The natural history of Parkinson's disease

被引:98
作者
Poewe, WH [1 ]
Wenning, GK [1 ]
机构
[1] Univ Innsbruck Hosp, Dept Neurol, A-6020 Innsbruck, Austria
关键词
D O I
10.1002/ana.410440703
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
There are still insufficient data on the natural course of Parkinson's disease (PD) owing to lack of standardized longitudinal follow-up studies. Reported progression rates in early PD vary considerably by a factor of 2 to 3. Similarly, data from sequential [F-18] dopa PET studies in PD patients have produced variable decline rates of PET indices ranging between 7 and 70% per decade. Risk factors fro rapid progression include old age at onset, concomitant major depression, dementia, andakinetic-rigid symptoms presentation. The introduction of levodopa into the routine treatment of PD patients had a dramatic impact on symptomatic control without affecting the underlying rate of disease progression. By contrast, monoamine oxidase (MAO) B inhibition by deprenyl monotherapy in early PD was shown to delay the need for levodopa by around 9 months. However, the neuroprotective action disappeared after 2 years of follow-up. Furthermore, deprenyl also failed to influence the subsequent development of levodopa-induced motor complications. Available studies on mortality in PD provide heterogeneous mortality rates, probably because of discrepancies between patient populations with respect to co-morbidity, disease stage at study entry, and diagnostic accuracy. However, the most recent follow-up from the DATATOP cohort suggests normal life expectancy in carefully selected patients without significant co-morbidity and with adequate treatment and expert follow-up.
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页码:S1 / S9
页数:9
相关论文
共 59 条
[1]  
[Anonymous], PROR NEUROENETICS
[2]   Prevalence of Parkinsonian signs and associated mortality in a community population of older people [J].
Bennett, DA ;
Beckett, LA ;
Murray, AM ;
Shannon, KM ;
Goetz, CG ;
Pilgrim, DM ;
Evans, DA .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (02) :71-76
[3]   SURVIVAL AND CAUSE OF DEATH IN A COHORT OF PATIENTS WITH PARKINSONISM - POSSIBLE CLUES TO ETIOLOGY [J].
BENSHLOMO, Y ;
MARMOT, MG .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1995, 58 (03) :293-299
[4]  
BERNHEIMER H, 1973, J NEUROL SCI, V20, P415, DOI 10.1016/0022-510X(73)90175-5
[5]   A CONTROLLED, LONGITUDINAL-STUDY OF DEMENTIA IN PARKINSONS-DISEASE [J].
BIGGINS, CA ;
BOYD, JL ;
HARROP, FM ;
MADELEY, P ;
MINDHAM, RHS ;
RANDALL, JI ;
SPOKES, EGS .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1992, 55 (07) :566-571
[6]   INCREASED LIFE EXPECTANCY RESULTING FROM ADDITION OF L-DEPRENYL TO MADOPAR TREATMENT IN PARKINSONS-DISEASE - A LONGTERM STUDY [J].
BIRKMAYER, W ;
KNOLL, J ;
RIEDERER, P ;
YOUDIM, MBH ;
HARS, V ;
MARTON, J .
JOURNAL OF NEURAL TRANSMISSION, 1985, 64 (02) :113-127
[7]   DOES AGING AGGRAVATE PARKINSONIAN DISABILITY [J].
BLIN, J ;
DUBOIS, B ;
BONNET, AM ;
VIDAILHET, M ;
BRANDABUR, M ;
AGID, Y .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1991, 54 (09) :780-782
[8]   DOES LONG-TERM AGGRAVATION OF PARKINSONS-DISEASE RESULT FROM NONDOPAMINERGIC LESIONS [J].
BONNET, AM ;
LORIA, Y ;
SAINTHILAIRE, MH ;
LHERMITTE, F ;
AGID, Y .
NEUROLOGY, 1987, 37 (09) :1539-1542
[9]   ETIOLOGY OF PARKINSONS-DISEASE [J].
CALNE, DB ;
LANGSTON, JW .
LANCET, 1983, 2 (8365) :1457-1459
[10]  
CURTIS L, 1984, LANCET, V2, P211