Does the absence of clinical expression of choreoathetosis, despite severe striatal atrophy, correlate with plasticity of neuropeptide synthesis?

Abstract

Neuropeptide and neurotransmitter plasticity has been demonstrated in the central nervous system. Modifications of their synthesis occur following receptor blockade or deafferentiation by surgical lesions. This concept should provid answers to some remaining open questions in human pathology especially in degenerative diseases of the basal ganglia. In a severely atrophied striatum we observed a selective increase in the number of detectable striatal substance P and met-enkephalin neurones which exhibited a striking increase in the intensity of labelling. This increase, instead of the well established reduction of substance P and enkephalins in the atrophied striatum of Huntington's disease, could explain the absence of choreoathetosis which was replaced by rigidity and bradykinesia in the patient. The absence of choreoathetosis, despite severe striatal atrophy, is described in several basal ganglia diseases and could also be related to neurotransmitter or neuropeptide plasticity rather than due to the primary lesion.

Cite this paper

@article{Schiffmann1991DoesTA, title={Does the absence of clinical expression of choreoathetosis, despite severe striatal atrophy, correlate with plasticity of neuropeptide synthesis?}, author={Serge N. Schiffmann and Jeroen Vanderhaeghen}, journal={Journal of neural transmission. Supplementum}, year={1991}, volume={33}, pages={99-103} }