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)

A 67-year-old man with a family history of parkinsonism had visual complaints due to difficulty in convergence, which was followed 2 years later by development of bradykinesia and rigidity. The diagnosis of Steele-Richardson-Olszewski syndrome was made on the basis of a supranuclear gaze palsy, bradykinesia, rigidity, and poor response to levodopa. However, subsequent neuropathological examination revealed diffuse Lewy body disease with no evidence of neurofibrillary tangles involving either subcortical or brain stem structures.
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PMID:Diffuse Lewy body disease presenting with supranuclear gaze palsy, parkinsonism, and dementia: a case report. 148 31

Patients with unilateral neglect may exhibit slowness in the initiation of contralesionally directed movements in peripersonal space (directional hypokinesia). The present study used a sequential movement task to characterize any such impairment in a group of 24 patients with right hemisphere lesions, 18 of whom had left neglect. A further five patients with left hemisphere lesions, one of whom had right neglect, were also tested. We measured movement initiation and execution times for leftward and rightward movements in either hemispace and across the body midline. Most left neglect patients, particularly those with lesions involving posterior cortex, showed directional hypokinesia. Left neglect patients with anterior and/or subcortical lesions also showed directional bradykinesia, i.e. a slowing in the execution phase of contralesionally directed movements. This impairment occurred regardless of the spatial location of the apparatus and was exacerbated as patients moved closer to their neglected side. The patient with right neglect showed directional hypokinesia but not directional bradykinesia. Right hemisphere and left hemisphere lesion patients without neglect performed in a manner comparable to controls, who did not exhibit directional hypokinesia or directional bradykinesia. These results suggest that directional hypokinesia is associated with both left hemisphere and right hemisphere damage, but only in the context of unilateral neglect. Moreover, the site of hemispheric lesion may determine the temporal characteristics of movement impairments in neglect. Damage to posterior cortex produces deficits in detecting contralesional targets and initiating movements toward them, while damage to anterior or subcortical structures may disrupt the internal representation of an intended trajectory.
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PMID:Impairments of movement initiation and execution in unilateral neglect. Directional hypokinesia and bradykinesia. 148 64

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

Parkinson's disease has been modeled in humans, lower primates, and to a lesser extent in some other vertebrates by administration of the potent neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine). The MPTP model has thus drawn considerable attention as a system to search for anti-Parkinson's disease drugs, although the cost and scarcity of primates has limited extensive applications. We now report that a parkinsonian syndrome can be elicited in the common goldfish (Carassius auratus) by a single dose of MPTP. The syndrome is characterized by profound bradykinesia (slow movement), the full extent of which is reached 3 days after MPTP administration. The reduction in movement is paralleled by loss of dopamine and norepinephrine from the forebrain and midbrain and in other brain regions as well. The toxic oxidative product of MPTP, MPP+, is also accumulated predominantly in forebrain and midbrain, and pretreatment with the monoamine oxidase blocker tranylcypromine substantially reduces accumulation of the toxic metabolite. A barely perceptible coarseness in balance adjustment also occurs in treated animals. The MPTP-treated goldfish recover normal movement and normal brain monoamine levels within 10-13 days after administration of the drug. We interpret these and other data to indicate that MPTP can induce a Parkinson's disease-like syndrome in the goldfish that is similar in many aspects to the syndrome induced by MPTP in humans and other primates. This remarkable parallel may permit the goldfish to supplement expensive and scarce primates for the purpose of searching and screening neuroprotective drugs with specific relevance to Parkinson's disease.
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PMID:A parkinsonian syndrome induced in the goldfish by the neurotoxin MPTP. 152 41

The paper describes the case of a 37-year woman, with no past history of measles infection, who initially showed behavioral disorders, interpretative and reference deliria with a persecutory content. Extrapyramidal rigidity, bradykinesia, myoclonia, dementia, hyperpyrexia and coma with decerebrate rigidity subsequently appeared. Instrumental tests showed a spinal fluid status with intrathecal IgG synthesis and oligoclonal pattern, aspecific signs of widespread electric anomalies in the EEG. Encephalic CT and NRM were altered showing multifocal damage to the white substance. Anti-measles antibody titres were high in both spinal fluid and serum. Post-mortem histological tests confirmed the clinical hypothesis of subacute sclerosing panencephalitis. The paper reviews existing reports and pays special attention to cases of SSPE in adults and those cases with a psychiatric outcome. Lastly, the role of neuroradiological methods in the diagnostic iter is assessed.
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PMID:[A personal case report of subacute sclerosing panencephalitis in an adult]. 152 74

Parkinson's disease, or paralysis agitans, is a central nervous system disease. Concentrations of dopamine and acetylcholine, neurotransmitters in the substantia nigra of the basal ganglia, become imbalanced. Bradykinesia, rigidity, rhythmic head nodding, and pill-rolling motion of the thumb and forefinger are characteristic. Difficulty verbalizing, dementia, and depression are also common. Levodopa, the medication of choice, restores dopamine to brain cells, reducing parkinsonian symptoms. Awareness by the PACU nurse of the potential for systemic effects of dopamine is one important element of postanesthesia care for the patient with Parkinson's disease. In addition, recognition of the unique physical limitations and medication combinations for each patient promotes optimal postanesthesia nursing assessment and intervention.
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PMID:The postanesthesia patient with Parkinson's disease. 153 Dec 38

Recent research has shown that Huntington's disease (HD) causes problems in the initiation and execution of movement (akinesia, bradykinesia): information which is useful in documenting the functional progression of the disease. The present experiment used a sequential movement task to characterize such impairments. Eighteen patients diagnosed as suffering from HD, and a similar number of matched At-Risk (AR) and Normal control subjects, performed sequential button pressing tasks, under varying amounts of visual advance information. Specific dimensions of motor control were examined (hand, direction). Movement initiation and in particular movement duration were useful indicators of the functional progression of the disease, and also detected anomalies of performance in some AR individuals. Impaired motor programming was indicated by patients' difficulty in initiating movements in the absence of external visual cues, and their problems in utilizing advance information to control movement. Patients had specific deficits in initiating movements with the nonpreferred hand, and directional movement asymmetries were accentuated. The results suggest that HD causes difficulties at three discrete levels: in utilizing advance information, in the initiation and in the spatial representation of movement.
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PMID:Initiation and execution of movement sequences in those suffering from and at-risk of developing Huntington's disease. 153 1

The ability of dopamine D1 antagonists to produce acute extrapyramidal syndromes (EPS) in nonhuman primates is unclear. Some studies in monkeys show that D1 antagonists produce acute dystonia, whereas other studies do not report these effects. The central issues that have yielded conflicting results revolve around prior treatment status (neuroleptic-naive versus neuroleptic sensitized) and route of administration (oral versus parenteral). In this study, separate groups of neuroleptic drug-naive cebus monkeys were tested once weekly with intramuscularly administered SCH 23390, a D1 antagonist, or haloperidol, a D2 antagonist, across a dose range of 0.01-0.25 mg/kg, and a saline control. Both active drugs, but not saline, produced clinically identical syndromes of acute dystonia and bradykinesia, though haloperidol induced higher symptom scores over a longer duration. Sedation and locomotor activity were unchanged by SCH 23390, but decreased with haloperidol. Factors regarding acute EPS liability in nonhuman primate models and clinical implications in man are discussed.
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PMID:Dopamine D1 (SCH 23390) and D2 (haloperidol) antagonists in drug-naive monkeys. 153 77

Decreased olfactory function is among the first signs of idiopathic Parkinson's disease (PD). Whether such dysfunction is present to the same degree on both sides of the nose, however, is unknown. Furthermore, whether the deficit results from or is influenced by anti-Parkinsonian medications has not been definitely established. Odour identification ability was evaluated on the left and right sides of the nose in 20 early-stage untreated PD patients, 20 early-stage treated PD patients, and 20 controls. In all cases, the PD related olfactory dysfunction was bilateral and no difference was observed between the test scores of patients taking or not taking drugs for PD. Although asymmetries of unsystematic direction were present in the test scores of some PD patients, similar asymmetries were observed in the controls and the asymmetries were not related to the side of the major motor dysfunction. As in earlier work, no relation was present between the olfactory test scores and the degree of tremor, rigidity, bradykinesia, or gait disturbance at the time of testing. These findings indicate that the olfactory dysfunction of early stage PD is robust, typically of the same general magnitude on both sides of the nose, and uninfluenced by anti-Parkinsonian medications.
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PMID:Bilateral olfactory dysfunction in early stage treated and untreated idiopathic Parkinson's disease. 153 21

Parkinsonian bradykinesia is defined by a slowness in the execution of movement. We studied the pathophysiology of this symptom in rapid arm-reaching movements to a visual target carried out in a reaction-time task. The major cause of bradykinesia was found to be depression in the rate of rise of electromyographic activity. The amplitude of the peak of this activity did not change significantly. There was no change either in the sequential activation of muscles, in the amount of co-contraction activity, in the accuracy of aim toward the visual target, or in the movement trajectory.
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PMID:Parkinsonian bradykinesia is due to depression in the rate of rise of muscle activity. 154 54


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