Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0233565 (bradykinesia)
2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate the influence of white matter hyperintensities (WMH) on clinical features of Parkinson's disease (PD) patients. The study subjects were 44 patients with PD who took a brain MRI. The severity of Parkinsonian symptoms was assessed in both 'on' and 'off' states, using the UPDRS-motor score. Thirteen patients (30%) showed WMH. The patients with WMH were significantly older than those without WMH (67 +/- 5.7 vs 60 +/- 6.4 years). In both 'off' and 'on' states, the gait scores were significantly higher in patients with WMH than in those without WMH (1.6 +/- 0.18 vs 1.1 +/- 0.12, P < 0.05), but other motor symptom (tremor, bradykinesia, rigidity) scores between the two patient groups were not statistically different. After taking a single dose of oral levodopa/benserazide (200mg/50mg), the patients with WMH showed significantly less improvement in bradykinesia score than those without WMH (25 +/- 4.1% vs 40 +/- 4.0%, P < 0.05), but the improvements in other symptoms were comparable between the two groups. These results suggest that WMH on MRI may influence Parkinsonian motor symptoms, particularly gait symptom and levodopa-responsiveness to bradykinesia symptom.
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PMID:The influence of white matter hyperintensities on the clinical features of Parkinson's disease. 952 85

The distinction between procedural and declarative memory is widely accepted in the memory literature. Converging evidence makes a strong case that the medial aspects of the temporal lobes and the diencephalon subserve the declarative memory system. However, the neuroanatomy of procedural memory is much less clear. In animal studies, damage to the basal ganglia has been found to affect procedural memory, but studies of patients suffering from degenerative diseases of the basal ganglia (e.g., Parkinson's and Huntington's disease) are less conclusive. Two groups of Parkinson's disease subtypes, with tremor (PDt) and bradykinesia (PDb) as the predominant motor symptom, were compared to controls on declarative and procedural memory tasks. The two patient groups did not differ from each other on the declarative tasks. However, in the procedural learning tasks, the PDb but not the PDt group, was significantly impaired compared to the control group. The results are discussed in terms of the differential involvement of discrete neuroanatomic loops connecting the basal ganglia and the prefrontal cortex.
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PMID:Declarative and procedural learning in Parkinson's disease patients having tremor or bradykinesia as the predominant symptom. 980 94

Intravenous application of amantadine sulphate induces a rapid improvement of motor symptoms in Parkinson's disease (PD), but there are no trials on the efficacy of this compound on bradykinesia, rigidity and tremor in detail in combination with standardized instrumental measurement of tapping and peg insertion abilities. We treated 31 stable non fluctuating PD patients with amantadine, scored motor symptoms of both arms and performed peg insertion and tapping under cued conditions before and after 3 days. Motor symptoms and peg insertion significantly improved in contrast to tapping. Tapping asks for repetitive performance of simple standardized movements, therefore it needs low cognitive efforts. Since peg insertion depends on more complex movements and thus more dopamine dependent cognitive processes, it improved after application of the indirect dopaminomimetic substance amantadine.
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PMID:Intravenous amantadine sulphate application improves the performance of complex but not simple motor tasks in patients with Parkinson's disease. 1261 92

During the past decade, dopamine transporter (DAT) imaging with single photon emission computerized tomography (SPECT) or positron emission tomography (PET) has evolved as an objective in vivo marker of nigrostriatal neuron loss in Parkinson's disease (PD). We investigate the relationship between striatal DAT binding, measured with [(123)I]beta-CIT SPECT, and parkinsonian motor handicap in a sample of 59 PD patients with minimal to severe disability, and review published cross-sectional studies on the correlation between DAT imaging and motor symptoms in PD. Earlier studies as well as the present results show a good correlation between overall striatal DAT binding and global measures of disease severity such as the Hoehn and Yahr scale, the total score on the Unified Parkinson's Disease Rating Scale (UPDRS), and UPDRS activities of daily living, with a progressive decline of DAT binding with increasing disability. A number of studies found a significant inverse correlation of striatal DAT binding with UPDRS motor score. Bradykinesia, posture, gait, and other midline symptoms, such as speech and facial expression, compared with rigidity, seem to be more closely related to striatal DAT binding. By contrast, neither the severity of parkinsonian rest nor of action tremor is related to the degree of dopaminergic denervation as measured by DAT imaging. Motor symptoms in the clinically less affected body side show a closer correlation with striatal DAT binding than do symptoms occurring in the dominantly affected body side. The correlation of putamen and caudate DAT binding with parkinsonian motor handicap seems to be similar. Although there have been limited comparative studies applying [(18)F]fluorodopa PET and DAT imaging in the same group of PD patients, available data suggest that putamen [(18)F]fluorodopa uptake, when compared with striatal DAT binding, may be more closely related to parkinsonian motor handicap.
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PMID:Correlation of dopamine transporter imaging with parkinsonian motor handicap: how close is it? 1453 Oct 46

PD (Parkinson's disease) is an aetiologically heterogeneous disorder characterized by a clinical phenotype consisting of resting tremor, rigidity and bradykinesia. Motor symptoms are associated with a progressive loss of dopaminergic neurons, with Lewy body inclusions within surviving neurons. Although heritability studies have shown evidence of familial aggregation, twin studies have provided limited support for a genetic aetiology. Nevertheless, classical linkage methods have nominated 11 regions of the genome and pathogenic mutations have been identified in several genes, including alpha-synuclein, parkin, ubiquitin C-terminal hydrolase L1, oncogene DJ-1, PTEN-induced protein kinase 1 and microtubule-associated protein tau. Most recently, heterozygous mutations in LRRK2 (leucine-rich repeat kinase 2) were found to cause late-onset, autosomal-dominant PD. Despite their consistent clinical phenotype, family members with LRRK2 mutations can have variable alpha-synuclein and tau pathologies. Lrrk2 is a member of the Roc (Ras of complex proteins) family, with Ras GTPase and MAPKKK (mitogen-activated protein kinase kinase kinase) catalytic domains. Thus its discovery highlights vesicle dynamics and secondary-messenger signalling in disease pathophysiology. To diagnose a disease accurately and effectively treat it, requires an understanding of its molecular pathogenesis. Herein, we provide an overview of the genetics of PD, how these discoveries are revolutionizing long-held beliefs and more importantly how this knowledge may be translated into patient therapy.
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PMID:Pathophysiology, pleiotrophy and paradigm shifts: genetic lessons from Parkinson's disease. 1604 50

It is well known that many patients with Parkinson's disease experience neuropsychological decline. However, the nature and extent of mental status change varies widely, with some patients showing mild or no cognitive impairments and others exhibiting frank dementia. Research has shown that several clinical disease parameters may differentially correlate with patterns of neuropsychological dysfunction. The present study examined side and type of motor symptom at disease onset and their relationship to cognition in idiopathic Parkinson's disease (PD). We identified 58 patients who initially presented with one of the following symptom profiles: right-side tremor onset (RSO-T; n = 15), right-side bradykinesia/rigidity onset (n = 12), left-side tremor onset (n = 19), and left-side bradykinesia/rigidity onset (n = 12). There were no differences between groups in disease duration, overall mental status, education, or depression severity. We administered a battery of neuropsychological measures to the four PD subgroups and a group of matched control subjects (n = 40). MANCOVAs controlling for age revealed patients with RSO-T performed significantly better than the other three PD subgroups across the entire neuropsychological battery. Further, the RSO-T subgroup performed comparably to controls. In contrast, the other three PD subgroups showed widespread cognitive deficits. These findings suggest an intricate relationship between motor symptom and side of disease onset and it is the combination of these factors that may influence the disease course and extent of cognitive deterioration. Furthermore, patients who develop tremor on the right side of their body represent a distinct subgroup of PD patients who exhibit relative sparing of cognitive function.
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PMID:Side and type of motor symptom influence cognition in Parkinson's disease. 1699 Nov 55

Parkinson's disease is known to result from basal ganglia dysfunction. Electrophysiological recordings in parkinsonian patients and animals have shown the emergence of abnormal synchronous oscillatory activity in the cortico-basal ganglia network in the pathological condition. In addition, previous studies pointed out an altered response pattern during movement execution in the pallidum of parkinsonian animals. To investigate the dynamics of these changes during disease progression and to relate them to the onset of the motor symptoms, we recorded spontaneous and movement-related neuronal activity in the internal pallidum of nonhuman primates during a progressive dopamine depletion process. Parkinsonian motor symptoms appeared progressively during the intoxication protocol, at the end of which both animals displayed severe akinesia, rigidity and postural abnormalities. Spontaneous firing rates did not vary significantly after intoxication. During the early phase of the protocol, voluntary movements were significantly slowed down and delayed. At the same time, the neuronal response to movement execution was modified and inhibitory responses disappeared. In contrast, the unitary and collective dynamic properties of spontaneous neuronal activity, as revealed by spectral and correlation analysis, remained unchanged during this period. Spontaneous correlated activity increased later, after animals became severely bradykinetic, whereas synchronous oscillatory activity appeared only after major motor symptoms developed. Thus, a causality between the emergence of synchronous oscillations in the pallidum and main parkinsonian motor symptoms seems unlikely. The pathological disruption of movement-related activity in the basal ganglia appears to be a better correlate at least to bradykinesia and stands as the best candidate to account for this motor symptom.
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PMID:Late emergence of synchronized oscillatory activity in the pallidum during progressive Parkinsonism. 1788 Apr 1

Most patients with idiopathic PD (IPD) show variable degrees of cognitive decline. The purpose of this study was to evaluate the relationship between the predominant motor symptom at the time of disease onset and the level of cognitive function in patients with IPD. A total of 159 patients with IPD were enrolled in this study. The patients' initial motor symptoms were classified into three types: tremor-dominant (TD), bradykinesia and rigidity-dominant (BRD), gait and postural instability-dominant (GPD). Disease severity was rated according to the Hoehn-Yahr classification (H&Y stage). Overall cognitive status was evaluated using the Korean versions of the Mini-Mental State Examination (K-MMSE) and the Modified Mini-Mental State (3MS) tests. The GPD group showed the lowest scores of the K-MMSE/3MS, and the patients with TD showed the best performance in the cognitive analysis (p<0.05). The patients who were older at disease onset showed worse cognitive performance than those the patients who were younger at disease onset (p<0.05). There was no difference in cognitive status according to H&Y stages. The accurate classification of initial motor symptoms and the detailed history, including the exact onset age of IPD, may allow us to predict cognitive decline in IPD.
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PMID:Relationship between clinical phenotypes and cognitive impairment in Parkinson's disease (PD). 1913 59

Visual perceptual problems are common in Parkinson's disease (PD) and often affect activities of daily living (ADLs). PD patients with non-tremor symptoms at disease onset (i.e., rigidity, bradykinesia, gait disturbance or postural instability) have more diffuse neurobiological abnormalities and report worse non-motor symptoms and functional changes than patients whose initial symptom is tremor, but the relation of motor symptom subtype to perceptual deficits remains unstudied. We assessed visual ADLs with the Visual Activities Questionnaire in 25 non-demented patients with PD, 13 with tremor as the initial symptom and 12 with an initial symptom other than tremor, as well as in 23 healthy control participants (NC). As expected, the non-tremor patients, but not the tremor patients, reported more impairment in visual ADLs than the NC group, including in light/dark adaptation, acuity/spatial vision, depth perception, peripheral vision and visual processing speed. Non-tremor patients were significantly worse than tremor patients overall and on light/dark adaptation and depth perception. Environmental enhancements especially targeted to patients with the non-tremor PD subtype may help to ameliorate their functional disability.
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PMID:Relation of Parkinson's disease subtypes to visual activities of daily living. 2181 30

Patients with Parkinson's disease (PD) receive therapies aimed at addressing a diverse range of motor symptoms. Motor complications in the form of symptom fluctuations and dyskinesias that commonly occur with chronic PD medication use may not be effectively captured by Unified Parkinson's Disease Rating Scale (UPDRS) assessments performed in the clinic. Therefore, home monitoring may be a viable adjunct tool to provide insight into PD motor symptom response to treatment. In this pilot study, we sought to evaluate the feasibility of capturing PD motor symptoms at home using a computer-based assessment system. Ten subjects diagnosed with idiopathic PD used the system at home and ten non-PD control subjects used the system in a laboratory. The Kinesia system consists of a wireless finger-worn motion sensor and a laptop computer with software for automated tremor and bradykinesia severity score assessments. Data from control subjects were used to develop compliance algorithms for rejecting motor tasks performed incorrectly. These algorithms were then applied to data collected from the PD subjects who used the Kinesia system at home to complete motor exams 3-6 times per day over 3-6 days. Motor tasks not rejected by the compliance algorithms were further processed for symptom severity. PD subjects successfully completed motor assessments at home, with approximately 97% of all motor task data files (1222/1260) accepted. These findings suggest that objective home monitoring of PD motor fluctuations is feasible.
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PMID:Feasibility of home-based automated Parkinson's disease motor assessment. 2197 87


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