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At least 19 recordsLinked to original sources
PubMed1998

Three-dimensional CT angiography of intracranial vasospasm following subarachnoid haemorrhage.

We evaluated the usefulness of three-dimensional CT angiography (3D-CTA) in the diagnosis of intracranial vasospasm following subarachnoid haemorrhage (SAH) in 13 patients suspected of having vasospasm on clinical grounds. The intracranial vessels were clearly shown by 3D-CTA in 12 patients. 3D-CTA revealed spasm in the vessels of nine patients. Catheter angiography performed in seven of these patients immediately after 3D-CTA confirmed vasospasm. A low-attenuation area was seen on CT in the other two patients, representing an ischaemic lesion due to the spasm. In nine patients, a second 3D-CTA was performed using the same technique 1 week after the first, showing no vasospasm. Initial 3D-CTA revealed no vasospasm change in three patients. Following 3D-CTA, one of these had conventional angiography, which also demonstrated no spasm.

Adult↗
PubMed1993

Role of transcranial Doppler in neuroradiological treatment of intracranial vasospasm.

BACKGROUND AND PURPOSE: The expanded role of interventional neuroradiological treatment for post-subarachnoid hemorrhage vasospasm has highlighted the diagnostic utility of transcranial Doppler studies in this condition. The role of transcranial Doppler in follow-up and determining the need for repeat intervention has not been previously emphasized. SUMMARY OF REPORT: Intracranial angioplasty for clinically evident vasospasm after subarachnoid hemorrhage was performed in four patients. In two patients, transcranial Doppler flow velocities remained elevated despite initial anatomic correction of the vasospasm. Reangiography revealed new areas of involvement by vasospasm. Reangioplasty or papaverine infusion treatment of the new lesions resulted in decreased flow velocities and clinical improvement in all patients. CONCLUSIONS: Transcranial Doppler has a more significant role than has been previously emphasized in the management of patients undergoing interventional neuroradiological treatment for intracranial vasospasm. Specifically, the persistence of elevated transcranial Doppler flow velocities after intracranial angioplasty suggests the need for repeat angiographic evaluation and possibly further therapy.

Aged↗
PubMed1993

Severe diffuse intracranial vasospasm as a cause of extensive migrainous cerebral infarction.

We report on a 47-year-old white female with a long history of recurrent episodes of migraine with aura, who progressed to develop a continuous intractable headache during the course of which cortical blindness and quadriparesis occurred due to extensive and bilateral hemispheric cerebral infarction. Severe diffuse intracranial major arterial vasospasm was demonstrated by arteriogram. All studies were negative for CNS vasculitis, including cerebral biopsy. The arterial spasm reversed itself, but the patient did not improve. Smoking was the only additional risk factor. Vasospasm is an important cause to be considered in migrainous infarctions. The use of vasoconstrictor agents such as DHE in patients with migraine with prolonged aura has to be carefully re-evaluated.

Blindness↗
PubMedDate not supplied

[Management of intracranial vasospasm in rupture of cerebral aneurysm].

This paper describes the methods of prevention of delayed neurological deficit (DND) in patients with subarachnoid haemorrhage (SAH) due to ruptured intracranial aneurysm. To prevent the decrease in the cerebral flow, vasodilators, inhibitors of platelet aggregation and synthesis of endogenous prostaglandins, stimulators of prostacyclin synthesis of its analogue should be applied. It is also recommended to use the inhibitors of phosphodiesterase, blockers of serotonin and of calcium channel (particularly nimodipine). Therapy with the immunosuppressive drugs helps to prevent DND. With all those therapeutical methods DND is still a serious complication following SAH.

Cerebral Arteries↗
PubMed1985

Early aneurysm operation and vasospasm. Intracranial Doppler findings.

Modern ultrasonic Doppler systems enable us for the first time to carry out intraoperative and pre- and postoperative investigations of the circle of Willis. The application of Doppler in acute aneurysm surgery provided the following information: During the first 3 days following subarachnoid bleeding from a cerebral aneurysm, no signs of vasospastic reaction were found by Doppler sonography. Thereafter, 90% of all patients operated on in the acute stage demonstrated localized acceleration as a sign of vasospasm, despite prophylactic nimodipine treatment. Thirty-eight percent of the patients developed delayed ischemic deficits, which, however, were only transient. These results may indicate that early surgery and nimodipine prophylaxis may not prevent vasospasm but do reduce its consequences.

Adult↗
PubMed1991

[A model for intracranial vasospasm in subarachnoid hemorrhage].

Cerebral vasospasm (V.S.P.) is a major complication of subarachnoid hemorrhage. In order to investigate this cerebral vasospasm, an intracisternal injection of autologous blood and topical application around the internal carotid artery was performed in the dog model. Thirty dogs were divided into five groups and a cerebral angiography was performed on D0, D2, D5, D7 and D9. In comparison with the control group (group 1), the angiography in group 2 (12 dogs) systematically exhibited severe V.S.P. In group 3 (intracisternal injection of venous blood: 5 dogs), the angiography exhibited no vasospasm at all. In group 4, a left frontoparietal flap was opened, allowing us to deposit blood around the carotid bifurcation. In these cases, a severe narrowing of cortical arteries was demonstrated. In group 5 (intracisternal injection of heparinated blood), no vasospasm was observed. These findings suggest that the vasospasm involves the circle of Willis' as well as the cortical arteries.

Animals↗
PubMed1979

Intracranial vasospasm: a study with iron compounds.

The effects of topically applied hemoglobin, methemoglobin, hemin, ferrous chloride (FeCl2) and ferric chloride (FeCl3) were investigated by observation through the operating microscope to determine their effect on the normal and spastic canine basilar artery. Following transclival exposure, the artery was made spastic by puncture or topical barium chloride. No consistent changes in arterial diameter were seen with topical hemoglobin, methemoglobin, or hemin. The buffered ferrous ion (Fe++) caused marked vasodilation at concentrations of 10 microgram/ml. The buffered ferric ion (Fe++) caused mild vasoconstriction at similar concentrations. The possible role of iron (a component of hemoglobin) in vasospasm following subarachnoid hemorrhage and subsequent hemoglobin degradation is discussed.

Animals↗
PubMed1975

The relief of intracranial vasospasm: an experimental study with methylprednisolone and cortisol.

The effects of topically applied soluble glucocorticosteroids (methyl-prednisolone and cortisol) were investigated by observation through the microscope to determine their effect on the canine basilar artery and the canine and monkey arterial circle of Willis made spastic by puncture or by topical barium chloride, prostaglandin (F-2alpha), or serotonin. The steroids were tested without their normal diluent; the diluent was tested separately. Marked vasodilatory effects of the major arteries and the smallest visible arteries were found with both of these steroids. Moderate vasodilatory effects also were found with the diluent alone. In addition methylprednisolone was injected into the vertebral artery (40 mg) and intravenously (10 mg/Kgm); vasodilation beyond that seen in the absence of drug injection was not observed. In monkeys whose circle of Willis was made spastic by arterial puncture, severe spasm persisted at 24 and 72 hours. If the puncture was followed by topical application of 10 mg of 4% methylprednisolone acetate, spasm was not seen at 24 or 72 hours.

Animals↗
PubMed1989

Risk factors in intracranial saccular aneurysms. Aspects on the formation and rupture of aneurysms, and development of cerebral vasospasm.

Intracranial saccular aneurysms have been a well-known clinical and pathological entity for over two centuries. The pathophysiological events that lead to aneurysm formation and rupture are, however, poorly understood. Besides an HLA-associated genetic factor, the most widely accepted risk factors are arterial hypertension, female gender, and increasing age. Some aneurysm patients have a deficient formation of Type III collagen. This seems to interfere with the mechanical integrity of the cerebral arterial wall encouraging aneurysm formation. While some of the risk factors may be involved in the process of aneurysm formation, others may be of importance in the actual aneurysm rupture. Medical and surgical developments have only had a slight impact on mortality rates from aneurysm rupture. The principal cause of death and disability is cerebral arterial spasm. Considerable effort has been expended in investigating the etiology of this phenomenon. Previous studies have failed to yield conclusive evidence of the causative agent(s) or the nature of cerebral artery narrowing. The time course of vasospasm after the onset of subarachnoid hemorrhage is consistent with an immune-mediated response, and more recent observations suggest that immunological processes including activation of the complement system may be involved. Missed minor bleeding episodes may thus be a risk factor for aneurysm patients in respect to the development of cerebral vasospasm.

Adolescent↗
PubMedDate not supplied

New microballoon device for transluminal angioplasty of intracranial arterial vasospasm.

A new microballoon device has been developed to treat intracranial arterial vasospasm by transluminal angioplasty. The balloon is composed of a unique silicone elastomer that will elongate and conform to the blood vessel lumen, thereby decreasing the risk of vessel rupture. The balloon device, which can be either flow-directed or catheter-guided, is permanently affixed to a 2.0-French microcatheter and introduced from a transfemoral arterial approach. Two balloon sizes are currently available. The smaller-sized balloon, used in most cases, measures 0.85 x 3.50 mm uninflated, will accept a volume of 0.10 ml, and will expand to 3.5 x 12.5 mm. The larger balloon, used in six of 14 cases, measures 1.5 x 3.9 mm uninflated, accepts a volume of 0.50 ml, and expands to 7.5 x 13.5 mm. In clinical trials, this device has been successful in dilating both focal and diffuse areas of vasospasm in multiple territories. Thus far, 40 vascular territories have been successfully treated in 14 patients 15-73 years old. In each case, there was angiographic evidence of successful dilatation, and in 10 patients (71%), clinical improvement in the neurologic condition. Transluminal angioplasty techniques may be useful for reversing some of the serious neurologic sequelae associated with acute intracranial arterial vasospasm.

Angioplasty, Balloon↗
PubMed1992

Intravascular balloon dilatation therapy for intracranial arterial vasospasm: patient selection, technique, and clinical results.

Patients presenting with symptomatic intracranial arterial vasospasm are now being treated by interventional neurovascular techniques in selected cases. From a percutaneous transfemoral approach, a custom-designed silicone microballoon can be guided through the intracranial vessels, and inflated to dilate the spastic vessel(s). This technique has been useful for both focal and diffuse areas of spasm. In clinical trials, 28 patients, ranging in age from 15-73 years have been treated. A total of 99 vascular territories have been successfully dilated in both the anterior and posterior circulations. Clinical improvement following treatment was observed in 17 cases (60.7%). Technical complications directly related to therapy included 2 cases (7.1%) of vessel rupture. In long term clinical follow-up 17 patients (60.7%) had good to excellent outcome, 2 patients (7.1%) remained in poor condition, and 9 patients (32.1%) died despite therapy. In patients presenting with symptomatic intracranial arterial vasospasm who are unresponsive to medical therapy, treatment by balloon angioplasty techniques may help to improve cerebral perfusion and clinical outcome of the patient.

Adolescent↗
PubMed2004

[The effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery].

OBJECTIVE: To evaluate the effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery. METHODS: Thirty consecutive patients under-going intracranial aneurysmal surgery were prospectively randomized into two groups: Isoflurane (group A, n = 15) and nimodipine (group B, n = 15). The patients in group A were maintained with 1 minimum alveolar concentration (MAC) isoflurane anesthesia during the whole procedure. The patients in group B were given nimodipine infusion continuously (20 microg.kg(-1).h(-1)) after induction of anesthesia and anesthetized with 1 MAC isoflurane. S100B levels in cerebrospinal fluid were determined before aneurysm clipping and 0, 2, 4 h after aneurysm clipping by enzyme linked immunosorbent assay. Assessment of mean blood flow velocity of parent arterial and arterial branches were performed before and after aneurysm clipping. RESULTS: (1) S100B in cerebrospinal fluid was increased significantly at 4 h after aneurysm was clipped in group A (F = 4.11, P < 0.05). However, S100B in cerebrospinal fluid was stable in group B in the whole procedure. (2) Mean arterial flow velocity of parent vessels in group B was lower significantly than that in group A (t = 2.08, P < 0.05). However, mean arterial flow velocity of distal vessels in both groups has no significant difference. CONCLUSION: Intraoperative nimodipine infusion may prevent cerebral vasospasm during intracranial aneurysm surgery.

Adult↗
PubMed2004

[The effect of isoflurane induced hypotension on intraoperative cerebral vasospasm in intracranial aneurysm surgery].

OBJECTIVE: To evaluate whether isoflurane induced hypotension increases the incidence of cerebral vasospasm in intracranial aneurysm surgery. METHODS: Thirty consecutive patients undergoing intracranial aneurysmal surgery without preexisting cerebral ischemia were prospectively randomized into 2 groups: isoflurane induced hypotension group (group A, n = 15) and isoflurane maintained anesthesia group (group B, n = 15). The patients in the group A were performed isoflurane induced hypotension after dura opening by increasing the inhaled concentration of isoflurane to decrease the mean arterial pressure (MAP) by 30 - 40 percent of that of baseline value. After the aneurysm was clipped, the concentration of inhaled isoflurane was decreased so as to stop blood pressure reduction. The patient in group B was given 1 minimum alveolar concentration (MAC) of isoflurane during the whole procedure. The indicators of blood circulation were measured before blood pressure reduction, 30 minutes after blood pressure reduction, just after the clipping of the aneurysm, and 30 minutes after stopping blood pressure reduction. The S100B protein level in cerebrospinal fluid was observed before the controlled hypotension and 0, 2, and 4 h after the aneurysm was clipped. Assessment of the mean blood flow velocity of parent artery and its main branches was performed by microvascular ultrasonics before and after the aneurysm was clipped. The patients were followed-up for one week after the operation to observe the neurological complication. RESULTS: The MAP was decreased from 95 mm Hg +/- 12 mm Hg to 59 mm Hg +/- 5 mm Hg 30 minutes after the induced hypotension, and resumed to 75 mm Hg +/- 8 mm Hg 30 minutes after the aneurysm was clipped. Compared with those in the group B, both the total systemic vascular resistance and myocardial contract acceleration were decreased in group A, whereas the cardiac output and heart rate remained stable. (2) 4 hours after the aneurysm was clipped the S100B protein level in CSF was increased significantly in both groups, and that in the group A being significantly higher than that in the group B (t = 2.854, P < 0.01). (3) In the group A, the mean arterial flow velocity of distal parent vessels increased by more than 30 percent in 8 out of the 15 patients and 3 of these 8 patients suffered from neurological deficits postoperatively. However, the mean arterial flow velocity of distal parent vessels in the group B increased by more than 30 percent in only 3 of the 15 patients and 2 of these 3 patients suffered from neurological deficits postoperatively. CONCLUSION: Isoflurane controlled hypotension may increase the incidence of cerebral vasospasm. Isoflurane induced hypotension for intracranial aneurysm surgery should be cautioned.

Adult↗
PubMed1994

The effect of surgery on the severity of vasospasm.

Intracranial aneurysm surgery performed between 4 and 12 days after subarachnoid hemorrhage (SAH) has been associated with an increased risk of delayed cerebral ischemia and poor outcome compared to surgery performed before or after this time. To investigate whether this increased risk is due to aggravation of vasospasm, the angiograms obtained before and after surgery in 56 patients operated on at various times after aneurysmal SAH were studied. Vasospasm was quantitated by measuring the diameters of intracranial arteries and expressed as the ratio of the diameters of the intracranial arteries to the diameter of the extracranial internal carotid artery. Aggressive surgical clot removal was not performed at surgery. To correct for differences in prognostic factors for vasospasm between patients operated on at different times after SAH, multiple regression analysis was performed using the arterial diameter ratio during vasospasm as the dependent variable and the prognostic factors for vasospasm, including the time of surgery, as independent variables. Equations predicting the severity of vasospasm could be generated using the clinical grade on admission, patient age, and preoperative arterial diameter ratio. The time of surgery had no effect on vasospasm. Cerebral infarction due to vasospasm developed in five (15%) of 34 patients operated on within 3 days after SAH and in four (20%) of 20 operated on between 4 and 12 days after SAH (p = 0.66). A good outcome for these two groups was achieved in 88% and 85%, respectively (p = 1.00). These results suggest that the timing of surgery does not affect the development of vasospasm. Any increased risk of cerebral ischemia associated with surgery performed between 4 and 12 days after SAH is due to factors other than aggravation of vasospasm.

Adult↗