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Parkinson's Disease? J7ournal ofNeurology, Neurosurgery, and Psychiatry 1996;61:4-16 NEUROEPIDEMIOLOGY J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.61.1.4 on 1 July 1996. Downloaded from How far are we in understanding the cause of Parkinson's disease? Y Ben-Shlomo generate suffi- ... the writer will repine at no censure which to have a large sample size to the precipitate publication of mere conjectural cient cases for analysis. The combined alumni suggestions may incur: but shall think himself cohorts of Harvard and Pennsylvania colleges fully rewarded by having excited the attention of consisted of 50 000 people and only generated those, who may point out the most appropriate Older cohorts will be more efficient means of relieving a tedious and most distress- 160 cases.6 ing malady. in terms of statistical power. Case- James Parkinson' control studies, although far more practical, are It is almost 180 years since James Parkinson more prone to bias. Particularly problematic is described his series of patients with what is the recruitment of control subjects and the now known as Parkinson's disease. His own measurement of putative exposures. Associa- astute clinical observations were unable to dis- tions must be treated with some caution and if cern any obvious aetiology. "On the subject possible verified using either historical data or a indeed of remote causes, no satisfactory cohort design. account has yet been obtained from any of the sufferers."' He noted an indulgence in alcohol, CASE DEFINITION lying on damp ground, and the possibility of The case definition for Parkinson's disease is trauma. He also reported the occupations of based on clinical criteria. Only two thirds of three of his patients; one was a gardener, potential cases of Parkinson's disease recruited another a sailor, and the third a magistrate. directly from primary care may truly have the Even in 1817, the disease affected a broad disease as validated by postmortem diagnosis.7 social range of society. We have made some Prevalence studies from various countries have progress in elucidating the cause of Parkinson's shown that potential cases will include patients disease over this period but this has been lim- with benign essential tremor, dementia, and ited. For instance, the role of trauma in the cerebrovascular disease.8 1' In Aberdeen, 15% aetiology of Parkinson's disease remains uncer- of potential cases were excluded after specialist http://jnnp.bmj.com/ a neuro- tain and disputed.2 4 Epidemiological research examination.8 A clinical diagnosis by has steadily increased, particularly over the logist or geriatrician is also limited. The United past 10 years, and more research has been Kingdom Parkinson's Disease Society Brain directed towards analytical rather than just Bank data have shown that the predictive value descriptive studies. More recently, work in the of an expert diagnosis is only around 75%.11 area of genetic epidemiology5 has begun and The use of stricter clinical criteria can improve value but this is at the cost researchers are now focusing on both molecu- the predictive on October 2, 2021 by guest. Protected copyright. lar and environmental risk factors. This review of excluding more genuine cases and is there- interprets the existing evidence and provides a fore only really of value for therapeutic trials personal view on what we definitively know rather than epidemiological studies.'2 The use about the epidemiology of Parkinson's disease, of complex investigations, such as PET, is what remains speculative, and what questions not suitable for large epidemiological studies. remain to be answered. The result of including other disorders as well as true cases of Parkinson's disease in a study will depend on the relation between Problems facing a neuroepidemiologist these diseases and the exposures of interest. If Department of It is important to appreciate the problems and this is no different to that found for Parkinson's Epidemiology and limitations faced by neuroepidemiologists disease, the results will not be biased. It is Public Health, 1-19 that do not Torrington Place, attempting to study Parkinson's disease. These more reasonable to assume they University College, drawbacks help to explain some of the rather share the same aetiological factors. In this case, London Medical inconclusive and often contradictory findings misclassification will bias the results towards School, London it will be harder to show a relation WC1E 6BT, UK between studies. the null; Y Ben-Shlomo between exposure and disease, even if it truly Correspondence to: STUDY DESIGN exists. Dr Y Ben-Shlomo, Department of Social Most analytical studies use a case-control Medicine, University of approach. This is because Parkinson's disease MEASUREMENT OF EXPOSURE Bristol, Canynge Hall, The measurement of exposure is also problem- Whiteladies Road, Bristol is relatively rare. Any prospective study needs BS8 2PR, UK. atic. It is unclear as to when in the lifecourse an Howfar are we in understanding the cause ofParkinson's disease? 5 Figure 1 Nigral cell loss: 100 neurons at a constant rate. It did, possible periods during the however, lifecourse for the role ofan exclude a process which resulted in either an J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.61.1.4 on 1 July 1996. Downloaded from environmentalfactor. Cell accelerating or decelerating cell death. loss is shown at a constant 80 Most exposures are measured by subjective ratefor simplicity; see text for details. (Modifiedfrom recall. This has two problems: low impact Langston"7.) exposure, such as past diet, is likely to be M 60 0 poorly recalled by both cases and controls ' 6 (non-differential misclassification). This will dilute any true relation and lead to erroneously _F 40 concluding that there is no relation. High 0 z impact exposures might be differentially recalled by cases and not controls, particularly if 20..._.... ............. there is pre-existing knowledge of a possible Clinical symptoms link between the exposure and disease. For oN example, a previous head injury might be more 0 20 40 60 80 100 salient in the minds of patients than in con- Age (y) trols, as they may link the trauma with their neurological disease (recall bias). exposure may be important (fig 1). Clinical GEOGRAPHICAL PATlERNS symptoms are thought to start once cell loss International comparisons have in the past has reached a threshold level of 70% to 80%. relied on mortality rates adjusted for demo- Normal age-related cell loss (a) is thought not graphic differences between countries. Early to result in disease unless current life findings showed a sevenfold to eightfold varia- expectancy is prolonged. A genetic model tion in mortality rates2223 suggesting an impor- might propose that cell loss from birth tant role for environmental factors as well as occurred in some people at a faster than nor- possible genetic differences. Mortality rates are mal rate (b) due to "aging genes"." susceptible to variations in diagnosis, survival, Intrauterine events, such as infection or pla- and certification practice, which could produce cental abnormalities,'4 15 might result in a per- large artefactual differences. This is best illus- son being born with a depleted cell count and trated by the fivefold mortality differences normal age related loss (c) would ensure that between Scotland and Japan.22 However, there disease would appear in later life. This devel- is little difference in the prevalence rates for opmental model has been proposed to explain patients between 60 and 69 years of age, when the discordance rate seen for monozygotic underascertainment should be less problematic twins.'5 Environmental factors could act (Scotland 254/100 0008; Japan 245/100 000).9 through an acute mechanism-for example, a More complex approaches differentiate head injury (d) destroying a finite number of between "multisource" prevalence studies, cells-followed by nornal age related loss (two which rely on the complete identification of stage hypothesis).'6 Alternatively a low level patients with a pre-existing diagnosis, and chronic exposure (e)-for example, a diet rela- "population based" surveys which screen a tively deficient in antioxidants-may simply act total defined population identifying both pre- http://jnnp.bmj.com/ by slightly accelerating the rate of cell death. existing and new cases.24 The population based Finally an acute event-for example, exposure survey method is particularly important for to a toxic chemical-may act by triggering cell developing countries because of limited med- death which results in a cascade of events and ical services or for communities in which there accelerated cell death (f). This final model may be differential access to health care. For would suggest that a long latency period may example, differential access to health care for not be essential for disease aetiology and would ethnic minorities is well recognised in the on October 2, 2021 by guest. Protected copyright. focus attention on later life. Most people United States25 and in the Copiah county believe that a long latency period for study, more previously undiagnosed black Parkinson's disease is most likely.'7-'9 However, patients (58%) than white patients (32%) were pathological data challenge the hypothesis that found.26 The population based survey method age related cell loss on top of an external insult also enables more valid comparisons between is important.20 It is also possible that causation is studies as ascertainment is
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