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)

Signs of a central nervous system disorder were observed following 2 instances of accidental ingestion of glucocorticoid in a young female Doberman Pinscher. The signs included transient aggressive and paranoid behavior, amaurosis, disorientation, ataxia with circling backward, and depression. Vomiting, weight loss, and abnormal drinking behavior persisted for several weeks following recovery from the acute illness.
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PMID:Central nervous system depression associated with glucocorticoid ingestion in a dog. 56 44

Three case histories of patients with large tumors in the posterior fossa who were operated on in a sitting position subsequently developed 1 or more symptoms referable to the temporoparietooccipital regions of the brain 24 to 48 hours postoperatively. Initially, it was believed that such symptoms were due to a stimulation of the association pathways causing firing of remote association areas (See Ch. 4). Subsequent studies of the rotation of blood vessels of the brain in the developing embryo and a review of the anatomical location of the arteries supplying the temporoparietooccipital region led to the conclusion that some compromise of the posterior cerebral artery was responsible for the symptoms. The symptomatology in these brain tumor patients was not unlike that seen in the cosmonauts and astronauts in space flight, designated as "motion sickness" in the space literature. A suggestion was made as to clarification of the definitions. This author advocated that the term "motion sickness" be confined to those symptoms of dizziness, nausea, and vomiting, due to involvement of the peripheral end organ, the inner ear. "Space sickness" might include these symptoms but also might have the addition of disorientation or the inversion of image in space and formed or unformed hallucinations. These relate to the temporoparietooccipital area, the midtemporal, and the occipital regions. In such instances, there must be central involvement or a stimulation of this interpretive cortex of the brain. The remote symptoms from the supratentorial cotex were believed to be due to hypoxia related to the posterior cerebral artery compromise, resulting in delayed "luxury perfusion" and the development of local lactic acidosis. Transaxial transmission of force with an uncal tentorial herniation causing compression of the posterior cerebral artery was suggested as a mechanism responsible for the vascular compression.
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PMID:Remote cerebral hemisphere symptoms from surgically treated patients with posterior fossa brain tumors; vascular factors: a basis for a theory concerning space sickness. 56 32

As a causative factor in spontaneous subarachnoid hemorrhage, vascular anomalies, especially aneurysm or arteriovenous malformation, have been generally recognized. On the other hand, subarachnoid hemorrhage from brain tumor and cryptic vascular malformation are rare. We experienced two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma as an initial symptom. Case 1: A 48-year-old woman, who complained of severe headache and vomiting on Feb. 10th, 1972, gradually became lethargic. Lumbar puncture revealed moderately hemorrhagic C.S.F.. On the fifth day after the onset, she was admitted to our hospital. On admission she showed disorientation and disturbance of resent memory. Aphasia and agnosia were slightly observed. On ophthalmologic examination right homonymous lower quadrant hemianopsia was observed. The carotid angiogram showed slight square shift of the anterior cerebral artery to the right side, elevation of the middle serebral artery and a homogeneous tumor stain in the occipital region in capillary phase. A walnut sized tumor invading the middle portion of the left lateral sinus and showing firm adhesion to the tentrium was found. There was an intracerebral hematoma behined the tumor. The tumor, the tentrium and the lateral sinus were extirpated en bloc and the intracerebral hematoma was aspirated. Histologically, the tumor was angioblastic meningioma. Case 2: A 7-year-old boy, who complained of severe abrupt headache, nuchal pain and vomiting on Sept. 17th, 1972, became gradually lethargic. Lumbar puncture revealed hemorrhagic C.S.F., On the tenth day after the onset, he was admitted to our hospital. He showed confusion and agitation. The carotid angiogram showed an unrolling of the pericallosal artery, but no findings of space taking lesions. An air study indicated a globular filling defect protruding into the anterior horn of the right lateral ventricle. The tumor located in the laterobasal wall of the anterior horn was removed picemiel by transventricular approach. Histologically, the tumor was vascular hamartoma. Furthermore, we discussed various brain tumors showing subarachnoid hemorrhage as an initial symptom, its frequency and bleeding mechanism on the literature.
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PMID:[Two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma (author's transl)]. 98 94

Siblings, aged 9 and 7 years, had simultaneous onset of vomiting, disorientation, ataxia, and coma. Both children had prodromal symptoms of upper respiratory tract infections, and had been treated with large doses of aspirin. Laboratory data showed evidence of hepatocellular dysfunction, with an elevated serum ammonia level in one patient; salicylate levels were 50 and 44 mg/100 ml. The child who died had autopsy evidence of cerebral edema and fatty liver. The difficulty in clinically differentiating Reye syndrome from salicylate intoxication is discussed.
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PMID:Acute encephalopathy in siblings. Reye syndrome vs salicylate intoxication. 125 38

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Toremifene is an antiestrogen that binds strongly to estrogen receptors (ER). A total of 19 previously treated postmenopausal women with metastatic breast cancer whose performance status was good and whose ER status was positive or unknown were studied to determine the maximum tolerated dose of toremifene. Cohorts of patients received 200, 300, or 400 mg/m2 p.o. daily until relapse or unacceptable toxicity had occurred. Nausea, vomiting, and dizziness were dose-related. Three of five patients receiving 400 mg/m2 experienced moderate or severe vomiting and another developed reversible disorientation and hallucinations. Mild sweating, peripheral edema, vaginal discharge, and hot flushes were encountered at all doses. Reversible corneal pigmentation was identified in seven cases but was not of clinical importance. The pharmacokinetics of toremifene was studied weekly and in detail on day 42 using a high-performance liquid chromatographic (HPLC) assay that identified the parent compound and three active metabolites, N-desmethyltoremifene, (deaminohydroxy)toremifene, and didemethyltoremifene. Steady state was achieved at 1-3 weeks. The toremifene area under the curve and the maximal concentration were dose-dependent at high doses. The recommended phase II dose is 300 mg/m2 p.o. daily.
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PMID:Phase I clinical and pharmacokinetics study of high-dose toremifene in postmenopausal patients with advanced breast cancer. 138 61

A military tank driving simulator has recently been introduced as a training aid for tank drivers in the Israel Defense Forces. Reports of nausea and vomiting among the first users of the simulator launched our investigation of the possible existence of a motion sickness-like syndrome among simulator drivers. Although the 59 subjects drove the simulator without any report of vomiting, other motion sickness-like symptoms were frequently reported. A comparison of symptoms reported after simulator and real tank driving show that dizziness, nausea, disorientation and hypersalivation were more frequently reported by simulator drivers and were of greater intensity. However, sweating and drowsiness were more prevalent among real tank drivers. The objective effect of driving the simulator was evaluated by instability and performance tests that were conducted before, during and after driving the simulator. A greater decrement in test results was observed among subjects reporting higher frequency of motion sickness-like symptoms.
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PMID:Motion sickness-like syndrome among tank simulator drivers. 142 18

Hypo- and hypertension, arrhythmias, bradycardia extending to cardiac arrest with circulatory failure, pneumothorax, allergic reactions with or without anaphylactic shock, production of methaemoglobin, vomiting, vertigo, disorientation, acoustic and visual disorders, tinnitus, slurred speech, muscle contractions, unconsciousness, and epileptic seizures are well-known complications associated with local anaesthetics. We have observed an additional central nervous system complication: a case of transient, total motor aphasia (Broca aphasia) in a 50-year-old patient after axillary blockade of the brachial plexus. Possible causes such as type and dosage of local anaesthetic or a transient ischaemic attack in the area of the prerolandic artery are discussed and related to the literature. Ultimately, however, it is still not apparent why this complication could appear although there was no overdosage intravascular injection, or abnormality of the pulse or blood pressure, and why its manifestation was limited to a motor aphasia.
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PMID:[Transient total motor aphasia. A complication of an axillary brachial plexus block]. 149 33

A case report of severe digitalis poisoning in a patient with prosthetic heart valve is presented. He complained of nausea, vomiting, drowsiness, temporal disorientation and lethargy. The electrocardiogram showed idioventricular rhythm, and plasma levels of digoxin were 6.78 ng/ml. Predisposing factors por digitalis poisoning were prerenal failure and concomitant quinidine therapy. Treatment with digoxin-immune antibody fragments (FAB) promptly lead to abolition of the ventricular arrhythmia and disappearance of every clinical symptoms in hours. Plasma digoxin levels showed a steep decrease until normal values at the fifth day. The favourable course of either clinical and electrocardiographic response to IV administration of FAB are discussed, stressing the fact of the high morbidity of digitalis poisoning in opposition to the relative safety of Fabs use in its therapy.
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PMID:[Severe poisoning with digitalis treated by the administration of anti-digoxin antibodies]. 178

We describe two female patients presenting with spontaneous peritonitis and fulminant Streptococcus pyogenes (Strep. pyogenes) septicemia and shock. Both patients recovered completely upon immediate antibiotic therapy, initially with broad range combination therapy effective against Strep. pyogenes, which was switched to penicillin G when culture results became available. This isolated strain in case 1 was M-type 28, which is the M-type most often isolated from vaginal swabs (as commensal) and from blood from patients with puerperal sepsis. Patient 1 had signs and symptoms of a toxic shock-like syndrome, including rapid onset of fever and shock, skin rash, desquamation of palms and soles, and multisystem involvement with vomiting, diarrhea, myalgia, renal failure, and severe disorientation without focal neurological deficits.
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PMID:Fulminant group A streptococcal infections. Report of two cases. 219 45


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