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

Three patients with severe postoperative hemiplegia and one with hemiplegia following a subarachnoid hemorrhage are presented. None had hematomas. All were treated with dopamine-induced hypertension, mannitol, and large quantities of intravascular fluids. All showed a remarkable degree of clinical improvement, presumably secondary to an increase in cerebral blood flow.
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PMID:Treatment of aneurysmal hemiplegia with dopamine and mannitol. 69 Jun 80

By using measurements of cerebral blood flow and internal carotid artery pressure it is possible to select patients in whom carotid ligation can be performed with a very low risk of post-operative cerebral ischaemia. A study has been carried out in 100 patients comparing this method with clinical predictions of the type used in aneurysm surgery based on age of the patient, arterial hypertension, time from latest subarachnoid haemorrhage, and neurological status on a modified Botterell scale. These clinical factors were found to be of little value in predicting which patients would and would not develop cerebral ischaemia after carotid occlusion.
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PMID:Safety of carotid ligation and its role in the management of intracranial aneurysms. 84 9

Sudden death is defined as any death that occurs less than 24 hours after the onset of first symptoms. Strokes account for 10 to 20% of all sudden deaths. The records of all residents of Rochester, Minn., who had their first stroke during the period 1955 through 1969 were analyzed. Among 255 deaths caused by the first stroke, 52 were sudden. Twenty-six of the deaths were due to primary intracerebral hemorrhage, and 20 to primary subarachnoid hemorrhage. Only two of the sudden deaths were caused by infarction: one by pontine and cerebellar infarct and the second by a cortical infarct, which resulted in death from status epilepticus. Among the nine patients who died within 2 hours of the onset of symptoms, six had primary subarachnoid hemorrhage. Hypertension was noted in 23 of the 26 patients (88%) who died of primary intracerebral hemorrhage; 8 patients with primary intracerebral hemorrhage were on long-term oral anticoagulant therapy, and all 8 were hypertensive.
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PMID:Sudden death from stroke. 87 Oct 28

The long-term evaluation of 60 patients who suffered a subarachnoid hemorrhage and survived 6 months is reported. By bilateral carotid arteriography, all patients were shown to have a single aneurysm at the vicinity of the posterior communicating artery at its junction with the internal carotid artery. The patients had previously been randomly assigned to treatment either by bed rest or by common carotid ligation. Average duration of survival among those followed is 8 years. Late rebleeding episodes were found to occur at a similar rate, irrespective of mode of treatment in the studied populations, but morbidity following operation continued to remain somewhat less over the ensuing years of follow-up study compared with the patients treated conservatively. On final assessment many years after the original hemorrhage, there is little improvement in degree of morbidity in either treatment group, and hypertension is noted to develop in the patients undergoing carotid ligation. A larger number of cases will be required to validate these findings.
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PMID:Late morbidity and mortality of common carotid ligation for posterior communicating aneurysms. A comparison to conservative treatment. 90 36

This paper reports a retrospective study of the microneurosurgical management of intracranial aneurysm in 133 patients. Good or fair results were obtained in 76%, 12% of patients had a poor result and the mortality was 12%. Major factors which were found to influence the outcome of surgery were: pre-operatively, the Botterell grade of the patient, pre-existing systemic hypertension and the time interval between the last subarachnoid haemorrhage and surgery. Post-operatively, the development of cerebral vasospasm was associated with a poor outcome from surgery. Better results might be obtained from the surgery of intracranial aneurysm by delaying operation to the second week after subarachnoid haemorrhage and by better management of hypertensive patients pre-operatively and patients who develop cerebral vasospasm post-operatively.
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PMID:Some observations on the microneurosurgical treatment of intracranial aneurysms. 96 9

Subarachnoid haemorrhage from intracranial aneurysms has a poor prognosis. Operative management of intracranial aneurysms was once considered ineffective. The first 100 cases treated by micorsurgery were analysed to see whether mortality and morbidity were reduced. Modern surgical techniques halved the total mortality but the morbidity was unaltered. Results can be improved by delaying surgery seven days and by treating any hypertension before surgery.
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PMID:Intracranial aneurysms: analysis of results of microneurosurgery. 96 61

The devastating natural history of 138 consecutive admissions for non-traumatic intracranial hemorrhage to a major emergency care municipal hospital is reviewed. Sixty-four percent of the patients had demonstrable intracranial hematomas while 36% had mainly subarachnoid hemorrhage. Hypertension was a related condition in 43% of the parenchymal hematoma patients, while proved aneurysms accounted for 74% of the subarachnoid hemorrhage patients. There was only a 14% survivorship for patients requiring emergent surgery. All operated hematoma patients survived delayed surgery with improved level of responsiveness. The overall mortality was 74% for intracranial hematoma patients and 58% for aneurysm-caused subarachnoid hemorrhage patients.
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PMID:Primary non-traumatic intracranial hemorrhage. A municipal emergency hospital viewpoint. 100 37

One case with Wallenberg's syndrome followed by the neck clipping of the posterior inferior cerebellar aneurysm was reported. The patient was 49 years old female with the subarachnoid hemorrhage, who had previously no history of the cardiovascular disease. The vertebral angiogram revealed a saccular aneurysm of the left vertebral artery at the origin of the posterior inferior cerebellar artery. The preoperative neurological examination were normal, except for the slight degree of the meningeal irritation. The surgical intervention was successfully performed on 39th day after the subarachnoid hemorrhage. Postoperative course was eventful, presenting the typical Wallenberg's syndrome, which was complicated the accompanying signs. The troublesome accompanying signs were chiefly automatic respiratory dysfunction (sleep-induced dyspnea), autonomic dysfunction (Horner's syndrome, perspiration, hypertension), and restless confusion. The postoperative vertebral angiogram showed the obliteration of the aneurysm and the sufficient circulation of the vertebrobasilar system, especially the posterior inferior cerebellar artery. The mechanism of "sleep-induced dyspnea" was discussed in detail from the literatures. In addition to the above mentioned, it should be stressed that the recognition of "sleep-induced dyspnea" and the other accompanying signs are important for the treatment of the patient with the brain stem lesion.
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PMID:[Wallenberg's syndrome with sleep-induced dyspnea--a case study]. 103 29

On the autopsy findings of the 140 consecutive stroke cases, some characteristics of cerebrovascular diseases in this district were discussed. Predominance of intracranial hemorrhage (cerebral hemorrhage and subarachnoid hemorrhage) over cerebral infarction was still evident. Ruptured intracranial aneurysms were demonstrated in 98% of fatal subarachnoid hemorrhage. Compared with the autopsy data of other institutions, the age of death was generally low, the median age for cerebral hemorrhage, subarachnoid hemorrhage and cerebral infarction falling in the fourth, fifth, and sixth decade, respectively. Cerebellar hemorrhage was relatively frequent, while blood dyscrasias and other symptomatic hemorrhage constituted only a small part in contrast with the report of American authors. A dominant role of hypertension in causing strokes was concluded from both the heart weight and the clinical records.
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PMID:Analysis of 140 consecutive autopsy cases of cerebrovascular strokes in northern Japan. 108 83

Due to the rapid evolution of vascular lesions it is not surprising that most causes of sudden death of cerebral origin are due to vascular pathology. Of the traumatic causes extradural haemorrhage is a fairly common clinical entity but as a cause of death declining in its frequency. Sources of diagnostic error can be attributed to the fact that not all patients with extradural haematomas have marked external evidence of trauma and a significant number, particularly children and adolescents, show no radiological, clinical or for that matter, post-mortem evidence of a fracture. Subdural haematomas of a chronic variety are usually produced by minor trauma and occur predominantly in the older person. Acute subdural haematomas are most frequently the result of trauma and may be rapidly fatal due to the associated massive cerebral damage. That intracranial aneurysm or angioma may rupture into the subdural space and cause an acute or chronic subdural haematoma, is less widely appreciated. The acute spontaneous arterial subdural haematoma due to the rupture of a cortical vessel, usually one affected by atheroma, into the subdural space is an uncommon entity. It should be looked for specifically in patients with minimal trauma and the clinical picture of an acute subdural haematoma. Subarachnoid haemorrhage due to aneurysmal rupture is still the common cause of unexpected rapid demise in young adults. There is very little evidence that antecedent trauma or exertion play a part as precipitating factors. Centrally placed aneurysms situated at the anterior communicating artery origin or terminal carotid seem to be particularly malignant in their effects. Cause of death is usually massive extrusion of blood into the intracranial cavity with increasing intracranial pressure, compressive haematoma formation and widespread arterial spasm with ischaemic consequences. Whether aneurysmal rupture can be caused by trauma cannot really be satisfactorily resolved. Intracerebral haemorrhage is most commonly due to hypertension but, as in the case of other haematomas, bleeding disorders may also be a cause. Intracerebral haematoma may, however, also result from rupture of micro-angiomata and the brain should be carefully examined for them in the young patient without evidence of hypertension. Hypertensive crises occurring in people on monoamine oxidase inhibitors should also be remembered as a cause of intracerebral haemorrhage.
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PMID:Unexpected natural death of cerebral origin in medicolegal practice. 113 58


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