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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare case of extracranial internal carotid occlusion with a coexisting ipsilateral internal carotid aneurysm is reported. A 50-year-old male had a sudden onset of severe headache, vomiting and right motor weakness on May 14, 1984. Two days later the patient was transferred to our hospital. On admission he was alert but presented with nuchal rigidity and right moderate hemiparesis. He had an episode of a blunt head injury 12 years previously, but no history of hypertension, diabetes mellitus or cerebral stroke. A computed tomography revealed mild subarachnoid hemorrhage and mild ventricular dilatation. A cerebral angiography did not demonstrate any aneurysms but it revealed occlusion of the right internal carotid artery at the cervical bifurcation. The repeated angiography on May 31 disclosed a saccular aneurysm arising anteromedially at the level of the junction of the right posterior communicating artery and the internal carotid artery. The cervical internal carotid artery remained occluded at the same site. The middle cerebral artery was supplied through the well-developed posterior communicating artery, and the right anterior cerebral artery was supplied through the anterior communicating artery. Clipping of the aneurysm was attempted but it was forcibly trapped because of premature bleeding on June 5. The right V-P shunt was performed for the progressive ventricular dilatation on June 12. The patient was discharged with no paresis on June 20. It has been well known that the uni- or bilateral carotid occlusion, whatever the origins are, are often associated with cerebral aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Extracranial internal carotid occlusion and coexisting ipsilateral intracranial internal carotid aneurysm]. 361 34

Thirteen patients with caudate hemorrhage are described. All the hemorrhages were in the head of the caudate nucleus, and all the hemorrhages but one ruptured in the anterior horn of the lateral ventricle. In 9 patients, the hemorrhage was related to hypertension and the patients were older. In the other 4 patients, the hemorrhage resulted from rupture of an arteriovenous malformation (AVM) and the patients were under 40 years old. Clinical manifestations were nearly the same in both groups, suggestive of subarachnoid hemorrhage and including hemiparesis in most patients. In patients with hypertension, good recovery was obtained by conservative treatment and in those with ruptured AVMs, resection of AVMs through an anterior transcallosal approach may be safe and recommended.
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PMID:Caudate hemorrhage. 370 14

We studied 50 patients with thalamic hemorrhage, 84% with hypertension. Five patients had hematomas less than 8 mm and signs that resolved within 4 days. Two patients had headache, papilledema, and hemorrhage contiguous with the lateral ventricles. Twenty-four had hemiparesis, parenchymal hemorrhage 9 to 30 mm, and no ventricular blood. Nineteen had a larger hemorrhage and intraventricular hemorrhage, impaired consciousness, hemiparesis, and pupillary abnormalities; 12 had vertical gaze impairment, and all 19 patients died.
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PMID:Thalamic hemorrhage: clinical-CT correlations. 376 49

Four boys and four girls with brain tumors who were admitted to our department in the last 8 years are herein described. They presented with epileptic fits, which began before the age of 14 years, with neither intracranial hypertension nor localizing signs during the first 6 months of the illness. The length of time between the first fit and the diagnosis of a tumor ranged from 2 months to 11 years (median of 3 years), during which period all patients but one received anticonvulsant therapy. The nontreated patient was under psychiatric treatment for 1 year. The electroencephalographic evolution was disconcerting, showing asymmetry of the recording with association of slow polymorphic waves and acute irregular waves, suggesting encephalitis. The neuroradiological diagnosis was made by cerebral arteriography in one patient and in the others by angiography and CT scans (which revealed hypodense cerebral areas in five cases and hyperdense areas in the other two). The histology of the tumor was that of a grade I astrocytoma in six cases; a grade III oligondendroglioma in one case, and a meningioma in the other. All patients underwent surgical treatment. Four also received radiation therapy, two for a partially excised astrocytoma and one each for an oligodendroglioma and a meningioma. Postoperatively, all patients were put on anticonvulsant drug therapy. There were no mortalities. To date, only one astrocytoma has recurred. The sequellae observed were hemiparesis in one case and marked psychomotor deficit in another. These two patients also still have epileptic fits. The others are all psychologically and neurologically normal, and two are now off antiepileptic drugs.
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PMID:Epilepsy and brain tumors in infancy and adolescence. 377 77

Fifty-four patients, aged 15 to 81 years had a spontaneous intracerebral haematoma surgically removed (51 patients) or had ventricular drainage. One-third had arterial hypertension. Two thirds were alert or drowsy preoperatively and two thirds presented with hemiparesis or decerebrate rigidity. Lobar haematomas constituted 72%, deep supratentorial constituted 21% and cerebellar haematomas 7%. Volume of the haematomas ranged from 10 to 205 ml. 10 patients died in the early postoperative phase and 8 patients died later. Among 36 survivors, 35 were evaluated 15-115 months postoperatively. 10 had resumed part of their earlier occupation. Another 12 were incapacitated and the remaining 13 patients needed nursing care. No patient was neurologically or neuropsychologically intact, but 19 had only slight disabilities. CT-changes at follow-up ranged from no abnormalities at all to low-density lesions, possibly associated with dilatation of a lateral ventricle or porencephaly depending on the size of the haematoma and possible ventricular penetration. Surgical evacuation of ICH is recommended in lobar or deep supratentorial haematomas exceeding 20 ml except in patients older than 60 already unconscious. Smaller haematomas with intraventricular extension may benefit from ventricular drainage or, in the fossa posterior, even from evacuation in case of increasing brain stem compression.
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PMID:Spontaneous intracerebral haematomas. Clinical and computertomographic findings and long-term outcome after surgical treatment. 381 43

Chronic intracranial hypertension in the presence of hydrocephalus and/or arachnoiditis is a rare presentation of neurobrucellosis. The present case is exceptional because neither hydrocephalus nor arachnoiditis were present. Brucellosis was diagnosed by serological tests. The patient developed asthenia, anorexia, weight loss, violent headaches, explosive vomiting, bilateral papilloedema, diplopia with paralysis of the abducens nerves, left supranuclear facial paralysis and left hemiparesis. A skull radiograph showed destruction of the sella turcica. Rapid recovery was attained with the use of antibiotics. The pathogenesis of this intracranial hypertension syndrome with destruction of sella turcica is discussed.
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PMID:Chronic intracranial hypertension secondary to neurobrucellosis. 381 88

Four men and four women, aged 16 to 43, developed dural sinus thrombosis, five patients with acute lymphoblastic leukemia (L.A.L.) and three with non Hodgkin malignant lymphoma (N.H.M.L.). All the cases of L.A.L. were F.A.B.-2 subtype without any unusual hematological features. In 6 cases, the disorders occurred during the phase of therapeutical induction (E.O.R.T.C.-A.L.L.-H.R. protocol) at D5, D10, D15, D26, D30, D38, and in 2 cases during maintenance after a period of remission. All patients had received Vincristine and Prednisone, intrathecal Methotrexate in 5 cases, encephalic irradiation in 3 cases and L-Asparaginase in one case. Three women were taking contraceptive drugs. The neurological symptoms and signs were headache due to intracranial hypertension in 6 cases, Grand Mal seizures in 5 cases, focal seizures in 2 cases, a regressive hemiparesis in 4 cases, stupor in 3 cases. CT scan was abnormal in 4 cases, displaying oedema in 3 cases and an hemorrhagic infarction in 1 case. Angiography showed in all cases occlusion of the superior sagittal sinus in 7 cases and of the transverse sinus on 1 case. Six patients received anticoagulant therapy. Outcome was fatal in 3 cases: in 2 cases of L.A.L., the condition worsened rapidly after the onset and death was related to a tentorial herniation; in 1 case of N.H.M.L. death resulted from an intercurrent infection.
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PMID:[Dural venous sinus occlusions in hemopathies]. 385 30

Of 44 children with hemolytic-uremic syndrome seen at Milwaukee Children's Hospital, 15 (34%) had neurological involvement. This group contained 8 boys and 7 girls, with a mean age of 3 1/4 years. Twelve patients had seizure within 48 hours of admission. Seizures were associated with hypertension, fever, hyponatremia, or hypocalcemia. Other neurological symptoms included altered consciousness, behavioral changes, diplopia, and dizziness. Hemiparesis (4 patients), eye involvement (7 patients), decerebrate posturing (2 patients), and ataxia (1 patient) were present on physical examination. Cerebrospinal fluid examination showed increased protein in 4 of 11 patients. Electroencephalograms were abnormal in all 9 patients tested. Computed tomographic and radionuclide scans showed evidence of vascular abnormalities in 4 of the 14 patients studied. Complete neurological recovery occurred in only 6 of the 15 children, while the remaining 6 demonstrated residual hemiparesis, seizures, and cortical visual defect. In those children with neurological involvement, there was a higher incidence of residual hypertension (49% versus 11%), chronic renal damage (40% versus 3.5%), and death (28% versus 0%), suggesting that central nervous system involvement indicates severe hemolytic-uremic syndrome.
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PMID:Neurological involvement in hemolytic-uremic syndrome. 394 42

A 76 year-old woman visited our university hospital with a complaints of dysphagia of 3 months duration and was discovered to have a right internal carotid aneurysm protruding to the right side of the larynx. A day prior to admission, dysarthria and left hemiparesis occurred with sudden onset. These ischemic attacks spontaneously remitted within 48 hours. A carotid arteriogram showed a saccular aneurysm located high in the right internal carotid artery. Four days after admission, aneurysmectomy with end-to-end anastomosis was carried out with the temporary internal shunt under the induced hypertension. There was no sign of ischemic brain damage after the operation. But she suffered from dysphagia due to the NO. 9, 10, and 12 cerebral nerve palsies, which took 5 months to recover completely. Despite several difficulties in the operation for a highly located internal carotid aneurysm, we emphasize in this report the necessity of aneurysmectomy and the establishment of vascular continuity with the aid of internal shunt to prevent the ischemic brain damage.
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PMID:[Successful surgical management of extracranial high internal carotid aneurysm. A case report]. 403 28

Most of "so-called" posterior communicating artery aneurysms previously reported, originated from the internal carotid-posterior communicating junction. Aneurysms arising from the posterior communicating artery itself are very rare. The abducens nerve palsy caused by cerebral aneurysm is also very rare. We are reporting a case with the saccular aneurysm arising directly from the distal half of the posterior communicating artery presenting the abducens nerve palsy. This 73-year-old woman who had no treatment with hypertension for several years was admitted for sudden onset of severe headache, vomitting and unconsciousness on March 1, 1984. She opened her eyes when addressed and had disorientation, urinary incontinence, right-hemiparesis and left-abducens nerve palsy. A 4-vessel angiography revealed the saccular aneurysm originating directly from the distal half of the posterior communicating artery. The patient underwent left-frontotemporal craniotomy on the 27th day after subarachnoid hemorrhage under Hunt & Kosnic Grade 3. The aneurysm originated directly from the distal half of the posterior communicating artery and directed inferior-posterior-laterally below the oculomotor nerve. The neck was successfully clipped. Immediate post-operative course was uneventful until the 7th day after surgery. On the 8th day she had hypertensive intraventricular hemorrhage and expired. The autopsy could not be obtained. The saccular "true" posterior communicating artery aneurysm with isolated unilateral abducens nerve palsy as seen in our case has not been reported. Considering the operative findings, we thought the aneurysmal dome contacted directly with the abducens nerve.
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PMID:["True" posterior communicating artery aneurysm presenting the abducens nerve palsy]. 408 54


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