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)

A 14-year-old boy, suffering from acute lymphoblastic leukemia with meningeal involvement, was treated with intraventricular methotrexate and cytosine arabinoside, administered via an Ommaya reservoir (OR). Three months later, right occipital headache, vomiting, and lethargy appeared. Cerebrospinal fluid specimens showed increased proteins and a right frontal slow-wave focus was evident on the EEG recording. The computed tomography scan revealed white matter hypodensity within the right frontal and rolandic regions. After injection of medium contrast, an abscesslike hyperdensity appeared, surrounding both a well-placed cannula tip and the right frontal horn of the lateral ventricle. Brain swelling and shift signs were also evident. Nine cases of focal methotrexate leukoencephalopathy have been previously reported, and in six of these there was a misplaced OR cannula tip. The focal methotrexate leukoencephalopathy seems to be related to the neurotoxicity of the drugs administered, and may also exist with a well-placed OR cannula tip. Immediate removal of the catheter may be associated with a benign evolution.
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PMID:Transient focal leukoencephalopathy following intraventricular methotrexate and cytarabine. A complication of the Ommaya reservoir: case report and review of the literature. 220 Jun 10

We report a 17-year-old female case of ornithine transcarbamylase (OTC) deficiency who died of brain edema due to hyperammonemic attack. The patient had a brother with OTC deficiency who had died of hyperammonemia at 17 years of age. She firstly had a symptom of headache, nausea, vomiting and myalgia at 14 years old and twice thereafter. On admission she had a severe disorientation and vomiting. The plasma ammonia level was 89 micrograms/dl, then increased to 400 micrograms/dl in five hours. In addition to plasma exchange, hemodialysis and then peritoneal dialysis for next 5 days, parenteral sodium benzoate and arginine were administered. Although the plasma ammonia level improved gradually, her consciousness never returned and she died of severe brain edema with uncontrollable hypotension on day 8. Histology of a necropsy liver sample showed fatty metamorphosis of hepatocytes mainly with fine lipid droplets. Electron micrograph of hepatocytes showed crystalloid inclusions in mitochondria. Significance of the clinical course and the treatment during hyperammonemic crisis was discussed.
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PMID:[Abrupt onset and rapid deterioration in the course of congenital ornithine transcarbamylase deficiency: a case report]. 221 May 91

The neurotoxicity of local administration of nitrosoureas in malignant gliomas was investigated clinicopathologically. Twenty patients were entered into this study: 13 were treated with 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and 7 with methyl 6-[3-(2-chloroethyl-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU). On the average, a single dose of 20 mg of ACNU was administered 15 times, for a total dose of 295 mg in each case, while a single dose of 11 mg of MCNU was given 2 times, for a total dose of 24 mg. These nitrosoureas provoked greater toxicity when the administration dose was larger or the indwelling multiperforated Silastic basket was in direct continuity with the ventricle or the basal cistern. Usually ACNU was well tolerated, whereas MCNU induced marked brain edema. Side effects consisted of headache, nuchal stiffness, vomiting, motor weakness, and cranial nerve palsy for ACNU, and headache, vomiting, abnormal respiration, and arrhythmia for MCNU. Pathological changes were represented by capsule formation, spongy degeneration and reactive gliosis of adjacent white matter, occlusion of neighboring arteries, and demyelination of cranial nerves in the patients treated with ACNU, while they were represented by focal brain necrosis in two patients treated with MCNU. The differences in neurotoxity of ACNU and MCNU conceivably derive from the different blood-brain delivery of these drugs.
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PMID:Neurotoxicity of local administration of two nitrosoureas in malignant gliomas. 235 97

Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension were presented. The first case was a 68-year-old man admitted for vomiting following headache for eight days. There was no history of head trauma. A CT scan revealed a high-density mass that had a concave inner margin in the left temporo-parietal region with a slight midline shift. No vascular lesion was noted on the angiogram. The consciousness of the patient deteriorated suddenly on the 12th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural clot was removed. The postoperative recovery was good. The patient was discharged 7 days later without any neurological deficit. The second case was a 69-year-old man who was admitted with sudden onset of headache. There was no history of head trauma. A CT scan showed a high density mass in the right temporoparietal subdural space with a slight midline shift. The consciousness of the patient deteriorated suddenly on the 15th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural hematoma was removed. Two days later, suddenly his consciousness deteriorated. A CT scan showed his severe brain edema with a marked midline shift without increased hematoma. External decompression was performed immediately. The postoperative recovery was very good and 40 days after the second operation, the patient was discharged with no neurological deficit. The delayed intracranial hypertension appeared in these two cases about 10 days after the initial symptom. Two kinds of mechanisms are suspected: 1) swelling of the hematoma because of the adsorption of cerebrospinal fluid, 2) the occurrence of secondary brain edema. From our experience, a repeated CT scan is necessary for 2 to 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension]. 322 89

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

A diagnosis based on the presumed mechanism of stroke onset is useful for management strategies in acute ischemic stroke. Ninety-two patients with embolic (cardiac or artery-to-artery) and 107 with non-embolic (thrombotic or hemodynamic) stroke were diagnosed on strict cerebral angiographic criteria alone. To clearly discriminate between these two groups, the neurological and computed tomographic (CT) findings were then compared. Rapidity of onset, vomiting, urinary incontinence, level of consciousness, cervical bruit, anisocoria, tongue deviation, sensory disturbance, and CT findings (location of hypodense area, findings of brain edema and hemorrhagic transformation) were discriminatory factors between the two groups (p<0.01). According to these 11 items, we prepared a numerical table for quantitative differential diagnosis. A diagnostic accuracy of 98.9% for embolic and 87.9% for non-embolic stroke in internal verification, and 90.0% and 82.9%, respectively, in external verification was observed. The differences in clinical features and CT findings between embolic and non-embolic stroke may reflect the pathophysiological mechanisms of the occlusive process of cerebral artery as well as the extent and severity of ischemia.
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PMID:Differences in clinical features and computed tomographic findings between embolic and non-embolic acute ischemic stroke: a quantitative differential diagnosis. 955 May 93

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
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PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77

A neonate presented in the first weeks after birth with vomiting. He was unresponsive, with hypotonia, macrocephaly, and lactic acidosis. The cranial computed tomographic scan revealed a hypodense brain, with increased brain volume and extensive cerebral edema. He died at 6 weeks of age; postmortem examination revealed necrotizing encephalopathy with marked brain edema, spongiosis, thalamic necrosis, and basal ganglia calcifications. Enzyme studies of the mitochondrial respiratory chain revealed complex I deficiency in both muscle and liver.
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PMID:Necrotizing encephalopathy and macrocephaly with mitochondrial complex I deficiency. 1032 81

Intracranial aneurysms associated with moyamoya disease are often reviewed. Aneurysms not around the circle of Willis but on the collateral vessels are rare. A 71-year-old woman presented with sudden onset of severe headache and vomiting. CT scan showed an intraventricular hemorrhage from bilateral lateral ventricle to fourth ventricle. Cerebral angiography showed the occlusion of the terminal portion of the bilateral internal carotid artery with moyamoya vessels and three aneurysms at the distal portion of the left lateral posterior choroidal artery. Clinical symptoms improved day by day, but 17 days later, due to rebleeding of the aneurysms the patient fell into coma. The day after rebleeding, endovascular embolization was performed using liquid particle, and the left lateral posterior choroidal artery and the aneurysm were occluded. Brain infarction with massive brain edema of the left cerebral hemisphere resulted in the patient's death. The management of the aneurysms in the basal ganglia and on the collateral vessels associated with moyamoya disease is controversial. We suggest positive intervention during the acute stage for the peripheral artery aneurysms taking endovascular embolization into consideration to prevent rupture or rebleeding.
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PMID:[Moyamoya disease with intraventricular hemorrhage due to rupture of lateral posterior choroidal artery aneurysm: case report]. 1056 52


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