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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of the literature on cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH) has shown that angiographic vasospasm occurs in 67.3% of cases when angiography is timed for the highest likelihood, and delayed ischaemic deficit or symptomatic vasospasm in 32.6%. The presence of vasospasm has a marked effect on overall outcome of SAH, and the outcome of delayed ischaemia itself is in about one-third death and in one-third permanent deficit. Management with fluid loading or induced hypertension and with calcium antagonists has been reported widely for both prevention and treatment, and can reduce the incidence and improve the outcome of vasospasm. Other forms of treatment including tissue plasminogen activator, aminosteroids and transluminal angioplasty also appear useful. In spite of these improved therapeutic possibilities, large numbers of patients are still being reported in whom no specific treatment is used.
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PMID:Cerebral arterial spasm--a clinical review. 754 61

Only 53%-58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. PATHOPHYSIOLOGY. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6-12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. CALCIUM ANTAGONISTS. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. HYPERVOLAEMIC HAEMODILUTION. Volume expansion and haemodilution to a hematocrit of 30%-33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10-12 mm Hg and 15-18 mm Hg, respectively. But there is no evidence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. INDUCED ARTERIAL HYPERTENSION. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. CONCLUSION. Treatment of cerebral vasospasm following a SAB aims to avoid any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
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PMID:[Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Therapeutic value of treatment with calcium antagonists, hypervolemic hemodilution and induced arterial hypertension]. 778 50

The two major neurological complications of subarachnoid haemorrhage (SAH) due to an intracranial aneurysm are rebleeding and delayed cerebral ischaemia related to cerebral vasospasm. The best way to prevent rebleeding is early surgery. Even when surgery is performed within the first 72 hours posthaemorrhage, the risk of cerebral ischaemia due to vasospasm is high. Conventional medical treatment of cerebral vasospasm includes haemodilution, hypervolaemia and increase of arterial blood pressure. Haemodilution is of limited value as the patients suffering from SAH have usually a low haematocrit. The effectiveness of hypervolaemia is controversial and it may worsen cerebral and pulmonary oedema. Systemic hypertension is an effective therapy of vasospasm, but which can only be used once the aneurysm is controlled. Nimodipine and nicardipine, two calcium antagonists, have a beneficial effect on neurologic outcome following SAH. Today, it is still debated whether the beneficial effect of nimodipine results from the vascular effect of the drug or from a direct cerebral cytoprotective mechanism. Early surgery implies that surgeons operate on brains in acute inflammatory state. Thus, it is mandatory to use peroperative techniques improving cerebral exposure. These techniques include infusion of mannitol, lumbar cerebrospinal fluid (CSF) drainage, administration of anaesthetic agents known to decrease cerebral blood flow (CBF) and hypocapnia. Usually, the effect of CSF drainage is very effective and sufficient by itself. The second objective in the peroperative period is to avoid ischaemia. In areas with decreased flow distal to vasospasm, autoregulation is impaired and CBF is directly dependent on cerebral perfusion pressure. Furthermore, the safe practice of transient clipping of vessels supplying the aneurysm has dramatically reduced the indications of controlled hypotension. During temporary clipping, some authors recommend a pharmacological brain protection using barbiturates, etomidate or propofol, but this practice has not been validated by randomized studies. However, it is generally agreed that the arterial pressure should be increased during temporary clipping to improve collateral blood flow and to maintain it after the aneurysm has been secured. To conclude, together with lumbar CSF drainage and transient clipping, the anaesthetic management of the patients should include: maintenance of the arterial blood pressure close to its preoperative level, maintenance of PaCO2 between 30 and 35 mmHg and of normovolaemia through replacement of fluid and blood losses. After completion of surgery, recovery from anaesthesia should be rapid to allow fast diagnosis of neurological complications. The monitoring of the status of consciousness is the key of the diagnosis of early postoperative complications.
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PMID:[Anesthesia in surgery for intracranial aneurysms]. 781 6

Because of their action as cerebral vasodilators, dihydropyridine calcium antagonists have received intense scrutiny for their potential benefit in ameliorating the devastating consequences of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). From October, 1987, to September, 1989, 41 North American neurosurgical centers in the Cooperative Aneurysm Study accrued 906 patients with recent (Days 0 to 7) aneurysmal SAH into a prospective randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine to test whether treatment with this agent improved overall outcome. Eligible patients received 0.15 mg/kg/hr of either nicardipine or placebo by continuous infusion for up to 14 days following hemorrhage. The 449 patients randomly assigned to the nicardipine-treated group and the 457 patients assigned to the placebo-treated group were balanced with regard to prognostic factors for ischemic deficits from vasospasm and for overall outcome. Other medical and surgical interventions were used with similar frequency in both groups, except that antihypertensive agents were used less frequently in the nicardipine-treated patients (26% of the nicardipine-treated group vs. 43% of the placebo-treated group, p < 0.001), and more patients in the placebo-treated group had intentional hypervolemia, induced hypertension, and/or hemodilution administered therapeutically for symptomatic vasospasm (38% of the placebo-treated group vs. 25% of the nicardipine-treated group, p < 0.001). The incidence of symptomatic vasospasm during the treatment period was higher in the placebo-treated group (46%) than in the nicardipine-treated group (32%) (p < 0.001). Despite the reduction in symptomatic vasospasm in the nicardipine-treated group, overall outcome at 3 months was similar between the two groups. Fifty-five percent of nicardipine-treated patients were rated as having a good recovery according to the Glasgow Outcome Scale at follow-up review and 17% were dead, compared to 56% and 18%, respectively, in the placebo-treated group (not statistically significant). These data suggest that high-dose intravenous nicardipine treatment is associated with a reduced incidence of symptomatic vasospasm in patients with recent aneurysmal SAH, but not with an improvement in overall outcome at 3 months when compared to standard management in North America. It is postulated that, while nicardipine prevents vasospasm, hypertensive/hypervolemic therapy may be effective in reversing ischemic deficits from vasospasm once they occur.
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PMID:A randomized controlled trial of high-dose intravenous nicardipine in aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study. 845 Mar 26

Calculation program software of the four rules of arithmetic in computed tomography (CT) has been introduced for clinical purposes since 1990. Evaluation of hemodynamic reserve and cerebral autoregulation can be calculated using this software in ischemic cerebrovascular diseases and delayed cerebral vasospasm after ruptured intracranial aneurysms. Eight hemodynamic maps can be entered and calculation based on the four rules of arithmetic can be performed between them and shown visually. For example, delta CBF [CBF after administration of acetazolamide (B)-CBF before its administration(A)] and % CBF [(B - A)/A x 100] maps are useful in evaluation of the capacity of hemodynamic reserve in ischemic cerebrovascular diseases. And delta CBF [CBF before induced hypertension using intravenous dopamine administration (B)-CBF during induced hypertension (A)] and % CBF [(B - A)/A x 100] also can be used in evaluation of cerebral autoregulation and decision concerning indication of the need for induced hypertension during the period of delayed cerebral vasospasm after subarachnoid hemorrhage.
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PMID:[Clinical application of calculation software of the four rules of arithmetic on computed tomography]. 847 85

Following subarachnoid haemorrhage, delayed cerebral ischaemia from cerebral vasospasm remains the most important cause of mortality and morbidity in patients with surgically secured aneurysms. Therapy with haemodilution, hypertension and volume expansion has been recommended to prevent and treat delayed cerebral ischaemia in these patients on the basis of uncontrolled clinical series (level of evidence III to V, grade C recommendation). Despite the lack of controlled studies, the maintenance of a cardiac index > 3.5 L.min-1.m-2 and a systolic arterial pressure between 120 and 150 mmHg before clipping and 160 to 200 mmHg thereafter is recommended as a prophylactic or therapeutic measure for vasospasm. Close monitoring of neurological and cardiorespiratory status is important to avoid neurologic and systemic complications.
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PMID:[Enhancement of cardiac performance for prevention and treatment of delayed cerebral ischemia caused by vasospasm]. 875 96

Noradrenaline (NA)-containing nerves, mainly originating in the sympathetic superior cervical ganglia, supply large and small cerebral arteries. In large cerebral arteries, nerves containing serotonin (5-hydroxytryptamine, 5-HT) may represent neuronal uptake of circulating 5-HT by sympathetic nerves. 5-HT-containing nerves supplying small pial vessels probably have a central origin in the dorsal raphe nucleus. In most species, NA is a weak vasoconstrictor (alpha 1- or alpha 2-adrenoceptors), while 5-HT is a potent vasoconstrictor (5-HT2 or 5-HT1-like receptors) of large cerebral arteries. In contrast, both NA and 5-HT tend to cause vasodilatation in small pial vessels and arterioles. Adrenergic and serotonergic transmission can be modulated by pH, a range of putative neurotransmitters and neuromodulators, and by the endothelium. Sumatriptan, a 5-HT1-like receptor agonist, has been shown to be effective in the treatment of migraine. Changes in NA- or 5-HT-containing nerves and/or in the responses of cerebral vessels to NA and 5-HT have been observed in a variety of vascular disorders, including cerebral vasospasm following subarachnoid haemorrhage, hypertension, and atherosclerosis.
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PMID:Innervation of cerebral arteries by nerves containing 5-hydroxytryptamine and noradrenaline. 878 67

Sixteen patients (6 women, 10 men; mean age: 52.5 years) suffering from spontaneous subarachnoid haemorrhage (SAH) of unknown origin underwent a protocol of initial and then weekly computed tomography (CT), initial four-vessel digital subtraction angiography (DSA) and at least one control pancerebral DSA. Fourteen patients had magnetic resonance imaging before undergoing first control DSA. All patients had calcium-antagonists (Nimodipine) via a central venous catheter, were kept on the neurosurgical intensive care unit and followed daily with transcranial Doppler ultrasonography (TCD). One patient (6.3%) developed moderate and 5 (31.1%) developed severe cerebral vasospasm as documented with TCD and exhibited deterioration of their level of consciousness. These 6 patients were treated with induced hypertension, hypervolaemia and haemodilution. Their blood flow velocities were elevated for a mean of 8 (5-17) days with a peak after 12.5 (9-17) days following SAH. No complications due to treatment were noted. One patient of the non-vasospastic group died of pulmonary embolism, another patient had an ischaemic incident during angiography, which has led to permanent disability. On follow-up 2-24 months after SAH 14 patients had returned to their premorbid state. It is concluded that patients suffering from SAH of unknown origin should undergo repeated angiographic investigation and subsequent daily monitoring of their neurologic status including daily TCD recordings so that haemodynamic treatment can be established in the event of cerebral vasospasm, which may occur in up to one third of these patients.
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PMID:Cerebral vasospasm after subarachnoid haemorrhage of unknown aetiology: a clinical and transcranial Doppler study. 880 Mar 32

Four consecutive patients with subarachnoid hemorrhage were studied by serial cranial CT and transcranial Doppler ultrasonographic recordings. Patients were in the age range 52 to 67 years. According to Hunt and Hess scale the clinical status varied between grade I and IV. Increase in intracranial pressure "masked" the hemodynamic signs of cerebral vasospasm, reappeared after normalization of intracranial pressure following therapeutic management. Based on the reported findings transcranial Doppler ultrasonography should be considered an indispensabile diagnostic procedure however inadequate for monitoring the natural history of vasospasm complicated by intracranial hypertension.
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PMID:[Cerebral vasospasm and intracranial hypertension: transcranial Doppler ultrasonographic findings]. 885 24

Since the discovery of the most potent vasoconstrictor peptide, endothelin, in 1988, explosive investigations have rapidly clarified much of the basic pharmacological, biochemical and molecular biological features of endothelin, including the presence and structure of isopeptides and their genes (endothelin-1, -2 and -3), regulation of gene expression, intracellular processing, specific endothelin converting enzyme (ECE), receptor subtypes (ETA and ETB), intracellular signal transduction following receptor activation, etc. ECE was recently cloned, and its structure was shown to be a single transmembrane protein with a short intracellular N-terminal and a long extracellular C-terminal that contains the catalytic domain and numerous N-glycosylation sites. In addition to acute contractile or secretory actions, endothelin has been shown to exert long-term proliferative actions on many cell types. In this case, intracellular signal transduction appears to converge to activation of mitogen-activated protein kinase. As a recent dramatic advance, a number of non-peptide and orally active receptor antagonists have been developed. They, as well as current peptide antagonists, markedly accelerated the pace of investigations into the true pathophysiological roles of endogenous endothelin-1 in mature animals; e.g., hypertension, pulmonary hypertension, acute renal failure, cerebral vasospasm, vascular thickening, cardiac hypertrophy, chronic heart failure, etc. Thus, the interference with the endothelin pathway by either ECE-inhibition or receptor blockade may provide an exciting prospect for the development of novel therapeutic drugs.
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PMID:Molecular pharmacology and pathophysiological significance of endothelin. 901 36


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