Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Marked advances in the treatment of neurological disorders which affect the elderly have been established in recent years. Cerebrovascular disorders including stroke and vascular dementia are still among the most frequent diseases in the Japanese elderly. For treatment of hypertensive patients with or without a history of stroke, slight decrease of blood pressure (BP) is recommended since recent PET studies have revealed that an excessive drop of BP markedly decreases cerebral blood flow. Furthermore, 24-hour-monitoring of BP revealed that physiological fluctuation of BP consisting of high daytime BP and low nocturnal BP disappears in hypertensive patients with vascular dementia and those with non-symptomatic vascular lesions on MRI. Recommendable BP levels for the hypertensive elderly must be established. The efficacy of both aspirin and ticlopidine for prevention of stroke has been established. Recent multi-centric trials have revealed that ticlopidine is more effective in preventing stroke but has more dangerous adverse effects than aspirin. Aspirin is reported to improve both the intellectual scale and cerebral blood flow in vascular dementia. In Parkinson's disease (PD), L-DOPA therapy, usually in combination with a dopa decarboxylase inhibitor, is common. Other dopaminergic drugs including bromocriptine, lisuride and pergolide are used clinically or are being studied. Recently selective monoamine oxidase (MAO) B inhibitors have been used in order to slow clinical progression of the disease, in addition to an attempt to increase the potential of dopamine through inhibition of MAO. Neural transplants to the striatum of PD were first applied using autografts of the adrenal medulla in 1985, but resulted in transient or only slight improvements.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recent therapeutic advances in geriatric neurology]. 143 48

Lacunes on brain MRI, causal blood pressure, 24-hour ambulatory blood pressure and common carotid blood flow measured by the doppler method were studied in 31 elderly patients with Parkinson's disease (mean age 67.5 +/- 7.3 years). Nineteen patients with Parkinson's disease (61%) had at least one lacune. Patients with lacunes (P(+)) were significantly higher in age than patients without lacune (P(-)). The difference of casual blood pressure between patients in the two groups was not significant. On the other hand, the average of ambulatory blood pressure measurements during a 24-hour period was significantly higher in the P(+) group than in the P(-) group. The average of carotid blood flow was also significantly lower in the P(+) group than in the P(-) group, however, after adjustment for age, the difference between them became insignificant. In conclusion, the incidence of silent lacunes on brain MRI was fairly common in elderly patients with Parkinson's disease. A high average 24-hour ambulatory blood pressure was suggested to be one of the risk factors of lacunar stroke in elderly cases of Parkinson's disease. The concept of "combine type" in Parkinsonism was supposed to be suitable as well as in senile dementia of Alzheimer type.
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PMID:[Silent lacunes in the elderly Parkinson's disease correlated with ambulatory blood pressure]. 143 50

We studied 18 patients with multiple system atrophy (MSA) by high field strength MRI: 6 striatonigral degeneration (SND), 4 Shy-Drager syndrome (SDS), and 8 olivo-ponto-cerebellar atrophy (OPCA). We also studied 30 Parkinson's disease (PD) and 10 age-matched controls. The diagnoses of SND, SDS, and OPCA were based on criteria after Hirayama et al (1985). Bradykinesia, rigidity, and tremor were assessed with the summed scores of the signs used as the extrapyramidal scores. The mean extrapyramidal scores were not significantly different in patients with SND, SDS, OPCA, and PD. MRI studies were performed on 1.5 tesla MRI unit, using a T2 weighted spin echo pulse sequence (TR2500 ms/TE40 ms). The width of the pars compacta signal in all subjects was measured by the method of Duguid et al (1986). Intensity profiles were made on a straight line perpendicular to the pars compacta through the center of the red nucleus on an image of the midbrain. We measured the width of the valley at half-height between the peaks of intensity representing the red nucleus and the crus cerebri-pars reticulata complex and used this measurement as an index of the width of the pars compacta signal. The mean widths of the pars compacta signal were: 2.8 +/- 0.4 mm (SND), 2.8 +/- 0.7 mm (SDS), 3.6 +/- 0.6 mm (OPCA), 2.7 +/- 0.3 mm (PD), and 4.3 +/- 0.6 mm (control). The mean widths of the pars compacta signal in PD, SND, and SDS were significantly narrower than that in the control group (p < 0.05), while the OPCA group was not significantly narrower.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Magnetic resonance imaging in multiple system atrophy]. 149 Mar 8

We report palilalia and acquired stuttering in a 60-year-old Japanese male with Parkinson's disease. At the age of 54, he presented with resting tremor in the hand and foot on the left, and gradual slowness in voluntary movements. Two years later, resting tremor involved the right foot, and an expressionless face and frozen gait occurred. A diagnosis of Parkinson's disease was made and treatment with L-dopa and carbidopa resulted in conspicuous improvement. At the age of 57, he developed compulsive repetitions of syllables, words and phrases, and sentences infrequently when he spoke. They have been persisting for four years. Repetitions increased in spontaneous speech while they decreased in oral reading and repetition of sentences. These repetitions in speech were symptomatologically diagnosed as palilalia and acquired stuttering. Brain CT showed slight brain atrophy, and brain MRI disclosed a few lesions indicating lacunae in the left substantia nigra, left putamen, and right internal capsule. SPECT showed a slight decrease in blood flow in the frontal lobes and basal ganglia bilaterally. Full IQ on WAIS was 105, and neither agnosia nor apraxia was detected. Palilalia and acquired stuttering, though the pathomechanism has not been clarified, have been reported to occur usually secondary to cerebral vascucular lesions and very rarely in Parkinson's disease. In the present case, they may have been produced by the parkinsonian nigro-striatal lesions. Alternatively, they may have been induced by the small vascular lesions demonstrated by MRI.
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PMID:[Palilalia and acquired stuttering in a case of Parkinson's disease]. 149 Mar 13

MRI is a relatively simple, safe, in vivo technique that has proved to be of great value in differentiating patients with Parkinson's disease from those with atypical parkinsonism, and it is the first laboratory marker to be able to do so. By permitting the in vivo detection of increased iron in the nigra and striatum of patients with parkinsonism, MRI may also have provided a clue into the mechanism of cell death in neurodegenerative disorders. Finally it is conceivable that MRI scanning may serve as a screening tool that permits the early recognition of pathologic iron accumulation before the development of clinical symptoms. This is reasonable to anticipate for patients with atypical parkinsonism in whom large quantities of iron appear to accumulate in the putamen early in the disease. It is possible that with some refinement, abnormalities in the nigra may be detected on MRI with a higher level of certainty. In an era in which we may be able to provide neuroprotective therapy, MRI might be an important technique for defining a population of patients at risk for the development of Parkinson's disease who might benefit from presymptomatic therapy.
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PMID:Magnetic resonance imaging in parkinsonism. 158 82

The causes of symptomatic parkinsonism are enumerated and discussed including drug-induced, vascular, toxic, postencephalitic and posttraumatic parkinsonism. The environmental hypothesis and the concept of oxidative stress in the pathogenesis of Parkinson's disease are illustrated. The clinical diagnosis, the differential diagnosis and the possible diagnostic errors originating from the cardinal symptoms akinesia, rigor und tremor in the early stages of the disease are delineated. At last the contributions of EEG, CCT, evoked potentials, MRI, PET und the apomorphine test to the diagnosis especially early diagnosis are evaluated.
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PMID:[Current aspects in diagnosis of Parkinson disease]. 158 88

The enzymatic activity of acetylcholinesterase (AchE) in the cerebrospinal fluid (CSF) is considered to be a marker of central cholinergic neuron integrity. Then, we evaluated CSF AchE activity in 90 cases of neurological diseases involving cholinergic system and their related disease, and 28 control cases without central organic lesions or abnormal findings in routine CSF study. AchE activity was evaluated according to Ellman's method using acetylthiocholine iodide as a substrate and tetraisopropyl-pyrophosphoramide, a specific inhibitor of butyrylocholinesterase. CSF AchE of Alzheimer type dementia (AD/SDAT, N = 12: 21.9 +/- 4.7 nmol/ml/min) showed no significant change from those of both control group (22.1 +/- 3.9) and vascular dementia (9: 21.7 +/- 6.7). In extrapyramidal diseases, reduction of the activity was observed in Huntington's chorea (HC, 4: 16.3 +/- 1.4) and progressive supranuclear palsy (PSP, 4: 17.6 +/- 1.7), whereas normal activity was shown in Parkinson's disease (PD, 19: 22.5 +/- 4.6), dentatorubropallidoluysian atrophy (DRPLA, 4: 22.6 +/- 4.2) and striatonigral degeneration (SND, 4: 20.4 +/- 4.3). In olivopontocerebellar atrophy (OPCA, N = 16), we disclosed reduced CSF AchE activity (15.8 +/- 2.4) which had significant correlations with the atrophy of the pontine base (r = 0.6017, p less than 0.02) and cerebellar vermis (r = 0.5450, p less than 0.05) in MRI. AchE activity in cerebellar cortical atrophy (CCA, 5: 20.6 +/- 2.2) remained within the control values. Normal activity was demonstrated in both amyotrophic lateral sclerosis (6: 24.3 +/- 7.3) and spinal muscular atrophy (4: 22.9 +/- 3.9).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[CSF acetylcholinesterase activity in central neurological diseases involving cholinergic systems]. 162 49

Parkinson's disease (PD) is often associated with dementia in elderly patients, and sometimes PD coexists with senile dementia of the Alzheimer type (SDAT) or cerebrovascular disease (CVD) in the elderly. However, since there are few previous clinical studies on the coincidence of, or relationship between PD and CVD, the authors evaluated these aspects in 34 elderly patients with PD using MRI and SPECT. All the patients were over 70 years old. The diagnosis of PD was based on the presence of three symptoms (resting tremor, cogwheel rigidity and bradikinesia) which are characteristic of PD, and the effectiveness of L-DOPA therapy. We therefore believe that patients with vascular Parkinsonism were excluded from our study. In 34 cases, 24 (71%) had MRI evidence of CVD (mainly the lacunar state). In the 10 cases who had no CVD, 2 (20%) had severe dementia and the decrease of regional cerebral blood flow (rCBF) in the temporal and parietal lobes bilaterally correlated with the SPECT findings commonly found in SDAT. A comparison of the rCBF and the results of Hasegawa's dementia score (HDS) (verbal intelligence score) was made between the patients with PD associated with CVD and the patients with PD who had no CVD and no SPECT findings which correlated with SDAT. The rCBF in the frontal lobes and the results of the HDS of the former group were significantly lower than those of the latter. As mentioned above, elderly patients with PD often had CVD, leading to dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinical study in elderly patients with Parkinson's disease using MRI and SPECT--Parkinson's disease and the lacunar state]. 179 37

We examined the magnetic resonance (MR) image of midbrain and striatum in 30 patients with Parkinson's disease (PD), 10 patients with vascular parkinsonism (VP) and 10 age-matched control subjects. Studies were performed on a high field strength (1.5 tesla) MRI unit. T2 weighted spin echo pulse sequence (TR2500ms/TE40ms) was used. We measured the width of the pars compacta signal in patients and controls on the basis of the method described by Duguid et al. Intensity profiles of a straight line perpendicular to the pars compacta through the center of the red nucleus were made on an image of the midbrain. We measured the width of the valley at half-height between the peaks of intensity representing the red nucleus and the crus cerebri-pars reticulata complex and used this as an index of the width of the pars compacta signal. The results were as follows: 1. The mean width of the pars compacta signal was 2.7 mm (SD = 0.3) in the PD group and 4.3 mm (SD = 0.6) in controls. The difference between the means was highly significant (p less than 0.01). While not significant statistically, there was a trend toward narrowing of the width of pars compacta signal of substantia nigra in the PD group as the Yahr's grade or disease duration progressed. In hemiparkinsonism, MRI revealed significant narrowing of the pars compacta signal on the contra-lateral side to the clinical predominant side compared with the ipsi-lateral side. 2. The mean width of the pars compacta signal was 3.9 mm (SD = 0.4) in the VP group, but the decrease was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[MRI in Parkinson's disease and vascular parkinsonism--study on the lesion of substantia nigra]. 193 76

It is known that the anticholinergic drug causes acute psychosis and memory disturbance, which may be due to cholinergic dysfunction. But it has not been well described that the anticholinergic drug causes chronic dementia after long administration. We describe six cases of chronic dementia, which is thought to be induced by anticholinergic drug. We conducted detailed neuropsychological and neuroradiological examination in these six cases. All of them were Parkinson's disease, and had used anticholinergic drug for more than six months without any side effect, and then their initial symptom of dementia appeared, followed by chronic dementia. All cases recovered reversibly from dementia within a few weeks after stoppage of taking anticholinergic drug. And any of our cases had no possibility in the cause of chronic dementia other than the side effect of anticholinergic drug. Detailed neuropsychological examinations (WAIS, WMSR, and so on) were conducted in all cases, SPECT was in two cases, and PET was in one case, before and after stoppage of the anticholinergic drug. And in all cases, brain MRI was conducted. The indices of attention, verbal memory, visual memory, and delayed recall were significantly elevated after stoppage of drug. And both verbal IQ and performance IQ were increased after stoppage of drug, too. SPECT and PET revealed significant improvement, which showed diffuse and generalized change, not localized change.
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PMID:[Chronic dementia in Parkinson disease treated by long-term administration of anticholinergic drug--evaluation of neuropsychological test, PET, and SPECT]. 193 77


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