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At least 19 recordsLinked to original sources
PubMed1997

Prevalence of parkinsonism and Parkinson's disease in Europe: the EUROPARKINSON Collaborative Study. European Community Concerted Action on the Epidemiology of Parkinson's disease.

OBJECTIVES: To assess and compare the prevalence of parkinsonism and Parkinson's disease in five European populations that were surveyed with similar methodology and diagnostic criteria. METHODS: Joint analysis of five community surveys--Gironde (France), eight centres in Italy, Rotterdam (The Netherlands), Girona (Spain), and Pamplona (Spain)--in which subjects were screened in person for parkinsonism. Overall, these surveys comprised 14,636 participants aged 65 years or older. RESULTS: The overall prevalence (per 100 population), age adjusted to the 1991 European standard population, was 2.3 for parkinsonism and 1.6 for Parkinson's disease. The overall prevalence of parkinsonism for the age groups 65 to 69, 70 to 74, 75 to 79, 80 to 84, and 85 to 89 years was respectively, 0.9, 1.5, 3.7, 5.0, and 5.1. The corresponding age specific figures for Parkinson's disease were 0.6, 1.0, 2.7, 3.6, and 3.5. After adjusting for age and sex, the prevalence figures did not differ significantly across studies, except for the French study in which prevalence was lower. Prevalence was similar in men and women. Overall, 24% of the subjects with Parkinson's disease were newly detected through the surveys. CONCLUSIONS: Prevalence of both parkinsonism and Parkinson's disease increased with age, without significant differences between men and women. There was no convincing evidence for differences in prevalence across European countries. A substantial proportion of patients with Parkinson's disease went undetected in the general population.

Age Distribution↗
PubMed1993

Pathological overlap in cases of parkinsonism associated with neurofibrillary tangles. A study of recent cases of postencephalitic parkinsonism and comparison with progressive supranuclear palsy and Guamanian parkinsonism-dementia complex.

In recent years a number of patients suffering from long-standing postencephalitic parkinsonism have donated their brains to the United Kingdom Parkinson's Disease Society Brain Bank, in London. In view of the paucity of detailed neuropathological reports of the disease since the 1940s, we have carried out a clinicopathological study of eight recent cases. A spectrum of pathological change was seen, with highly variable involvement of cortical, subcortical and brainstem structures. There was no correlation between severity of disease and severity of pathology. The anatomical distribution of lesions was compared with that seen in progressive supranuclear palsy and Guamanian Parkinson-dementia complex. No definite histological features were identified that could distinguish any of the three disease entities. While the pathogenesis of postencephalitic parkinsonism, progressive supranuclear palsy and Guamanian Parkinson-dementia complex remains unknown, the presence of similar pathologies in these conditions suggests a common disease mechanism, despite the distinctive clinical features.

Aged↗
PubMed1999

A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe. French Parkinson's Disease Genetics Study Group and the European Consortium on Genetic Susceptibility in Parkinson's Disease.

Autosomal recessive juvenile parkinsonism (AR-JP, PARK2; OMIM 602544), one of the monogenic forms of Parkinson's disease (PD), was initially described in Japan. It is characterized by early onset (before age 40), marked response to levodopa treatment and levodopa-induced dyskinesias. The gene responsible for AR-JP was recently identified and designated parkin. We have analysed the 12 coding exons of the parkin gene in 35 mostly European families with early onset autosomal recessive parkinsonism. In one family, a homozygous deletion of exon 4 could be demonstrated. By direct sequencing of the exons in the index patients of the remaining 34 families, eight previously undescribed point mutations (homozygous or heterozygous) were detected in eight families that included 20 patients. The mutations segregated with the disease in the families and were not detected on 110-166 control chromosomes. Four mutations caused truncation of the parkin protein. Three were frameshifts (202-203delAG, 255delA and 321-322insGT) and one a nonsense mutation (Trp453Stop). The other four were missense mutations (Lys161Asn, Arg256Cys, Arg275Trp and Thr415Asn) that probably affect amino acids that are important for the function of the parkin protein, since they result in the same phenotype as truncating mutations or homozygous exon deletions. Mean age at onset was 38 +/- 12 years, but onset up to age 58 was observed. Mutations in the parkin gene are therefore not invariably associated with early onset parkinsonism. In many patients, the phenotype is indistinguishable from that of idiopathic PD. This study has shown that a wide variety of different mutations in the parkin gene are a common cause of autosomal recessive parkinsonism in Europe and that different types of point mutations seem to be more frequently responsible for the disease phenotype than are deletions.

Binding Sites↗
PubMedDate not supplied

Comparison of the Unified Parkinson's Disease Rating Scale and the Short Parkinson's Evaluation Scale in patients with Parkinson's disease after levodopa loading.

The Short Parkinson's Evaluation Scale has been compiled and validated previously (Clinical Neuropharmacology, 1997). In the present study, we have assessed and compared the motor scoring of the Unified Parkinson's Disease Rating Scale and the Short Parkinson's Evaluation Scale in 23 patients (mean age, 61.8 years) with Parkinson's disease. Patients were 12 hours off medication at the beginning of the series. They were then given levodopa, 125 mg and 250 mg, on different days and were evaluated each 30 minutes for 2 hours. In addition, patients' motor skills (finger tapping and walking velocity) were measured at each time. Analysis of variance with repeated measures was applied. The results presented show that both scales have the same ability to measure levodopa-dose effect within time. In addition, Spearman's correlation coefficients showed a negative correlation between finger tapping and upper-limb impairment and a positive correlation between walking velocity and lower-limb impairment in both scales. In summary, the present results suggest that Short Parkinson's Evaluation Scale is a useful tool in assessing the effect of medication, having the advantage of being easier and quicker.

Aged↗
PubMed2000

Importance of familial Parkinson's disease and parkinsonism to the understanding of nigral degeneration in sporadic Parkinson's disease.

We review here familial Parkinson's disease (PD) from clinical as well as molecular genetic aspects. The contribution of genetic factors to the pathogenesis of PD is supported by the demonstration of the high concordance in twins, increased risk among relatives of PD patients in case control and family studies, and the existence of familial PD and parkinsonism based on single gene defects. Recently, several genes have been mapped and/or identified in patients with familial PD. Alpha-synuclein is involved in a rare dominant form of familial PD with dopa responsive parkinsonian features and Lewy body positive pathology. In contrast, parkin is responsible for autosomal recessive form of early-onset PD with Lewy body-negative pathology. This form is identified world-wide among patients with young-onset PD. Furthermore, ubiquitin carboxy terminal hydrolase L1 gene is responsible for an autosomal dominant form of typical PD, although only a single family has so far been identified with a mutation of this gene, and tau has been identified as a causative gene for frontotemporal dementia and parkinsonism. In addition, five other chromosome loci have been identified to be linked to familial PD or dystonia-parkinsonism. The presence of different loci or different causative genes indicates that PD is not a single entity but a highly heterogeneous. Identification and elucidation of the causative genes should enhance our understanding of the pathogenesis of sporadic PD.

Animals↗
PubMed1993

Suppression of dyskinesias in advanced Parkinson's disease. I. Continuous intravenous levodopa shifts dose response for production of dyskinesias but not for relief of parkinsonism in patients with advanced Parkinson's disease.

We characterized the clinical dose-response curves for relief of parkinsonism and production of dyskinesias as a function of plasma levodopa and 3-O-methyldopa levels in six patients with advanced Parkinson's disease (PD) and fluctuating responses to oral levodopa/carbidopa. Dose response to ramped intravenous levodopa infusion was measured after overnight drug withdrawal on two occasions: first after chronic, intermittent oral levodopa/carbidopa, and second after 3 to 5 days of continuous intravenous levodopa. Continuous intravenous levodopa shifted the dyskinesia dose-response curve to the right, reduced maximum dyskinesia activity, but did not significantly alter dose response for relief of parkinsonism. Improvement in dyskinesia was apparent by the second day of continuous levodopa, during which ratios of plasma dopa/3-O-methyldopa remained constant. Our results support the hypothesis that relief of parkinsonism and production of dyskinesia by levodopa occur by separate mechanisms.

Aged↗
PubMed1995

Epidemiological, genetic, pharmacological, kinesiological, nuclear medical (IBZM-SPECT), standard and functional MRI studies on Parkinson's disease and related disorders and economic evaluation of Parkinson's disease therapy--clinical projects in the BMFT-research program Munich: "Parkinson's disease and other basal ganglia disorders".

The results of selected clinical research projects related to epidemiological, genetic, pharmacological, kinesiological, and neuroimaging aspects (SPECT, PET, MRI, functional MRI) of basal ganglia disorders such as Parkinson's disease, Progressive Supranuclear Palsy, Multiple System Atrophy and Wilson's disease are summarized. A retrospective pharmacoeconomic analysis of Parkinson's disease is presented. These studies are part of a nationwide research program of the German ministry of research and technology (BMFT) entitled "Parkinson's disease and other basal ganglia disorders" and were carried out at the Department of Neurology, LMU München.

Basal Ganglia Diseases↗
PubMed1998

Chromosome 6-linked autosomal recessive early-onset Parkinsonism: linkage in European and Algerian families, extension of the clinical spectrum, and evidence of a small homozygous deletion in one family. The French Parkinson's Disease Genetics Study Group, and the European Consortium on Genetic Susceptibility in Parkinson's Disease.

The gene for autosomal recessive juvenile Parkinsonism (AR-JP) recently has been mapped to chromosome 6q25.2-27 in Japanese families. We have tested one Algerian and 10 European multiplex families with early-onset Parkinson disease for linkage to this locus, with marker D6S305. Homogeneity analysis provided a conditional probability in favor of linkage of >.9 in eight families, which were analyzed further with eight microsatellite markers spanning the 17-cM AR-JP region. Haplotype reconstruction for eight families and determination of the smallest region of homozygosity in two consanguineous families reduced the candidate interval to 11.3 cM. If the deletion of two microsatellite markers (D6S411 and D6S1550) that colocalize on the genetic map and that segregate with the disease in the Algerian family is taken into account, the candidate region would be reduced to <1 cM. These findings should facilitate identification of the corresponding gene. We have confirmed linkage of AR-JP, in European families and in an Algerian family, to the PARK2 locus. PARK2 appears to be an important locus for AR-JP in European patients. The clinical spectrum of the disease in our families, with age at onset <=58 years and the presence of painful dystonia in some patients, is broader than that reported previously.

Age of Onset↗
PubMed1999

Possible relation of atypical parkinsonism in the French West Indies with consumption of tropical plants: a case-control study. Caribbean Parkinsonism Study Group.

BACKGROUND: In Europe and North America, Parkinson's disease is the major form of parkinsonism; less than 4% of cases are progressive supranuclear palsy (PSP) and about 20% are atypical parkinsonism. The distribution of these subgroups is different in the French West Indies. We aimed to define the clinical and demographic specificity of these disorders in Guadeloupe and to investigate a postulated link with consumption of herbal tea and fruits from the Annonaceae family (Annona muricata and Annona squamosa), which contain neurotoxic benzyltetrahydroisoquinoline alkaloids. METHODS: Between September, 1996, and August, 1998, 87 consecutive patients with parkinsonism were referred to the single neurological department in Guadeloupe. After detailed clinical, neurophysiological, cognitive, and neuroradiological assessment, they were classified by generally accepted criteria as having Parkinson's disease, PSP, or atypical parkinsonism. We compared the amount of tropical fruits and herbal tea consumed by the various parkinsonian subgroups and by frequency-matched controls (patients with benign symptoms and no neurodegenerative disease). FINDINGS: Of the 87 patients, 22 had Parkinson's disease, 31 had PSP, 30 had atypical parkinsonism, and four had atypical parkinsonism associated with motor neuron disease, 44 of the patients with PSP or atypical parkinsonism were male. The patients with atypical parkinsonism had symmetrical rigidity and bradykinesia, and no levodopa peak-dose dyskinesias. Patients with PSP differed from those with atypical parkinsonism because they had supranuclear vertical down-gaze palsy, severe gait and balance problems, and frontal-lobe syndrome. 29 patients with PSP reported regular consumption of pawpaw fruit, and 26 drank herbal tea. 30 patients with atypical parkinsonism reported regular consumption of pawpaw fruit, and 24 drank herbal tea. Both of these groups consumed significantly more fruit and herbal tea than patients with Parkinson's disease (fruit: odds ratio 23.6; herbal tea: 28.2); and controls (fruit: 20.7; herbal tea: 6.48). INTERPRETATION: Our study confirms the over-representation of atypical parkinsonism and PSP in patients with parkinsonism in the French West Indies. Chronic exposure to neurotoxic alkaloids could be an important aetiological factor because these compounds induce parkinsonism in animals. A larger epidemiological study, to clarify the link between these fruits with atypical parkinsonism and PSP, is proposed.

Aged↗
PubMed1991

Striatal blood flow, glucose metabolism and 18F-dopa uptake: difference in Parkinson's disease and atypical parkinsonism.

Striatal blood flow, glucose metabolism and 18F-Dopa uptake were studied with positron emission tomography (PET) in eight non-demented patients with idiopathic Parkinson's disease and eight with atypical Parkinsonism. Patients with atypical Parkinsonism had no specific cause for the Parkinsonian symptoms and were clinically different from Parkinson's disease with lack of resting tremor and a poor response to dopaminergic drugs. Decreased 18F-Dopa uptake in the putamen was observed in patients with Parkinson's disease and atypical Parkinsonism compared with normal controls. 18F-Dopa uptake in the head of the caudate was also significantly reduced in both conditions but relatively less in Parkinson's disease. Decreased blood flow and glucose metabolism in the striatum associated with a global cerebral decrease were also observed in patients with atypical Parkinsonism compared with controls, while they were preserved in patients with Parkinson's disease, indicating affected neurons not only in the striatum but also in the cerebrum in patients with atypical Parkinsonism compared with patients with Parkinson's disease. The differences in the caudate 18F-Dopa uptake, and blood flow and glucose metabolism in the cerebrum including the striatum between Parkinson's disease and atypical Parkinsonism assessed by PET may be due to the differences in the pathophysiological mechanism between Parkinson's disease and atypical Parkinsonism.

Adolescent↗
PubMed1988

Electrophysiological differences between Parkinson's disease and vascular parkinsonism.

Short-latency somatosensory evoked potentials (SSEPs) and brainstem auditory evoked potentials (BAEPs) were recorded in 30 patients with Parkinson's disease (mean age 66.3 years), 17 patients with vascular parkinsonism (mean age 70.5 years) and 22 normal subjects (mean age 66.7 years). In patients with vascular parkinsonism, the interpeak latencies between N13 and N20(CCTs) were significantly longer than those of patients with Parkinson's disease and normal subjects (p less than 0.005 and p less than 0.001, respectively). Patients with Parkinson's disease and normal subjects did not show any significant differences with regard to CCT. The significant differences between left and right CCT were revealed between patients with vascular parkinsonism and patients with Parkinson's disease or normal subjects (p less than 0.001 and p less than 0.001, respectively). Patients with vascular parkinsonism disclosed significant prolongation of interpeak latencies between waves I and V (I-V IPLs) compared to patients with Parkinson's disease and normal subjects (p less than 0.005 and p less than 0.001, respectively). Furthermore, the I-V IPLs in patients with Parkinson's disease were significantly longer than those of the normal subjects (p less than 0.01). The mean left-right differences of I-V IPLs in patients with vascular parkinsonism were longer than those of the other two groups. Present results indicate that there were some differences between Parkinson's disease and vascular parkinsonism from the electrophysiological aspects and suggest that assessments of SSEPs and BAEPs may be helpful in differentiating Parkinson's disease from vascular parkinsonism.

Adult↗
PubMed2005

Is Parkinson's disease a homogeneous disorder--what is the burden of Parkinson's disease in India.

Movement disorders are common neurological illnesses among the elderly. These include essential tremor, Perkinsonian disorders and chorea of different aetiologies. Parkinsonian disorders can be divided into two major groups of disorders--classical idiopathic Parkinson's disease and Parkinson plus syndrome. The most common and important cause of Parkinsonism is idiopathic Parkinson's disease. Idiopathic Parkinson's disease is most confidently clinically diagnosed if we follow the United Kingdom Parkinson's Disease Society Brain Bank Diagnostic Criteria for Parkinson's disease. The most common degnerative diseases, which minic idiopathic Parkinson's disease are collectively called Parkinson plus syndrome. The most important diseases comprising Parkinson plus syndrome are: progressive supranuclear palsy, multiple system atrophy, cortical-basal ganglionic degneration, diffuse Lewy body disease and Parkinson-dementia-ALS complex. In India the prevalence of Parkinson's disease varied markedly from one study to another. The prevalence rate is high among the urban Parsi community of Mumbai. Incidence and prevalence of Parkinson's disease increase with increasing age. Some risk factors for Parkinson's disease have been narrated briefly. As the number of cases of Parkinsonism is likely to increase along with increasing population, the general practitioners or consultant physicans should have to play a greater role referring the cases to attend neurologists or movement disorder clinic early.

Aged↗
PubMed2005

Identifying and distinguishing cases of parkinsonism and Parkinson's disease using ICD-9 CM codes and pharmacy data.

Administrative databases have the potential to assess quality and cost of care for parkinsonism and Parkinson's disease. However, the validity of findings is limited by our understanding of how cases are identified. Patient records listing International Classification of Diseases, Version 9, Clinical Modification (ICD-9 CM) codes for parkinsonism (n = 2,076) and dopaminergic medications (n = 2,798) were pulled from fiscal years 1999 to 2001 for patients in the Pacific Northwest Veterans Administration. Samples of these records (n = 397) and records without these ICD-9 CM codes (n = 500) were reviewed, and clinical data were extracted. The accuracy of administrative data to identify and distinguish between Parkinson's disease and parkinsonism was calculated. A total of 37.9% of parkinsonism cases were detected using pharmacy data and ICD-9 CM codes compared to 18.7% by using ICD-9 CM codes alone. The ICD-9 CM code for paralysis agitans (332.0) did not distinguish between probable Parkinson's disease and other causes of parkinsonism, whereas the ICD-9 CM code for degenerative basal ganglia disorder (333.0) predicted having secondary parkinsonism (odds ratio [OR] = 5.0) as well as dopa-responsiveness in patients without secondary parkinsonism (OR = 4.5). Administrative data are limited in the ability to identify parkinsonism. The ICD-9 CM code, 332.0, which is generally considered the code to identify Parkinson's disease, did not distinguish between parkinsonism and Parkinson's disease.

Confidence Intervals↗
PubMed2002

Identification of parkinsonism and Parkinson's disease.

Parkinson's disease is a common movement disorder associated with considerable disability. The clinical syndrome of parkinsonism is based on the presence of core clinical features of rest tremor, bradykinesia, rigidity and impaired postural reflexes or gait. Parkinsonism is most often caused by Parkinson's disease, but can also be caused by other disorders, including cerebrovascular disease, multiple-system atrophy, progressive supranuclear palsy and other disorders. Parkinsonism can be identified by questionnaires and confirmed in person or by videotaped clinical examinations. The identification of presymptomatic cases remains problematic but is motivated by the hope for treatment before symptoms appear. Quantitative approaches to the diagnosis of parkinsonism based on the measurement of the cardinal features are available. Clinical approaches should include identification of features atypical for Parkinson's disease, which exclude the diagnosis, and documentation of a response to dopaminergic medications, which support a diagnosis of Parkinson's disease. Loss of smell and visual dysfunction are found in early patients and may be useful in screening protocols. In addition, behavioral changes, including depressive symptoms, may be detected in presymptomatic cases. Cognitive changes, such as impaired set shifting, have been observed in early Parkinson's disease, but can be seen with other causes of parkinsonism. Neuroimaging techniques, including positron emission tomography or single-photon emission computed tomography, are available to quantify dopaminergic neurons, while magnetic resonance imaging may be helpful in differentiating other forms of parkinsonism from Parkinson's disease. There are numerous approaches available to the identification of parkinsonism and Parkinson's disease. The gold standard remains a clinical diagnosis, confirmed by autopsy.

Humans↗
PubMed2000

Parkinson's disease and parkinsonism in a longitudinal study: two-fold higher incidence in men. ILSA Working Group. Italian Longitudinal Study on Aging.

OBJECTIVE: To determine the incidence of parkinsonism and PD in the Italian elderly, and to explore the relation with age and gender. METHODS: In eight Italian municipalities, a population-based, parkinsonism-free cohort was followed for an average of 3 years. At the end of the follow-up, the cohort survivors were directly contacted (screening and clinical examination). Cohort members who had died were studied using death certificates, clinical records, and information gathered from relatives and general practitioners. Parkinsonism diagnosis and subtyping were made according to specified diagnostic criteria. RESULTS: The cohort consisted of 4,341 individuals (65 to 84 years of age): 596 died before the examination, 2,863 (76.4% of the survivors) completed the screening procedure, and 882 refused to participate. The authors found 68 incident cases of parkinsonism: 42 PD (62%), 7 drug-induced parkinsonism (10%), 8 parkinsonism in dementia (12%), 8 vascular parkinsonism (12%), and 3 parkinsonism, unspecified (5.8%). Average annual incidence rate (per 100,000 person-years) in the population aged 65 to 84 years, adjusted to the 1992 Italian population, was 529.7 (95% CI, 400.5 to 658.9) for parkinsonism, and 326.3 (95% CI, 224.1 to 427.5) for PD. Incidence rates for both parkinsonism and PD increased with age in both men and women; men had higher rates in every age group. Age-adjusted relative risk in men compared with women was 1.66 (95% CI, 1.02 to 2.70) for parkinsonism and 2.13 (95% CI, 1.11 to 4.11) for PD. CONCLUSIONS: Incidence of parkinsonism and PD increased with age, PD was the most common type of parkinsonism, and men had a risk of developing PD twice that of women.

Aged↗
PubMed2000

Ropinirole versus bromocriptine for levodopa-induced complications in Parkinson's disease.

BACKGROUND: Long-term levodopa therapy for Parkinson's disease is complicated by the development of motor fluctuations and abnormal involuntary movements. One approach is to add a dopamine agonist at this stage of the disease to reduce the time the patient spends immobile or off and to reduce the dose of levodopa in the hope of reducing such problems in the future. OBJECTIVES: To compare the efficacy and safety of adjuvant ropinirole therapy with bromocriptine in patients with Parkinson's disease already established on levodopa therapy and suffering from motor complications. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with SmithKline Beecham. SELECTION CRITERIA: Randomised controlled trials of ropinirole versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data was abstracted independently by the authors and differences settled by discussion. The outcome measures used included Parkinson's disease rating scales, levodopa dosage, 'off' time measurements and the frequency of withdrawals and adverse events. MAIN RESULTS: No significant differences between ropinirole and bromocriptine were found in off time reduction, dyskinesia as an adverse event, motor impairment and disability, or levodopa dose reduction. Withdrawal rates and adverse event frequency were similar with the two agents apart from significantly less nausea with ropinirole (odds ratio 0.50; 0.29, 0. 84 95% CI; p =0.01). REVIEWER'S CONCLUSIONS: Ropinirole is at least as good as bromocriptine in patients with Parkinson's disease with motor complications in terms of improving off time and reducing levodopa dose, without increasing adverse events including dyskinesia. However, these comparitor studies may have been underpowered to detect clinically meaningful differences between the agonists. Further, much larger, phase IV studies are required to examine the efficacy, effectiveness, and safety of all of the dopamine agonists as adjuvant therapy in Parkinson's disease.

Antiparkinson Agents↗
PubMed1992

Control of simultaneous movements distinguishes depressive motor retardation from Parkinson's disease and neuroleptic parkinsonism.

Patients with depressive motor retardation, neuroleptic induced parkinsonism or Parkinson's disease were tested on movement tasks requiring control of simultaneous movements. This was in order to determine whether these three groups of patients, who all show slowing of movements, also share the distinctive impairment of simultaneous movement control that is observed in Parkinson's disease. Though all three patient groups showed equivalent slowing on the motor tasks that were studied, the patterns of impairment were different. Only the patients with parkinsonism, either neuroleptic induced or from Parkinson's disease, showed additional slowing of a rapid ballistic elbow flexion movement when it was performed simultaneously with a rapid squeeze of the ipsilateral hand. Only patients with parkinsonism showed a significant increase in dual task interference on a bimanual bead and tapper task, compared with controls. The bead and tapper interference in patients with depressive motor retardation was between that of controls and parkinsonism. Having a bimanual skill had a large effect on the subjects' dual task interference on this task. The measures of dual task interference for the two tasks did not correlate with one another; difficulty running simultaneous motor programs does therefore not explain the interference that is observed when tapping is performed while the other hand simultaneously performs a dextrous motor task. Only patients with parkinsonism showed increased fatigue on the tapping task. The patients with depressive motor retardation did have elevated scores on a clinical rating of parkinsonism. Nevertheless there are clearly defined differences between the movement disorder observed in patients with depression, and that observed in in parkinsonism. The patterns of impairments in patients with neuroleptic parkinsonism were very similar to those of Parkinson's disease.

Adult↗
PubMed2001

Differential diagnosis of Parkinson's disease and vascular parkinsonism by (99m)Tc-TRODAT-1.

UNLABELLED: The aim of this study was to use brain SPECT to differentiate vascular parkinsonism (VP) from Parkinson's disease. METHODS: Fourteen VP patients (age range, 59-87 y; mean age, 70 +/- 7.5 y), 30 Parkinson's disease patients (age range, 54-84 y; mean age, 65 +/- 8.8 y), and 26 healthy (control) individuals (age range, 50-85 y; mean age, 60 +/- 9 y) were examined. A 925-MBq (25 mCi) dose of (99m)Tc-TRODAT-1 was injected intravenously, and brain SPECT images were acquired 4 h after injection. The ratio of specific to nonspecific striatal (99m)Tc-TRODAT-1 binding was measured and compared. RESULTS: After a region-of-interest analysis of the images from VP patients, Parkinson's disease patients, and healthy volunteers was performed to obtain ratios of putamen to occipital and striatal to occipital binding as a measurement of specific binding to the dopamine transporters in these regions of the brain, where dopamine neurons are concentrated, the specific binding in the 14 VP patients was slightly lower than but not statistically different from that of the healthy individuals in both putamen and caudate areas. A significant decrease in uptake of (99m)Tc-TRODAT-1 in the striatum (P<0.01) was found in Parkinson's disease patients. Reduction of the uptake was more pronounced in the contralateral putamen of Parkinson's disease patients than that of VP patients (P<0.001). A significant bilateral striatal asymmetry was also observed in Parkinson's disease patients but not in VP patients (P< 0.01). CONCLUSION: Our findings clearly show that, for VP patients, (99m)Tc-TRODAT-1 SPECT is a reliable method to differentiate VP from Parkinson's disease. Further studies, including those to differentiate Parkinson's disease from arteriosclerotic parkinsonism and patients with both VP and Parkinson's disease, are needed to help rule out the possibility of Parkinson's disease as early as possible.

Aged↗