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The Neuropathology of Parkinson's Disease
Author(s) -
Eadie M. J.
Publication year - 1971
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1971.tb02559.x
Subject(s) - substantia nigra , parkinsonism , globus pallidus , basal ganglia , putamen , neuropathology , neuroscience , substantia innominata , lewy body , caudate nucleus , medicine , pathology , parkinson's disease , biology , central nervous system , cholinergic neuron , disease
Summary: For almost 100 years after Parkinson's original description there was uncertainty as to whether there was any structural brain pathology in idiopathic Parkinsonism, or, if there was, whether the lesions were situated in (a) the spinal cord (b) the mid‐brain and substantia nigra (c) the striatum, pallidum, thalamus and mid‐brain Then, in 1913, Lewy 2 studied 20 Parkinsonian brains and found changes in the cerebral cortex, caudate nucleus, putamen, globus pallidus, certain fibre tracts in the basal ganglia, the substantia innominata and the dorsal vagal nucleus. As well as cell loss and gliosis there were neurofibrillary changes in neurons, and laminated inclusion bodies (Lewy bodies). Except for changes in the substantia nigra Lewy described practically all the microscopic lesions of idiopathic Parkinsonism. The nigral changes were emphasised by many later authors, and came to be regarded as the most common, if not the essential, lesions of Parkinsonism. However, the currently available evidence suggests that bilateral substantia nigra lesions alone are not a sufficient explanation for Parkinsonism. At the present time, at least three problems face those who would interpret the neuropathology of Parkinsonism: (i) what is the meaning of the Lewy body? (ii) what is the correlation between regional brain lesions and different aspects of Parkinsonian dysfunction ? (iii) could Parkinsonism be the clinical expression of a chemical disorder in monoaminergic neurons, with structural alterations a late effect of the underlying chemical changes?