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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following subarachnoid hemorrhage using a uniform management protocol over a 24-month period. One hundred eighteen consecutive patients were admitted to the neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not attributed to trauma, tumor, or vascular malformation (113 patients had aneurysms). Early surgery was performed whenever possible, and hypertensive hypervolemic hemodilution therapy was instituted at the first sign of clinical vasospasm. Forty-two patients (35.6%) developed characteristic signs and symptoms of clinical vasospasm with angiographic verification of spasm in 39 cases. All patients with clinical vasospasm received hypervolemic hemodilution therapy aiming for a hematocrit of 33-38%, a central venous pressure of 10-12 mm Hg (or a pulmonary wedge pressure of 15-18 mm Hg), and a systolic arterial pressure of 160-200 mm Hg (120-150 mm Hg for unclipped aneurysms) for the duration of clinical vasospasm. Over the course of treatment, 60% of patients with clinical vasospasm had sustained improvement by at least 1 neurologic grade, 24% maintained a stable neurologic status, and 16% continued to worsen. At the end of hypervolemic hemodilution therapy, 47.6% had become neurologically normal, 33.3% had a minor neurologic deficit, and 19% had a major neurologic deficit or were dead. There were 3 instances of cardiopulmonary deterioration (7%), all of which were in patients without Swan-Ganz catheters, and all resolved with appropriate diuresis. One patient rebled and died while on hypervolemic hemodilution therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension. 356 92

Because previous reports have suggested that IgE-mediated events may lead to both platelet activation and arterial spasm, a population-based study of 262 men and 315 women, aged 38 to 82, was conducted to investigate the association of serum IgE levels with myocardial infarction, stroke, and noninvasively diagnosed large-vessel peripheral arterial disease. In men with previous myocardial infarction, previous stroke, or current large-vessel peripheral arterial disease, geometric mean serum IgE levels were increased 119 percent, 164 percent, and 78 percent, respectively. These associations were statistically significant (p less than 0.05). Because IgE was positively or inversely correlated with several traditional cardiovascular disease risk factors, logistic regression was used to evaluate the independent association of IgE with any cardiovascular disease (myocardial infarction, stroke, or large-vessel peripheral arterial disease). In a model including age, cigarette smoking, fasting plasma glucose level, diastolic blood pressure, and low-density lipoprotein cholesterol level as covariates, IgE was positively and independently associated with any cardiovascular disease (p = 0.03). Similar evaluations in women revealed no correlation between IgE and cardiovascular disease by either univariate or multivariable analysis. These data indicate that IgE may be an independent marker for cardiovascular disease in men, and thus suggest IgE-mediated events may play a role in the pathogenesis of cardiovascular disease.
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PMID:IgE and cardiovascular disease. Results from a population-based study. 357 66

Cocaine use has increased rapidly over the past few years. This has led to an increase in the number and variety of cocaine-related conditions for which medical attention is sought. Among these have been several cases of intracranial hemorrhage. Four cases reported in the literature and 6 from our own institution are presented here. They represent different diagnoses including hemorrhage from aneurysms and arteriovenous malformations, hemorrhage into a tumor, and spontaneous hemorrhage with no underlying lesion with and without preexisting hypertension. Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. Cocaine may also cause arterial spasm. Although the pathophysiology has not been entirely resolved, the clinical significance of this association is clear. Intracranial hemorrhage should be considered in the differential diagnosis whenever a patient presents with an acute alteration in neurologic examination associated with cocaine use.
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PMID:Intracranial hemorrhage and cocaine use. 360 97

Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
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PMID:[Vascular spasms in microsurgery]. 362 68

The authors report a case of pituitary apoplexy associated with oculomotor defects and focal cerebral signs; the visual pathways were intact. Computed tomography documented a mass of heterogeneous density within an enlarged sella turcica and a right parietal infarct. Angiograms revealed bilateral carotid spasm and occlusion of the right angular artery. Treatment was conservative. Control angiograms showed spontaneous resolution of the vasospasm and recanalization of the cortical artery. The patient made a complete neurological recovery; he needed only treatment with vasopressin due to transient diabetes insipidus. The risk of vasospasm and brain ischemia should be kept in mind when treating pituitary apoplexy. The early occurrence of vasospasm in our case suggests the participation of powerful vasoactive agents liberated from the tumor.
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PMID:Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. 380 76

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic vasospasm. Lesioning at the level of the mesencephalon of the ascending catecholamine pathways from locus coeruleus in the pons and the A1 and A2 nuclei in the medulla oblongata prior to cisternal blood injection prevents the development of both acute and late spasm. Selective lesioning in the medulla oblongata of ascending fibres from A1 and A2 also prevents development of spasm, indicating that these nuclei, which project to the hypothalamus-pituitary, are essential for the spasm syndrome. It is suggested that a substance vasospasm is produced by a substance liberated either by the hypothalamus or by the pituitary is involved in the occurrence of spasm.
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PMID:Subarachnoid haemorrhage in the rat: effect on the development of vasospasm of selective lesions of the catecholamine systems in the lower brain stem. 389 91

An overview of the possible factors that might contribute to the development of cerebral vasospasm is presented, with particular emphasis on the possibility that spasm arises from a malfunction of the regulatory or contractile processes in smooth muscle cells. This possibility is emphasized because the evidence for cellular damage and the delayed occurrence of vasospasm are suggestive of pathological alteration. Data regarding the development of spasm in vivo has been reviewed and, to the extent possible, correlated with in vitro studies of cerebrovascular smooth muscle contractility. Short-term in vitro studies of normal cerebral arteries may be of little relevance to the prolonged and severe cerebral vasoconstriction that occurs only after a delay of several days from the initial insult.
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PMID:The relevance of in vitro smooth muscle experiments to cerebral vasospasm. 389 90

In the rat an intracisternal injection of blood induces an angiographically demonstrable biphasic cerebral arterial vasospasm. Chemical destruction of the central serotoninergic and dopaminergic pathways prior to the cisternal blood injection does not affect the spasm pattern after the subarachnoid haemorrhage. It is suggested that neither system plays a role in the development of spasm.
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PMID:Subarachnoid haemorrhage in the rat: effect on the development of cerebral vasospasm of lesions in the central serotoninergic and dopaminergic systems. 394 90

We examined the relationship between the biological protective mechanisms of scavengers and free radicals that are elicited by subarachnoid hemorrhage (SAH) in the pathogenesis of prolonged vasospasm following ruptured intracranial aneurysm. The study included 25 patients treated by early surgery (within 72 hours after SAH). Lipid peroxides concentrations and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px) in the cerebrospinal fluid (CSF) were measured. The concentration of lipid peroxides increased significantly more (p less than 0.05) during the first 4 days after SAH in patients with symptomatic vasospasm than in those without. Patients with symptomatic vasospasm had a marked decrease in SOD activity on Days 3 and 4 followed by a gradual decrease, whereas the patients without spasm showed little change (difference between the groups, p less than 0.05). There was a significant difference in catalase activity reversal to SOD activity, but no difference in GSH-px activity. Thus, correlation was close between the increased lipid peroxides concentration and the decrease in SOD activity in CSF (p less than 0.05), suggesting an important mechanism in the pathogenesis of vasospasm.
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PMID:Biological defence mechanism in the pathogenesis of prolonged cerebral vasospasm in the patients with ruptured intracranial aneurysms. 396 28

A subarachnoid haemorrhage (SAH) in the rat was produced by the injection of blood via a previously implanted catheter connected to the cisterna magna. Repeated angiographical examinations of the vertebro-basilar arteries revealed a biphasic vasospasm with a maximal acute spasm at ten minutes and a maximal late spasm at two days after cisternal blood injection. Fluorescence microscopical examination of the major cerebral arteries at day two after the SAH revealed a reduction in the fluorescence intensity and in the number of histochemically visible sympathetic nerve terminals.
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PMID:Subarachnoid haemorrhage in the rat: angiography and fluorescence microscopy of the major cerebral arteries. 402 74


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