Abstract
Parkinson’s syndrome or parkinsonism, involving the clinical symptoms first described by James Parkinson (1817) occurs in a variety of disorders of the central nervous system (CNS), basically characterized by dysfunction of the dopaminergic nigrostriatal system. It may or, rarely, may not be associated with distinct anatomic damage to the melanin-containing neurons of the substantia nigra, changes to the neuronal cytoskeleton, including the Lewy bodies, and pathology in other non-nigral neuronal systems, often as part of a more widespread process. The term Parkinson’s disease (PD) is restricted to paralysis agitans, the idiopathic form of parkinsonism associated with formation of Lewy bodies and loss of neurons in the pars compacta of the substantia nigra, known since TréTiakoff (1919) as the principal at-risk system in this disorder. It can be accompanied by nonspecific or age-related brain pathology and a variety of other coincidental lesions elsewhere in the CNS. Unilateral parkinsonism is associated with predominant damage to the contralateral brain stem or substantia nigra (Blocq and Marinesco 1893; Lindenberg 1964; Martinez and Utterback 1973; Oppenheimer 1984), while only in exceptional cases of parkinsonism no morphological lesions of the substantia nigra can be found (Denny-Brown 1960; Leverenz and Sumi 1986; Morris et al. 1987). On the other hand, moderate or even considerable damage to the substantia nigra, e.g., in aged subjects or senile dementia of the Alzheimer type (SDAT), may not be necessarily associated with parkinsonian symptoms (Hakim and Mathieson 1979; Jacob 1983; Heilig et al. 1985; Leverenz and Sukmi 1986; Jellinger 1987b; Ditter and Mirra 1987).
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Jellinger, K. (1989). Pathology of Parkinson’s Syndrome. In: Calne, D.B. (eds) Drugs for the Treatment of Parkinson’s Disease. Handbook of Experimental Pharmacology, vol 88. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73899-9_2
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