Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal studies have indicated a "vomiting center" situated in the dorsal portion of the lateral reticular formation of the medulla at the level of the dorsal nucleus of the vagus. There is also a chemoreceptor trigger zone in the floor of the fourth ventricle in the area postrema which influences the vomiting center. A 63 year old man with a three year history of metastatic malignant melanoma presented with nausea, projectile vomiting, gait ataxia and diplopia associated with horizontal and vertical nystagmus. CT scan showed a solitary brainstem metastasis without hydrocephalus and he was treated with radiotherapy with resolution of his vomiting after four weeks. At post mortem three months later a metastasis was found in the right middle cerebellar peduncle and lateral tegmentum of the pons; there was no pathological change in the area of the vomiting center or area postrema. It is postulated that this lesion caused projectile vomiting because of involvement of either afferent projections to the vomiting center. The neuroanatomy of vomiting is discussed.
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PMID:The neuroanatomy of vomiting in man: association of projectile vomiting with a solitary metastasis in the lateral tegmentum of the pons and the middle cerebellar peduncle. 407 83

A 46-year-old man developed sudden dysarthria and atactic gait and was noted to be unable to get up even on the bed about one year prior to his death. By following several days, he started to have scanning speech, nausea, trancal ataxia and dysmetria in succession. The cerebro-spinal fluid yielded moderate pleocytosis. There were no sensory disturbance, pathological reflexes and Romberg's sign. Half a year later, submandibular tumor was noted. The biopsy showed metastatic small cell undifferentiated carcinoma, presumably of pulmonary origin, and paraneoplastic cerebellar degeneration was suspected. He died of bronchopneumonia, superimposed on lung cancer on February 25 in 1979. The necropsy showed a large tumor in the right lung which was histologically verified small cell undifferentiated carcinoma (so-called oat-cell carcinoma). The cerebellum disclosed diffuse cortical atrophy, chiefly of Purkinje cell type. Moderate demyelination with reparative gliosis and foamy macrophages was seen in the white matter, which was considered secondary to cortical devastation. The morphometric study on Purkinje cell loss showed interesting distribution of the lesions. The severely affected portions were the central lobe and culmen in the vermis, and the ala lobuli centralis and quadrangular lobe in the hemisphere, respectively. The lingula was strikingly spared. The finding was compared with that of other cerebellar disease in reviewing the literature.
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PMID:[An autopsy case of carcinomatous subacute cerebellar degeneration--on distribution of cerebellar cortical lesions]. 609 6

Forty female out-patients undergoing therapeutic abortion participated in a double-blind study comparing flunitrazepam 0.05 mg . kg-1 with thiopentone 6.0 mg . kg-1 as induction agents for general anaesthesia. Induction time, as measured by the time to loss of lid reflex and voluntary speech, was not only significantly longer in patients receiving flunitrazepam, but also much more variable and imprecise than with thiopentone. The Steward recovery room scores and psychomotor drawing test results revealed that recovery was significantly slower in the flunitrazepam group. Anterograde amnesia was observed in all patients who had received flunitrazepam and in one patient who had received thiopentone. No retrograde amnesia was found in either group. Flunitrazepam produced postoperative drowsiness, sedation, ataxia and nausea while with thiopentone discomfort from surgery and discomfort at the intravenous injection site were the main complaints. Because of the slowness of induction with flunitrazepam and marked individual variation, we do not feel that this drug can be considered a suitable agent for routine induction of general anaesthesia.
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PMID:Comparison of flunitrazepam and thiopentone for induction of general anaesthesia. 610 7

When a patient with a peripheral monocular paresis is forced to look with the paretic eye, head movements induce the sensation of an unstable visual world. The patient behaves as if he had acute bilateral labyrinthine lesions. These symptoms are due to the lack of compensatory ocular movement and the patients complain that the visual objects move in the direction opposite to the head. The patients develop ataxia, nausea, vomiting and past pointing. The symptoms, however, are transient and consistently disappear after approximately 48 hours. The central adaptation to looking and seeing with the paralysed eye is associated with a plastic change of the VOR. This plastic adaptation is probably induced by the large retinal slip produced by the lack of compensatory movement of the eye and can be studied in the normally mobile eye in the dark. The psychophysical adaptation is probably generated by an efferent copy or corollary discharge of the vestibular system to the visual system that cancels the retinal error.
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PMID:Looking with a paralysed eye: adaptive plasticity of the vestibulo-ocular reflex. 647 Jul 22

A report is given on 113 tumours of the 4th ventricle in children (up to the age of 18 years) observed among a total of 1028 cerebellar operations. Of these, 87 (= 77%) tumours were exclusively tumours of the 4th ventricle, in 26 cases the tumour also encroached on adjacent structures (cerebellar hemisphere and vermis, pons and Medulla oblongata). Medulloblastomas were predominant (55%), they mainly occurred in school age. Leading clinical symptom of the tumours of the 4th ventricle - especially in child age - is the increase in intracranial pressure which can often be demonstrated radiologically in this age group. Besides there are coordination disturbances and disturbances of the cerebral nerves; relatively frequently one sees a "vermis syndrome". The initial symptoms, which are in most cases non-characteristic (nausea, headache, also ataxia), are more often than not misinterpreted. Surgically treatment aims at a radical removal of the tumour whenever of possible, which is frequently problematic in children, and the restoration of the pathways the cerebrospinal fluid. Microsurgical techniques clearly contributed to a decrease in the mortality rate which, however, still is very high. This stresses the importance of an improvement of early recognition of these tumours.
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PMID:[Special diagnostic and surgical problems in tumors of the 4th ventricle in childhood]. 663 59

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.
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PMID:Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation. 663 51

We report four cases of carbamazepine toxicity in children associated with the concurrent administration of erythromycin. They all developed clinical toxicity (ataxia, dizziness, nausea, and vomiting) when erythromycin administration was begun; symptoms disappeared after erythromycin was discontinued. Serum carbamazepine levels were measured before, during, and, in most cases, after the toxic episodes. In all cases, there was a sharp increase in carbamazepine concentration after erythromycin therapy was begun and a rapid fall once erythromycin was discontinued. Our data support the previous suggestion that erythromycin interferes with the liver microsomal metabolism of carbamazepine with a subsequent increase in blood levels of the drug.
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PMID:Carbamazepine--erythromycin interaction leading to carbamazepine toxicity in four epileptic children. 665 14

A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3-4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.
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PMID:Acute trazodone poisoning: clinical signs and plasma concentrations. 671 57

Eight psychiatric patients with tardive dyskinesia (TD) were treated with single doses of the synthetic met-enkephalin analogue FK 33-824 (1, 2, and 3 mg IM) morphine (10 mg SC) and naloxone, an opiate receptor antagonist (0.8 mg IM). The drug effects were assessed by blind evaluation of randomly sequenced videotapes made before and during treatment. FK 33-824 (1, 2, and 3 mg IM) slightly reduced TD (P < 0.05) and increased preexisting bradykinesia. The effect on TD, however, was pronounced only in patients concurrently treated with neuroleptics in relatively high doses. Morphine had a similar although weaker antihyperkinetic effect, whereas naloxone had no effect. Side effects of FK 33-824 included dizziness, heaviness in the extremities, slurred speech, and dryness of mouth. Morphine caused drowsiness, dizziness, ataxia, and nausea, and naloxone had no side effects. The results do not point to a primary role of enkephalin in the pathophysiology of TD, but enkephalin may interact with dopamine functions and potentiate some of the effects of neuroleptic drugs.
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PMID:Enkephalin, morphine, and naloxone in tardive dyskinesia. 677 5

Acivicin, an L-glutamine antagonist, was administered to 37 evaluable patients with refractory advanced solid tumors in a phase I trial. A total of 67 evaluable 72-hr iv infusions were given at 3- to 4-week intervals. Doses ranged from 3.0 to 90 mg/m2/course. Reversible CNS toxicity was dose-limiting and included lethargy, somnolence, anxiety, hallucinations, and paranoid psychoses. Four of five patients experienced unacceptable CNS toxicity at 90 mg/m2. Three of eight patients experienced reversible diaphoresis and chills without fever at 75 mg/m2, and two had dizziness and ataxia. Hematopoietic toxicity, nausea, emesis, and diarrhea were mild and dose-related. One patient developed a blue-green discoloration of the infusion arm. Serial plasma and urine specimens from 13 patients were assayed for acivicin using a microbiologic method. Peak plasma levels at the end of the 72-hr infusions correlated with dose and ranged from 0.09 to 1.10 microgram/ml. When data from six patients were fitted to a two-compartment open model, alpha-half-life ranged from 1.1 to 63 mins, while beta-half-life ranged fro 338 to 629 mins. Renal clearance ranged from 6 to 24 mL/min, and nonrenal clearance accounted for 58%-83% of the total drug clearance. CNS toxicity correlated with plasma acivicin levels which exceeded 0.9 microgram/ml for greater than 16 hrs, but not with peak plasma levels or with the integrals of the concentration x time curves. Minor responses were seen in one patient with melanoma, in one with epidermoid pulmonary carcinoma, and in two with colon carcinoma. A starting dose of 60 mg/m2/course was recommended for phase II trials, with possible escalation to 75 mg/m2 in the second course if the drug was well-tolerated.
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PMID:Phase I trial and pharmacokinetics of acivicin administered by 72-hour infusion. 687 83


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