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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

An oral liquid form of ivermectin was administered to 14 purebred Collies (12 rough coated, 2 smooth coated). All Collies were given ivermectin at dosages of 100 and then 200 micrograms/kg of body weight. Three of the dogs developed mild clinical signs of toxicosis (salivation, vomiting, confusion, ataxia, and tremors) with the 100 micrograms/kg dosage. After the 200 micrograms/kg dosage, 7 dogs (including 1 smooth-coated Collie) developed severe toxicosis (seizure-like activity, recumbency, nonresponsiveness, and coma). Because dogs that developed severe toxicosis were not retreated, only the 7 remaining dogs were given ivermectin at 600 micrograms/kg. Severe toxic signs were not observed in the dogs given the 600 micrograms/kg dosage, and only 1 of these 7 dogs developed severe toxicosis when given ivermectin at 2,500 micrograms/kg. Dogs that developed severe toxicosis were given supportive care while in the comatose state. All dogs recovered completely. The results indicated that Collies (including the smooth-coated Collies) have a wide range of sensitivity to ivermectin-induced toxicosis.
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PMID:Clinical observations in collies given ivermectin orally. 359 67

A three-year-old boy with a progressive history of headache, vomiting and ataxia in the course of 2 months, was admitted on August 1983, when he was lethargic. Neurological examination revealed dysphagia, scanning speech and tremor in the bilateral hand. CT scan showed a very large enhanced mass in the center of posterior fossa with central necrosis in it and the dilatation of whole ventricular system. Suboccipital craniectomy was immediately performed and the tumor that occupied the vermis and invaded into both cerebellar hemisphere was subtotally removed. Postoperative irradiation was well performed: 4140 rads to the whole brain and 3162 rads to the spinal cord. However, 5 months later, facial palsy in the left side and progressive ataxia became prominent. CT scan showed multiple enhanced masses in the left trigonum and right anterior horn of the lateral ventricles and in the left cerebellopontine angle. In spite of chemotherapy, the patient had a down-hill course, especially after the ventricular hemorrhage, and died on June 9th, 1984. Histologically, the tumor had a lobulated appearance with an aggregation of tumor cells encircled by vascular septae. The cells within lobules generally had vesicular nuclei, which were arranged in parallel row. Occasionally smaller hyperchromatic cells with scant cytoplasm were present along the vascular septae. Reticulin was present within the septa, but was not observed within the lobules. Scattered astrocytic cells and processes were identified within the lobules by the immunoperoxidase technique for GFAP. The fibrillary cytoplasmic processes within the lobules were stained by immunoperoxidase technique for neurofilament (68K).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cerebellar neuroblastoma]. 361 40

Reaction to rapid intravenous administration (RIA) of rifampicin in a dose of 10 mg/kg was studied on 173 healthy dogs. Immediately after the first RIA of rifampicin there were observed vomiting and ataxia of various levels in 5.2 per cent of the animals. After the drug administration their arterial pressure (AP) lowered to 50-60 mm Hg. By the 9th-11th minute it restored to the initial level. A collapse-like condition was recorded immediately after rifampicin RIA in 2.3 per cent of the dogs with marked decreasing of their AP up to 15-20 mm Hg. Its restoration to the initial level was slow and required 35-40 min. It was noted that after the third consecutive RIA of rifampicin the observed reaction disappeared. Probably this was due to adaptation of the host to rifampicin intravenous injections. Mezaton is an efficient agent rapidly arresting the reaction within 1-3 min.
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PMID:[Complications and their elimination during the rapid intravenous administration of rifampicin in an experiment]. 367 42

Appropriate use of carbamazepine for the treatment of epilepsy is based on correct identification of the patient's seizure type. Carbamazepine is effective against partial seizures and against generalized tonic clonic seizures. Therapy should begin gradually, with initial doses increased slowly over 1 or 2 weeks, as tolerated. Side effects include fatigue, dizziness, ataxia, double vision, nausea, and vomiting. Most practitioners agree that, because of carbamazepine's relatively short half-life, the total dosage should be administered in at least two divided doses. This avoids too high a peak blood level that would occur with a single dose. Carbamazepine therapy is associated with the development of two hematologic conditions. Leukopenia, which may be transient or persistent, requires careful monitoring but is not cause for immediate discontinuation of therapy. Aplastic anemia occurs rarely but is potentially fatal, and therefore diligent monitoring of hematologic function is indicated. Aplastic anemia is an idiosyncratic, non-dose-related side effect that is most likely to occur within the first 3 or 4 months of initiating therapy. Once seizures are controlled, plasma levels of carbamazepine should be measured to establish optimum levels for individual patients being treated with this drug.
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PMID:How to initiate and maintain carbamazepine therapy in children and adults. 369 21

The effect on behavior of eight anticholinergic agents: atropine, scopolamine, trihexyphenidyl, biperiden, homatropine, eucatropine, hexocyclium and propantheline, injected into the cerebral ventricle (ICV) of the cat was investigated and compared. The anticholinergic agents evoked: (1) psychomotor stimulation such as miaowing, loud calling, restlessness, impelling locomotion, jumping, vacant staring, apprehension and loss of interest of the surroundings; (2) aggression, hissing, threat, attack, defense, fighting with paws and flight; (3) autonomic responses including mydriasis, tachypnea, dyspnea, licking, vomiting, salivation, micturition and defection; and (4) motor phenomena comprising scratching, ataxia, rigidity, tremor, weakness with adynamia or myoclonic jerks. Convulsions appeared only after ICV injections of atropine and homatropine. The most characteristic behavioral effect of anticholinergic agents was psychomotor stimulation accompanied by mild aggressive responses. The only exception was propantheline which caused a muscular weakness and adynamia. Atropine and scopolamine alone induced a dose-dependent impelling locomotion as well as fighting behavior. Carbachol and eserine injected intracerebroventricularly reversed the locomotion autonomic and motor phenomena produced by anticholinergic agents administered similarly. It is suggested that anticholinergic agents acting as partial agonists, can produce their behavioral effects through central cholinoceptive sites.
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PMID:Comparative behavioral effects of anticholinergic agents in cats: psychomotor stimulation and aggression. 370 93

We report the case of a Mexican man who suddenly developed severe occipital headache, vomiting, vertigo, and ataxia. Neurologic examination showed nystagmus and cerebellar findings. Computed tomography of the brain demonstrated a large left cerebellar cystic lesion consistent with the diagnosis of cysticercosis. The patient was treated with dexamethasone and praziquantel and required surgical removal of the lesion to prevent herniation. He recovered without neurologic sequelae. The abrupt onset of cerebellar findings is an unusual presentation of this disease. Central nervous system cysticercosis is being recognized with increasing frequency in the United States, where it is found primarily in Hispanic and Asian immigrants. The literature of central nervous system cysticercosis is reviewed and the pathogenesis, clinical presentation, and therapy are discussed.
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PMID:Central nervous system cysticercosis simulating an acute cerebellar hemorrhage. 372 11

Acute spontaneous cerebellar hemorrhage presenting with ataxia, dysarthria, vomiting, dizziness, and coma is commonly the result of hypertension. Early diagnosis is possible, and appropriate treatment, if timely executed, may be lifesaving.
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PMID:Acute spontaneous cerebellar hemorrhage. 373 46

Among 100 childhood brain tumors treated at Kobe Children's Hospital from May 1970 to June 1985, 18 of the children presented with symptoms during the first year of life. This paper analyzes these 18 cases. Supratentorial tumors (78%) were more common than infratentorial ones, and 67% of all the tumors were located in the central neural axis. Initial symptoms were cranial enlargement (56%), vomiting (17%), cranial deformity (11%), blepharoptosis, respiratory distress, and ataxia. Histological diagnosis of the tumors was as follows: teratoma (3 cases), medulloblastoma (3), glioblastoma (2), astrocytoma (2), ependymoma (2), craniopharyngioma (1), choroid plexus papilloma (1), hamartoma (1), lipoma (1), melanotic progonoma (1), and an undetermined type, probably medulloblastoma (1). Seventeen of the patients underwent craniotomy for tumor resection (4 total, 4 subtotal and 7 partial removal, and 2 biopsies). Additional therapeutic methods used separately and in various combinations included ventriculoperitoneal shunt, subduralperitoneal shunt, ventricular drainage, radiotherapy and chemotherapy. Nine patients died (average 98 days) after surgery. Of the 9 survivors, 6 are still alive after more than 5 years. Five of the 6 are mentally retarded and 4 are physically handicapped to some degree.
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PMID:Intracranial tumors in the first year of life. 377 67

The authors report a case of erythromycin-induced carbamazepine toxicity in a 6-year-old child following use of erythromycin ethylsuccinate (50 mg/kg/day). Within 5 days of erythromycin use, vomiting, weakness, lethargy, ataxia, nystagmus, and cogwheeling movements developed. A serum carbamazepine concentration had increased from 11.9 mg/L (measured 1 week prior to antibiotic use) to 25.8 mg/L. Following erythromycin withdrawal, serum concentrations returned toward baseline, and symptoms resolved. Erythromycin has known effects on hepatic enzyme function, with altered cytochrome P-450 function. The dramatic reduction in carbamazepine clearance observed in this patient is similar to that reported when erythromycin is used concurrently with other drugs. A brief review of potentially significant erythromycin drug interactions is presented.
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PMID:Erythromycin-induced drug interactions. An illustrative case and review of the literature. 381 8


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