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)

The authors reported a case of subdural effusion secondary to dural metastasis of prostatic cancer. A 61-year-old man was referred for headache, vomiting and gait disturbance. He had undergone hormonal therapy for prostatic cancer. He showed a mild left hemiparesis and anemia without bleeding. CT-scan disclosed a multilobular crescent shaped low density area in the right hemisphere. Under the diagnosis of chronic subdural hematoma, burr hole irrigation therapy was performed. Xanthochromic fluid was evacuated from the subdural space, in which no tumor cells were shown to exist. CT-scan on the 21st day disclosed a low density area, which was diagnosed as recurrent chronic subdural effusion. Therefore, craniotomy was performed to evacuate the subdural fluid and to explore the dura mater. Removal of the red hemorrhagic tumor at the dura mater and the fluid was performed. The patient died of heart failure in the 16th month despite complete recovery after the second operation. Histopathological examination of the tumor revealed adenocarcinoma at the outer part of the dura mater and the adjacent skull bone, where capillaries were embolized with tumor cells. However, no tumor cells were found in the subdural fluid. The authors could find in the literature 30 cases of subdural hematoma or effusion secondary to dural metastasis of carcinoma. The pathogenesis of the subdural hematoma in this case might be due to circulatory disturbance at the dura mater brought about by the invasion of the tumor or tumor cells emboli in the capillaries.
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PMID:[A case of subdural effusion secondary to dural metastasis of prostatic cancer: case report]. 239 13

A 49-year-old male was hospitalized with a 1-month history of persistent headache and vomiting. Computed tomography (CT) revealed left middle fossa arachnoid cysts and a chronic subdural hygroma. The cysts were excised after evacuation of the subdural hygroma. Postoperatively, the patient did not regain consciousness and CT showed multiple intracerebral hemorrhages in both the supra- and infratentorial spaces. Three months postoperatively, he was discharged with mental deficits and right hemiparesis. A review of the literature indicates that the possible pathogenic mechanism in this case was a sudden increase in cerebral blood flow due to faulty autoregulation. This devastating complication may have been avoided by simple drainage of the subdural hygroma, perhaps with the addition of cyst-peritoneal shunting.
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PMID:[Multiple intracerebral hemorrhages immediately after surgical excision of middle fossa arachnoid cysts and evacuation of chronic subdural hygroma. Case report]. 247 5

Four cases of brain tumors associated with hemorrhage from tumors as their first manifestation were reported. These were malignant astrocytoma in two cases, brain metastasis of hepatocellular carcinoma in one case and skull metastasis of hepatocellular carcinoma in one case. Clinical symptoms and sings were generalized convulsion, sudden onset of headache, vomiting and hemiparesis. It was difficult to confirm the diagnosis of brain tumors in such cases. Therefore it is important to perform follow-up plain and enhanced CT repeatedly and it is also important to make adequate biopsy of hematoma wall and surrounding tissue during operation.
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PMID:[Brain tumors associated with hemorrhage from tumors as their first manifestation]. 255 50

Eighteen patients with subcortical lobar hematomas were reviewed. Arterial hypertension was the leading cause and three had arteriovenous malformation and were treated surgically. More than half of cases had hematomas of either the temporooccipital or occipital lobes. Common neurologic findings were headaches, vomiting, alertness, dysarthria, hemiparesis and hemianopsia. All patients survived and had better resolution of neurological deficits, suggesting that surgical intervention is not necessary.
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PMID:Subcortical lobar hematomas: clinico-computed tomographic correlations. 270 3

A 12-year-old boy with corticosteroid-responsive mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is described. His mother proved to have an asymptomatic mitochondrial myopathy on examination of a muscle biopsy specimen. Three weeks after the onset of vomiting, headache, ataxia and visual and speech impairment, he presented with a background of somatic growth retardation, deafness and school failure. Examination revealed disorientation, dysphasia, dyspraxia, optic atrophy, hemianopia, hemiparesis and sensory inattention. A cranial computed tomographic scan disclosed a large, low-density area, which was consistent with infarction, in the left posterior hemisphere and marked calcification of the basal ganglia bilaterally. Within two weeks of the commencement of corticosteroid treatment, the neurological dysfunction resolved. Attempts to decrease the dosage of dexamethasone caused an exacerbation of symptoms repeatedly. Two weeks after ceasing corticosteroid therapy, the patient developed a serious neurological relapse and a new, large, low-density area, which resembled an infarction, in the right posterior hemisphere on a computed tomographic scan. The reintroduction of corticosteroid therapy again resulted in the rapid resolution of all symptoms. It became evident that the patient had an exquisitely sensitive corticosteroid dependency, whereby a reduction in the dexamethasone dosage of even 0.25 mg a day caused confusion, headaches and increasing lactic acidaemia. Although it is difficult to assess the impact of various therapies in MELAS because of the episodic natural course of the disease, this remarkable corticosteroid responsiveness also has been noted in four previously reported patients with MELAS syndrome; therefore, it would seem reasonable to suggest that corticosteroid therapy now should be considered as standard treatment for this condition. However, corticosteroid therapy in other forms of mitochondrial disorders still awaits careful evaluation.
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PMID:Mitochondrial encephalomyopathy with corticosteroid dependence. 273 98

A female in whom systemic lupus erythematosus had been diagnosed 5 years before suddenly developed headache and recurrent vomiting. Cranial computed tomography (CT) was consistent with subarachnoid hemorrhage, and cerebral arteriography disclosed cerebral aneurysms, multiple microaneurysms and cerebral vasculitis. After 7 days she developed left hemiparesis, and a cerebral infarct area was apparent in a new CT scan. Despite the poor prognosis of these lesions, the patient had a favorable outcome, without residual neurological deficit, after having been treated with intravenous corticosteroid boluses and oral cyclophosphamide.
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PMID:[Multiple aneurysms and cerebral vasculitis in systemic lupus erythematosus]. 275 31

A series of 22 patients with thalamic bleeding with CT confirmation is reported. Sixteen patients had hypertension and 7 experienced headaches and vomiting. Twenty patients had hemiparesis, and 14 had hemianesthesia. More than half the cases had hematomas in the posterior thalamus. Twenty-one had hematomas less than 3 cm. No patient displayed the characteristic pupil signs. One patient died and mortality rate was 4.5% (died from respiratory arrest). None of the 7 patients who had ventricular rupture died, indicating that the prognosis of the patients may not be affected by the ventricular extension.
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PMID:Thalamic bleeding: clinico-computed tomographic correlations. 317 77

We examined case of intracerebral hemorrhage presenting as lacunar syndrome. Of 115 cases, 10 presented with a lacunar syndrome: 3 presented with pure motor hemiparesis, 1, pure sensory stroke, 1, ataxic hemiparesis, 5, sensorimotor stroke, and, none, dysarthria--clumsy hand syndrome. The sites of hemorrhage were capsular in 1, pontine in 1, thalamic in 4, and putaminal in 4. In these 10 patients, 9 were hypertensive, and the signs characteristics of parenchymal hemorrhage, e.g., headache, nausea, vomiting, and stiffness of neck, were absent or rare.
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PMID:Lacunar syndrome and intracerebral hemorrhage: clinico-computed tomographic correlations. 320 39

A 19-month-old boy was found to have an optico-hypothalamic tumor with obstructive hydrocephalus, and received a ventriculoperitoneal (V-P) shunt followed by irradiation to the hypothalamic area. Although his visual disturbances continued, general conditions improved subsequently and he enjoyed normal life with only a visual disturbance. Four years later, however, he developed vomiting, left hemiparesis and dysuria, and died at the age of 6.5 years. Autopsy revealed a huge tumor occupying the hypothalamus, thalamus, basal ganglia and the right temporal lobe. Histologically, the tumor was composed of pilocytic astrocytes with Rosenthal fiber in the hypothalamus, where the tumor is considered to have developed initially, and poorly differentiated cells with some astrocytic and neuronal differentiation in other areas. Dissemination of the tumor was extensive in the whole CSF spaces, and in the peritoneum through the V-P shunt. We consider this a rare case of a childhood hypothalamic pilocytic astrocytoma undergoing delayed malignant evolution.
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PMID:Anaplastic evolution of childhood optico-hypothalamic pilocytic astrocytoma: report of an autopsy case. 320 64

A case of ruptured cerebral aneurysm with hemophilia B is reported, and discussion is made concerning the management of mild type hemophilia in surgical operations. A 41-year-old male came to our hospital with complaints of severe headache, vomiting, and transient consciousness disturbance. His dentist said the patient had a mild bleeding tendency when he was 30 years old, however no postoperative hemorrhage was repeated in appendectomy in his childhood. He also had had no episodes of spontaneous bleeding. CT scan on admission showed subarachnoid hemorrhage, and angiography revealed a ruptured aneurysm at the trifurcation of the left middle cerebral artery. His coagulation screening tests (bleeding time, clotting time, prothrombin time, and activated partial thromboplastin time) were normal. An aneurysmal neck clipping was carried out, and operators did not detect any bleeding tendency during the surgery. CT scan on the next day showed no remarkable finding. On the third postoperative day, right hemiparesis occurred. Left putaminal hemorrhage took place. His coagulation tests and FDP were also normal. The hematoma was partially evacuated. After the second operation his condition was good, and rehabilitation program started. On the 15th hospital day his consciousness deteriorated suddenly, and CT scan showed a massive epidural hematoma on the left. His prothrombin time elongated mildly, but other tests were normal. Coagulation factors VIII and IX were examined and the factor IX was 22.5% of control. He was thought to be a patient with mild type hemophilia B. Despite a third operation for hematoma removal he died on the 20th hospital day. Mild type hemophilia B does not bleed spontaneously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Unusual postoperative hemorrhage in a patient with ruptured aneurysm and hemophilia B]. 321 Dec 77


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