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 6-year-old boy developed a flaccid hemiplegia and dysarthria following several transient episodes of nausea, vomiting, and ataxia. An anomly of the dens was discovered, permitting subluxation of C-1 on C-2. A segmental occlusion of the right vertebral artery and an aneurysm of the left vertebral artery were found at the C-2 level, as well as a thromboembolic occlusion of the rostral end of the basilar artery. It appeared that the repeated cervical subluxation produced occlusive, aneurysmal, and embolic vascular disease, and that clinical symptoms were the result of ischemia in the territory perfused by the vertebrobasilar arteries.
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PMID:Occlusive vertebrobasilar artery disease associated with cervical spine anomaly. 113 Mar 56

The clinical manifestations of 20 cases of insular cistern hematoma were characterized by sudden onset violent headache, vomiting, bloody CSF, and subhyaloid hemorrhage (1/3 cases). CT scan showed semilunar high density image centering on the insular cistern with serrate internal edge. The average volume of the hematoma was 20 ml. By means of cerebral angiography, operation and/or autopsy, 7 cases were identified as aneurysm of middle cerebral artery, 6 as aneurysm of posterior communicating artery, and 2 as amyloid angiopathy. In the other 5 cases, the etiology was unknown.
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PMID:Insular cistern hematoma. A special type of subarachnoid hemorrhage. 128 72

Presented here are case reports of two patients who became completely blind in both eyes following acute systemic hypotension - in one following bouts of vomiting and in the other after repeated gastrointestinal bleeding. Both patients had severe degree of anemia. There were no other risk factors for vascular disease such as arteriosclerosis or vasculitis.
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PMID:Bilateral optic nerve infarction following acute systemic hypotension and anemia--a case report. 145 87

Clinical and computed tomographic findings in 24 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type were reviewed. The common initial symptoms were headache and vomiting. Computed tomographic scans showed 50 hypodense and 49 hyperdense cortical lesions and in 20 patients the scans also showed generalized white matter hypodensity. Impairment of consciousness was related to the size of the hemorrhagic lesion. Dementia, seen in 11 patients, was related to the duration of the disease and the number of focal lesions on the computed tomographic scans, but not to the presence of white matter hypodensity. It is concluded that in hereditary cerebral hemorrhage with amyloidosis-Dutch type, lobar hemorrhages account predominantly for the acute clinical syndromes. The hemorrhages often have an irregular shape and are responsible for progression of the symptoms after an acute onset. Furthermore, cerebral amyloid angiopathy leads to a generalized abnormality of the white matter, probably due to chronic hypoperfusion.
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PMID:Hereditary cerebral hemorrhage with amyloidosis-Dutch type. Clinical and computed tomographic analysis of 24 cases. 234 93

Alzheimer's disease is a degenerative brain disorder with a progressive dementia which develops in middle or late life. The pathological findings of this disease are characterized by neurofibrillary tangles, senile plaques and cerebrovascular amyloidosis. However, cerebral hemorrhage caused by amyloid angiopathy rarely occurs. A 71-year-old woman, who had been suffering from an impairment of her cognitive ability for the past several months, suddenly developed a severe headache with vomiting and gait disturbance. Brain CT disclosed a hemorrhagic lesion in the right parieto-occipital region. In the following two years she had experienced two episodes of the similar subcortical hemorrhage which occurred in the right parietal lobe and bilateral parieto-occipital regions. She died at the age of 73. Histopathological examinations of the brain revealed a decreased number of neurons with diffuse distribution of senile plaques and neurofibrillary tangles in the neocortex and hippocampus. Severe cerebrovascular amyloid deposits were also seen. Immunostaining for amyloid was carried out using a monoclonal antibody to amyloid beta protein. The senile plaque and cerebrovascular amyloid was strongly immunoreactive to anti-beta protein antibody. Cerebral amyloid angiopathy is commonly seen in the brains with Alzheimer's disease and severe cerebrovascular degeneration secondary to heavy amyloid deposits may cause recurrent subcortical hemorrhages in the patients with this disorder.
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PMID:[An Alzheimer's disease case showing recurrent subcortical hemorrhage: an autopsy findings with immunohistochemical studies of cerebral amyloid deposits]. 280 20

Angioedema is characterized by a well-demarcated swelling on the skin, oropharyngolaryngeal tissue, or the gastrointestinal wall. Underlying mechanisms may include IgE-mediated reactions, complement activation, inhibition of the cyclo-oxygenase pathway of arachidonic acid metabolism, direct release of mediators from mast cells, and activation of the kinin-forming system. Foods, drugs, inhalants, insect bites, blood transfusion, collagen vascular disease, infections, physical factors, neoplasms, and hereditary factors can cause angioedema through one or more of these mechanisms. Chronic angioedema lasts more than 6 weeks or recurs during this period. Acute angioedema is a self-limited disorder and resolves spontaneously, or with simple therapy, in several days; the patient rarely requires a complete work-up. Chronic angioedema may necessitate a detailed history, physical examination, and limited clinical or laboratory tests to exclude serious underlying illnesses. The H1 antihistamines are used for the treatment of both acute and chronic angioedema. An H2 antihistamine, a second H1 antihistamine, or rarely even a low dose of corticosteroid may be added to the regimen if H1 antihistamine alone fails to control chronic angioedema. Hereditary angioedema is an autosomal dominant disease that is caused by C1INH deficiency. In patients with this disorder, swelling of the lip, pharynx, and extremities may follow trauma to soft tissue. Other clinical manifestations include abdominal pain, nausea, vomiting, and suffocation because of laryngeal swelling. Diagnosis can be confirmed by the finding of low levels of C4 and C2 and the absence of nonfunction of C1INH. Androgens reverse the biochemical defects.
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PMID:Angioedema. 286 18

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.
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PMID:[Benign cerebral angiopathies and phenylpropanolamine]. 304 37

A case of multiple cerebral hemorrhage in the bilateral parietal lobes related to cerebral amyloid angiopathy (CAA) is reported. A 66-year-old man was admitted to our hospital because of headache and vomiting on Feb. 21, 1983. He had no history of hypertension, diabetes mellitus, recent head injury, or dementia. Four days prior to admission, he had behaved as if he were blind, but, had denied any blindness. On examination, he was confused and disoriented. Blood pressure was 130/80 mmHg. Abnormal findings on neurological examination included memory disturbance, apraxia for dressing, right-left disorientation, finger agnosia and Balint's syndrome. A CT scan showed multiple subcortical hematomas in the bilateral parietal lobes. Intracerebral hemorrhage related to CAA was suspected. Confirmation of the presence of amyloid in the cerebral vessels was established by examination of brain biopsy specimens. The characteristics of cerebral hemorrhage related to CAA are as follow--occurrence in elderly, sometimes demented people; localization to the cortex and subcortical white matter, with direct extension into the subarachnoid space; frequent multiple occurrence in time and/or at several sites within the cerebral hemispheres; sometimes occurrence after operative procedures or head injuries. A specific diagnosis of CAA can only be made by histological examination, but the indication of brain biopsy should be carefully decided because of hemostatic difficulty and tendency to rebleed. In conclusion, CAA should be considered as a cause of hemorrhage in elderly patients who are often normotensive and demented.
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PMID:[A case of multiple cerebral hemorrhage related to cerebral amyloid angiopathy]. 339 10

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
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PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31

Seven cases of lobar cerebral haemorrhage due to amyloid angiopathy were found among 60 necropsy cases of intracerebral haemorrhage. Clinically five patients were demented and two had hypertension. Immediately after the onset of stroke there was a high incidence of headache and vomiting, followed by nuchal rigidity. Amyloid angiopathy was most prominent in the cerebral cortex and the leptomeninges. Senile plaques were noted in all cases. One should suspect that a haemorrhage may be due to amyloid angiopathy, when lobar cerebral haemorrhage occurs in an aged, normotensive patient with or without dementia. Surgical evacuation of the haematoma is inadvisable, because of the diffuse nature of amyloid angiopathy, high recurrence rate and less tendency to cause brain stem compression.
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PMID:Amyloid angiopathy and lobar cerebral haemorrhage. 650 78


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