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)

The purpose of this study was to analyze the kinematic properties of upper limb trajectories in Parkinson's disease (PD) patients and to investigate the role of visual feedback from the moving limb. Beyond the characteristic bradykinesia, PD patients differed from controls by generating hand trajectories with asymmetrical velocity profiles that lacked smoothness and were composed of a short initial accelerative phase, followed by a prolonged interval composed of alternating decelerative and accelerative phases. In both groups, the reaction times for movements directed away from the body were longer than for movements directed toward the body; this effect was accentuated in PD. In both groups, initial peak accelerations were significantly larger for distally as compared to proximally directed movements. In the absence of visual feedback from the limb a deterioration in the accuracy of reaching the target was observed in both control and PD patients only for distally directed movements. However, this deterioration and the effect of target location on final accuracy was substantially larger in PD. Taken together, our study suggests that in PD visual information is continuously relied upon for ongoing movement correction, therefore accentuating the bradykinesia. The deficit in final accuracy in the absence of visual feedback reflects the important role played by the basal ganglia in sensorimotor integration.
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PMID:Kinematic analysis of upper limb trajectories in Parkinson's disease. 142 28

Many authorities have drawn attention to the difficulties in clinically distinguishing Parkinson's disease (PD) from other parkinsonian syndromes. We assessed the clinical features of 100 patients diagnosed prospectively by a group of consultant neurologists as having idiopathic PD according to their pathologic findings. Seventy-six percent of these cases were confirmed to have PD. By using selected criteria (asymmetrical onset, no atypical features, and no possible etiology for another parkinsonian syndrome) the proportion of true PD cases identified was increased to 93%, but 32% of pathologically confirmed cases were rejected on this basis. These observations suggest that studies based on consultant diagnosis of PD, using standard diagnostic criteria, will include cases other than PD, thus distorting results from clinical trials and epidemiologic studies. The strict use of additional criteria can reduce misdiagnosis but at the cost of excluding genuine PD cases.
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PMID:What features improve the accuracy of clinical diagnosis in Parkinson's disease: a clinicopathologic study. 835 Oct 36

Regional metabolic rate for glucose (rCMRGlc) was estimated using [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) in five patients (four men, one woman; mean age 68; mean disease duration 2.4 years) with clinical findings consistent with the syndrome of cortico-basal ganglionic degeneration (CBGD). Left-right rCMRGlc asymmetry, (L-R)/(L + R) x 100, was calculated for 13 grey matter regions and compared with regional metabolic data from 18 normal volunteers and nine patients with asymmetrical Parkinson's disease (PD). In the CBGD group mean metabolic asymmetry values in the thalamus, inferior parietal lobule and hippocampus were greater than those measured in normal control subjects and patients with asymmetrical PD (p less than 0.02). Parietal lobe asymmetry of 5% or more was evident in all CBGD patients, whereas in PD patients and normal controls, all regional asymmetry measures were less than 5% in absolute value. Measures of frontal, parietal and hemispheric metabolic asymmetry were found to be positively correlated with asymmetries in thalamic rCMRGlc (p less than 0.05). The presence of cortico-thalamic metabolic asymmetry is consistent with the focal neuropathological changes reported in CBGD brains. Our findings suggest that metabolic asymmetries detected with FDG/PET may support a diagnosis of CBGD in life.
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PMID:The metabolic landscape of cortico-basal ganglionic degeneration: regional asymmetries studied with positron emission tomography. 174 38

Fifty four patients with idiopathic Parkinson's disease receiving levodopa therapy were studied. Thirty three of these patients displayed peak-dose dyskinesia. Neither the duration of Parkinson's disease nor the duration of levodopa therapy discriminated between patients with and patients without peak-dose dyskinesia. Consequently, these criteria could not determine whether the first appearance of peak-dose dyskinesia depends on the duration of Parkinson's disease--a factor that is related to the severity of the disease--or on the duration of levodopa therapy. A subgroup of nineteen patients with unilateral or unequivocally asymmetrical peak-dose dyskinesia was examined 12 hours after withdrawal of levodopa. A levodopa testdose provoked unilateral or unilateral preponderant peak-dose dyskinesia which always involved the most severely affected side and which also happened to be the side of onset of the disease. This demonstrates that the severity of Parkinson's disease is the main risk factor for peak-dose dyskinesia.
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PMID:Severity of Parkinson's disease is a risk factor for peak-dose dyskinesia. 232 54

A pathological study of 21 patients with Parkinson's disease of asymmetrical onset revealed significant asymmetry of degeneration of the substantia nigra with greater neuronal loss contralateral to the initially affected body side. It has previously been suggested that decline in duration of effectiveness of levodopa doses in Parkinsonian patients with motor oscillations is caused by loss of nigro-striatal dopaminergic terminals with consequent reduction in striatal dopamine storage capacity. If this is true, duration of levodopa motor response should be shorter on the more severely affected body side in patients with asymmetrical disease, as loss of contralateral striatal dopamine storage capacity should be greater. Serial motor evaluations in 20 patients with asymmetrical Parkinson's disease failed to reveal any such asymmetry of duration of motor response to levodopa. It is suggested that striatal dopamine storage is not an important determinant of duration of clinical response to levodopa doses.
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PMID:Asymmetry of substantia nigra neuronal loss in Parkinson's disease and its relevance to the mechanism of levodopa related motor fluctuations. 270 38

The parkinsonian syndrome rests on the clinical tripod: akinesia, rigidity, tremor. Akinesia is the key symptom, broadly defined as a difficulty in initiating and performing movements in proportion to their complexity (sophisticated, simultaneous movements) and their duration (repetitive movements). The most frequent cause of the syndrome is Parkinson's disease. Although this diagnosis needs to be confirmed in pathological terms by the loss of neurons and the presence of Lewy's bodies in the substantia nigra, some clinical data enable it to be envisaged with a minimum of errors; these are pure parkinsonian triad, good response to dopatherapy and asymmetrical symptoms. The other causes of parkinsonian syndrome are usually related to the administration of neuroleptic drugs and to degenerative diseases with lesions that are more diffuse than those of Parkinson's disease. In Steele-Richardson-Olzewski disease a parkinsonian syndrome is associated with supranuclear ophthalmoplegia. Multiple systematized atrophy presents under three different clinical aspects: a parkinsonian syndrome without tremor and resistant to L-dopa, suggesting atrophy of the strionigral tract; a parkinsonian syndrome associated with a cerebellar syndrome, suggesting olivo-cerebellar-pontine atrophy, and Shy-Drager disease which includes primary dysautonomy and other neurological syndromes.
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PMID:[Parkinson's disease and parkinsonian syndromes]. 272 71

The control of unimanual and bimanual aiming movements by Parkinson's disease and control subjects was examined. Despite greater bimanual movement initiation asynchrony and overall bradykinesia, the Parkinson's disease subjects were affected by the experimental manipulations in the same way as controls. Symmetrical and, more especially, asymmetrical bimanual movements required more preparation time and were executed more slowly by both groups than were unimanual movements. Both groups also showed temporal linkage of movements to targets of different extents--movements which have different movement times when performed unimanually, as well as of the faster and slower limbs. A majority in both groups over-compensated for asynchrony in bimanual movement initiation by modulation of movement times, but there was no group difference in this tendency. The results are discussed in terms of underlying motor control processes and with regard to previous evidence for impaired control of simultaneous movements in Parkinson's disease.
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PMID:The control of bimanual aiming movements in Parkinson's disease. 334 87

Regional and mean cerebral blood flow (rCBF, CBF) were measured by tomography of inhaled 133Xe in 18 hemiparkinsonian patients before and after levodopa (L-dopa). Baseline mean CBF was 55 ml/ (100 g X min) after an L-dopa-free interval of at least 10 h (range 10-13) and remained unchanged at 56.1 ml/ (100 g X min) after optimal clinical improvement was achieved by L-dopa. However, L-dopa reduced rCBF significantly (P less than 0.05) in the striatum contralateral to the symptomatic limbs. In patients with adverse reactions such as hyperkinesias and on/off symptoms, flow tended to increase bilaterally in striatum and often markedly in midline structures anatomically related to globus pallidus and thalamus. Compared with a normal population, the subcortical rCBF distribution was asymmetrical with a reduced flow (-18%) in the striatum contralateral to the symptomatic limbs and in midline structures anatomically related to globus pallidus and thalamus (-12%). Cortical CBF was inverse related to the duration of Parkinson's disease (P less than 0.05), probably reflecting an increasing mental deterioration with time.
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PMID:Regional cerebral blood flow in hemiparkinsonian patients. Emission computerized tomography of inhaled 133Xenon before and after levodopa. 387 79

Hereditary dysphasic dementia is described in terms of its clinicopathological, ultrastructural, and transmissibility characteristics. Its mode of inheritance is autosomal dominant, and its clinical manifestations of progressive dementia and severe dysphasic disturbances are expressed in late adulthood. Complete neuropathological examination of four patients reveals findings typical for Pick's disease (asymmetrical focal cerebral atrophy), Alzheimer's disease (profuse neuritic plaques), and paralysis agitans (neuronal depigmentation, depletion, and Lewy body formation in substantia nigra) in addition to a striking but nonspecific spongiform degeneration of superficial cortical layers. This unique combination of gross morphological and histopathological features qualifies hereditary dysphasic dementia as a distinct entity, but its precise relationship to the well-recognized adult cortical dementias has been difficult to establish by conventional classification methods. This disorder and other unusual dementing illnesses may be best considered as part of a Pick-Alzheimer spectrum of cortical neuronal degenerations.
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PMID:Hereditary dysphasic dementia and the Pick-Alzheimer spectrum. 649 55

Parkinson's disease is characterized by a depletion of dopamine (DA) neurons in the nigrostriatal pathway. Stereotaxic injections of 6-hydroxydopamine (6-OHDA), a selective neurotoxin, into either the medial forebrain bundle or the substantia nigra result in a massive DA denervation of the nigrostriatal pathway. Following unilateral nigrostriatal DA depletion, hemiparkinsonian animals develop a stereotypical rotational behavior when challenged with DA agonists such as apomorphine. The drug-induced rotational behavior has been widely used as the behavioral index of hemiparkinsonian animals, but it has some limitations. Although asymmetries in the rotational behavior may indicate an imbalance of DA contents and release capacity in the bilateral nigrostriatal pathway, the behavior is a pharmacological reaction. Accordingly, the drug-induced rotation test is subject to sensitization effects. The present study proposes the elevated body swing test (EBST) as a measure of asymmetrical motor behavior of hemiparkinsonian animals in a drug-free state. The EBST simply involves elevating the animal by handling its tail and recording the frequency and direction of the swing behavior. Unilateral nigral 6-OHDA-lesioned rats exhibited significant biased swing activity with the direction contralateral to the lesioned side, corresponding to the direction of apomorphine-induced rotations. A 30 sec EBST was noted as the peak time for biased swing activity. At 7 d postlesion (the start of testing), and every week thereafter for a period of 2 months, a fairly stable biased swing activity level was observed. At 1 and 2 months postlesion, the same animals were also challenged with apomorphine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated body swing test: a new behavioral parameter for rats with 6-hydroxydopamine-induced hemiparkinsonism. 762 59


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