Neurological disorders are now the leading source of disability globally, and ageing is increasing the burden of neurodegenerative disorders, including Parkinson's disease. We aimed to determine the ...global burden of Parkinson's disease between 1990 and 2016 to identify trends and to enable appropriate public health, medical, and scientific responses.
Through a systematic analysis of epidemiological studies, we estimated global, regional, and country-specific prevalence and years of life lived with disability for Parkinson's disease from 1990 to 2016. We estimated the proportion of mild, moderate, and severe Parkinson's disease on the basis of studies that used the Hoehn and Yahr scale and assigned disability weights to each level. We jointly modelled prevalence and excess mortality risk in a natural history model to derive estimates of deaths due to Parkinson's disease. Death counts were multiplied by values from the Global Burden of Disease study's standard life expectancy to compute years of life lost. Disability-adjusted life-years (DALYs) were computed as the sum of years lived with disability and years of life lost. We also analysed results based on the Socio-demographic Index, a compound measure of income per capita, education, and fertility.
In 2016, 6·1 million (95% uncertainty interval UI 5·0–7·3) individuals had Parkinson's disease globally, compared with 2·5 million (2·0–3·0) in 1990. This increase was not solely due to increasing numbers of older people, because age-standardised prevalence rates increased by 21·7% (95% UI 18·1–25·3) over the same period (compared with an increase of 74·3%, 95% UI 69·2–79·6, for crude prevalence rates). Parkinson's disease caused 3·2 million (95% UI 2·6–4·0) DALYs and 211 296 deaths (95% UI 167 771–265 160) in 2016. The male-to-female ratios of age-standardised prevalence rates were similar in 2016 (1·40, 95% UI 1·36–1·43) and 1990 (1·37, 1·34–1·40). From 1990 to 2016, age-standardised prevalence, DALY rates, and death rates increased for all global burden of disease regions except for southern Latin America, eastern Europe, and Oceania. In addition, age-standardised DALY rates generally increased across the Socio-demographic Index.
Over the past generation, the global burden of Parkinson's disease has more than doubled as a result of increasing numbers of older people, with potential contributions from longer disease duration and environmental factors. Demographic and potentially other factors are poised to increase the future burden of Parkinson's disease substantially.
Bill & Melinda Gates Foundation.
This overview of population-based studies of incidence, prevalence, mortality, and case-fatality of stroke was based on studies from 1990. Incidence (first stroke in an individual's lifetime) and ...prevalence were computed by age, sex, and stroke type. Age-standardised incidence and prevalence with the corresponding 95% CI were plotted for each study to facilitate comparisons. The review shows that the burden of stroke is high and is likely to increase in future decades as a result of demographic and epidemiological transitions in populations. The main features of stroke epidemiology include modest geographical variation in incidence, prevalence, and case-fatality among the—predominantly white—populations studied so far, and a stabilisation or reversal in the declining secular trends in the pre-1990s rates, especially in older people. However, further research that uses the best possible methods to study the incidence, risk factors, and outcome of stroke are urgently needed in other populations of the world, especially in less developed countries where the risk of stroke is high, lifestyles are changing rapidly, and population restructuring is occurring.
Understanding how prevalence, incidence, and mortality of motor neuron diseases change over time and by location is crucial for understanding the causes of these disorders and for health-care ...planning. Our aim was to produce estimates of incidence, prevalence, and disability-adjusted life-years (DALYs) for motor neuron diseases for 195 countries and territories from 1990 to 2016 as part of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016.
The motor neuron diseases included in this study were amyotrophic lateral sclerosis, spinal muscular atrophy, hereditary spastic paraplegia, primary lateral sclerosis, progressive muscular atrophy, and pseudobulbar palsy. Incidence, prevalence, and DALYs were estimated using a Bayesian meta-regression model. We analysed 14 165 site-years of vital registration cause of death data using the GBD 2016 cause of death ensemble model. The 84 risk factors quantified in GBD 2016 were tested for an association with incidence or death from motor neuron diseases. We also explored the relationship between Socio-demographic Index (SDI; a compound measure of income per capita, education, and fertility) and age-standardised DALYs of motor neuron diseases.
In 2016, globally, 330 918 (95% uncertainty interval UI 299 522–367 254) individuals had a motor neuron disease. Motor neuron diseases have caused 926 090 (881 566–961 758) DALYs and 34 325 (33 051–35 364) deaths in 2016. The worldwide all-age prevalence was 4·5 (4·1–5·0) per 100 000 people, with an increase in age-standardised prevalence of 4·5% (3·4–5·7) over the study period. The all-age incidence was 0·78 (95% UI 0·71–0·86) per 100 000 person-years. No risk factor analysed in GBD showed an association with motor neuron disease incidence. The largest age-standardised prevalence was in high SDI regions: high-income North America (16·8, 95% UI 15·8–16·9), Australasia (14·7, 13·5–16·1), and western Europe (12·9, 11·7–14·1). However, the prevalence and incidence were lower than expected based on SDI in high-income Asia Pacific.
Motor neuron diseases have low prevalence and incidence, but cause severe disability with a high fatality rate. Incidence of motor neuron diseases has geographical heterogeneity, which is not explained by any risk factors quantified in GBD, suggesting other unmeasured risk factors might have a role. Between 1990 and 2016, the burden of motor neuron diseases has increased substantially. The estimates presented here, as well as future estimates based on data from a greater number of countries, will be important in the planning of services for people with motor neuron diseases worldwide.
Bill & Melinda Gates Foundation.
It has been reported that nimodipine reduces the frequency of secondary ischemia and improves outcome after aneurysmal SAH, but definitive evidence concerning all available calcium antagonists is ...lacking.
Systematic overview of randomized trials that were completed by January 1996 compared calcium antagonists with control and started treatment within 10 days after onset of subarachnoid hemorrhage (SAH) was performed. All calcium antagonists studied thus far (nimodipine, nicardipine, and AT877) were included.
We analyzed 10 trials totaling 2756 patients. The relative risk (RR) reduction of poor outcome (death or dependency) was 16% (95% CI, 6 to 27%) and that of case fatality was 10% (95% CI, -6 to 25%). To prevent one poor outcome, 19 (12 to 59) patients need to be treated. Calcium antagonists give a 33% (95%, CI 25 to 41) RR reduction in the frequency of ischemic neurologic deficit and a 20% (95% CI, 11 to 28) RR reduction in the frequency of CT-scan documented cerebral infarction. Eight (6 to 11) patients need to be treated to prevent one ischemic neurologic deficit. In the analyses for nimodipine only, treatment was associated with a 24% RR reduction of poor outcome (95% CI, 12 to 38). To prevent one poor outcome, 13 (8 to 30) patients need to be treated with nimodipine. The RR reduction of angiographically detected cerebral vasospasm was statistically significant for AT877 (38%; 95% CI, 17 to 54%) and nicardipine (21%; 95% CI, 6 to 34%) but not for nimodipine (9%; 95% CI, -2 to 19%).
Calcium antagonists reduce the proportion of ischemic neurologic deficits and nimodipine improves overall outcome within 3 months of aneurysmal SAH; evidence for a reduction of poor outcome from all causes by nicardipine and AT877 is inconclusive. The intermediate factors by which nimodipine exerts its beneficial effect remain uncertain.
Drawing on the experience of conducting the Brain Injury Incidence and Outcomes New Zealand in the Community study, this article aims to identify the issues arising from the implementation of ...proposed guidelines for population-based studies of incidence and outcomes in traumatic brain injury (TBI).
All new cases of TBI (all ages and severities) were ascertained over a 1-year period, using overlapping prospective and retrospective sources of case ascertainment in New Zealand. All eligible TBI cases were invited to participate in a comprehensive assessment at baseline and at 1-month follow-up.
Our experience to date has revealed the feasibility of case ascertainment methods. Consultation with community health services and professionals resulted in feasible referral pathways to support the identification of TBI cases. 'Hot pursuit' methods of recruitment were essential to ensure complete case ascertainment for this population with few additional cases of TBI identified through cross-checks.
This review of proposed guidelines in relation to practical study methodology provides a framework for future comparable population-based epidemiological studies of TBI incidence and outcomes in developed countries.
Objective: Depression is common post-TBI, yet has not been studied longitudinally, nor at a population level. This study examined prevalence of depression in a population-based sample across the ...first year post-TBI.
Design and methods: Prospective follow-up of 315 adults (>16 years) with assessments (Hospital Anxiety Depression Scale, DSM-IV criteria) at 1-, 6- and 12-months post-TBI. Demographic and injury-related predictors of depression at 1-year post-TBI were also explored.
Results: The number of individuals identified as depressed reduced significantly between baseline and 12-months post-TBI from 21-12.4% using the HADS and 49-34% using DSM-IV criteria; with only 10 of the 28 individuals initially meeting criteria on the HADS continuing to do so at 12-month follow-up. Meeting HADS depression criteria was linked to pre-morbid depression and/or anxiety; while those meeting DSM-IV criteria were older, but not significantly so.
Conclusions: The findings suggest depression is common post-TBI and that clinicians/researchers use caution in its diagnosis, as existing criteria have significant overlap with common TBI sequels.
After a 1996 review from our group on risk factors for subarachnoid hemorrhage (SAH), much new information has become available. This article provides an updated overview of risk factors for SAH.
An ...overview of all longitudinal and case-control studies of risk factors for SAH published in English from 1966 through March 2005. We calculated pooled relative risks (RRs) for longitudinal studies and odds ratios (ORs) for case-control studies, both with corresponding 95% CIs.
We included 14 longitudinal (5 new) and 23 (12 new) case-control studies. Overall, the studies included 3936 patients with SAH (892 cases in 14 longitudinal studies and 3044 cases in 23 case-control studies) for analysis. Statistically significant risk factors in longitudinal and case-control studies were current smoking (RR, 2.2 1.3 to 3.6; OR, 3.1 2.7 to 3.5), hypertension (RR, 2.5 2.0 to 3.1; OR, 2.6 2.0 to 3.1), and excessive alcohol intake (RR, 2.1 1.5 to 2.8; OR, 1.5 1.3 to 1.8). Nonwhite ethnicity was a less robust risk factor (RR, 1.8 0.8 to 4.2; OR, 3.4 1.0 to 11.9). Oral contraceptives did not affect the risk (RR, 5.4 0.7 to 43.5; OR, 0.8 0.5 to 1.3). Risk reductions were found for hormone replacement therapy (RR, 0.6 0.2 to 1.5; OR, 0.6 0.4 to 0.8), hypercholesterolemia (RR, 0.8 0.6 to 1.2; OR, 0.6 0.4 to 0.9), and diabetes (RR, 0.3 0 to 2.2; OR, 0.7 0.5 to 0.8). Data were inconsistent for lean body mass index (RR, 0.3 0.2 to 0.4; OR, 1.4 1.0 to 2.0) and rigorous exercise (RR, 0.5 0.3 to 1.0; OR, 1.2 1.0 to 1.6). In the studies included in the review, no other risk factors were available for the meta-analysis.
Smoking, hypertension, and excessive alcohol remain the most important risk factors for SAH. The seemingly protective effects of white ethnicity compared to nonwhite ethnicity, hormone replacement therapy, hypercholesterolemia, and diabetes in the etiology of SAH are uncertain.
The last few years have seen a considerable increase in the amount of information available concerning blood pressure (BP) and stroke associations. This article provides an overview of published ...reviews of the effects on stroke seen in trials of BP-lowering drugs and compares these with the results available from cohort studies.
We present a review of major overviews of prospective cohort studies and an updated meta-analysis of >40 randomized controlled trials of BP lowering, which included >188 000 participants and approximately 6800 stroke events. Cohort studies now indicate that in the Asia Pacific region as well as in North America and Western Europe, each 10 mm Hg lower systolic BP is associated with a decrease in risk of approximately one third in subjects aged 60 to 79 years. The association is continuous down to levels of at least 115/75 mm Hg and is consistent across sexes, regions, and stroke subtypes and for fatal and nonfatal events. The proportional association is age dependent but is still a strong and positive association in those aged 80 years. Data from randomized controlled trials, in which mean age at event was approximately 70 years, indicate that a 10 mm Hg reduction in systolic BP is associated with a reduction in risk of stroke of approximately one third. Per mm Hg systolic BP reduction, the benefits for stroke appear similar between agents, by baseline BP levels, and whether or not individuals have a past history of cardiovascular disease. There is, however, evidence of greater benefit with a larger BP reduction.
The epidemiologically expected benefits of BP lowering for stroke risk reduction are broadly consistent across a range of different population subgroups. There are greater benefits from larger BP reductions, and initiating and maintaining BP reduction for stroke prevention is a more important issue than choice of initial agent.
Secondary ischaemia is a frequent cause of poor outcome in patients with subarachnoid haemorrhage (SAH). Its pathogenesis has not been elucidated yet, but may be related to vasospasm. Experimental ...studies have indicated that calcium antagonists can prevent or reverse vasospasm and have neuroprotective properties. Several types of calcium antagonists have been studied in several clinical trials.
To determine whether calcium antagonists improve outcome in patients with aneurysmal SAH.
We searched the Cochrane Stroke Group Trials Register (September 2003). In addition, we searched MEDLINE (1966 to October 2003) and EMBASE (1980 to October 2003), handsearched two Russian journals (1990 to 2003) and contacted trialists and pharmaceutical companies (in 1995 and 1996) to identify further studies.
All unconfounded, truly randomised controlled trials comparing any calcium antagonist with control.
Two reviewers independently extracted the data and assessed trial quality. Trialists were contacted to obtain missing information.
We analysed 12 trials totalling 2844 patients with SAH (1396 in the treatment group and 1448 in the control group). The drugs analysed were: nimodipine (eight trials, 1574 patients), nicardipine (two trials, 954 patients), AT877 (one trial, 276 patients) and magnesium (one trial, 40 patients). Overall, calcium antagonists reduced the risk of poor outcome: relative risk (RR) 0.82 (95% confidence interval (CI) 0.72 to 0.93); the absolute risk reduction was 5.1%, the corresponding number of patients needed to treat to prevent a single poor outcome event was 20. For oral nimodipine alone the RR was 0.70 (0.58 to 0.84). The RR of death on treatment with calcium antagonists was 0.90 (95% CI 0.76 to 1.07), that of clinical signs of secondary ischaemia 0.67 (95% CI 0.60 to 0.76), and that of CT or MR confirmed infarction 0.80 (95% CI 0.71 to 0.89).
Calcium antagonists reduce the risk of poor outcome and secondary ischaemia after aneurysmal SAH. The results for 'poor outcome' depend largely on a single large trial with oral nimodipine; the evidence for nicardipine, AT877 and magnesium is inconclusive. The evidence for nimodipine is not beyond every doubt, but given the potential benefits and modest risks of this treatment, against the background of a devastating natural history, oral nimodipine (60 mg every 4 hours) is currently indicated in patients with aneurysmal SAH. Intravenous administration of calcium antagonists cannot be recommended for routine practice on the basis of the present evidence.
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