Symptomatic Vasospasm Research Articles

Complications and adverse events associated with Neuroform stent-assisted coiling of wide-neck intracranial aneurysms

<title/>Background: Successful experiences of the Neuroform stent-assisted coiling have been reported by many teams in endovascular neurosurgery centers throughout the world. However, most of the reported complications involved a limited number of patients.Objective: To systematically report the complications of Neuroform stent-assisted coiling of intracranial aneurysms and to tentatively assess the efficacy and safety of this method.Methods: A retrospective study of 232 consecutive patients with 239 wide-neck aneurysms treated with Neuroform stent-assisted coil embolization at our institution over a 6-year period was performed. Angiographic results and clinical outcome were evaluated. Cases with complications were analyzed.Results: Stenting was successful in 237 of 239 aneurysms. Favorable clinical outcome (modified Rankin score: 0-2) was observed in 88·3% of the patients. Procedure-related complications included thromboembolism (n = 13), intraprocedural rupture (n = 8), coil protrusions (n = 5), new mass effect (n = 3), vessel injury (n = 3), and stent dislodgement (n = 2). Procedure-related morbidity and mortality were 4·2 and 1·3%, respectively. Non-procedural complications attributable to subarachnoid hemorrhage in 129 patients with ruptured aneurysms were symptomatic vasospasm (18·6%) and shunt-dependent hydrocephalus (6·9%). Angiography follow-up was obtained in 67·1% of the treated aneurysms. The overall recanalization rate was 14·5%. Delayed complications included in-stent stenosis (n = 2) and penetrating artery occlusion (n = 2) in follow-up period.Conclusion: Neuroform sent-assisted coiling of intracranial aneurysm is a safe technique with relatively low recanalization rate. The main cause of morbidity and mortality is thromboembolism. Long-term effect on parent artery should be observed carefully.

Asymmetric Posterior Reversible Encephalopathy Syndrome Complicating Hemodynamic Augmentation for Subarachnoid Hemorrhage-Associated Cerebral Vasospasm

Posterior reversible encephalopathy syndrome (PRES) is a rare complication of hemodynamic augmentation for subarachnoid hemorrhage (SAH)-associated vasospasm. The roles of hyperperfusion and hypoperfusion in the genesis of PRES remain uncertain. Case report. We admitted a 35-year-old woman with Hunt & Hess grade II SAH secondary to rupture of a right middle cerebral artery (MCA) aneurysm. This was surgically clipped. Beginning on hospital day 3, she developed recurrent symptomatic vasospasm of the right MCA despite hemodynamic augmentation to a MAP as high as 130mmHg and endovascular therapy. On hospital day 7, after 36h of sustained MAP120-130mmHg, her level of arousal progressively declined, culminating in stupor and two generalized tonic-clonic seizures. MRI showed widespread, yet markedly asymmetric changes consistent with PRES largely sparing the right MCA territory. After the MAP was decreased to 85-100mmHg, she had no further seizures. 2days later she was fully alert with mild left hemiparesis. PRES is a rare complication of hemodynamic augmentation that should be considered in the differential diagnosis of delayed neurological decline in patients with aneurysmal SAH-associated cerebral vasospasm. The markedly asymmetric distribution of PRES lesions with sparing of the territory affected by vasospasm supports the hypothesis that hyperperfusion underlies the pathophysiology of this disorder.

Plasma Platelet-Activating Factor–Acetyl Hydrolase Activity and the Levels of Free Forms of Biomarker of Lipid Peroxidation in Cerebrospinal Fluid of Patients With Aneurysmal Subarachnoid Hemorrhage

Free radicals and lipid peroxidation are thought to be related to the vasospasm generation after subarachnoid hemorrhage (SAH). Plasma platelet-activating factor-acetyl hydrolase (PAF-AH) degrades phospholipids with an oxidatively modified fatty acyl chain. To compare plasma PAF-AH activity and free forms of biomarker of lipid peroxidation in cerebrospinal fluid (CSF) between patients with and without symptomatic vasospasm (SVS) after SAH. The identification of PAF-AH in CSF was performed by Western blotting. The genotype at position 279 of the plasma PAF-AH gene was determined. The activities of PAF-AH and the levels of free 8-iso-prostaglandin F2α (free isoPs), free hydroxyoctadecadienoic acid (free HODE), and free hydroxyeicosatetraenoic acid (free HETE) in CSF were measured. The PAF-AH in CSF was confirmed to be only the plasma type. The genotype of the plasma PAF-AH was not different between patients with and without SVS. Free isoPs, free HODE, and free HETE showed higher values in patients without SVS in 0 to 4 days and 5 to 9 days after SAH. The PAF-AH activity also was higher in patients without SVS in 0 to 4 days and 5 to 9 days after SAH. The associations between PAF-AH activity and free isoPs, and between PAF-AH activity and free HODE were significant. Oxidized lipids of lipoproteins and blood cell membranes produced by reactive oxygen species in CSF when SAH occurs may be the main source of lipid peroxidation. Plasma PAF-AH can hydrolyze oxidized phospholipids, and may attenuate the spreading of lipid peroxidation and participate in defense mechanisms against vasospasm after SAH.

In Response

Drummond et al.1 are concerned that proscribing the use of albumin in head injury patients is not warranted by the strength of a post hoc 2-year follow-up analysis of a subgroup from the SAFE trial (SAFE–TBI)2 and cite several studies suggesting that albumin has no harmful effects and may even be beneficial in these patients. However, the cited clinical studies have severe methodological limitations. They are uncontrolled or retrospective cohort studies with small patient numbers in different clinical conditions yielding much less convincing data than does the SAFE–TBI study. Naredi et al.3 and Rodling Wahlstrom et al.4 both reported outcomes from patients with TBI receiving treatment based on the hypothesis that posttraumatic vasogenic edema is the major factor causing late intracranial hypertension and transcapillary filtration and is therefore controlled by reducing mean arterial blood pressure and maintaining normal colloid osmotic pressure (“Lund concept”). The first study3 included 31 patients prospectively receiving prostacyclin infusions along with unspecified amounts of albumin, crystalloids, or both, and the second study4 retrospectively analyzed a cohort of 93 patients receiving a similar treatment regimen. In contrast to these nonrandom observations on a total of 124 patients without any control group, and given that there are no clinical data from randomized controlled trials showing benefit for albumin in these patients, Myburgh et al.2 reported primary outcome data from 420 patients with TBI, prospectively and randomly enrolled to receive exclusively either 4% albumin or normal saline. Myburgh et al.'s findings that albumin—after confirmation of equivalence in baseline and injury-specific parameters—was associated with a significantly greater 2-year mortality in comparison with saline (33.2% vs 20.4%; relative risk, 1.63; 95% confidence interval, 1.2 to 2.38; P = 0.003), and a significantly greater proportion of patients with unfavorable neurological outcomes should raise considerable concern. The authors suggest albumin extravasation through an impaired blood–brain barrier with increased intracranial edema and hypertension as a possible mechanism.5 Palesch et al.6 reported outcomes from an uncontrolled study with 82 patients with acute ischemic stroke receiving 25% albumin in different doses and used historical cohort data as control. The study of Frontera et al.7 was an uncontrolled cohort study in 95 patients with subarachnoid hemorrhage (SAH) and symptomatic vasospasm treated with hypervolemic hemodilution and received 5% albumin, crystalloid solution, or both. Suarez et al.8 retrospectively analyzed data from 84 patients with SAH before and after albumin was abandoned for hypervolemic hemodilution. Of note, according to 2 Cochrane reviews, there is no scientific support from randomized controlled trials either for hemodilution in the routine treatment of patients with acute stroke9 nor for the use of volume expansion therapy in patients with aneurysmal SAH,10 and findings from uncontrolled observations are merely hypotheses that need to be verified by adequately designed clinical trials. Christiane S. Hartog, MD Michael Bauer, MD Konrad Reinhart, MD Department of Anesthesiology and Intensive Care Friedrich Schiller University Jena, Germany [email protected]

Routine Management of Volume Status After Aneurysmal Subarachnoid Hemorrhage

Prophylactic use of hypervolemia and hypertension is believed to present an option to decrease the incidence of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage and improve neurologic outcome. A Medline literature search was conducted to review available evidence regarding volume management after subarachnoid hemorrhage. Quality of selected studies was evaluated, using the standardized GRADE system. Eleven studies focused on prophylactic hypervolemic therapy after aneurysmal subarachnoid hemorrhage were identified, including four randomized controlled trials. Available studies showed a large heterogeneity in physiologic treatment goals and interventions applied. The oldest and smallest randomized controlled trial suggested a positive effect, but had severe limitations in trial design. Neither of the other randomized controlled studies showed outcome benefit with hypervolemic therapy. Results from observational studies were not found to support the use of prophylactic hypervolemia and hypertension. Complication frequency was repeatedly reported to be higher with the application of prophylactic hypervolemia. In summary, prophylactic hyperdynamic therapy after subarachnoid hemorrhage has not been adequately shown to effectively raise cerebral blood flow or improve neurological outcome. In contrast, there is evidence for harm using overly aggressive hydration.

Age-Associated Vasospasm in Aneurysmal Subarachnoid Hemorrhage

The relationship between age and vasospasm caused by subarachnoid hemorrhage (SAH) is controversial. We evaluated this relationship in a contemporary sample from a single institution. In a retrospective study design, we included patients with SAH caused by ruptured intracranial aneurysms. All patients underwent an evaluation that included head imaging, cerebral angiography, and treatment for the underlying aneurysm. Vasospasm was classified as absent, any vasospasm, or symptomatic vasospasm. Age was classified into 2 categories with a cutoff of 50 years, and also was stratified by decade. All patients had received preventative and therapeutic measures for vasospasm. Logistic regression analysis was used to assess the association between age and the occurrence of vasospasm. A total of 108 patients were included in this analysis, 67 of whom were age ≥50 years. The older patients had a higher incidence of vascular risk factors, and the younger patients had a higher incidence of smoking and illicit substance abuse. The mean age of the patients with any vasospasm (n = 41) was 48.51 ± 11.23 years, compared with 59.67 ± 13.30 years in those without vasospasm (P < .0001). Adjusted analysis found a greater risk of vasospasm in the younger patients compared with the older patients (odds ratio, 5.83; 95% confidence interval, 2.41-14.12 for any vasospasm; odds ratio, 2.66; 95% confidence interval, 1.008-7.052 for symptomatic vasospasm). This risk of vasospasm decreased with advanced age (P < .0001). Our findings suggest that patients age <50 years are at 5-fold greater risk of any vasospasm compared with older patients, and that age-adjusted prevention protocols may need to be considered.

Cilostazol Improves Outcome after Subarachnoid Hemorrhage: A Preliminary Report

Background: Cerebral vasospasm (VS) is the most common cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). Reversal of VS by intra-arterial infusion of cyclic adenosine monophosphate (cAMP)-elevating agents has been reported; however, the preventive role in the development of VS is not fully understood. This study is designed to evaluate the possible efficacy of using cilostazol, a selective inhibitor of phosphodiesterase type 3 and a cAMP-elevating agent, in patients with SAH. Methods: In this prospective randomized study, we enrolled 100 SAH patients who met the following criteria: neck clipping within 72 h after onset, Hunt and Hess (HH) score ≤4, modified Rankin scale (mRS) score ≤2 prior to ictus, and no serious cardiovascular complications. Patients were divided into control and cilostazol groups; we focused on the effects of cilostazol on the decrease in the incidence of symptomatic VS, cerebral infarction, and the mRS score at discharge. Result: Patients’ age, male/female ratio, mRS score prior to ictus, HH grade, Fisher group, site of the aneurysm, drugs prescribed during the observation period, and length of hospital stay were not different between the groups. Cilostazol did not significantly decrease the incidence of symptomatic VS (37.3% in the control vs. 22.4% in the cilostazol group, p = 0.183) and cerebral infarction (27.5% in control vs. 10.2% in the cilostazol, p = 0.091). However, mRS score was significantly improved at discharge (2.6 in controls vs. 1.5 in the cilostazol group, p = 0.041). Patients’ age being ≤65 years (OR = 8.47, 95% CI = 2.45–29.32, p = 0.0007), Fisher group ≤3 (OR = 4.64, 95% CI = 1.00–21.45, p = 0.049), HH grade ≤2 (OR = 4.31, 95% CI = 1.27–14.59, p = 0.019), no hydrocephalus (OR = 8.55, 95% CI = 1.72–19.23, p = 0.0046), and cilostazol use (OR = 5.52, 95% CI = 1.61–18.90, p = 0.0065) were independent predictors of good outcomes (mRS score ≤2). Conclusion: Cilostazol may improve outcomes after SAH, but further double-blind, placebo-controlled studies are required for a definitive conclusion.

Risk Factors for Heparin-Induced Thrombocytopenia Type II in Aneurysmal Subarachnoid Hemorrhage

Heparin-induced thrombocytopenia type II (HIT II) correlates with a higher incidence of thromboembolic complications and unfavorable outcome. To examine the risk factors and outcomes for patients with HIT II with aneurysmal subarachnoid hemorrhage. Demographics, risk factors, treatments, and outcomes data of 600 aneurysmal subarachnoid hemorrhage patients admitted to the University of Illinois Medical Center in Chicago between June 2002 and July 2007 were retrospectively reviewed. Patients meeting the clinical criteria for HIT II were compared with those who did not develop thrombocytopenia. Twenty-five patients (6%) met the clinical criteria for HIT II, and 396 (94%) did not develop thrombocytopenia. Both groups were the same with respect to age, Hunt-Hess score and Fisher grade on admission, medical conditions, and social risk factors. The HIT II patients had significantly more unfavorable outcomes (modified Rankin Scale score >3), deep vein thrombosis, stroke, pulmonary embolism, and death. Development of HIT II was strongly associated with symptomatic vasospasm (odds ratio, 5.7; 95% confidence interval, 2.5-13.1; P < .001) and number of angiographic procedures (odds ratio, 1.7; 95% confidence interval, 1.3-2.2; P < .001). Forward buildup selection modeling demonstrated the latter to be the strongest predictor for HIT II development (odds ratio, 2.3; 95% confidence interval, 1.7-3.2; P = .02). Heparin-induced thrombocytopenia type II correlates with a worse outcome and higher risk of thromboembolic complications in aneurysmal subarachnoid hemorrhage patients. In addition, HIT II was strongly associated with the number of angiographic procedures performed during the same hospitalization.

A proposed definition of symptomatic vasospasm based on treatment of cerebral vasospasm after subarachnoid hemorrhage in Japan: Consensus 2009, a project of the 25 Spasm Symposium.

Background:There is a lack of unified information on diagnosis and treatment of cerebral vasospasm (CV) after subarachnoid hemorrhage (SAH) among the hospitals in Japan. Thus, the aim of the study was to define the current practice in this area based on a survey by Japanese neurosurgeons.Methods:A survey on diagnosis and treatment of CV was sent to 414 hospitals each of which performs >100 neurosurgeries annually.Results:Responses were received from 240 hospitals (58.0%). Because accurate criteria for diagnosis of symptomatic vasospasm (SVS) were used in only 33.8% of the hospitals, we proposed a clinical definition of SVS that was approved at the 25th Spasm Symposium (Consensus 2009). This definition is simplified as follows: (1) the presence of neurological worsening; (2) no other identifiable cause of neurological worsening; and (3) confirmation of vasospasm by medical examinations. The results also showed that the Fisher CT scale is used differently for patients with ICH or IVH, with 41.3% of cases with ICH/IVH based on SAH that met Fisher criteria classified into Fisher group 1, 2 or 3, and 46.3% classified into Fisher group 4. There were no major differences in prophylactic therapies of CV and therapy for cerebral ischemia among the hospitals. Endovascular treatment for vasospasm was performed in most hospitals (78.7%); however, the criteria differed among the hospitals: (1) angiographic vasospasm and SVS appeared (37.9%), (2) only when aggressive therapy was ineffective (41.4%).Conclusion:We established a clinical definition of SVS based on the results of this survey (Consensus 2009).

Intra-Arterial Nimodipine Infusion for Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage

This study evaluated the efficacy of intra-arterial nimodipine infusion for symptomatic vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). Clinical data collected from 42 consecutive patients with symptomatic vasospasm after aSAH were retrospectively reviewed. Forty-two patients underwent 101 sessions of intra-arterial nimodipine infusion. Angiographic response, immediate clinical response, and clinical outcome were evaluated at discharge and six months later. Angiographic improvement was achieved in 82.2% of patients. The immediate clinical improvement rate was 68.3%, while the deterioration rate was 5.0%. A favorable clinical outcome was achieved in 76.2% at discharge and 84.6% six months. Vasospasm-related infarction occurred in 21.4%. There was no drug-related complication. The nimodipine group showed satisfactory outcomes. Nimodipine can be recommended as an effective and safe intra-arterial agent for the treatment of symptomatic vasospasm after aSAH.

Continuous Local Intra-arterial Nimodipine Administration in Severe Symptomatic Vasospasm After Subarachnoid Hemorrhage

Cerebral vasospasm (CV) is a potentially disastrous consequence of subarachnoid hemorrhage despite medical treatment. Nimodipine is a potent drug for vessel relaxation, but side effects may preclude a sufficient dose. To explore whether continuous local intra-arterial nimodipine administration (CLINA) can reverse vasospasm and prevent delayed ischemic neurological deficit. Six consecutive subarachnoid hemorrhage patients (5 women; mean age, 47.2 years) with severe CV despite maximum medical therapy underwent CLINA within 2 hours after the onset of clinical symptoms. After anticoagulation, microcatheters were inserted distally in the concerning supra-aortic vessels. Glyceryl trinitrate injection (2 mg) was followed by CLINA (nimodipine 0.4 mg/h for 70-147 hours). Duration of CLINA was determined by neurological status, transcranial Doppler sonography, and partial tissue oxygen pressure values. In all patients, neurological deficits improved or partial tissue oxygen pressure values returned to normal and transcranial Doppler sonography confirmed a reduced blood flow velocity within 12 hours. Magnetic resonance imaging showed no ischemic lesion caused by CV. Neurological outcome was good (modified Rankin Scale score, 0-2) in 3 patients, whereas 1 patient had a moderate clinical outcome (modified Rankin Scale score, 3-4) and 2 patients had a poor outcome (modified Rankin Scale score, 5) because of the SAH. Preliminary data show that CLINA is a straightforward, effective, and safe option for patients with severe CV refractory to medical therapy. Dilation of spastic arteries starts within a few hours and is lasting. Indication for CLINA is peripheral and diffuse CV at any location.

Influences of early hyperbaric oxygenation on postoperative recovery of intracranial aneurysms patients

Objective To explore the effects of early hyperbaric oxygenation (HBO) on postoperative recovery of intracranial aneurysms patients.Methods The chnical data of 120 postoperative intracranial aneurysms patients were divided into HBO group and control group.The determination of average blood stream speed of middle cerebral artery(MCA) of operation side were recorded at the 1st,3th,7th,14th and 21st day after operation.The operative regional abnormity density volume of CT re - examination were calculated at the 1st,7th,14th and 21st day.The number of cases associated with “symptomatic cerebral vasospasm” was counted at the 3st,7th and 14st day.The functional state ( KPS score) was evaluated at the 3th and 21st day.Result There was no significant difference of MCA average blood stream speed,number of cases associated with “symptomatic cerebral vasospasm” and KPS score between two groups at 3rd day after operation( P ＞ 0.05 ).The MCA average blood stream speed of HBO group was lower than that of control group at the 7th and 14th day after operation ( P ＜ 0.05 and P ＜ 0.01 ).The abnormity density volume of HBO group was less than that of control group at the 14th and 21st day after operation ( P ＜ 0.05 ).The number of cases associated with “symptomatic cerebral vasospasm” of HBO group was smaller than that of control group at the 7th and 14th day after operation ( P ＜0.05).The KPS score of HBO group was higher than that of control group at the 21 st day after operation ( P ＜ 0.05 ).Conclusion The effects of early hyperbaric oxygenation therapy on postoperative intracranial aneurysms patients are good.One of the possible mechanism is release of cerebral vasospasm. Key words: Intracranial aneurysm ; Cerebral vasospasm ; Hyperbaric oxygen therapy ;

Proof of Concept: Endogenous Antiangiogenic Factors Predict the Occurrence of Symptomatic Vasospasm Post Subarachnoid Hemorrhage

The pathogenesis of vasospasm (VS) post aneurysmal subarachnoid hemorrhage (SAH) is multifactorial and not completely understood. The authors hypothesize that circulating antiangiogenic factors play an important role in brain injury post SAH and that elevated levels predict the occurrence of symptomatic vasospasm. In this study the authors measured the serum and cerebrospinal fluid (CSF) levels of soluble endoglin (sEng) and soluble fms-like tyrosine kinase 1 (sFlt1) in controls and SAH patients within 48h of the bleed. Patients were prospectively followed and subcategorized into those with (sVS) and without symptomatic vasospasm (no-sVS). Compared to healthy controls, SAH patients had higher CSF levels of sEng (0.037 vs. 0.251ng/ml; P=0.02) and sFlt1 (0.068 vs. 0.679ng/ml; P=0.001). In the subgroup analysis, sVS patients had higher CSF levels of sEng and sFlt1 than no-sVS patients (sEng: 0.380 vs. 0.159ng/ml, P=0.02; sFlt1: 1.277 vs. 0.343ng/ml, P=0.01). The serum levels of sEng and sFlt1 were not statistically different among the different groups. Based on these results the authors conclude that elevated CSF levels of sFlt1 and sEng herald the occurrence of symptomatic VS post SAH.

Endovascular Treatment of Severe Vasospasm in Nonaneurysmal Perimesencephalic Subarachnoid Hemorrhage

Nonaneurysmal perimesencephalic subarachnoid hemorrhage (SAH) has usually a benign prognosis and uneventful course; however, recent reports suggest that these patients may develop severe symptomatic vasospasm. Description of the clinical course of one patient with nonaneurysmal perimesencephalic SAH who required intraarterial infusion of calcium antagonists and transluminal balloon angioplasty for treatment of symptomatic vasospasm. The perimesencephalic clot burden was quantified to determine if there is a relationship with the development of symptomatic vasospasm. Despite maximized clinical management, the patient described in this report developed vasospasm and delayed cerebral ischemia (DCI), requiring multiple endovascular interventions. The volumetric quantification of subarachnoid blood was 15.4ml, and was mostly localized in the cisternal space. Nonaneurysmal perimesencephalic SAH may have a "malignant" course requiring close neurocritical care monitoring and multiple clinical and endovascular interventions. Moreover, large cisternal hemorrhage was correlated with the development of DCI in this patient with non-aneurysmal SAH.

Search for Genetic Variants in the Ryanodine Receptor 1 Gene in Patients with Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm is one of the most serious complications after subarachnoid hemorrhage (SAH). The cerebral artery diameter is regulated by complex physiological mechanisms. Among them the regulation of intracellular calcium homeostasis seems to play a crucial role. Recent data suggest that ryanodine receptors (RYRs) are involved in regulating the luminal calcium concentration in vascular smooth muscle cells. In this gene association investigation, we studied the question as to whether variants in the gene for the ryanodine receptors subtype 1 (RYR1) are associated with symptomatic cerebral vasospasm following SAH. After informed consent genomic DNA analysis was performed from a whole blood sample in 46 patients suffering from aneurysmal SAH. 16 Patients were affected by symptomatic vasospasm. The RYR1 gene was screened for possible genetic variants by means of direct sequencing. The association of these variants was correlated to the development of symptomatic vasospasm, which was confirmed by clinical examination combined with cerebral angiography, transcranial doppler sonography, or CT scan. Three different genetic RYR1 variants (c.5360C>T, c.6178G>T, and c.7244G>A) were identified in the study. The G/T genotype of RYR1 c.6178G>T was associated with an increased risk for development of symptomatic vasospasm (odds ratio 6.4; 95% CI 1.1-37.8; P=0.04). Our pilot study suggests that RYRs are involved in the complex pathophysiology of vasospasm development following SAH. The potential role of RYR1 as a biomarker for prediction of cerebral vasospasm after SAH has to be confirmed in a larger clinical trial.

Cerebral artery restenosis following transluminal balloon angioplasty for vasospasm after subarachnoid hemorrhage.

Background:Although percutaneous transluminal angioplasty (PTA) is a widely used less invasive method to treat coronary artery stenosis, 10% of treated patients experience restenosis. Restenosis also occurs in approximately 5% of patients subjected to carotid artery stenting. Animal and human data suggested that restenosis is a response to injury incurred during PTA. As PTA has come into wide use to manage symptomatic cerebral vasospasm after subarachnoid hemorrhage (SAH) we studied the incidence of restenosis after PTA for cerebral vasospasm.Methods:Our study population consisted of 32 patients who had undergone PTA. They were followed by cerebral or 3DCT angiography or MRA for 6 126 months post-PTA (mean 48.65 months) to diagnose restenosis of the cerebral artery. We compared the size of the cerebral artery on the PTA and the contralateral side.Results:All 32 patients underwent successful PTA of 38 vascular territories and all manifested angiographic improvement of vasospasm. None suffered restenosis during the follow up period.Conclusion:PTA resulted in a significant improvement in the vessel diameter in patients with vasospasm after SAH and they did not suffer restenosis in the course of prolonged follow-up.

Lower Incidence of Transcranial Doppler and Symptomatic Vasospasm After Aneurysmal Subarachnoid Hemorrhage and Aneurysm Clipping in the Elderly Patient?

Vasospasm is the major cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage. It is well known that the vasoreactivity decreases with advancing age, but it is not well investigated in a large patient cohort whether, as a consequence, the incidence of vasospasm is lower in elderly patients. To investigate whether transcranial Doppler vasospasm, delayed ischemic neurological deficits, and vasospasm-associated ischemic lesions are less frequent in older patients. Seven hundred fifty-eight patients who suffered from subarachnoid hemorrhage were included in this study. Clinical presentation, Hunt and Hess score, Fisher grade, incidence of vasospasm, neurological deficits and ischemic lesions on radiographic imaging, transcranial Doppler blood flow velocities, medical complications, and outcome were registered. Four hundred seventy-eight patients < 60 years of age and 280 patients ≥ 60 years of age were identified; 55.2% of the younger and 25.7% of the older age group developed post-hemorrhagic vasospasm (P < .001). Older patients developed less vasospasm (P = .00), fewer neurological deficits (P < .001), and fewer ischemic lesions on computed tomography imaging (P = .06). On the other hand, older patients had significantly worse outcomes than younger patients (P = .01) and more frequently died of medical complications (P = .01). Vasospasm, delayed ischemic neurological deficits, and vasospasm-associated ischemic lesions are more likely to occur in patients < 60 years of age than in older patients. The lower incidence of vasospasm and vasospasm-related ischemia in the elderly patient does not translate into better outcome because of the higher rate of fatal medical complications in patients ≥ 60 years of age.

Fate of Clots in Patients With Subarachnoid Hemorrhage After Different Surgical Treatment Modality: A Comparison Between Surgical Clipping and Guglielmi Detachable Coil Embolization

Subarachnoid clot is important in the development of delayed vasospasm after subarachnoid hemorrhage (SAH). To compare the clearance of subarachnoid clot and the incidence of symptomatic vasospasm in surgical clipping and embolization with Guglielmi detachable coils for aneurysmal SAH. The subjects were 115 patients with Fisher group 3 aneurysmal SAH on computed tomography scan at admission whose aneurysm was treated by surgical clipping (clip group; n = 86) or Guglielmi detachable coil embolization (coil group; n = 29) within 72 hours of ictus. Software-based volumetric quantification of the subarachnoid clot was performed, and the amount of hemoglobin in drained cerebrospinal fluid was measured. Clearance of the subarachnoid clot on the computed tomography scan was rapid in the clip group until the day after the operation but slow in the coil group (58.9% removed vs 27.8% removed; P = .008). However, postoperative clearance of the clot occurred more rapidly in the coil group. Reduction of the clot until days 3 through 5 did not differ significantly between the 2 groups (72.9% removed vs 75.2% removed). The amount of hemoglobin in the clip group was > 0.8 g/d until day 3 and then gradually decreased (n = 15), but hemoglobin in the coil group remained at > 0.8 g/d until day 5 (n = 17). The incidence of symptomatic vasospasm did not differ between the groups. Subarachnoid clot can be removed directly during surgical clipping, which is not possible with endovascular treatment. However, the percentage reduction of the clot on days 3 through 5 did not differ between the 2 groups.

The clinical study of preoperative external lumbar drainage in patients with aneurysmal subarachnoid hemorrhage in Hunt and Hess grades I～III undergoing early surgery

Objective To explore the therapeutic effect of preoperative external hunbar drainage in Hunt and Hess grade Ⅰ～Ⅲ patients with subarachnoid hemorrhage ( SAH ) undergoing early surgery for intracranial aneurysms. Method The 101 cases of grade Ⅰ～Ⅲ patients according to the classification of Hunt and Hess with early surgical treatment were devided into preoperative external lumbar drainage group(47 cases) and postoperative external lumbar drainage group(54 cases).Outcome of patients with different external drainage of cerebrospinal fluid was analyzed. Results There was no case of aneurysm rebleeding could be associated with preoperative spinal drain placement. Tne incidences of intraoperative aneurysm rapture in preoperative external lumbar drainage group was 8. 5%,which was lower than 11. 1% in postoperative external lumbar drainage group. The incidences of symptomatic cerebral vasospasm and chronic hydrocephalus in preoperative external lumbar drainage group were 12. 8% and 12.8% ,which were lower than 20. 4% and 14. 8% in postoperative external lumbar drainage group. There all were not significant differences between the two groups. Conclusions Preoperative external lumbar drainage wont increase a risk of rebleeding for grade Ⅰ～Ⅲ patients with aneurysmal SAH undergoing early surg ery. Furthermore, it can decrease the incidences of symptomatic cerebral vasospasm and chronic hydrocephalus,which is a safe and useful method of removing bloody cerebrospinal fluid. Key words: Intracranial aneurysm; Subarachnoid hemorrhage; External lumbar drainage

Transluminal Balloon Angioplasty for Symptomatic Distal Vasospasm Refractory to Medical Therapy in Patients With Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm (VSP) is a major cause of morbidity and mortality associated with subarachnoid hemorrhage. The current endovascular paradigm for VSP refractory to medical therapy is to perform angioplasty for proximal vessel VSP and vasodilator infusion for distal vessel VSP. To report our experience with a large series of balloon angioplasty for distal VSP refractory to medical therapy in patients with aneurysmal subarachnoid hemorrhage. This was a retrospective series of 32 patients with subarachnoid hemorrhage and symptomatic VSP refractory to medical therapy who were treated with balloon angioplasty for distal vessel VSP. Immediate angiographic results, procedure-related complications, and clinical outcomes were assessed. From September 2001 to January 2010, 32 patients with symptomatic VSP refractory to medical therapy underwent angioplasty for distal arterial VSP. There were 26 women (81.3%); patients were 29 to 67 years of age. A total of 175 vessels were angioplastied (95 proximal and 80 distal). The only complication was rupture of an incompletely clipped aneurysm that was treated by immediate coiling and did not result in any clinical worsening. Repeated treatment was needed for 6 arteries (6 of 80, 7.5%). There were no procedure-related symptomatic complications. Good outcomes (modified Rankin Scale score ≤ 2) were observed in 23 of 28 patients (82.1%) with follow-up. Balloon angioplasty for distal VSP is safe and effective and decreases the need for repeated intraarterial treatments seen with infusion of vasodilator.