Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine monkeys (Macaca fascicularis) were used in this study. Four monkeys were rendered parkinsonian by administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) 0.5 mg/kg intravenously. Three animals were injected once daily for 4 days, and one animal once weekly for 4 weeks. Five animals were used as controls. All MPTP-treated animals demonstrated the same clinical features which included akinesia, bradykinesia, a flexed posture of the trunk and all extremities, decreased initiation of the threat response, decreased vocalization and difficulty in swallowing. An increase in rigidity and reflexes was noted in all extremities. Tremor was present in all animals. Determination of the local spinal metabolic rate of glucose (LSMRg) utilization revealed an increase (P less than 0.05) in LSMRg in Rexed layer I in all cord segments and in Rexed layer II in both cervical and lumbar segments. Rexed layer X demonstrated a significant (P less than 0.05) increase in LSMRg at the cervical cord. The LSMRg in the animal that received weekly injections was similar to the daily injected animals.
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PMID:Spinal cord metabolism of the 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine-treated monkey. 387 82

We demonstrate that injections of 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP), 1-methyl-4-phenyl-pyridinium ion (MPP+) and Paraquat (PQ+) produce in Rana Pipiens different behavioral, biochemical and skin pigmentation changes. MPTP causes in frogs the main symptoms of Parkinsonism (rigidity, akinesia and tremor) and it darkens the skin of animals. It also decreases brain and, less so, adrenal medulla dopamine. These effects are blocked by Pargyline. MPP+ causes the same symptoms but more rapidly. In contrast, skin pigmentation is clearly lightened. Brain and particularly adrenal dopamine reserves are nearly abolished. Pargyline increases these effects. Paraquat, in a cumulative fashion, eventually causes the same behavioral changes and a slight increase in pigmentation. It initially produces an increase in brain and adrenal dopamine concentrations, but later a significant dopamine concentration decrease. Pargyline potentiates these long term effects, blocks the dopamine increase, but reverses the PQ+ effect upon melanin, producing the same depigmentation as MPP+ alone.
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PMID:Comparative behavioral, biochemical and pigmentary effects of MPTP, MPP+ and paraquat in Rana pipiens. 387

A peripheral and cerebral cholinergic syndrome was induced in mice by oxotremorine administration; pretreatment orally with cytidine diphosphocholine (CDP-choline) does not potentiate this syndrome and even antagonizes oxotremorine-induced salivation. Levodopa antagonizes the oxotremorine-induced cerebral symptoms (akinesia + tremor); however this antagonism disappears when mice are chronically pretreated orally with CDP-choline, confirming the action of CDP-choline on dopaminergic pathways. The proven efficacy of CDP-choline in Parkinsonism could then be mediated by a hypersensitivity of some cerebral dopamine receptors, and not by a direct stimulating effect of the striatal dopaminergic receptors.
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PMID:Oxotremorine-induced cholinergic syndrome: modifications by levodopa and/or oral cytidine diphosphocholine. 399 Apr 45

In 15 patients (8 men, 7 women), aged 44-81 years, with idiopathic parkinsonism, the effects of mesulergine (CU 32-085) were observed for up to 3 years. Of these patients, four had been without previous levodopa treatment, five had been on levodopa/decarboxylase inhibitor for 6.4 years and six patients had been on levodopa/decarboxylase inhibitor and bromocriptine for a period of 7.5 years. Mesulergine proved to be effective in all three groups of patients and for each main symptom of the disease. Rigidity and tremor showed a better response than akinesia. A decline in efficacy could be observed after 18 months of treatment. By increasing the levodopa dosage, the worsening of the symptomatology could be reduced again and after 3 years patients were slightly better off than before the introduction of mesulergine. Fine motor performance showed a longer-lasting improvement than walking, which was affected by an increase of freezing. Mesulergine was not fully sufficient when given in monotherapy and the levodopa saving effect was only temporary. Parallel with the decline in the therapeutic response as assessed by the rating scales, there was a worsening in the on/off symptomatology. The on/off symptoms, evaluated by patients themselves, had shown very small or no improvement at the beginning of mesulergine administration, contrasting with the findings reflected in the assessment scales. The most frequent side-effects were hallucinations and dyskinesias. Orthostatic hypotension did not prove a problem. Dyskinesias were not seen during monotherapy with mesulergine in de novo patients.
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PMID:Three-year observation of mesulergine (CU 32-085) in advanced and newly treated parkinsonism. 399 71

1. The pA2 anti-acetylcholine activity in vitro for benapryzine was 6.55 compared with 9.02 for benzhexol.2. In vivo, the anti-acetylcholine activity of benapryzine relative to benzhexol was 0.038 as assessed by the mydriatic response of mice after subcutaneous administration. The relative activity assessed by the inhibition of pilocarpine-induced salivation was 0.13 after oral administration and 0.056 following subcutaneous administration of the drugs.3. Benapryzine had the same order of activity as benzhexol in inhibiting oxotremorine-induced tremors in mice.4. Benapryzine had anticonvulsant properties but no analgesic activity, whilst in high doses it antagonized the extrapyramidal symptoms induced by perphenazine in rats.5. In patients benapryzine was effective in reducing the symptoms of Parkinson's disease without overt anti-cholinergic effects or central hallucinogenic actions.6. Benapryzine abolished the excess tremor and reduced the rigidity and akinesia induced by physostigmine in Parkinsonian subjects.
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PMID:Some initial animal and human pharmacological studies with benapryzine (BRL 1288). 458 Dec 46

Fourteen slightly disabled patients with Parkinsonism were treated separately with benzhexol, amantadine, and levodopa. Benzhexol and amantadine both gave a 15% reduction in functional disability and levodopa a 36% reduction. Benzhexol lessened the rigidity and improved the flexion of posture of Parkinson's disease, but had little or no effect on akinesia and tremor. Amantadine and levodopa caused improvement in all these symptoms. The combination of benzhexol and amantadine was as effective after four weeks of treatment as levodopa was after six months.
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PMID:Comparative trial of benzhexol, amantadine, and levodopa in the treatment of Parkinson's disease. 483 13

One hundred patients with Parkinson's disease were treated with levodopa for more than a year at UCLA Medical Center. They were examined at given intervals and their improvement was graded. The optimum therapeutic dose was attained by balancing side effects against relief of symptoms and ranged from 1.5 grams to 8.0 grams per day (average 4.3 grams). There is no doubt that levodopa is the most effective treatment now available for Parkinson's disease. At the end of the first year, 60 percent of the patients improved 50 percent or better, and 10 percent were considered symptom-free. All major symptoms of this disease, including rigidity, akinesia and tremor, improved in variable degree. There were no serious abnormalities in the routine clinical laboratory tests. The comon side effects included nausea, vomiting and choreoathetoid dyskinesias. The side effects were not life threatening, but occasionally were major therapeutic challenges. Maximal benefits with minimal side effects were achieved only by careful adjustments of the levodopa dosage as the months went by. This needed careful management by the physician and cooperation by the patient. Anticholinergic medications or amantadine hydrochloride, sometimes both, usually supplemented the effect of the levodopa.
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PMID:One to two year treatment of Parkinson's disease with levodopa. 508 81

25% of patients with Parkinson's disease demonstrate the first symptoms with 70 years. The deficiency of Tyrosinhydroxylase is the trigger of the decreased level of Dopamin in the basal ganglia. The implications are the typical symptoms (tremor, rigor and akinesia) and the psychopathological decompensations as depression, delirs and bradyphrenie.
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PMID:[Senile Parkinsonism: its motor and psychological defects]. 612 32

3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA) as well as homovanillic acid (HVA) and cyclic AMP were estimated in the morning urine of 41 drug-free parkinsonian patients and 25 hospitalized controls. In 29 patients, the estimations were repeated after 2 weeks treatment with L-dopa plus decarboxylase inhibitor. Drug-free patients excreted more MHPG and less 5-HIAA than controls. The difference from controls was significant for MHPG, only for the subgroup of patients with akinesia as the main symptom (P = 0.001) and for 5-HIAA only for the tremor subgroup (P = 0.03). 2 weeks treatment with L-dopa plus decarboxylase inhibitor, increased the MHPG excretion significantly only for the akinesia subgroup, where the pretreatment MHPG values were high, while there was no change in MHPG excretion in the tremor and the rigidity subgroups. The treatment caused no change in the 5-HIAA excretion in the tremor subgroup, where the pretreatment values were low, while in the rigidity and akinesia subgroups 5-HIAA excretion was significantly decreased. These results, as well as our previous results on HVA and cyclic AMP, show that there are considerable differences among the subgroups of parkinsonian patients regarding the metabolism of dopamine, noradrenaline and serotonin.
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PMID:Urinary noradrenaline and serotonin metabolites in drug-free Parkinson patients and the effect of L-dopa treatment. 618 30

The long-term effects of bromocriptine as an adjuvant were investigated in 32 patients (20 male, 12 female), aged 43-76 years (mean 65.4), suffering from parkinsonism for 3-20 years (mean 9.3). Patients were pretreated with levodopa/decarboxylase inhibitor for 24-116 months (mean 74.9). Bromocriptine was given because of a decline in the response to levodopa, various kinds of "on-off" phenomena, and disabling dyskinesias. Levodopa was reduced by 18%, while bromocriptine was added with a mean dose of 29 mg. The results showed a marked tremor and rigidity response, clearly greater than that of bradykinesia of the hands. The improvement after 4 weeks of bromocriptine treatment was maintained over 12 months. Only gait disturbances tended to increase. At the same time the self-ratings of the patients showed an increase in disability as far as daily activities were concerned. Likewise, the "on-off" symptoms with regard to the wearing-off effects worsened in comparison with the condition during the 4-week period. Akinesia paradoxica was never definitely influenced. An increase in dyskinesias was avoided and serious side-effects could be kept under control.
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PMID:Long-term experience with bromocriptine in advanced parkinsonism. Results after one year's treatment. 618 12


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