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Physiopathology of Experimental Parkinsonism in the Monkey

Published online by Cambridge University Press:  18 September 2015

Louis J. Poirier ,
Michel Filion ,
Louis Larochelle  and
Jean-Claude Péchadre
Louis J. Poirier*
Affiliation:
Laboratoires de Neurobiologie, Faculte de Medicine, Universite Laval, Quebec, Que., Canada
Michel Filion
Affiliation:
Laboratoires de Neurobiologie, Faculte de Medicine, Universite Laval, Quebec, Que., Canada
Louis Larochelle
Affiliation:
Laboratoires de Neurobiologie, Faculte de Medicine, Universite Laval, Quebec, Que., Canada
Jean-Claude Péchadre
Affiliation:
Laboratoires de Neurobiologie, Faculte de Medicine, Universite Laval, Quebec, Que., Canada
*
Laboratoires de Neurobiologie, Université Lava, Quebec, Canada G1K 7P4
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Postural or Parkinson-like tremor, which results from the impairment of mechanisms which are predominantly lateralized in the brain, is most likely related to the combined impairment of the dopaminergic nigrostriatal pathway and the corresponding rubro-olivo-cerebello-rubral loop (without excluding the possibility that other nervous mechanisms interconnected with these structures may represent an alternative disturbance). The integrity of the internal division of the pallidum and the ventrolateral area of the thalamus and their efferent fibers as well as the motor cortex and certain of its cortico-subcortico-spinal pathways (Figures 1 and 2) is apparently an essential feature for the elaboration of the rhythmic bursts associated with the appearance of postural tremor. The integrity of the spinal sensory roots and the rubro-tegmentospinal tract is not a prerequisite for the expression of postural tremor, a condition which seems essential for the production of rigidity. The latter facts suggest that the disturbances which subserve these two types of motor impairment, often concomitantly present in Parkinsonism, partially involve the impairment of different mechanisms although the loss of the DA fibers originating in the substantia nigra and ending in the neostriatum (Figure 1) appears to represent a disturbance common to both types of disorders.

Bradykinesia which may be associated with an impairment of catecholamine metabolism (and more especially the neostriatal DA mechanisms) on both sides of the brain may also result from bilateral lesions of the pallidum or of its outflow corresponding, in the main, to the pallidothalamic fibers ending in the ventrolateral thalamus. The latter types of lesion most likely exclude the influence of the monoaminergic, cholinergic and gabaminergic activities normally originating in the striopallidal system and influencing the activity transmitted to other CNS mechanisms. Severe akinesia, however, apparently depends on more profound and generalized disturbances of brain monoamine metabolism with or without the involvement of other ill-defined mechanisms. At any rate the impairment of the brain DA mechanisms (and especially those of the neostriatum) seems to represent a major feature in the production of the Parkinsonian type of akinesia. Further work is needed to establish the relative importance of the loss of catecholaminergic mechanisms other than those of the neostriatum in the production of akinesia.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 2 , Issue 3 , August 1975 , pp. 255 - 263
Copyright
Copyright © Canadian Neurological Sciences Federation 1975

References

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