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)

In this work, we have attempted to reproduce dyskinesia similar to tardive dyskinesia by two methods. In the first experiment, we have administered to 6 macaca mulatta, haloperidol 0.25 mg/kg daily for six months. During that period we observed in all monkeys, after each dose: restlessness, akinesia and tremor. One monkey developed choreoathetoid movements, which were seen each day after the first month. They disappeared however upon cessation of the drug administration. Only one animal developed a bucco lingual dyskinesia after two months which was still present when they were sacrificed six month after the drug administration was discontinued. At that time, harmaline 3 mg/kg induced a postural tremor in all monkeys suggesting a lesion of the rubro-olivo-cerebello rubral loop. Histological analysis of the brains revealed no gross abnormality. In a second experiment, a left midbrain electrolytic lesion was performed in twelve monkeys. One monkey, developed a contralateral tremor but five including the trembling one developed a buccolingual dyskinesia which has now lasted more than a year. This dyskinesia is present at rest but increased by dopaminergic agents and blocked by haloperidol. Histological analysis of the brain of one of the monkeys revealed a dorsal lesion involving the region of the nucleus parafascicularis thalami. The substantia nigra was spared.
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PMID:Experimental tardive dyskinesia. 689 21

Intermittent stimulation of the parvocellular portion of the nucleus ventralis posterolateralis (V.P.L.) by means of chronically implanted electrodes and stimulus generator was performed in 124 patients for the control of chronic intractable pain. Among these, 11 showed spontaneous abnormal movements within the painful area: 6 post amputation "jumping stumps"; 4 pseudothalamic syndromes and 1 Von Benedikt's syndrome following a cerebrovascular accident. Electrical stimulation of the V.P.L. was able to control both pain and abnormal movements in all cases. The technique was applied with an equally good result in a case of choreoathetotic syndrome without pain but with severe sensory disturbances following a demyelinating process. Attempts made to control action tremor, parkinsonism and other dyskinesias not associated with sensory deafferentation in 12 cases failed. The same mechanism seems to be responsible for pain and dyskinesia in cases of sensory deafferentation, and thalamic stimulation might work as a substitute for sensory information delivered to the nucleus ventralis posterolateralis.
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PMID:Control of dyskinesias due to sensory deafferentation by means of thalamic stimulation. 697 May 2

Clinical characteristics of ten patients with metoclopramide hydrochloride-induced parkinsonism were studied. This condition was found to be more common in aged women and developed subacutely with bilateral symptoms. Clinically, metoclopramide-induced parkinsonism is sometimes accompanied by a rest tremor and may therefore be confused with Parkinson's disease. It is distinct from the latter in that orolingual dyskinesia and postural tremor are often found before the administration of antiparkinsonian drugs. The patients with metoclopramide-induced parkinsonism made a complete recovery within a few months after administration of the drug was discontinued.
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PMID:Metoclopramide-induced Parkinsonism. Clinical characteristics of ten cases. 710 98

Bromocriptine (Parlodel) was given for 2 years to 17 parkinsonian patients showing inadequate response to treatment over a mean of 7 years with levodopa combined with a decarboxylase inhibitor. 11 of the patients had developed dyskinesia and 13 the on-off phenomenon during levodopa therapy. When the dose of bromocriptine reached 30 mg daily, after 4 weeks' treatment, a highly significant improvement (p less than 0.001) was observed in the following six variables: bradykinesia, rigidity, tremor, feeding, dressing and speech. These improvements have now been maintained for 2 years. The on-off phenomenon disappeared in 9 out of 13 patients. Side effects were mild and transient. Involuntary movements existing prior to bromocriptine administration were improved by reducing the dose of levodopa. The mean daily dose--after progressive and individual adjustment--was 46 mg bromocriptine combined with 435 mg levodopa plus decarboxylase inhibitor.
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PMID:Bromocriptine combined with levodopa in Parkinson's disease. 711 8

An acute administration of various doses of apomorphine, a dopaminergic agonist, and of dopaminergic receptor blockers (domperidone, sulpiride, haloperidol), was double-blindly achieved in a parkinsonian patient also suffering from dyskinesia. Apomorphine improved tremor and dyskinesia proportionnally to the dose. Domperidone did not prevent from this beneficial effect whereas sulpiride or haloperidol revealed a competitive antagonism versus apomorphine.
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PMID:[Modification of extrapyramidal signs by apomorphine associated with various dopaminergic antagonists]. 714 25

Essential tremor (ET) has been described in association with major dyskinesias, such as dystonia musculorum deformans, torticollis, and dystonic writer's cramp. In a series of 104 patients affected by ET, the incidence of buccolinguofacial dyskinesias (BLFD) has been investigated, including a comparison with another dyskinesia involving the facial muscles--mimic muscle tremor. The association of ET and BLFD may be casual; however, on the other hand, it might suggest the existence of a subgroup of patients suffering from a non-specific sign of motor control impairment, such as ET, in which other non-specific disorders of voluntary movement, such as BLFD, can gradually develop, particularly late in life.
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PMID:Essential tremor and buccolinguofacial dyskinesias. 716 71

Extrapyramidal syndromes have been described after administration of phenytoin and primidone. Although asterixis, dystonia, and tremor have been described with carbamazepine (Tegretol), there is no report of orofacial dyskinesia. We report a case in which a dose-related lingual-facial-buccal extrapyramidal reaction occurred in association with carbamazepine intoxication.
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PMID:Carbamazepine-induced orofacial dyskinesia. 719 14

In a double-blind trial with a placebo phase, low-dose bromocriptine therapy (average dose, 15 mg per day) produced a significant improvement in 25 idiopathic parkinsonian patients. Tremor and bradykinesia were equally and significantly improved in both the levodopa-treated and the de novo patients. Rigidity was most improved in the levodopa-treated subjects. Age was not a factor in determining the dose of bromocriptine or the degree of improvement. Adverse effects occurred in 30% but were mild and dose-dependent. Four subjects, unable to tolerate initial doses of bromocriptine, withdrew from the trial. A low initial dose (1 mg per day) and slow escalation in dosage produced an optimal, though delayed improvement. Low-dose bromocriptine therapy is effective, does not induce significant dyskinesia nor on-off phenomenon, and is probably an alternative to levodopa as a drug of first choice in Parkinson disease.
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PMID:Bromocriptine: low-dose therapy in Parkinson disease. 720 Oct 89

Lisuride is a soluble ergolene derivative with endocrine effects similar to but more potent than those of bromocriptine. In nine subjects with idiopathic, postencephalitic, or drug-induced parkinsonism, lisuride at a dosage of 0.05 to 0.15 mg intravenously caused an immediate improvement in tremor, rigidity, akinesia, and postural deformity, but also caused chorea and orofacial dyskinesia. Improvement lasted 2 to 3 hours. Lisuride had little or no effect in a single patient with progressively supranuclear palsy. Oral lisuride therapy, 0.8 to 4.8 mg daily, had similar effects but occasionally caused reduced awareness and hallucinations.
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PMID:Lisuride in parkinsonism. 721 65

Two patients are reported presenting with incoordination mimicking cerebellar disease in the upper and lower limbs, ataxia of gait, absent tendon reflexes and little or no clinically detectable wasting. Motor conduction velocity in the upper limbs was substantially reduced in one patient whereas it was normal and slightly reduced in the other. It is concluded that in Charcot-Marie Tooth disease incoordination may mimic cerebellar disease and when this is so it is due to the association of varying degrees of proprioceptive deafferentation and a dyskinesia similar to that produced by familial (essential) tremor.
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PMID:Unusual presentation of Charcot Marie-Tooth disease-incoordination with absent of minimal wasting-Report of 2 cases. 722 62


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