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)

The paper is concerned with a study of the effect of metamizil in 45 patients with different forms of vascular parkinsonism. It was established that metamizil exerts a positive effect on the development of neurological symptoms (rigidity, bradykinesia, tremor) in mild and moderately expressed degrees of lesions. In most of the cases the drugs appeared effective in doses of 0.001 g thrice daily, and in separate cases 0.001 g 6 times daily. In the majority of patients metazil was tolerated without significant side effects. In some patients the side effects (vertigo, dryness in the mouth) were slightly expressed. The effect of treatment was seen after 2 days up to 2 weeks and lasted during the whole course of treatment and sometimes after it. Metamizil possessing a moderate sedative action, as well as spasmolytical and hypotensive is indicated for patients with vascular parkinsonism.
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PMID:[Experience in treating vascular parkinsonism with metamysil]. 64 11

The electrical activity of single motor units was recorded from the first dorsal interosseous muscles of nine patients with Parkinson's disease. Six of these patients had a combination of the following abnormal motor unit properies: (1) a variable delay period of 20 seconds to 3 minutes between the initiation of voluntary effort and the recruitment of the first group of motor units; (2) after recruitment, some of the motor units stopped firing for durations of 10s, 40s, 75s... 3 min.; (3) some of the motor units fired at abnormally low frequencies of 2-3 per second. All these six patients had slowed finger movement, and five of the six were studied while off levodopa for two to seven days. One of these patients, reinvestigated after levodopa therapy had been restarted, demonstrated improvement in motor unit control. The three remaining patients who were studied while on uninterrupted levodopa therapy could make rapid finger movements, could recruit motor units without delay, and could fire recruited motor units continuously at normal frequencies of 6-14 per second. These results suggest that levodopa therapy is effective in Parkinson's disease at least partly because of its ability to correct abnormalities in the recruitment of motor units. Levodopa also corrects the abnormal motor unit firing pattern. The abnormal motor unit properties found in these patients could account for some aspects of bradykinesia.
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PMID:Electrical properties of motor units in Parkinsonism and a possible relationship with bradykinesia. 76 83

Postural or Parkinson-like tremor, which results from the impairment of mechanisms which are predominantly lateralized in the brain, is most likely related to the combined impairment of the dopaminergic nigrostriatal pathway and the corresponding rubro-olivo-cerebello-rubral loop (without excluding the possiblity that other nervous mechanisms interconnected with these structures may represent an alternative disturbance). The integrity of the internal division of the pallidum and the ventrolateral area of the thalamus and their efferent fibers as well as the motor cortex and certain of its cortico-subcortico-spinal pathways (Figures 1 and 2) is apparently an essential feature for the elaboration of the rhythmic bursts associated with the appearance of postural tremor. The integrity of the spinal sensory roots and the rubro-tegmentospinal tract is not a prerequisite for the expression of postural tremor, a condition which seems essential for the production of rigidity. The latter facts suggest that the disturbances which subserve these two types of motor impairment, often concomitantly present in Parkinsonism, partially involve the impairment of different mechanisms although the loss of the DA fibers originating in the substantia nigra and ending in the neostriatum (Figure 1) appears to represent a disturbance common to both types of disorders. Bradykinesia which may be associated with an impairment of catecholamine metabolism (and more especially the neostriatal DA mechanisms) on both sides of the brain may also result from bilateral lesions of the pallidum or of its outflow corresponding, in the main, to the pallidothalamic fibers ending in the ventrolateral thalamus. The latter types of lesion most likely exclude the influence of the monoaminergic, cholinergic and gabaminergic activities normally originating in the striopallidal system and influencing the activity transmitted to other CNS mechanisms. Severe akinesia, however, apparently depends on more profound and generalized disturbances of brain monoamine metabolism with or without the involvement of other ill-defined mechanisms. At any rate the impairment of the brain DA mechanisms (and especially those of the neostriatum) seems to represent a major feature in the production of the Parkinsonian type of akinesia. Further work is needed to establish the relative importance of the loss of catecholaminergic mechanisms other than those of the neostriatum in the production of akinesia.
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PMID:Physiopathology of experimental Parkinsonism in the monkey. 80 27

Eight patients developed a syndrome marked by features of catatonia (including posturing, waxy flexibility, withdrawal and regression) and parkinsonism (including bradykinesia and rigidity) while receiving high-potency neuroleptic drugs. The syndrome had a gradual onset, responded slowly to withdrawal of the neuroleptic or use of an anticholinergic agent, but seemed to respond more rapidly to amantadine. The syndrome may easily be confused with a worsening of schizophrenic symptoms.
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PMID:Catatonic reactions to high-potency neuroleptic drugs. 88 19

The occurence of extranuchal dystonia, facial spasm, parkinsonian symptoms (facial masking, bradykinesia, rigidity), tremor and family history of tremor was tabulated in a group of 30 patients with IST. The incidence of extranuchal dystonia increased as severity of IST increased. There was a strong trend for severity of extranuchal dystonia to increase as severity of torticollis increased, which was significant (p less than 0.001). There was a similar trend for severity of facial spasm to increase with increasing severity of torticollis (p less than 0.025). Parkinsonian features were seen in 10 of 30 patients, and in three the diagnosis of Parkinson's disease could be entertained. Tremor was seen in 26 of 30 patients being mild in 12, moderate in 11, and severe in three. A family history of tremor was present in 16 of 28 cases for whom history was available (12 primary, four secondary relations). The results are most consistent with the hypothesis that IST is a variant of DMD with tremor as an integral part of the disease and tremor represents a forme of the disease in family members.
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PMID:Dystonia and tremor in spasmodic torticollis. 94 73

The post-mortem examination of the nervous system of a patient with Shy-Drager syndrome successfully treated with levodopa (Sharpe et al, 1972) revealed features of striato-nigral degeneration and amyotrophic lateral sclerosis, a cerebellar system degeneration and a loss of approximately 75% of sympathetic preganglionic neurons. Lewy bodies were not present and no detectable changes were observed in the sympathetic prevertebral ganglia. While the limited and transient beneficial effect of levodopa on the bradykinesia in our case is possibly due to the progressive loss of striatal dopaminergic receptors seen in striatonigral degeneration, we propose that in Shy-Drager syndrome, levodopa therapy benefits orthostatic hypotension because of a suppression of the central depressor action of this drug. This suppression is attributable to functional disconnection of sympathetic ganglia secondary to the loss of preganglionic neurons or to degeneration of central autonomic catecholaminergic systems.
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PMID:Shy-Drager syndrome. Neuropathological correlation and response to levodopa therapy. 96 36

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P less than 0.01) improvement in rigidity, tremor, bradykinesia, gait disturbance and total score. In seven patients levodopa with carbidopa was completely replaced by bromocriptine (mean dose, 70 mg), with improvement in four. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance (on-off effect) were decreased whereas orthostatic hypotension and mental changes were increased. Bromocriptine appears to be a major new agent in Parkinson's disease that is especially promising in patients no longer responding to levodopa.
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PMID:Treatment of parkinson's disease with bromocriptine. 98 85

On the basis of a reassessment of the aetiopathogenetic problem and the neuroendocrine implications, the therapeutic effectiveness of a prolactin inhibitor, 2-alpha-Br-ergocryptine (CB 154), in Parkinson's disease is assessed. Five patients were treated for a total of two weeks using doses between 10 and 15 mg/die. CB 154 was found to act as a dopaminergic receptor agonist at nigro-striatal level, considerably improving tremor and rigidity and to a lesser extent bradykinesia and total disability.
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PMID:[Neuroendocrine aspects of Parkinson's disease. Therapeutic/effect of a prolactin inhibitor]. 103 12

Nine patients with Parkinsonism were studied before and after treatment with piribedil, a dopamine-receptor stimulator. Piribedil appeared to have a slight anti-Parkinsonism effect upon bradykinesia, and possibly upon tremor, but did not improve rigidity. The chief toxic effects were drowsiness and confusion, and two patients experienced nausea. Changes in homovanillic acid in the cerebrospinal fluid indicated that the drug reduced the turnover of endogenous dopamine. In spite of this definite neuropharmacological action, no clear-cut associated clinical benefit was demonstrated. The significance of these findings is discussed.
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PMID:Clinical and pharmacological evaluation of the effects of piribedil in patients with parkinsonism. 109 Nov 22

The concept of akinesia deserves to be looked at again in the light of recent work on Parkinsonism, particularly those findings which have resulted from the use of L-dopa in Parkinsonian syndromes. Akinesia and bradykinesia are integral parts of such syndromes, at times even constituting their essential element. Akinesia belongs to a group of psychomotor syndromes, the semiology and pathogenesis of which were the subject of numerous discussions at the beginning of this century. As we have pointed out elsewhere, akinesia cannot be defined solely in terms of its own characteristics: it must be understood equally in its paradoxical aspects--"paradoxical kinesia" in post-encephalitic Parkinsonism in particular, and "paradoxical akinesia" in Parkinsonian patients treated with L-dopa.
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PMID:The concept of akinesia. 116 51


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