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

8-Chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazol[1,5-a][1,4]benzodiazepine (midazolam maleate, Ro 21-3981, Dormicum) or thiopental were administered to 99 women undergoing short gynecological surgical procedures for induction and maintenance of anesthesia along with 67% nitrous oxide. Either fentanyl 1.5 microgram kg-1 or a saline placebo were given i.v. as acute premedication 5 min before induction. We measured the quality of induction and maintenance. Induction was more rapid after thiopental but thiopental produced more apnea especially when combined with fentanyl. Fentanyl premedication reduced the dose of hypnotics necessary to keep patients asleep. It was difficult to keep patients from moving during the procedure when only the hypnotics and nitrous oxide were used, so the use of these drugs for both induction and maintenance is recommended only when combined with narcotics or other analgesics. Although recovery after midazolam was slower than after thiopental, it was without untoward reactions such as hallucinations or excitement. Vomiting was less frequent after midazolam. Midazolam produced a profound period of amnesia for 1-2 h, so important instructions could not be given to patients during this time. All patients were awake enough to discharge from the hospital 200 min after the last dose of hypnotic was given. We would recommend a combination of midazolam, fentanyl and nitrous oxide for induction and maintenance of anesthesia for short surgical procedures except when a rapid induction is desired, then thiopental is preferred as the hypnotic.
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PMID:Awakening characteristics following anesthesia induction with midazolam for short surgical procedures. 719 31

Early reports on space exploration suggested that cosmonauts and astronauts sustained "motion sickness" symptoms described as "dizziness, nausea, vomiting, flashes of light, formed hallucinations or illusions of inversion of image in space." Hallucinations may be due to many causes but most of the above symptoms were similar to those experienced by some patients with expanding intracranial lesions whose symptomatology was referable to the temporoparieto-occipital cortex of the brain. On the basis of our observations, it is suggested that the term "motion sickness" might be applied to earthly symptoms of dizziness, nausea, and vomiting--such as encountered ascending in an elevator or tossing about on the sea--for they are primarily related to the inner ear, the peripheral or end organ. However, when inversion of body image and formed and unformed visual hallucinations are superimposed upon these, there must be interpretation by the temporoparieto-occipital cortex and this might be designed as "motion sickness in space."
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PMID:Motion sickness: part I--a theory. 736 50

Three patients who had large, benign cerebellar tumors were operated upon in the sitting position and developed symptoms referable to the temporoparieto-occipital region of the brain 24-48 h postoperatively. They consisted of dizziness, nausea, vomiting, formed and unformed hallucinations, and inversion of image or disorientation in space, some of which were experienced by some of the astronauts and cosmonauts during space flight. Such findings are not due to stimulation of the cerebellum, the site of the lesion, but must come from the cerebral hemisphere. The symptoms were believed to be caused by "the luxury perfusion" of Lassen with the development of local lactic acidosis secondary to vascular insufficiency to the brain in the distribution of the posterior cerebral artery thus stimulating the temporoparieto-occipital region. This theory is suggested to some degree by the work of Endo et al. using CT scans, which showed the shifting of increased blood flow from the frontal region to the temporoparieto-occipital region following removal of a benign posterior fossa tumor. The mechanism for the compression of the posterior cerebral artery may be due to uncal herniation at the tentorium. The authors believe that it might be well to consider further testing in a vertical or oblique plane rather than only in a centrifugal horizontal one. This method would tend to cause uncal herniation more readily. Monitoring of such effects could be done with the colored CT scan.
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PMID:Motion sickness: part III--a clinical study based on surgery of posterior fossa tumors. 736 52

Your recent lead article on toxic shock and tampons (November 1, p. 1161) prompts me to report a case of pelvic infection and staphylococcal septicemia 8 days after the insertion of a Lippes loop. Pelvic infection is a recognized complication of IUDs; although there have been 2 reports of endocarditis occurring in susceptible patients following the insertion of an IUD, septicemia is rare. A previously healthy 31-year old married woman had a loop inserted at a family planning clinic. 3 days later she developed sweating, vomiting, confusion, and cough and during the following 48 hours became disoriented with hallucinations. She was referred to the hospital with suspected encephalitis and on admission was febrile (38.8 degrees Celsius) and stuporose but responded to simple commands. Blood pressure was 95/60 mmHg but there were no other abnormal signs. Hemoglobin was 12.2 g/dl, white blood count 4.0x109/1 (80% neutrophils), erythrocyte sedimentation rate 70mm in the 1st hour; cerebrospinal fluid normal. Chest x-ray examination revealed patchy consolidation in the upper lobes of both lungs and an electroencephalogram showed bilateral nonspecific abnormality. 3 blood cultures taken on admission yielded penicillin-resistant Staphylococcus aureus. She was treated with high-dose intravenous cloxacillin and 24 hours after starting the antibiotic had improved markedly and the IUD was removed. Culture from the coil and also from a high vaginal swab yielded Staph aureus with a similar antibiogram to that of the organism cultured from the blood. Subsequent recovery was uneventful, although repeat chest x-ray examination showed small abscess cavities in the upper lobes of both lungs. The patient was discharged 4 weeks after admission and serial chest radiographs have confirmed complete resolution of the pneumonia and abscesses. There is little doubt that this patients' septicemia with lung abscess formation and encephalopathy originated in the genital tract. The patient was both toxic and shocked but was different from patients with the recently described toxic shock syndrome in that her blood culture was positive for Staph aureus. The case provides another example of the importance of this organism as a cause of infection associated with the insertion of foreign bodies into or through the vagina.
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PMID:Staphylococcal septicaemia after insertion of an intrauterine contraceptive device. 744 49

Dextrorphan HCl (Ro 01-6794/706) is an NMDA receptor antagonist with clinical potential for administration in an elderly population of acute ischemic stroke patients. In vivo experience with such patients demonstrated a consistent pharmacologic effect/adverse experience profile that is typical of an NMDA receptor antagonist (e.g., nystagmus, nausea, vomiting, agitation, somnolence, hallucinations and hypertension). For the most part, these pharmacologic effects were mild to moderate in severity; short-lived; reversible; not life-threatening and subjectively tolerated. The most serious pharmacologic effect produced by dextrorphan administration was hypotension, which occurred within a well-defined window of 90 minutes from the start of the loading dose infusion in patients who received 200 mg/hr or greater loading dose infusions. In all cases it was reversible without neurologic sequelae. Careful review of demographic and pharmacokinetic parameters did not demonstrate any overriding factor(s) to the production of hypotension other than the rate of the loading dose infusion. Severe hypotension, severe decreased levels of consciousness and respiratory depression should not be generally expected at loading doses less than 200 mg/hr. In summary, dextrorphan can be safely given to an elderly population of ischemic stroke patients as a loading dose rate below 200 mg/hr and as a maintenance dose rate between 50-90 mg/hr for 24 hours when patients are monitored carefully for pharmacologic effects.
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PMID:Safety, tolerability and pharmacokinetics of the N-methyl-D-aspartate antagonist Ro-01-6794/706 in patients with acute ischemic stroke. The Dextrorphan Study Group and Hoffmann-La Roche. 748 11

The diagnosis, evaluation and assessment, supportive care, and pharmacologic treatment of acute alcohol withdrawal are reviewed. Patients in alcohol withdrawal have decreased or stopped their heavy, prolonged ingestion of alcohol and have subsequently begun to have at least two of the following symptoms: autonomic hyperactivity, tremor, nausea or vomiting, hallucinations, psychomotor agitation, anxiety, and grand mal seizures. Evaluation of the patient at risk for alcohol withdrawal should include a complete history and physical examination; laboratory tests are often indicated. The patient's progress should be assessed before, during, and after therapy, preferably with a validated instrument. After the initial evaluation and assessment but before the administration of dextrose-containing solutions, a 100-mg dose of thiamine hydrochloride should be given by i.m. or i.v. injection. Routine supplementation with calcium, magnesium, and phosphate is questionable. The need for fluid and electrolyte administration varies depending on losses. Most patients in alcohol withdrawal can be managed with supportive care alone, but for more severe or complicated withdrawal, pharmacologic therapy may be necessary. Benzodiazepines, especially diazepam and chlordiazepoxide, are the drugs of choice. Barbiturates, beta-blockers, and antipsychotics are generally not recommended as first-line therapy. Several drugs in other classes, including carbamazepine and clonidine, have been shown to be about as effective as benzodiazepines in a few studies, but the studies were small, the patients were usually in mild withdrawal, and validated instruments for assessing withdrawal were often not used. Some agents, such as beta-blockers, may play a role as adjuncts to, not replacements for, benzodiazepine therapy. For patients in alcohol withdrawal who do not respond to supportive care, benzodiazepines are the treatment of choice.
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PMID:Management of alcohol withdrawal. 762 38

The withdrawal of heterocyclic antidepressants and antipsychotic agents can produce nausea, emesis, anorexia, diarrhoea, rhinorrhoea, diaphoresis, myalgias, paraesthesias, anxiety, agitation, restlessness and insomnia. The withdrawal of monoamine oxidase (MAO) inhibitors may result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, cognitive impairment, delirium, suicidality and delusions of persecution. The withdrawal of antipsychotic agents may give rise to symptoms preceding the onset of psychosis. These potential harbingers of relapse include anxiety, agitation, restlessness and insomnia. The withdrawal phenomena reviewed are usually prevented by gradually reducing the total daily dosage of the pertinent drug. Antimuscarinic agents often alleviate the distress produced by the withdrawal of tricyclic antidepressants and antipsychotic agents. MAO inhibitor withdrawal syndromes may constitute medical emergencies. The prevention of the evolution of a MAO inhibitor withdrawal-precipitated syndrome is a high priority.
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PMID:Withdrawal phenomena associated with antidepressant and antipsychotic agents. 791 78

The approach to drug treatment of vertigo is almost exclusively symptomatic. There are 3 major goals for drug treatment of vertigo. The first one is to eliminate the hallucination of motion. Drugs with vestibular 'suppressant' properties are used for this purpose. The major vestibular suppressants are anticholinergic and antihistamine drugs. The second goal is to reduce the accompanying neurovegetative and psychoaffective signs (nausea, vomiting, anxiety). Antidopaminergics are used for this purpose. The third goal is to enhance the process of 'vestibular compensation' to allow the brain to find a new sensory equilibrium in spite of the vestibular lesion. Until now, the pharmacological manipulation of vestibular compensation has been assessed in animals but not in humans with vestibular lesions. Vestibular suppressant drugs delay rather than enhance compensation. A variety of other drugs is also used in the treatment of vertigo, including benzodiazepines, histaminergic agents, sympathomimetics and calcium antagonists. Their mechanism of action is poorly understood. The data base derived from clinical trials evaluating antivertigo medications is often questionable because of methodological limitations. This explains why habits of prescription are mainly empirical, and why striking differences can be noticed from one country to another. We can hope that new treatments may emerge from the present interest in receptor subclasses and neuromodulators of the vestibular system, and we must be ready to evaluate these potential new pharmacological agents with reliable clinical methods in humans.
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PMID:Antivertigo medications and drug-induced vertigo. A pharmacological review. 858 26

Alcohol withdrawal syndrome (AWS) may result in nausea, vomiting, diarrhea, weakness, sweating, tremors, tachycardia, hypertension, agitation, delirium, hallucinations, seizures, and death beginning 6 hours after alcohol cessation in alcoholics. Benzodiazepines are cross-tolerant with ethanol and are considered first-line therapy for treating AWS. Chlordiazepoxide and diazepam are first metabolized by hepatic oxidation, then glucuronidation. Lorazepam and oxazepam undergo only hepatic glucuronidation. Benzodiazepine oxidation is decreased in persons with liver disease and the elderly. Accumulation with resultant excessive sedation and respiratory depression may be significant when administering chlordiazepoxide or diazepam to patients with impaired oxidative metabolism. Lorazepam and oxazepam metabolism is minimally affected by age and liver disease. Chlordiazepoxide and diazepam are erratically absorbed by the intramuscular route. Lorazepam is predictably absorbed by the intramuscular route. Oxazepam is not available in parenteral form. Lorazepam appears to be the safest empiric choice among the various benzodiazepines for treating AWS in the elderly and in patients with liver disease, or those who require therapy by the intramuscular route.
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PMID:Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. 870 Jul 92

We report a rare case of relapsing polychondritis with an initial symptom of inner ear involvement. This 53-year-old Japanese man experienced a hearing difficulty, tinnitus in both ears, and dizziness of sudden onset, but lacked auricular chondritis at that time, which is the most frequent finding in relapsing polychondritis. Thus it was difficult to reach a correct diagnosis. Steroid therapy, with oral prednisolone 15 mg daily, was effective. Almost two months after we began the steroid therapy, the patient complained of losing interest in his work and reported a hallucination vision on the TV screen, so the dose of prednisolone was decreased to 10 mg. The hallucinations then disappeared, but the serum level of C-reactive protein increased highly. To reduce the dose of prednisolone, we tried low-dose oral methotrexate. However, we had to discontinue it when the patient experienced severe vomiting and diarrhoea. As adjuvant therapy, we then administered Sho-saiko-to, Chinese herbal medicines with few side effects. Symptoms and laboratory abnormalities then improved markedly.
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PMID:Relapsing polychondritis presented as inner ear involvement. 872 1


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