Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(+)-4-propyl-9-hydroxynaphthoxazine (PHNO) is a novel selective D2 agonist. The efficacy and safety of PHNO was studied in 10 Parkinsonian patients (Hoehn and Yahr Stage II or III) who continued to receive levodopa/carbidopa. At the lowest dose administered (0.25 mg tid), nine of the 10 patients improved with respect to rigidity, bradykinesia and tremor. At this dose there was one dropout because of severe orthostasis. Although there was a trend towards improvement in motor scores with the higher doses (0.5-1.0 mg tid), this was not statistically significant. At higher doses there were a total of four dropouts because of adverse effects such as nausea, vomiting and orthostatic hypotension. It appears that PHNO may prove to be efficacious in the treatment of Parkinson's disease.
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PMID:The efficacy of (+)-4-propyl-9-hydroxynaphthoxazine as adjunctive therapy in Parkinson's disease. 274 65

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

Twenty Parkinson's disease patients, who had not yet received levodopa, were treated with low-dose bromocriptine. At a mean daily bromocriptine dose of 13.2 mg, 13 patients (65%) improved and had a 32% reduction in the combined score for tremor rigidity and bradykinesia. Adverse effects were frequent, and 25% of the patients were taken off the drug because of nausea or vomiting. After 30 months follow-up, only three patients continued on bromocriptine alone. Ten patients were eventually maintained on low-dose bromocriptine and levodopa-carbidopa, and a clear synergistic effect of bromocriptine in this drug combination was documented in eight patients. Low-dose bromocriptine does not replace levodopa as initial therapy for Parkinson's disease. The potential long-term benefit of the early use of combined low-dose levodopa-dopamine agonist therapy needs to be further studied.
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PMID:Bromocriptine: problems with low-dose de novo therapy in Parkinson's disease. 397 51

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
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PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

This randomized, double-blind trial was designed to evaluate the efficacy of a transdermal system of piribedil on the motor symptoms of Parkinson's disease during 3 weeks of treatment administered to three different groups: placebo, one piribedil patch (1 PP), and two (2 PP) piribedil patches. Twenty-seven patients with idiopathic Parkinson's disease, treated with L-dopa but not sufficiently controlled, were included in this trial. The test treatment did not demonstrate any clinical efficacy on either the main end point (Unified Parkinson's Disease Rating Scale motor score) or the secondary end points (rigidity, bradykinesia, postural, and resting tremor scores). The main adverse events were nausea (11%), vomiting (7.4%), and malaise (7.4%) mainly observed in the placebo group (four of seven patients). The local acceptability of the transdermal system was good. Plasma piribedil concentrations at the end of treatment were 6.74+/-1.10 and 9.31+/-3.33 ng/mL in the 1 PP and 2 PP groups, respectively. These plasma levels could account for the lack of clinical efficacy, because a previous pharmacokinetics-PD study conducted in parkinsonian patients and treated with the intravenous route demonstrated that the critical limits of activity on tremor were between 10 and 30 ng/mL.
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PMID:A randomized, double-blind study of a skin patch of a dopaminergic agonist, piribedil, in Parkinson's disease. 1009 30

We report a 73-year-old Japanese woman with familial Parkinson's disease. The patient was well until her 67 years of the age, when she noted rest tremor in her right hand. Soon after her gait became short stepped. She visited our clinic on October 6, 1992 when she was 68 years old. She was alert and well oriented without dementia. She showed masked face, small voice, small stepped gait, retropulsion, resting tremor in her right hand, rigidity in the neck, and bradykinesia. She was treated with 400 mg/day of levodopa-carbidopa, which improved her symptoms, however, she developed wearing off phenomenon 3 years after the initiation of levodopa treatment. On August 26, 1998, she developed abdominal pain, diarrhea, and vomiting. She was admitted to another hospital, where abdominal plain x-ray revealed an evidence of intestinal obstruction (ileus). She was treated with nasogastric suction and intravenous fluid. Her condition did not improve and she was transferred to our hospital on August 29, 1998. Her family history revealed no consanguineous marriage. She had two elder brothers and three elder sisters. One of her brothers had been diagnosed as Parkinson's disease. Her husband also suffered from Parkinson's disease, however, her parents apparently did not have Parkinson's disease. On admission, she appeared to be drowsy. Her blood pressure was 102/70 mmHg, body temperature 36.2 degrees C. The lungs were clear and no cardiac murmur was present. Abdomen was flat and bowel sound was audible. No abnormal mass was palpable. Neurologic examination revealed mild consciousness disturbance, masked face, and small voice. No motor paralysis was noted. Muscle tone was hypotonic. No abnormal involuntary movement was noted. Abnormal laboratory findings on admission were as follows; WBC 11,300/microliter, amylase 1,373 IU/l, CK 446 IU/l, BUN 50 mg/dl, creatinine 1.17 mg/dl, CRP 22.7 mg/ dl, Na 134 mEq/l, K 3.1 mEq/l, and Cl 81 mEq/l. A chest x-ray film revealed pneumonic shadows in both lower lung fields. She was treated by nasointestinal suction, intravenous fluids, and chemotherapy for her infection. Her BP started to drop on September 2 and she developed cardiac arrest on the same day. She was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had a form of autosomal dominant familial Parkinson's disease. As parents did not have Parkinson's disease, some of the participants raised the possibility of autosomal recessive inheritance. But the age of onset was too late for autosomal recessive inheritance. Majority thought that the mode of inheritance was autosomal dominant with low penetrance. alpha-Synuclein mutation causes an autosomal dominant familial Parkinson's disease, but this type is very rare in non-Greek populations and the penetrance is high. Chromosome 2-linked autosomal dominant familial Parkinson's disease shows low penetrance. There are many other autosomal dominant forms of familial Parkinson's disease linked to yet unknown chromosome loci. Majority thought that this patient also had a form of Lewy-body positive autosomal dominant familial Parkinson's disease of unknown chromosome locus. Post mortem examination revealed ischemic intestinal lesion with strangulation. This was thought to be the cause of her death. In the central nervous system, the brain appeared to be normal by inspection. In the coronal sections, the substantia nigra and the locus coeruleus showed marked depigmentation. Histologic examination revealed marked neuronal loss and Lewy body formation in the remaining neurons. Pathologic examination was consistent with Parkinson's disease. Mutational analysis for the parkin gene was negative.
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PMID:[A 73-year-old woman with familial Parkinson's disease]. 1065 9

We present a clinicopathological report of a recent fatal case of a 27-year-old woman whom we consider to have had encephalitis lethargica. Clinical features of note were a presentation with vertigo, persistent vomiting and sleep disturbance including marked daytime somnolence and vivid nightmares. On examination, she had impaired slow pursuit vertical eye movements, dysarthria, an expressionless face and slow tongue movements. She went on to develop gross supranuclear gaze palsy, neck rigidity, bradykinesia, blepharospasm, profound somnolence and anarthria but no tremor, weakness or impairment of cognition. She died after an illness lasting 12 months. On investigation, the cerebrospinal fluid was found to contain a very high level of IgG with oligoclonal bands but no cells. Post-mortem examination revealed an active encephalitis, mainly centered on the upper brainstem and diencephalon with extensive Purkinje cell loss and marked plasma cell infiltrates and morula cells. No virus was recovered.
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PMID:A contemporary case of encephalitis lethargica. 1122 Jun 91

Headache makes one of the most common side effects of frequently pesticide application. This is to be taken care of in rural areas. Headaches have been reported with the use of ivermectin, ivermectin-diethylcarbamazine, organophosphates, and also with the fungicide maneb and copper sulfate, carbofuran, hexonal, dioxin, methomyl and its salts, as well as rare cases of poisoning with the fungicide combination of propineb and cymoxanil. Headache often occurs after long term work with pesticides and/or in laboratories. There are numerous symptoms accompanying headache in pesticide poisoning the most common being elevated body temperature, lassitude, dizziness, irritability, nausea, vomiting, epigastric pain, diarrhea, myalgia, pains in the arms and legs, sleepiness, pains in joints, irritation of eyes/face/skin, sweating. Much less common are respiratory disturbances, tachycardia, tachypnea and other cardiac distur bances, fall of blood pressure, gastrointestinal discomforts, constipation, poor appetite, significant decrease in leukocyte count, anemia, albuminuria, azotemia, fasciculations, miosis, blurred vision, memory disturbances and other neurologic disturbances, postural tremor, signs of cerebral function damage, bradykinesia, etc.
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PMID:[Headache caused by pesticides--a review of the literature]. 1871 90

Parkinson's disease, the most common neurological disorder in the elderly, is characterized by progressive extrapyramidal motor dysfunction including resting tremors, muscle rigidity, hypolocomotion (bradykinesia and akinesia) and postural instability. Various non-motor features are also seen such as cognitive impairments (deficits in learning and memory) and mood disorders (depression and anxiety). While the 5-HT(1A) receptor has long been implicated in the pathogenesis and treatment of anxiety and depression, recent research has revealed new therapeutic roles for 5-HT(1A) receptors in the treatment of Parkinson's disease. These include the modulation of parkinsonian motor symptoms, L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia, cognitive impairments and emesis. Thus, 5-HT(1A) agonists improve the various motor disorders associated with dopaminergic deficits, dyskinesia induced by chronic L-DOPA treatment, mood disturbances (anxiety and depression) and dopamine agonist-induced emesis. In addition, partial 5-HT(1A) agonists are expected to improve cognitive impairment in Parkinson's patients. These findings encourage research into new 5-HT(1A) receptor ligands, which will improve efficacy and/or ameliorate adverse reactions in the treatment of Parkinson's disease.
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PMID:Improving the Treatment of Parkinson's Disease: A Novel Approach by Modulating 5-HT(1A) Receptors. 2342 44

We report the case of a mother and two children who shared a mitochondrial DNA A3243G mutation. The mother had diabetes mellitus, neurogenic bladder, bradykinesia, dystonia, and slowly progressive cerebellar ataxia. Her two daughters were diagnosed with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes at adolescence. They all presented with gastrointestinal symptoms at an advanced clinical stage. They were diagnosed with chronic intestinal pseudo-obstruction, and they were resistant to therapy. The mother and her youngest daughter died from aspiration pneumonia because of vomiting. The determination of chronic intestinal pseudo-obstruction is an important prognostic factor in patients with the mitochondrial DNA A3243G variant.
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PMID:Familial Pernicious Chronic Intestinal Pseudo-obstruction with a Mitochondrial DNA A3243G Mutation. 2915 41


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