Cases reported "Vasospasm, Intracranial"

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1/17. Fatal severe vasospasm due to rewarming following hypothermia--case report.

    A 37-year-old female died of cerebral vasospasm as a complication of rewarming following hypothermia therapy for severe head injury. She presented with severe consciousness disturbance and anisocoria after falling down a flight of stairs. Computed tomography (CT) revealed a right acute subdural hematoma and temporal contusion. Following surgery, mild hypothermia was started and rewarming was completed by the 11th day. Neurological examination showed no abnormalities, but intracranial pressure (ICP) suddenly increased and she manifested anisocoria on the 13th day. Repeat CT revealed a low density area in the right middle cerebral artery region and cerebral angiography showed diffuse narrowing of the main arterial trunks. A cerebrospinal fluid (CSF) sample was collected using an intraventricular ICP monitoring catheter. The CSF level of 8-hydroxy-2'-deoxyguanosine was elevated during the rewarming period, indicating substantial deoxyribonucleic acid (DNA) oxidation. She died on the 15th day due to uncontrollable ICP. Histological examination at autopsy of the narrowed artery found the waving phenomenon in the internal elastic lamina and invasion of inflammatory cells into the adventitia. These findings constitute the possible evidence that free-radical-mediated oxidative dna damage may be important in the genesis of severe vasospasm due to rewarming following hypothermia.
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2/17. Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage.

    OBJECT: The mechanism of reduction of cerebral circulation and metabolism in patients in the acute stage of aneurysmal subarachnoid hemorrhage (SAH) has not yet been fully clarified. The goal of this study was to elucidate this mechanism further. methods: The authors estimated cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), O2 extraction fraction (OEF), and cerebral blood volume (CBV) preoperatively in eight patients with aneurysmal SAH (one man and seven women, mean age 63.5 years) within 40 hours of onset by using positron emission tomography (PET). The patients' CBF, CMRO2, and CBF/CBV were significantly lower than those in normal control volunteers. However, OEF and CBV did not differ significantly from those in control volunteers. The significant decrease in CBF/CBV, which indicates reduced cerebral perfusion pressure, was believed to be caused by impaired cerebral circulation due to elevated intracranial pressure (ICP) after rupture of the aneurysm. In two of the eight patients, uncoupling between CBF and CMRO2 was shown, strongly suggesting the presence of cerebral ischemia. CONCLUSIONS: The initial reduction in CBF due to elevated ICP, followed by reduction in CMRO, at the time of aneurysm rupture may play a role in the disturbance of CBF and cerebral metabolism in the acute stage of aneurysmal SAH.
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3/17. brain tissue PO(2), PCO(2), and pH during cerebral vasospasm.

    BACKGROUND: The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients. methods: After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies. RESULTS: Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO(2)) remained above 20 mmHg, carbon dioxide pressure (PCO(2)) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO(2) was not different from the control group. However, PCO(2) increased to 60 mmHg and pH decreased to 6.7 (p < 0.001). CONCLUSION: In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO(2) compared to controls. However, there was no significant change in PO(2) levels associated with vasospasm. brain tissue monitoring can provide an indication of ischemia during vasospasm.
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4/17. susac syndrome: a vasospastic disorder?

    PURPOSE: The susac syndrome is a microangiopathy that leads to visual symptoms, hearing loss and neurological symptoms. CASE REPORT: We report on a young woman suffering from this syndrome who also presented the following signs and symptoms typical of a vasospastic syndrome; 1) a history of cold hands, low blood pressure and migraine; 2) a typical alteration of conjunctival vessels; 3) prolonged flow arrest time after cooling in nailfold capillaromicroscopy; 4) increased resistivity in the orbital vessels measured by color Doppler imaging; and 5) an increased plasma level of endothelin-1. CONCLUSIONS: We postulate that the Susac syndrome is a manifestation of the vasospastic syndrome.
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5/17. cerebral revascularization using radial artery grafts for the treatment of complex intracranial aneurysms: techniques and outcomes for 17 patients.

    OBJECTIVE: The goal of this report is to illustrate the use of radial artery grafts as bypass conduits in the management of complex intracranial aneurysms and to describe a new "pressure distension technique" to eliminate postoperative vasospasm, which was a common problem early in our experience. methods: This study included a series of 17 patients who were surgically treated between 1994 and January 2001 for complex intracranial aneurysms. Five patients were surgically treated without the pressure distension technique; for 12 patients, the technique was used to reduce postoperative vasospasm. Fourteen of the patients had anterior circulation aneurysms, and three had posterior circulation aneurysms. Five of the patients had undergone previous attempts at direct clipping or excision and reconstruction of the aneurysm in question, and embolization had been performed for one patient with a carotid-cavernous fistula. Thirteen patients underwent permanent revascularization combined with proximal occlusion, trapping, or clipping, and four patients underwent temporary revascularization for cerebral protection during anticipated prolonged occlusion of the parent vessel during aneurysm dissection. Surgical techniques are described, with particular reference to vessel collection and bypass techniques. RESULTS: The outcomes for this group of patients, considering the complexity of the aneurysms and their "inoperability," with respect to direct clipping, were satisfactory. The aneurysms were completely obliterated for all patients, and the grafts were patent for all except one patient on postoperative angiograms. There were two deaths, one attributable to systemic sepsis and the other attributable to cardiac arrest during a transbronchial biopsy. The postoperative glasgow outcome scale scores were either better or the same for all other patients, compared with their preoperative scores. Three of the five patients treated before the institution of the pressure distension technique experienced vasospasm of the graft, with two of those patients requiring angioplasty. For one of those patients, angioplasty led to rupture of the graft. Vasospasm was not observed for any of the 12 patients for whom the pressure distension technique was used. We observed no morbidity related to radial artery collection. CONCLUSION: Revascularization techniques are occasionally necessary for the surgical treatment of complicated intracranial aneurysms. The merits of the use of the radial artery as a bypass conduit are discussed. radial artery grafts should be considered as alternatives to saphenous vein and superficial temporal artery grafts. The problem of vasospasm of the artery has been solved with the pressure distention technique.
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6/17. Reduction of vasopressor requirement by hydrocortisone administration in a patient with cerebral vasospasm.

    A 67-yr-old female received hypertensive, hypervolaemic treatment for cerebral vasospasm after severe subarachnoid haemorrhage. After 3 days of continuous vasopressor infusion and despite adequate hydration and normal cardiac function, the phenylephrine dose had to be increased to obtain the same systolic blood pressure. This tachyphylaxis to phenylephrine infusion was probably caused by down-regulation of alpha adrenoceptors, and was reversed by giving i.v. hydrocortisone.
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7/17. Intra-arterial papaverine-induced seizures: case report and review of the literature.

    BACKGROUND: Microcatheter-guided intra-arterial (IA) papaverine infusion in conjunction with balloon angioplasty is an available therapy for patients with symptomatic vasospasm after subarachnoid hemorrhage (SAH) that is refractory to hypertensive, hypervolemic therapy. However, side effects and complications have been reported in association with its use. CASE DESCRIPTION: We report on a patient who developed symptomatic vasospasm after subarachnoid hemorrhage due to rupture of a left terminal internal carotid artery (ICA) saccular aneurysm. Seven days after the hemorrhage and 4 days after surgical clipping, the patient developed aphasia and right hemiparesis due to vasospasm, which was refractory to maximal medical treatment with volume and blood pressure elevation. cerebral angiography identified severe narrowing of distal ICA and proximal middle cerebral artery segments bilaterally. These findings partially resolved after balloon angioplasty. However, after 300 mg of IA papaverine, the patient developed generalized convulsions. This occurred despite therapeutic serum levels of phenytoin. Twenty-four hours later, after brief neurologic improvement, recurrent neurologic deficits prompted repeat papaverine administration. seizures again occurred after the administration of 240 mg of IA papaverine and prevented administration of the full dose. The patient did not develop further seizures and her neurologic deficits continue to resolve. CONCLUSIONS: IA papaverine-induced seizures are infrequently reported. This potential complication should be considered when papaverine administration is entertained in the treatment of anterior circulation refractory symptomatic vasospasm after SAH.
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8/17. Transluminal balloon angioplasty improves brain tissue oxygenation and metabolism in severe vasospasm after aneurysmal subarachnoid hemorrhage: case report.

    OBJECTIVE AND IMPORTANCE: The effect of transluminal balloon angioplasty on cerebral biochemical monitoring during treatment of severe cerebral vasospasm after subarachnoid hemorrhage (SAH) was investigated. CLINICAL PRESENTATION: In a 36-year-old man, an anterior communicating artery aneurysm caused an SAH (Hunt and Hess Grade IV, Fisher Grade III). After clipping, intraparenchymal monitoring (intracranial pressure, brain tissue oxygen tension [P(ti)O(2)], and microdialysis sampling of extracellular glucose, lactate, pyruvate, and glutamate) was initiated. Flow velocities obtained by transcranial Doppler sonography increased in the internal carotid artery (ICA)/middle cerebral artery bilaterally. INTERVENTION: After a decrease of P(ti)O(2) to less than 2 mm Hg and an increase of the lactate-to-pyruvate ratio to 44 in the territorial region of the left ICA, angiography demonstrated a 70 to 80% stenosis of the left ICA, which was dilated by a temporary occlusion balloon. This maneuver normalized the ICA diameter, P(ti)O(2) increased immediately from 1.5 to 40 mm Hg, the lactate-to-pyruvate ratio decreased from 44 to 30, and extracellular glucose increased from 0.4 to 0.9 mmol/L. No major changes in glutamate or intracranial pressure were seen. In the clinical follow-up, the patient showed a good recovery 6 months after SAH. CONCLUSION: Transluminal balloon angioplasty led to a continuous and effective resolution of cerebral vasospasm observed by sustained, improved cerebral biochemical parameters. Both P(ti)O(2) and lactate-to-pyruvate ratio might provide an early diagnosis of severe cerebral vasospasm after SAH and continuous surveillance of threatened tissue regions after transluminal balloon angioplasty.
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9/17. Intravenous magnesium sulfate administration in a patient with refractory vasospasm following subarachnoid hemorrhage.

    OBJECTIVE: magnesium sulfate is being investigated for the prevention or treatment of vasospasm following subarachnoid hemorrhage. PATIENT: A 45-year-old woman suffered subarachnoid hemorrhage and developed after 8 days symptomatic vasospasm in the left middle cerebral artery (MCA) while she was receiving nimodipine prophylactically. methods AND RESULTS: Transcranial Doppler monitoring was performed. Cerebral autoregulation was abolished in the left MCA. Despite this finding the administration of a bolus dose of MgSO(4), followed by a continuous infusion in order to achieve serum magnesium levels in the range of 4-4.5 mg/dl (1.65-1.85 mmol/l), resulted in a marked decrease (12.2%) of the left MCA mean blood flow velocity, without clinically relevant change in systemic blood pressure (3%). This effect was maintained for at least 4 h. It did not prevent the development of ischemic lesions.
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10/17. Regional cerebral blood flow monitoring in the diagnosis of delayed ischemia following aneurysmal subarachnoid hemorrhage.

    OBJECT: The goal of this study was to evaluate regional cerebral blood flow (rCBF) monitoring, performed using thermal-diffusion (TD) flowmetry, as a novel means for the bedside diagnosis of symptomatic vasospasm. methods: Fourteen patients with high-grade subarachnoid hemorrhage (SAH) who underwent early clip placement for anterior circulation aneurysms were prospectively entered into the study. Thermal-diffusion microprobes were implanted into the white matter of vascular territories that were deemed at risk for developing symptomatic vasospasm. Data on arterial blood pressure, intracranial pressure, cerebral perfusion pressure, rCBF measurement obtained using a TD probe (TD-rCBF), cerebrovascular resistance (CVR), and blood flow velocities were collected at the patient's bedside. The diagnosis of symptomatic vasospasm was based on the manifestation of a delayed ischemic neurological deficit and/or a reduced territorial level of CBF as assessed using stable Xe-enhanced computerized tomography (CT) scanning in combination with vasospasm demonstrated by angiography. Bedside monitoring of TD-rCBF and CVR allowed the detection of symptomatic vasospasm. In the 10 patients with vasospasm the TD-rCBF decreased from 21 /- 4 to 9 /- 1 ml/100 g/min (mean /- standard error of the mean), whereas in the four other patients the TD-rCBF value remained unchanged (mean TD-rCBF = 25 /- 4 compared with 21 /- 4 m/100 g/min). A comparison of the results of TD-rCBF and Xe-enhanced CT studies, as well as the calculation of sensitivities, specificities, predictive values, and likelihood ratios, identified a TD-rCBF value of 15 ml/100 g/min as a reliable cutoff for the diagnosis of symptomatic vasospasm. In addition, TD flowmetry was characterized by a more favorable diagnostic reliability than transcranial Doppler ultrasonography. CONCLUSIONS: Thermal-diffusion flowmetry represents a promising method for the bedside monitoring of patients with SAH to detect symptomatic vasospasm. This is of major clinical interest for patients with high-grade SAH, who often cannot be assessed neurologically.
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