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

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.
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PMID:[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case]. 225 22

Treatment of hypertension may prevent many of the complications attributable to blood pressure elevation, particularly those that are "pressure-related," such as stroke. However, the atherosclerotic complications of hypertension, e.g., coronary artery disease manifested as coronary morbidity and mortality, have not been reduced significantly with antihypertensive therapy. This disappointing outcome may reflect the adverse metabolic effects of the traditional therapies, diuretics and beta blockers, and their lack of specific vasoprotective properties. Increasing attention is thus being paid to the newer antihypertensive agents, which typically have fewer adverse effects and perhaps more physiologic mechanisms of antihypertensive action. Since calcium plays a key role in the genesis of atherosclerosis, calcium antagonists may positively affect the course of vascular disease. Investigators have observed that calcium antagonists display clear antiatherosclerotic properties in experimental as well as clinical studies. In one recently published clinical study, coronary artery disease was shown to develop more slowly, with a slower progression of individual stenoses, higher regression rate and less frequent occurrence of new lesions in patients treated chronically with verapamil compared to those receiving conventional therapies. Other similar investigations are currently under way to evaluate the antiatherogenic properties of calcium antagonists, including the Frankfurt Isoptin Progression Study (FIPS), the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS), the International Nifedipine Trial on Atherosclerosis Coronary Therapy (INTACT), and the large-scale Montreal Heart Institute Study. Results of these studies, which use precise end points such as myocardial infarction, cerebral infarction and peripheral vascular disease, may revolutionize the treatment of hypertension by identifying therapeutic approaches that control both the pressure-related and atherosclerotic complications of the disease.
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PMID:Anti-atherosclerotic and vasculoprotective actions of calcium antagonists. 225 66

We evaluated the effect of nicardipine, a calcium channel blocker, on somatosensory evoked potentials (SEP) in 26 patients with acute cerebral infarction. Post treatment, 58% (15/26) of the N20 and P25 latencies were prolonged in the affected hemispheres; 8% (2/26) were shortened; and 35% (9/26) did not change. The mean N20 and P25 latencies were significantly prolonged two hours post treatment in the affected hemisphere (N20, P less than 0.01, P25 P less than 0.01). Nicardipine (Ni) had no effect on SEP components in the intact hemispheres. Seventy five per cent of the 12 patients with hypertension had a decrease in blood pressure (BP) after taking nicardipine, but there were no undesirable side effects or worsening of neurological signs. Our study demonstrates that nicardipine prolongs the latencies of short-latency components of SEP in the affected hemisphere after acute ischaemic stroke and also decreases BP. These observations suggest that nicardipine therapy might impair neuronal function in the ischaemic zone.
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PMID:Effect of nicardipine on somatosensory evoked potentials in patients with acute cerebral infarction. 226 63

The effects of cigarette smoking on cardiovascular disease were investigated in the Japanese community of Hisayama. This long-term prospective study assessed the occurrence of coronary heart disease and non-embolic cerebral infarction in relation to smoking habits at entry. The study population comprised 1603 subjects aged greater than or equal to 40 years. Seventy-six per cent of 699 men and 17% of 904 women were smokers. During 23 years of follow-up, 73 cases of coronary heart disease and 175 cases of non-embolic cerebral infarction developed. In both sexes, coronary heart disease occurred more frequently in those who smoked greater than 10 cigarettes per day than in those who never smoked. There was no relationship between smoking status and the incidence of non-embolic cerebral infarction. When more than one of the major risk factors (smoking, hypertension and elevated cholesterol) was present in the same person, the risk of coronary heart disease increased 2.4-7.7 times. Cox's proportional hazards model showed that cigarette smoking was an independent and significant risk factor for coronary heart disease, but not for non-embolic cerebral infarction.
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PMID:Smoking and cardiovascular disease in the general population in Japan. 228 56

Recent findings on the relation between alcohol abuse and ischaemic brain infarction are reviewed. Much of the association has hitherto been explained by the effects of confounding factors such as smoking. Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. Analysis of case histories shows that alcohol abuse has precipitated cerebral embolism in conjunction with cardiac diseases including alcoholic cardiomyopathy and paradoxical embolism due to deep vein thrombosis via atrial septal defect. Among young adults, falling when intoxicated with alcohol has caused traumatic dissection of the carotid artery and consequent brain infarction. Alcohol may predispose individuals to cerebral embolism, thrombosis and ischaemia via its effects on the coagulation cascade, platelet count and function and contractility of the cerebral vessels. Further studies are needed to prove that these mechanisms are significant and to identify any other mechanisms which may mediate the risk associated with alcohol abuse. On the basis of current data, alcohol should be considered as an independent risk factor for ischaemic cerebral infarction in young adults.
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PMID:Alcohol abuse and brain infarction. 229 43

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.
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PMID:Are hypertension or cardiac embolism likely causes of lacunar infarction? 230 60

Strokes in young adults are uncommon and often a diagnostic challenge. A retrospective study of strokes due to intracerebral hemorrhage, subarachnoid hemorrhage, or cerebral infarction was undertaken. We reviewed the medical records of 113 young patients aged 15-45 years who were admitted to the Medical Center Hospital of Vermont with a diagnosis of stroke between 1982 and 1987. This group comprised 8.5% of patients of all ages admitted for stroke, 2.3 times the proportion observed in the National Survey of Stroke. Nontraumatic intracerebral hemorrhage was diagnosed in 46 young patients (41%); the main causes included aneurysms, arteriovenous malformations, hypertension, and tumors. Subarachnoid hemorrhage was found in 19 young patients (17%); the majority were due to aneurysms. The remaining 48 young patients (42%) had cerebral infarction, the majority due to cardiogenic emboli and premature atherosclerosis. Mitral valve prolapse, the use of oral contraceptives, alcohol drinking, and migraine were infrequent sole causes of cerebral infarction in the absence of other risk factors. The case-fatality rate for this group of young patients with stroke was 20.4% compared with 23.9% for the National Survey of Stroke. Young adults with stroke deserve an extensive but tailored evaluation, which should include angiography and echocardiography.
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PMID:Stroke in young adults. 230 61

Preliminary experience with the occasional good survival of patients in Hunt and Hess Grade IV or V with aneurysmal subarachnoid hemorrhage (SAH) led to a prospective management protocol employed during a 2 1/2-year period. The protocol utilized computerized tomography (CT) scanning to diagnose SAH and to obtain evidence for irreversible brain destruction, consisting of massive cerebral infarction with midline shift or dominant basal ganglia or brain-stem hematoma. These patients, along with those who exhibited poor or absent intracranial filling on CT or angiography, were excluded from active treatment and given supportive care only. All other patients had immediate ventriculostomy placement and, if intracranial pressure (ICP) was controllable (less than or equal to 30 cm H2O without an intracranial clot or less than or equal to 50 cm H2O in the presence of a clot), went on to have craniotomy for aneurysm clipping. Aggressive postoperative hypertensive, hypervolemic, hemodilutional therapy was subsequently employed. Of 54 patients with poor-grade aneurysms, ventriculostomy was placed in 47 (87.0%) and yielded high ICP's in the overwhelming majority, with the mean ICP being 40.2 cm H2O. Nineteen poor-grade aneurysm patients received no surgical treatment and survived a mean of 31.8 hours with 100% mortality. Thirty-five patients underwent placement of a ventriculostomy, craniotomy for aneurysm clipping and intracranial clot evacuation, and postoperative hypertensive, hypervolemic, hemodilutional therapy. The outcome at 3 months of the 35 patients who were selected for active treatment was good in 19 (54.3%), fair in four (11.4%), poor in four (11.4%), and death in eight (22.9%). It is concluded that poor-grade aneurysm patients usually present with intracranial hypertension, even those without an intracranial clot. Based on radiographic rather than neurological criteria, a portion of these patients can be selected for active and successful treatment. Increased ICP can be present without ventriculomegaly, and immediate ventriculostomy should be performed. As long as ICP is controllable, craniotomy and postoperative intensive care can effect a favorable outcome in a significant percentage of these patients.
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PMID:Management morbidity and mortality of poor-grade aneurysm patients. 231 14

Cerebral infarction, headache, and hypertension are well-known complications of carotid endarectomy (CEA). Seizures are a less frequent, but important complication. We describe eight patients with focal and generalized seizures following CEA. Seizures occurred 6 to 13 days after CEA. All began as focal motor seizures contralateral to the side of the CEA, and six patients developed generalized tonoclonic seizures. Lorazepam and phenytoin sodium controlled the seizures. Five patients without evidence of stroke on computed tomographic scan were normal in follow-up and had no further seizures. The other three patients had mild deficits. One developed a chronic seizure disorder. The pathogenesis of this syndrome following CEA remains unclear, but may involve cerebral hyperperfusion, cerebral embolization, or both.
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PMID:Seizures following carotid endarterectomy. 199 2

That non-rheumatic atrial fibrillation is an independent risk factor for cerebral infarction has not been established with certainty. The rationale underlying contemporary clinical trials of warfarin therapy for the prevention of stroke in patients who have non-rheumatic atrial fibrillation is that the majority of strokes in such patients are due to cardiogenic cerebral embolism. However, there is evidence to suggest that the increased probability of stroke attributed to this arrhythmia is due to its association with other risk factors such as hypertension, diabetes mellitus, and atherosclerosis. The question of who should be anticoagulated is a major public health issue since atrial fibrillation is present in approximately ten per cent of the general population aged 65 or more years.
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PMID:Is atrial fibrillation an independent risk factor for stroke? 235 52


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