigrostriatal neurons. Akinesia also results from inhalation of toxic substances inducing bilateral lesions of the two pallidal nuclei and of the pars reticulata of the substantia nigra, and not of the pars compacta. Most of the recent studies of the anatomo-physiological substratum of akinesia used MPTP injections. Deoxyglucose studies have shown a clear increase in the neuronal activity of the medial nucleus of the pallidum and of its thalamic projection territory. Electrophysiological studies have shown a major modification of the spontaneous activity of medial pallidal neurons which is influenced in an excessive and non selective manner by sensorimotor inputs. Analysis of the relative three dimensional geometry of nervous arborizations have shown that the striato-pallido-nigral system is extremely convergent. Akinesia consecutive to nigrostriate lesions could be linked to an excessive and anarchic activation of this system. The contradiction which exists between akinesia with an abnormal activity of the medial pallidum and akinesia with bilateral pallidal lesions could only be apparent if akinesia was linked to the ineffective emission or to the interruption of messages to the thalamus.
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