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)

In 12 rhesus monkeys the injection of alumina cream into the temporal cortex, amygdala or hippocampus induced seizures after a latent period of six weeks to three months. Clinically the attacks are characterized by an arrest of movement, staring, unresponsiveness to most stimuli, wandering conjugate eye movements, automatisms, twitching of the contraleteral ear and less commonly commonly vocalization, chewing, hiccoughing, vomiting, adversive head movements and twitching of the face. The spiking from the amygdala and hippocampus, which usually fire together, propagates to the temporal cortex and multiple subcortical structures including the hypothalamus, anterior perforated space, anteromedial thalamus, cingulate gyrus, putamen, globus pallidus, subthalamus and mesencephalic reticular formation; from the temporal cortex to the amygdala and hippocampus, and secondarily to the diencephalic centers. There is a fairly consistent sequence of preferential propagation. Although there are some differences in the occurrences of clinical manifestations depending upon the sites of the focus, no specific structural correlation with clinical manifestations could be established. This experimental condition may provide a proper model for the study of clinical psychomotor epilipsy.
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PMID:Experimental studies on the pathogensis of temporal lobe epilepsy. 82 23

The clinical features and management of nine cases of mushroom poisoning due to Amanita pantherina (eight cases) and Amanita muscaria (one case) admitted to a children's hospital are described. Most ingestions were in the toddler age group with males being more frequently involved. Symptoms occurred between 30-180 min with the onset of central nervous system depression, ataxia, waxing and waning obtundation, hallucinations, intermittent hysteria or hyperkinetic behavior. Vomiting was rare. Seizures or myoclonic twitching occurred in 4/9 patients, but was controlled with standard anticonvulsant therapy. No other anticholinergic or cholinergic signs were prominent. Recovery was rapid and complete in all patients.
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PMID:Mushroom poisoning in infants and children: the Amanita pantherina/muscaria group. 134 20

A combination of metoclopramide, dexamethasone, droperidol, lorazepam, and diphenhydramine was used in prophylaxis of high-dose (greater than or equal to 100 mg/m2) or moderate dose (greater than or equal to 50 mg/m2) cisplatin. Sixty minutes prior to starting cisplatin, 16 mg dexamethasone, 50 mg diphenhydramine, and 0.5 mg lorazepam were given orally (PO). Droperidol 1 mg was given intramuscularly (IM) 15 minutes prior to beginning cisplatin. Repetitive doses of intravenous (IV) metoclopramide, 2 mg/kg in 75 ml 5% dextrose in water over 15 minutes was given 30 minutes prior to, and at 1 1/2, 4 1/2, and 7 1/2 hours after beginning cisplatin chemotherapy. Only patients with nausea and/or vomiting received subsequent doses of 2 mg/kg metoclopramide IV every 3 hours as needed. Patients refractory to metoclopramide were given 1 mg droperidol IM and 50 mg of diphenhydramine PO every 6 hours. There were 19 men and 9 women with a median age of 58 (range 31-75) years. Complete protection from nausea and vomiting in all courses of treatment occurred in 17 (61%) patients. In 63% and 70% of the 57 evaluable courses, there was neither nausea nor vomiting, during the first 24 hours after cisplatin. When present, nausea was mild and the median number of vomiting episodes was 2 (range 1-3). This antiemetic regimen was well tolerated. Toxicities were mild and occurred in 3 patients (angioneurotic edema, transient episode of facial twitching, and heaviness of tongue, respectively). The 5-drug antiemetic combination can prevent cisplatin-induced nausea and vomiting in a majority of patients.
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PMID:Five-drug antiemetic combination for cisplatin chemotherapy. 158 29

We assessed the antiemetic efficacy and safety of three different oral doses of ondansetron (GR 38032F), a novel serotonin type-3 receptor antagonist, in three consecutive series of 20 breast cancer patients receiving cyclophosphamide-doxorubicin-based chemotherapy for the first time. Patients received oral doses of 8 mg, 4 mg, or 1 mg of ondansetron three times daily for 2 days, with the first dose given 30 minutes before the cyclophosphamide infusion. We then evaluated the efficacy of a conventional antiemetic regimen of intravenous lorazepam, metoclopramide, and diphenhydramine given before chemotherapy and 10 mg prochlorperazine given orally twice on study day 1 and three times on study day 2 in a fourth series of 20 patients with comparable characteristics. The number of emetic episodes, assessment of nausea and appetite, and adverse events were recorded throughout the 2-day study period. Pretreatment and posttreatment clinical laboratory data were also collected. No emesis was observed during the 2-day study period in 17 (85%), 13 (65%), and 11 (55%) patients treated with 8-mg, 4-mg, and 1-mg ondansetron doses, respectively, and in seven (35%) patients who received conventional therapy. The incidence and intensity of nausea were lower with increasing doses of ondansetron and were lower than in the conventional group. Ondansetron-related side effects were generally mild and reversible and did not appear to increase in a dose-dependent manner. These effects included headache, stomach cramps, diarrhea, fatigue, and elevated serum transaminase concentrations. One patient who received three 1 mg doses of ondansetron experienced tremors and muscle twitching. Oral ondansetron is an effective and safe antiemetic for patients receiving noncisplatin cyclophosphamide-doxorubicin-based chemotherapy, and its antiemetic activity appears to be dose-related.
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PMID:Evaluation of three oral dosages of ondansetron in the prevention of nausea and emesis associated with cyclophosphamide-doxorubicin chemotherapy. 182 99

The sedative effects of medetomidine at doses of 20 and 40 micrograms/kg im given alone or followed 16-18 min later by fentanyl (2 micrograms/kg iv) was investigated in 6 bitches of mixed breeds. The higher dose of medetomidine alone caused the greater degree of sedation, but two bitches were only lightly sedated with either dose. Side effects noted in some cases included apparent pain on injection, vomiting on induction of sedation, bradycardia, slowing of respiratory rate, cyanosis and muscular twitching. The intravenous injection of fentanyl caused a marked increase in depth of sedation in all animals, inducing a condition similar to neuroleptanaesthesia in which the eyes were rotated downward and the pedal reflex abolished. Slight twitching and sensitivity to sound occurred immediately after fentanyl injection, but this was transient. The cardiopulmonary effects of medetomidine (40 micrograms/kg im) followed 20 min later by either fentanyl (2 micrograms/kg iv) or a saline placebo were investigated in 4 beagle dogs. Medetomidine caused bradycardia, hypotension and reduced respiratory rate, inducing an intermittent respiratory pattern. The iv injection of fentanyl did not further alter the heart or respiratory rate or blood pressure. However there was a small but significant decrease in arterial oxygen tension and rise in arterial carbon dioxide tension. indicating some respiratory depression. We conclude that the use of intravenous fentanyl to dogs already sedated with medetomidine could prove useful in clinical cases where the initial sedation with medetomidine has proved inadequate.
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PMID:The use of medetomidine/fentanyl combinations in dogs. 257 Dec 71

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

It is well known that vitamin K deficiency is an important cause of the spontaneous intracranial hemorrhage in infancy. A 60-day-old male infant with spontaneous intracerebral hematomas due to vitamin K deficiency was presented. He was breast-fed. He had been medicated oral antibiotic agent for diarrhea and fever. Three days later he developed petechien, vomiting and twitching, and became drowsy. The blood studies showed anemia, and advance of ESR. He was administered of vitamin K immediately. CT scan was showed four intracerebral hematomas with niveau, which were surrounded by high-density rings. The ring-like figures were unique for this case. The reason may be next, we think. Under the states in which blood can separate easily with advance of ESR, blood clot would adhere to the wall of the hematomas. So these hematomas showed ring-like figures and had niveau in them. CT scan of this case was also interesting because there was little deviation in spite of the big hematomas. The reason of this may be that the brain of infancy is incomplete in myelination and contains much water, and that the possibility of bleeding due to vitamin K occurs slowly. We examined 84 cases of intracranial hemorrhage due to vitamin K deficiency from literatures, and they were all identified for the hemorrhage sites by CT scan. Subarachnoidal hemorrhage was in 72 cases (85.7%), subdural hemorrhage was in 41 cases (48.8%), intracerebral hematomas was in 36 cases (42.9%) and intraventricular hemorrhage was in 9 cases (10.7%). In 52 cases the CT findings were described.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intracranial hemorrhage in infancy due to vitamin K deficiency: report of a case with multiple intracerebral hematomas with ring-like high density figures]. 382 41

A 68-year-old woman with a history of mild hypertension developed a toxic encephalopathy following myelography with metrizamide. Concomitant with the symptoms of vomiting, headache, muscle twitching, and hallucinations was a sudden and marked increase in arterial pressure. Treatment with parenteral vasodilators caused a partial, but transient lowering of the blood pressure. The mental status abnormalities were resolved by treatment with parenteral lorazempam and, subsequently, the blood pressure returned to the premyelography levels. This report demonstrates that metrizamide can induce a severe, accelerated form of hypertension.
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PMID:Accelerated hypertension associated with the central nervous system toxicity of metrizamide. 394 59

The authors present the results of own investigations on the occurrence of side effects following myelography with the contrast medium Amipaque administered usually by the lumbar route. Sixty patients aged 21-65 years with various diseases of the spinal cord and cauda equina were studied. Clinical and myelographic investigations were performed before and after myelography. In 6 out of 60 cases (10%) transient neurological disturbances developed including epileptic seizures, speech disturbances of the type of aphasia and dysartria, visual disturbances and twitching of lower extremities. Other symptoms and signs included: headaches, vomiting, collapse. One patient with cardiorespiratory failure died hours after myelography with evidence of increased symptoms of cardiorespiratory failure. EEG changes appeared after myelography in 2/3 of cases and persisted for up to 12 days. The authors call attention to the high proportion of neurological complications and EEG changes which must be taken into account when indications to myelography are considered. Particular caution is necessary in cases with coexistent cardiorespiratory failure.
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PMID:[Clinical and electroencephalographic signs of side effects in patients after myelography using "amipaque"]. 404

Vomiting, ear twitching and panting produced by either nicotine or dimethylphenylpiperazinium (DMPP) administered intracerebroventricularly (ICV) to the unanesthetized cat were studied and compared. On a molar basis, nicotine evoked stronger effects overall in terms of the three responses studied, but the DMPP-induced vomiting and ear twitching responses, while weaker, were of longer duration. No significant differences were found in the duration of panting evoked by these nicotinic agonists. The nicotinic blocker hexamethonium injected ICV abolished the vomiting and ear twitching caused by either ICV nicotine or ICV DMPP, but vomiting and ear twitching persisted following the ICV administration of the muscarinic blocker, atropine. Both hexamethonium and atropine depressed or abolished the panting response evoked by either ICV nicotine or ICV DMPP. In cats with ablations of the area postrema, nicotine and DMPP injected ICV did not produce the vomiting response, but ear twitching and panting still occurred. It is concluded that the ICV injection of nicotine or DMPP evoked vomiting and ear twitching in the cat by way of an action on the central nicotinic receptors. However, panting produced by these nicotine agonists is mediated by the mimicking action of acetylcholine on central receptors having mixed nicotinic and muscarinic properties.
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PMID:Central nicotinic receptors: vomiting, ear twitching and panting. 613 55


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