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A population-based investigation of Parkinson's disease with
and without dementia. Relationship to age and gender.
Because the prevalence of idiopathic Parkinson's disease (PD) with or without
dementia remains controversial, we initiated a population-based investigation
in the Washington Heights-Inwood section of New York , NY , so that nearly complete
case ascertainment could be achieved. A "registry" was developed for
the study, and we advertised in periodicals and on radio and television. Subjects,
or their records, were examined by experienced neurologists, and most underwent
a battery of neuropsychological tests specifically designed for assessment in
this community. All data were reviewed by a team of clinicians to achieve a consensus
diagnosis. The crude prevalence of idiopathic PD, with and without dementia,
was 99.4 per 100,000, increasing from 2.3 per 100,000 for those younger than
50 years to 1144.9 per 100,000 for those aged 80 years and older. The crude prevalence
for PD with dementia alone was 41.1 per 100,000 and also increased with age from
zero for those younger than 50 years to 787.1 per 100,000 for those aged 80 years
and older. Prevalence ratios were comparable with those of other published population-based
studies in similar settings. After standardization, men had PD with and without
dementia more frequently than did women. The major difference between patients
with and without dementia was a later estimated age at onset of motor manifestations.
We conclude that PD is a frequent disorder in the elderly population that affects
men and whites more frequently than women and nonwhites. Moreover, dementia in
patients with PD is more frequent than previously recognized and is strongly
related to the age at onset of motor manifestations.
Arch Neurol . 1992 May;49(5):492-7
Worldwide occurrence of Parkinson's disease: an updated review.
Comparison of Parkinson's disease (PD) prevalence and incidence in various
parts of the world is difficult because methods of case ascertainment, diagnostic
criteria, classification, medical facilities, and age distribution of the
populations vary broadly in different studies. We minimized these differences
by adjusting available data to a single standard population. Using this we
calculated age-adjusted rates for 27 regional populations and analyzed PD
frequency from 45 communities. We conclude: (1) with the exception of China,
Japan and Africa, which have the lowest prevalence ratios, the actual prevalence
variation for PD is probably lower than previously reported in geographically
diverse populations; (2) geographic variation is unlikely to be due exclusively
to racial factors, and (3) environmental risk factors for PD might differ
regionally.
Neuroepidemiology. 1993;12(4):195-208
Twin study of Parkinson disease.
Zero concordance for Parkinson disease was found in the first 12 monozygotic
twin pairs examined in an ongoing twin study. One co-twin (subject without
Parkinson disease) had essential tremor, another had cerebral vascular disease,
and a third was an alcoholic. Cigarette smoking appeared to be less frequent
in the probands than in the co-twins (11.9 versus 16.1 pack-years). There
was also evidence of premorbid personality differences between probands and
co-twins dating back to late adolescence or early adult years. These preliminary
findings suggest that genetic factors do not play a major role in the etiology
of Parkinson disease and point to a prodromal onset of the disease as early
as late adolescence or early adult life.
Neurology . 1981 Jan;31(1):77-80
Effect of deprenyl on the progression of disability in early
Parkinson's disease. The Parkinson Study Group.
In a clinical trial that is still in progress, we studied
the ability of deprenyl and tocopherol, antioxidative agents that act
through complementary mechanisms, to delay the onset of disability necessitating
levodopa therapy (the primary end point) in patients with early, untreated
Parkinson's disease. Eight hundred subjects were randomly assigned in
a two-by-two factorial design to receive deprenyl, tocopherol, a combination
of both drugs, or placebo, and were followed up to determine the frequency
of development of the end point. The interim results of independent
monitoring prompted a preliminary comparison of the 401 subjects assigned
to tocopherol or placebo with the 399 subjects assigned to deprenyl,
alone or with tocopherol. Only 97 subjects who received deprenyl reached
the end point during an average 12 months of follow-up, as compared
with 176 subjects who did not receive deprenyl (P less than 10(-8).
The risk of reaching the end point was reduced by 57% for the subjects
who received deprenyl (Cox hazard ratio, 0.43; 95% confidence limits,
0.33 and 0.55; P less than 10(-10]. The subjects who received deprenyl
also had a significant reduction in their risk of having to give up
full-time employment (P = 0.01). We conclude from these preliminary
results that the use of deprenyl (10 mg per day) delays the onset of
disability associated with early, otherwise untreated cases of Parkinson's
disease.
N Engl J Med. 1989 Nov 16;321(20):1364-71
Ropinirole for the treatment of early Parkinson's disease.
The Ropinirole Study Group.
A prospective, randomized, placebo-controlled, double-blind, parallel-group,
6-month study assessed the efficacy and safety of ropinirole, a nonergoline
D2-dopamine agonist, in patients with early Parkinson's disease (n = 241; Hoehn & Yahr
stages I to III) with limited or no prior dopaminergic therapy. Patients (mean
age, 62.8 years), stratified by concomitant use of selegiline, were randomized
to ropinirole (n = 116) or placebo (n = 125). The starting dose of ropinirole
was 0.25 mg tid with titration to at least 1.5 mg tid (maximum dose, 8 mg tid).
Primary efficacy endpoint was the percentage improvement in Unified Parkinson's
Disease Rating Scale (UPDRS) motor score. Ropinirole-treated patients had a
significantly greater percentage improvement in UPDRS motor score than patients
who received placebo (+24% vs -3%; p < 0.001). Ropinirole was well tolerated
and patient withdrawals were infrequent. Most adverse experiences were related
to peripheral dopaminergic activity. Ropinirole monotherapy is an effective
and well-tolerated therapeutic option for treatment of early Parkinson's disease.
Neurology . 1997 Aug;49(2):393-9
Smoking, alcohol, and coffee consumption preceding Parkinson's
disease: a case-control study.
OBJECTIVE: To study the association of PD with preceding smoking, alcohol,
and coffee consumption using a case-control design. METHODS: The authors used
the medical records linkage system of the Rochester Epidemiology Project to
identify 196 subjects who developed PD in Olmsted County , MN , during the
years 1976 to 1995. Each incident case was matched by age (+/-1 year) and sex
to a general population control subject. The authors reviewed the complete
medical records of cases and control subjects to abstract exposure information.
RESULTS: For coffee consumption, the authors found an OR of 0.35 (95% CI =
0.16 to 0.78, p = 0.01), a dose-effect trend (p = 0.003), and a later age at
PD onset in cases who drank coffee compared with those who never did (median
72 versus 64 years; p = 0.0002). The inverse association with coffee remained
significant after adjustment for education, smoking, and alcohol drinking and
was restricted to PD cases with onset at age <72 years and to men. The OR
for cigarette smoking was 0.69 (95% CI = 0.45 to 1.08, p = 0.1). The authors
found no association between PD and alcohol consumption. Extreme or unusual
behaviors such as tobacco chewing or snuff use and a diagnosis of alcoholism
were significantly more common in control subjects than cases. CONCLUSIONS:
These findings suggest an inverse association between coffee drinking and PD;
however, this association does not imply that coffee has a direct protective
effect against PD. Alternative explanations for the association should be considered.
Neurology. 2000 Nov 14;55(9):1350-8
Diet and Parkinson's disease. II: A possible role for the
past intake of specific nutrients. Results from a self-administered
food-frequency questionnaire in a case-control study.
In a case-control study, we compared the past dietary habits of 342 Parkinson's
disease (PD) patients recruited from nine German clinics with those of 342
controls from the same neighborhood or region. Data were gathered with a structured
interview and a self-administered food-frequency questionnaire. Nutrient intakes
were calculated from the reported food intakes through linkage with the German
Federal Food Code and analyzed using multivariate conditional logistic regression
to control for total energy intake, educational status, and cigarette smoking.
At the macronutrient level, patients reported higher carbohydrate intake than
controls after adjustment for total energy intake, smoking, and educational
status (OR = 2.74, 95% confidence interval [CI]: 1.30-6.07, for the highest
versus lowest quartile, p trend = 0.02). This was reflected in higher monosaccharide
and disaccharide intakes at the nutrient level. There was no difference between
patients and controls in protein and fat intake after adjustment for energy
intake. We found an inverse association between the intakes of beta-carotene
(OR = 0.67, 95% CI: 0.37-1.19, p trend = 0.06) and ascorbic acid (OR = 0.60,
95% CI: 0.33-1.09, p trend = 0.04) by patients, although only the trend for
ascorbic acid intake reached statistical significance. There was no difference
between groups for alpha-tocopherol intake after adjustment for energy intake.
We also found that patients reported a significantly lower intake of niacin
than controls (OR = 0.15, 95% CI: 0.07-0.33, p trend < 0.00005). Our results
suggest that if antioxidants play a protective role in this disease, the amounts
provided by diet alone are insufficient. Although the interpretation of the
inverse association between niacin intake and PD is complicated by the high
niacin content in coffee and alcoholic beverages, which were also inversely
associated with PD in this study, the strength of this association and its
biologic plausibility warrant further investigation.
Neurology . 1996 Sep;47(3):644-50 |