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Value of Perfusion CT, Transcranial Doppler Sonography, and Neurological Examination to Detect Delayed Vasospasm after Aneurysmal Subarachnoid Hemorrhage  [PDF]
Ekkehard Kunze,Mirko Pham,Furat Raslan,Christian Stetter,Jin-Yul Lee,Laszlo Solymosi,Ralf-Ingo Ernestus,Giles Hamilton Vince,Thomas Westermaier
Radiology Research and Practice , 2012, DOI: 10.1155/2012/231206
Abstract: Background. If detected in time, delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) may be treated by balloon angioplasty or chemical vasospasmolysis in order to enhance cerebral blood flow (CBF) and protect the brain from ischemic damage. This study was conceived to compare the diagnostic accuracy of detailed neurological examination, Transcranial Doppler Sonography (TCD), and Perfusion-CT (PCT) to detect angiographic vasospasm. Methods. The sensitivity, specificity, positive and negative predictive values of delayed ischemic neurological deterioration (DIND), pathological findings on PCT-maps, and accelerations of the mean flow velocity (MVF) were calculated. Results. The accuracy of DIND to predict angiographic vasospasm was 0.88. An acceleration of MFV in TCD (>140?cm/s) had an accuracy of 0.64, positive PCT-findings of 0.69 with a higher sensitivity, and negative predictive value than TCD. Interpretation. Neurological assessment at close intervals is the most sensitive and specific parameter for cerebral vasospasm. PCT has a higher accuracy, sensitivity and negative predictive value than TCD. If detailed neurological evaluation is possible, it should be the leading parameter in the management and treatment decisions. If patients are not amenable to detailed neurological examination, PCT at regular intervals is a helpful tool to diagnose secondary vasospasm after aneurysmal SAH. 1. Introduction Among other variables, cerebral infarction and symptomatic vasospasm are the most important postoperative risk factors for poor outcome after aneurysmal SAH [1] Both are consequences of a decreasing and insufficient brain perfusion that eventually causes a loss of neurological function and, finally, structural damage of brain tissue [2]. A variety of measures is undertaken to enhance cerebral blood flow (CBF) in SAH-patients developing delayed cerebral vasospasm (DCV). These include hyperdynamic therapy, intra-arterial and intrathecal drug infusion, intra-aortic balloon counterpulsation, and new experimental methods [3]. Endovascular treatment of DCV—balloon angioplasty and chemical vasospasmolysis—has proven to effectively enhance CBF and has been increasingly used for treatment of DCV in the last years [4]. The application of these modalities or their combination may be very helpful if treatment is started in time. However, the routine use of repeated four-vessel angiography is not justifiable because of high-radiation exposure. Therefore, other monitoring tools have to indicate upcoming vasospasm after aneurysmal SAH. If DCV is
Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage
Salah G Keyrouz, Michael N Diringer
Critical Care , 2007, DOI: 10.1186/cc5958
Abstract: Vasospasm is a common complication that follows aneurysmal subarachnoid hemorrhage (SAH). Ecker was first to point out the occurrence of arterial spasm following SAH [1]. Before him, Robertson had attributed ischemic brain lesions found on autopsy of patients with SAH to probable 'spasm of arteries' [2]. Despite growing literature, skepticism regarding the association between angiographic vasospasm and clinical findings persisted [3], until CM Fisher and colleagues published a synopsis on the matter in 1977 [4]. This seminal publication comprehensively described the deficits accompanying vasospasm and, most importantly, made the association between vasospasm and neurological deficits, also known as delayed ischemic deficits (DID).The term vasospasm implies a reduction in the caliber of a vessel; however, in SAH it has multiple meanings. SAH-induced vasospasm is a complex entity due in part to a delayed and reversible vasculopathy, impaired autoregulatory function, and hypovolemia causing a regional reduction of cerebral perfusion to the point of causing ischemia [5,6].Radiographic evidence of vasospasm develops in 50% to 70% of patients with SAH, but only half of those experience symptoms of DID [7-12]. Proximal vessels, situated at the base of the brain, are preferentially affected; however, more distal arteries could also develop impaired vascular reactivity (autoregulation), further reducing cerebral blood flow [5,13,14]. A tendency toward spontaneous intravascular volume contraction can further compound the deleterious effect of a marginal cerebral blood flow (CBF) caused by vasoconstriction. These factors are probably in play in a subset of patients with DID who show no evidence of radiographic vasospasm.Vasospasm adversely affects outcome in patients with SAH; it accounts for up to 23% of disability and deaths related to SAH [8,9,15-17]. However, given its predictable delayed onset between day 5 and 15 after bleeding, it is a potentially modifiable factor. Use
Treatment of Intracranial Vasospasm Following Subarachnoid Hemorrhage  [PDF]
Andrew M. Bauer
Frontiers in Neurology , 2014, DOI: 10.3389/fneur.2014.00072
Abstract: Vasospasm has been a long known source of delayed morbidity and mortality in aneurysmal subarachnoid hemorrhage patients. Delayed ischemic neurologic deficits associated with vasospasm may account for as high as 50% of the deaths in patients who survive the initial period after aneurysm rupture and its treatment. The diagnosis and treatment of vasospasm has still been met with some controversy. It is clear that subarachnoid hemorrhage is best cared for in tertiary care centers with modern resources and access to cerebral angiography. Ultimately, a high degree of suspicion for vasospasm must be kept during ICU care, and any signs or symptoms must be investigated and treated immediately to avoid permanent stroke and neurologic deficit. Treatment for vasospasm can occur through both ICU intervention and endovascular administration of intra-arterial vasodilators and balloon angioplasty. The best outcomes are often attained when these methods are used in conjunction. The following article reviews the literature on cerebral vasospasm and its treatment and provides the authors’ approach to treatment of these patients.
Effect of N-acetylcysteine on vasospasm in subarachnoid hemorrhage
Pereira Filho, Nelson de Azambuja;Pereira Filho, Arthur de Azambuja;Soares, Fabiano Pasqualotto;Coutinho, Ligia Maria Barbosa;
Arquivos de Neuro-Psiquiatria , 2010, DOI: 10.1590/S0004-282X2010000600017
Abstract: vasospasm remains an extremely serious complication that affects patients presenting with subarachnoid hemorrhage (sah) due to ruptured intracranial aneurysms. the current therapeutic armamentarium is still insufficient in many cases, and the search for new therapies is necessary. in this study, we evaluated the effect of n-acetylcysteine (nac) on cerebral arterial vasospasm using an experimental model. twenty-four wistar rats were divided into 4 groups: [1] control, [2] sah, [3] sah+nac and [4] sah+placebo. the experimental model employed double subarachnoid injections of autologous blood. the proposed dose of nac was 250 mg/kg intraperitoneally per day. we analyzed the inner area of the basilar artery to assess the action of nac. the experimental model proved to be very adequate, with a mortality rate of 4%. the inner area of the basilar artery in the sah group showed significant difference to the control group (p=0.009). the use of nac significantly reduced vasospasm as compared to the untreated group (p=0.048) and established no significant difference to the control group (p=0.098). there was no significant improvement with the administration of placebo (p=0.97). the model of the dual hemorrhage proved to be very useful for vasospasm simulation, with overall low mortality. the administration of nac significantly reduced vasospasm resulting from sah, and may represent a new therapeutic alternative.
Cerebral vasospasm following traumatic subarachnoid hemorrhage  [cached]
Bahram Aminmansour,Abbas Ghorbani,Davood Sharifi,Hamidreza Shemshaki
Journal of Research in Medical Sciences , 2009,
Abstract: Background: Cerebral vasospasm is a preventable cause of death and disability in patients who experience aneurysmal subarachnoid hemorrhage (SAH). The aim of this study is to investigate the incidence of cerebral vasospasm following traumatic SAH and its relationship with different brain injuries and severity of trauma. Methods: This cross-sectional study was conducted from October 2006 to March 2007 in department of Neurosurgery in Al-Zahra Hospital. Consecutive head-injured patients who had SAH on the basis of an admission CT scan were prospectively evaluated. The severity of the trauma was evaluated by determining Glasgow Coma Scale (GCS) score on admission. Transcranial Doppler ultrasonography evaluations were performed at least 48 hours after admission and one week thereafter. Vasospasm in the MCA and ACA was defined by mean flow velocity (FV) of more than 120 cm/sec with a Lindegaard index (MVA/ICA FV ratio) higher than 3. Basilar artery vasospasm was defined by FV higher than 85 cm/sec. Results: Seventy seven patients with tSAH were enrolled from whom 13 were excluded. The remaining were 52 (81.2%) men and 12 (18.7%) women, with a mean age of 37.89 years. Trauma was severe in 11 (17.2%), moderate in 13 (20.3%), and mild in 40 (62.5%) patients. From all, 27 patients (42.1%) experienced at least one vasospasm during the study period and MCA vasospasm was the most common in the first and second weeks (55.5%). Conclusions: Traumatic SAH is associated with a high incidence of cerebral vasospasm with a higher probability in patients with severe TBI. Keywords: Cerebral Vasospasm, Subarachnoid Hemorrhage, Trauma, Traumatic Brain Injury.
Cerebral vasospasm after subarachnoid hemorrhage  [PDF]
Milojevi? T.M.,Baljozovi? B.V.,Raki? M.Lj.,Nestorovi? B.D.
Acta Chirurgica Iugoslavica , 2008, DOI: 10.2298/aci0802055m
Abstract: Cerebral vasospasm causes permanent neurolological deficit or death occurrence in 13% of clinical cases. Peak frequency is from 8-10th day after SAH. The purpose of this study is factor analysis that may have influence on vasospasm development , as well as predictor determination. The study is prospective and analysis 192 patients treated in Institute of Neurosurgery, Clinical Centre of Serbia, Belgrade. The majority of patients were admitted in hospital in first four days after SAH, and 184 had GCS over 7. Univariate methods of factor analysis were used, and for significance of predictors influence testing multivariante regression analysis was used . Vasospasm occurred in 22,40% of all cases. No relationships have been found between sex, age, previous hypertension, timing of surgery, appearance of hydrocephalus and intracerebral hematoma, hypertermia or mean arterial blood pressure, with occurrence of cerebral vasospasm. Factors with significantly associated with the occurrence of vasospasm were: hearth disease, hypernatriemia, Hct, clinical grade on admission as well as preoperative clinical grade and Fisher CT scan grade. In the first four days after SAH, Fisher scan grade, preoperative clinical grade and Hct, appeared as predictors. After four days, clinical grade on admission and hypernatiemia, showed as predictors.
Matrix Metalloproteinases in Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage  [PDF]
Vivek Mehta,Jonathan Russin,Alexandra Spirtos,Shuhan He,Peter Adamczyk,Arun P. Amar,William J. Mack
Neurology Research International , 2013, DOI: 10.1155/2013/943761
Abstract: Delayed cerebral vasospasm is a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). While the cellular mechanisms underlying vasospasm remain unclear, it is believed that inflammation may play a critical role in vasospasm. Matrix metalloproteinasees (MMPs) are a family of extracellular and membrane-bound proteases capable of degrading the blood-rain barrier (BBB). As such, MMP upregulation following SAH may result in a proinflammatory extravascular environment capable of inciting delayed cerebral vasospasm. This paper presents an overview of MMPs and describes existing data pertinent to delayed cerebral vasospasm. 1. Background Delayed cerebral vasospasm is a devastating complication of subarachnoid hemorrhage (SAH). It typically occurs within fourteen days of aneurysmal rupture, and it is associated with significant morbidity and mortality [1, 2]. While pathophysiology remains incompletely understood, the interplay between inflammation and the innate immune response is strongly implicated. Following SAH, increased blood-brain barrier (BBB) permeability engenders a proinflammatory milieu in the cerebral cisterns and extravascular space. Subarachnoid blood initiates leukocyte transmigration via cellular margination, adhesion, rolling, and diapedesis [3]. The process necessitates violation of the tight junctions between endothelial cells of the BBB and typically occurs in response to stimulatory chemoattractants or chemokines. Coupled with concurrent physiologic derangements, these molecular alterations can incite delayed cerebral vasospasm. Regulation of the extracellular matrix and basal lamina by matrix metalloproteinase (MMP) enzymes may play a critical role in vasospasm. MMPs have been studied extensively in the pathogenesis of ischemic stroke and the development of aortic and cerebral aneurysms [4]. Recently, investigations have examined the role of MMPs in the setting of SAH. In this paper, we specifically review the function of MMPs in cerebral vasospasm. Understanding the complex interactions between inflammation and degradation of the extracellular matrix may ultimately allow for better development of diagnostic markers and targeted therapies relevant to the management of delayed cerebral vasospasm. 2. MMP Review MMPs are a family of extracellular and membrane-bound proteases capable of degrading or proteolytically modifying the extracellular matrix (ECM) through interactions with collagenases, laminins, and proteoglycans [5]. They utilize zinc-dependent endopeptidases to regulate physiologic
Pharmacological treatment of delayed cerebral ischemia and vasospasm in subarachnoid hemorrhage
Diego Castanares-Zapatero, Philippe Hantson
Annals of Intensive Care , 2011, DOI: 10.1186/2110-5820-1-12
Abstract: Delayed cerebral ischemia (DCI) is a common and serious complication following subarachnoid hemorrhage (SAH) after ruptured cerebral aneurismal [1,2]. Although this complication is at times reversible, it may develop into a cerebral infarction [3]. DCI occurs in approximately 20% to 40% [4] of patients and is associated with increased mortality and poor prognosis [5,6]. It is usually caused by a vasospasm [7], which, although preventable, remains a major cause of poor neurological outcome and increased mortality in the course of SAH [4-6].Vasospasm is defined as a reversible narrowing of the subarachnoid arteries occurring between the third to fifth and fifteenth day after the hemorrhage, with a peak at the tenth day. It is observed in 70% of patients on angiographic scans and causes symptoms in 50% [7-10]. Angiographic vasospasm is defined as evidence of arterial narrowing compared with the parent vessels [11]. It preferentially involves the vessels of the cranial base but also may affect small-caliber vessels or diffusely the entire cerebral vascularization. The severity of vasospasm is variable. The subsequent decrease in cerebral blood flow (CBF) in the spastic arteries leads to DCI, which may develop into cerebral infarction [7,12,13].The etiology of vasospasm is complex and still poorly understood. Several factors have been shown to be involved, such as endothelial dysfunction, loss of autoregulation, and a hypovolemic component leading to a decrease in CBF [14-16]. At the acute phase, the presence of oxyhemoglobin in the subarachnoid spaces causes a local and systemic inflammatory reaction [17] with activation of platelets and coagulation [8-10]. The products derived from red blood cells (bilirubin) and endothelium (endothelin-1, free radicals) are considered to be mediators of the vasospasm [18-22] Structural anomalies in endothelial and smooth muscle cells also have been reported [23].Treatments of DCI consist of preventing or minimizing secondary injuries
Post-Aneurysmal Subarachnoid Hemorrhage Vasospasm, Clinical Correlation between the Aneurysm Site and Clinical Vasospasm  [PDF]
Ahmed Ali, Mohamed A.R. Soliman
Open Journal of Modern Neurosurgery (OJMN) , 2018, DOI: 10.4236/ojmn.2018.83025
Abstract: Background: Intracranial vasospasm is a common complication following subarachnoid hemorrhage (SAH). The radiographic vasospasm can reach up to 90% of aneurysmal SAH. Materials and Methods: 139 consecutive patients admitted to Cairo University Hospitals from June 2013 to September 2014 with SAH who had been enrolled in a retrospective controlled study were analyzed retrospectively for the occurrence of vasospasm. The data collected from the charts of Cairo University Hospitals were the patient’s demographics, clinical presentation, aneurysm location, treatment modality, and Glasgow Outcome Scale (GOS) scores. We excluded 24 patients with nonaneurysmal SAH, 3 internal carotid artery (ICA) aneurysms, 7 with multiple aneurysms and 4 patients died before treatment. Results: 72 males and 29 females were included in the study, mean age 53.5 ± 11.5 years. Twelve patients had aneurysms located in the vertebral artery group, 24 had middle cerebral artery aneurysms, 11 had pericallosal aneurysms, and 54 patients had anterior communicating artery (ACoA) complex aneurysms. Radiographic vasospasm occurred in 62.4% with the highest incidence (75.9%) at the ACoA complex group. Symptomatic vasospasm occurred in 48.5% with the highest incidence (63%) at the anterior communicating artery complex aneurysm location. The mean GOS at 6 months follow-up was 4.2. The worse GOS was found in the vertebral artery (VA) aneurysm group with a mean of 3.75. Conclusion: Aneurysms of the anterior communicating artery complex group have a greater risk of both radiographic and clinical vasospasm. Also, the worse 6 months follow-up GOS when an aneurysm was located in the VA group.
Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea Perspectives in the treatment of subarachnoid-hemorrhage-induced cerebral vasospasm  [cached]
J. Fandino,A.R. Fathi,T. Graupner,S. Jacob
Neurocirugía , 2007,
Abstract: El vasospasmo cerebral sigue siendo la causa más importante de invalidez y muerte posterior a la ruptura de aneurismas saculares intracerebrales. Las estrategias terapéuticas en el vasospasmo inducido por la hemorragia subaracnoidea pueden ser agrupadas en cuatro categorías a saber: 1) terapias de prevención; 2) terapias de reversión; 3) terapias para el aumento de la perfusión cerebral; y 4) terapias de neuroprotección y rescate. Estudios experimentales recientes han permitido la realización de estudios clínicos fase II que sugieren resultados positivos con medicamentos que incluyen estatinas (simvastatina y pravastatina) y antagonistas de receptores tipo A de la endotelina-1 (clasozentan). De igual manera, evidencias experimentales y clínicas han mostrado las ventajas del drenaje de líquido cefalorraquídeo, administración intratecal de donadores de óxido nítrico, y los efectos desinhibidores de la Ca2+ Protein Kinasa C (Fasudil) y catecolaminas sobre la vascularización cerebral. Este artículo resume el estado de investigación actual de posibles agentes y estrategias terapéuticas relevantes en el tratamiento del vasospasmo cerebral. Cerebral vasospasm is still the most important cause of death and disability after rupture of intracranial aneurysms. The therapeutic strategies in the treatment of subarachnoid hemorrhage induced vasos pasm include four groups: 1) prevention of vasospasm; 2) reversion of vasospasm; 3) improvement of cerebral perfusion; and 4) neuroprotection and rescue therapies. Recent experimental studies allowed the design of phase II clinical studies which demonstrated positive results with medications and compounds such as statins (simvastatin and pravastatin) and endothelin-1 receptor antagonists (clasozentan). Moreover, experimental and clinical evidences showed the advantages of early cerebrospinal fluid drainage, intrathecal administration of NO-donors, effects of Ca2+ protein kinase inhibitor (Fasudil) and catecholamines on the cerebral vessels. This review article summarizes the stage of investigation of these medications and therapeutic strategies which will be relevant in the treatment of cerebral vasospasm. " I would caution that vasospasm is still around, it is still alive and living in every neurosurgical unit. Hence my plea that our scientists not falter or lose interest for a final understanding and solution" C.G. Drake,1990 9
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