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)

A case of severe life-threatening tardive dyskinesia resulting in esophageal and respiratory difficulties due to metoclopramide therapy is presented. A 66-year-old man with a primary diagnosis of clear cell carcinoma of the biliary duct was treated with metoclopramide for gastrointestinal symptoms related to his chemotherapy regimen. The patient initially presented with tremor and rigidity in the upper extremities. On antiparkinsonian therapy, symptoms progressed to hemiballism and involuntary movements of the face, mouth, and tongue, with respiratory and esophageal dyskinesia. Despite discontinuance of metoclopramide, severe tardive dyskinetic symptoms resulted in placement of a gastrostomy tube to maintain nutritional support. This case along with others in the literature should emphasize the need for continuous reevaluation of metoclopramide during long-term therapy, since serious side effects have been reported to occur.
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PMID:Life-threatening tardive dyskinesia caused by metoclopramide. 350 64

Tremor and drug-induced dyskinesia are major involuntary movements in Parkinson's disease. The rhythm of resting tremor is 4-6 cycles/s, driven by generators in the brain, and stabilized by reflex arcs involving the spinal cord, nerves and muscles. Its frequency is fixed: it is the same in proximal and distal muscles in each case and does not change in the course of amplitude reduction of tremor by levodopa injection. An approximate doubling of frequency occurs in action tremor which suggests a central mechanism liable to produce harmonics. In postural tremor as observed in the lower limbs while on standing, the frequency of grouped discharges falls into ranges of rhythm with either resting or action tremor. Levodopa-induced dyskinesia has a similar nature to chorea in both clinical observation and EMG. With EMG choreic discharges may appear concomitant with regular parkinsonian tremors in the same muscle, suggesting that the two are not opposites as expressions of dysfunction of the dopaminergic system.
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PMID:Pathophysiology of involuntary movements in Parkinson's disease. 355 88

This paper presents a review of the literature on the therapeutic action and the side effects of the two main dopaminergic agents: L-DOPA/decarboxylase inhibitor (L-DOPA/DI) and bromocriptine (Parlodel used either as monotherapy or in combination in patients with Parkinson's disease. The combination of L-DOPA/DI and bromocriptine gives the best therapeutic efficacy (49% improvement) in the total score (bradykinesia, rigidity and tremor). However, treatment by monotherapy or combination gives the same pattern of activity: greatest improvement in tremor, followed by rigidity and bradykinesia. Improvement observed in the short term is not sustained over longer periods of time for monotherapy with either drug. The short-term side effects are similar for each treatment, whereas long-term complications (dyskinesia, end-of-dose deterioration and on-off phenomenon) appear only when levodopa is used, alone (high incidence) or in combination with bromocriptine (low incidence). The overall optimum treatment is obtained with a combination of L-DOPA/DI and bromocriptine.
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PMID:Optimum symptomatic control of Parkinson's disease with dopaminergic therapy. 367 21

Low-dose bromocriptine therapy (average dose 14.5 mg/day at 2 years) produced significant improvement in 25 of 39 parkinsonian patients. Bradykinesia was less in de novo subjects; tremor and rigidity improved most in the levodopa subjects. Five of six patients improved after a low-dose bromocriptine drug "holiday." After the addition of bromocriptine any reductions in levodopa dosage were small, with repeated cuts made gradually over months preventing the deterioration commonly seen with larger sudden reductions in levodopa dosage. Five patients withdrew because of intolerable adverse effects, two because of worsening response. Adverse effects were mild and generally dose dependent, and in some patients they disappeared without reduction in continuing bromocriptine therapy. Eighty percent of those who tolerated bromocriptine maintained response over 2 years. Bromocriptine did not induce dyskinesia, the wearing-off response, or the on-off phenomenon in de novo subjects and was used as a first choice drug in these parkinsonian patients. Best results were obtained from a combination of bromocriptine and levodopa.
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PMID:Bromocriptine: long-term low-dose therapy in Parkinson's disease. 370 99

The long-term effects of mesulergine, a new drug with dopamine agonistic properties, were studied in 28 patients with Parkinson's disease. In 18 patients with late side effects of levodopa, the addition of mesulergine (10.9 mg/day) induced significant decreases in the global (-48%), rigidity (-62%), and akinesia (-37%) scores. The drug was found to be very effective on tremor (-71%). Mesulergine was useful in cases of inefficacy of levodopa alone or persistent intolerable side effects. The decrease in levodopa dose and the addition of mesulergine permitted a significant reduction in dyskinesia. Used as sole therapeutic agent (10.9 mg/day), mesulergine was found to be active on tremor and rigidity scores but not on akinesia or global scores. Mesulergine induced few side effects. These results show the antiparkinsonian properties of mesulergine that seem to be of significant therapeutic value in patients with tremor or in combination with levodopa.
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PMID:Mesulergine (CU 32-085) in the treatment of Parkinson's disease. 370

Metoclopramide hydrochloride is an antiemetic and gastric motility stimulant with a wide variety of extrapyramidal side effects, including parkinsonism. We describe two patients with end-stage renal disease secondary to diabetes mellitus treated with hemodialysis who developed extrapyramidal symptoms during treatment with metoclopramide. One patient with preexisting, well-controlled Parkinson's disease developed increasing rigidity and bradykinesia that became completely refractory to treatment with L-dopa and bromocriptine while taking metoclopramide for diabetic gastroparesis. A second patient with no history of Parkinson's disease developed a resting tremor and facial dyskinesia during treatment with metoclopramide. In both cases, discontinuation of metoclopramide therapy led to prompt improvement of symptoms.
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PMID:Metoclopramide-induced parkinsonism in hemodialysis patients. Report of two cases. 376 55

We used a new D2 dopamine agonist, mesulergine (8-alpha-amino-ergoline, CU 32-085), to treat 20 patients (12 men and 8 women), mean age 62.6 (SEM = 1.7) and mean duration of illness 5.9 (SEM = 1.0) years. Wearing-off effect was the principal indication for new therapy in 15 patients, and the others had inadequate response to levodopa. All continued on levodopa therapy, and 10 patients were studied in a double-blind controlled test. The mean motor disability decreased from 2.8 (SEM = 0.12) to 1.6 (SEM = 0.18) with mesulergine (p less than 0.0001) and increased to 1.9 (SEM = 0.20) with placebo (p less than 0.001). Tremor improved most, followed by rigidity, bradykinesia, gait, and postural instability. Side effects included dyskinesia, light-headedness, hallucinations, nausea, vomiting, drowsiness, and ankle edema, but, in general, mesulergine was tolerated well.
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PMID:Placebo-controlled study of mesulergine in Parkinson's disease. 388 92

A 58-year-old woman was receiving chemotherapy for carcinoma of the breast. She was given 1,700 mg metoclopramide IV for 2 months to prevent nausea and vomiting. Within hours after metoclopramide was given, she had hand tremor, akathisia, and truncal and orofacial dyskinesia. These symptoms resolved, but she was left with persistent shoulder stump chorea, the perception of the phantom left arm involuntarily adducted at the shoulder and flexed at the elbow, and dystonic pronation and extension of the hand away from her body. The motor aspects of the phantom dyskinesia will be emphasized.
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PMID:Metoclopramide-induced phantom dyskinesia. 397 6

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

In 144 patients receiving prolonged treatment with levodopa for Parkinson's disease, an attempt was made to establish possible correlations between the incidence of levodopa-induced dyskinesias and the age of the patient at the onset of the disease, the clinical form of the disease, the duration of symptoms before initiation of the levodopa therapy, the duration of the levodopa therapy and the influence of the concomitant treatment. Levodopa-induced dyskinesia was observed in 92 patients (64%). The age at onset of the disease of patients with dyskinesia was significantly different from the age at onset of those without dyskinesia, the means being 54.8 and 68.9 years respectively. Levodopa-induced dyskinesia occurred less often in the group with preponderant tremor than in those with preponderant bradykinesia (29% vs. 69%). The patients treated with levodopa from the very beginning of their disease were less susceptible to dyskinesia than those who had parkinsonism for some time before receiving levodopa. The influence of the duration of levodopa treatment on the manifestation of dyskinesia could not be confirmed because this side-effect usually appeared during the first year of treatment. The concomitant anti-parkinsonian treatment appeared to have no influence on the incidence of dyskinesia. Biochemical and practical implications of these observations are discussed.
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PMID:Levodopa-induced dyskinesia: clinical observations. 399 72


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