TY  - JOUR
T1  - Isolated Intraventricular Hemorrhage Associated with Cerebral Vasospasm and Delayed Cerebral Ischemia following Arteriovenous Malformation Rupture
A1  - Amuluru, Krishna
A1  - Al-Mufti, Fawaz
A1  - Romero, Charles E.
A1  - Gandhi, Chirag D.
Y1  - 2018///
KW  - arteriovenous malformation
KW  - cerebral vasospasm
KW  - delayed cerebral ischemia
KW  - intraventricular hemorrhage
KW  - stroke
KW  - subarachnoid hemorrhage
KW  - vasospasm
JF  - Interventional Neurology
VL  - 7
IS  - 6
SP  - 479
EP  - 489
DO  - 10.1159/000490583
UR  - https://www.karger.com/Article/FullText/490583
N2  - <b><i>Background:</i></b> Although it is well characterized in aneurysmal subarachnoid hemorrhage, vasospasm is exceedingly rare following cerebral arteriovenous malformation (AVM) rupture. Subsequently, this complication is poorly characterized with regard to delayed cerebral ischemia (DCI). We review cases of ruptured AVM to assess the frequency and severity of vasospasm on cerebral angiography, and DCI. <b><i>Summary:</i></b> We reviewed our institutional database of acute intracranial hemorrhages between 2005 and 2014. We identified patients with cerebral AVM rupture and evidence of vasospasm, which was confirmed with digital subtraction angiography (DSA). Cerebral angiograms were evaluated by 2 blinded neurointerventionalists for vasospasm. Statistical analyses were conducted on the angiographic results and variables of interest to determine predictors and associations of vasospasm and DCI. Thirty-six patients with acute intracranial hemorrhage due to ruptured cerebral AVM subsequently underwent cerebral angiography. The interrater reliability for vasospasm was 0.81. The incidence of vasospasm was 13.9% and the incidence of subsequent DCI was 11.1%. A significant relationship existed between isolated intraventricular hemorrhage and vasospasm (<i>p</i> = 0.001) and subsequent DCI (<i>p</i> = 0.006). Radiographic vasospasm was associated with DCI in 80% of the patients (<i>p</i> &#x3c; 0.0001). No statistical significance existed between subarachnoid hemorrhage and the development of vasospasm or DCI (<i>p</i> = 1.000 and <i>p</i> = 0.626, respectively). All differences were significant at a 99% level of significance. <b><i>Key Message:</i></b> In cases of ruptured AVM, isolated intraventricular hemorrhage appears to be an independent risk factor for vasospasm and DCI. Vasospasm must be considered during late neurological deterioration following AVM hemorrhage, especially in the setting of isolated intraventricular hemorrhage.
ER  - 
TY  - JOUR
T1  - Cerebral vasospasm due to arteriovenous malformation-associated hemorrhage: Impact of bleeding source and pattern
A1  - Dinc, Nazife
A1  - Won, Sae Yeon
A1  - Eibach, Michael
A1  - Quick-Weller, Johanna
A1  - Konczalla, Jürgen
A1  - Berkefeld, Joachim
A1  - Seifert, Volker
A1  - Marquardt, Gerhard
Y1  - 2019///
KW  - AVM hemorrhage
KW  - Cerebral vasospasm
KW  - Subarachnoid hemorrhage
JF  - Cerebrovascular Diseases
VL  - 47
IS  - 3-4
SP  - 165
EP  - 170
DO  - 10.1159/000500596
N2  - Objective: Cerebral vasospasm (CVS) after a ruptured arteriovenous malformation (AVM) is rarely reported. This study is aimed at evaluating the predictive variables in AVM hemorrhage for CVS. Methods: A total of 160 patients with ruptured AVMs were admitted to our neurosurgical department from 2002 to 2018. The frequency of cerebral vasospasm after AVM hemorrhage and the impact of AVM-associated aneurysms were evaluated. We compared different bleeding patterns, such as intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH) or a combination of both (ICH + SAH) and evaluated predictive variables for outcome in last follow-up. Results: A total of 62 (39%) patients had AAA, mostly located prenidal (75.8%). AVMs with ruptured aneurysms often resulted in ICH with SAH component (p < 0.001). Eighty-two patients (51%) presented a SAH component, and CVS occurred in 6 patients (7.3%), mostly due to a ruptured infratentorial AVM (p < 0.03). Infratentorial location and the amount of SAH component (p < 0.001) predicted the incidence of CVS significantly. Cerebral infarction was significantly associated with CVS (p < 0.02). Conclusion: SAH component and infratentorial location of ruptured AVMs may harbor a higher risk for CVS. Follow-up with angiographic imaging should be considered in patients with infratentorial AVM hemorrhage and delayed neurologic deterioration to rule out CVS.
ER  - 
TY  - JOUR
T1  - Methodological guidance for systematic reviews of observational epidemiological studies reporting prevalence and cumulative incidence data
A1  - Munn, Zachary
A1  - Moola, Sandeep
A1  - Lisy, Karolina
A1  - Riitano, Dagmara
A1  - Tufanaru, Catalin
Y1  - 2015/09//
KW  - Epidemiology
KW  - Incidence
KW  - Observational
KW  - Prevalence
KW  - Systematic review
JF  - International Journal of Evidence-Based Healthcare
VL  - 13
IS  - 3
SP  - 147
EP  - 153
SN  - 0000000000000
DO  - 10.1097/XEB.0000000000000054
UR  - https://journals.lww.com/01787381-201509000-00006
N2  - Aim: There currently does not exist guidance for authors aiming to undertake systematic reviews of observational epidemiological studies, such as those reporting prevalence and incidence information. These reviews are particularly useful to measure global disease burden and changes in disease over time. The aim of this article is to provide guidance for conducting these types of reviews.Methods: A methodological working group of the Joanna Briggs Institute, Adelaide, South Australia, Australia, was formed to create guidance for conducting systematic reviews of studies reporting prevalence and cumulative incidence information. All methodological output of the group was subject to peer review and feedback by members of the international evidence synthesis community.Results: Systematic reviews of prevalence and incidence data should follow the same structured steps as systematic reviews of effectiveness. However, many of these steps need to be tailored for this type of evidence, particularly surrounding the stages of critical appraisal and synthesis.Conclusion: Prevalence and incidence systematic review and meta-analysis is an emerging methodology in the field of evidence synthesis. These reviews can provide useful information for healthcare professionals and policymakers on the burden of disease, show changes and trends over time in disease, and inform geographical distributions of disease and conditions.
ER  - 
TY  - JOUR
T1  - Secondary S100B Protein Increase Following Brain Arteriovenous Malformation Rupture is Associated with Cerebral Infarction
A1  - Garzelli, Lorenzo
A1  - Jacquens, Alice
A1  - Amouyal, Caroline
A1  - Premat, Kevin
A1  - Sourour, Nader
A1  - Cortese, Jonathan
A1  - Haffaf, Idriss
A1  - Mathon, Bertrand
A1  - Lenck, Stéphanie
A1  - Clarençon, Frédéric
A1  - Degos, Vincent
A1  - Shotar, Eimad
Y1  - 2020/11//
KW  - arteriovenous malformations
KW  - biomarker
KW  - brain
KW  - cerebrovascular malformations
KW  - intracranial hemorrhage
KW  - prognosis
KW  - stroke
JF  - Molecules
VL  - 25
IS  - 21
SP  - 5177
EP  - 5177
DO  - 10.3390/molecules25215177
UR  - https://www.mdpi.com/1420-3049/25/21/5177
L1  - file:///Users/julianamayorga/Desktop/Secondary S100B Protein Increase Following Brain Arteriovenous Malformation Rupture is Associated with Cerebral Infarction.pdf
N2  - Early S100B protein serum elevation is associated with poor prognosis in patients with ruptured brain arteriovenous malformations (BAVM). The purpose of this study is to determine whether a secondary elevation of S100B is associated with early complications or poor outcome in this population. This is a retrospective study of patients admitted for BAVM rupture. A secondary increase of S100B was defined as an absolute increase by 0.1 μg/L within 30 days of admission. Fisher’s and unpaired t tests followed by multivariate analysis were performed to identify markers associated with this increase. Two hundred and twenty-one ruptures met inclusion criteria. Secondary S100B protein serum elevation was found in 17.1% of ruptures and was associated with secondary infarction (p < 0.001), vasospasm-related infarction (p < 0.001), intensive care (p = 0.009), and hospital length of stay (p = 0.005), but not with early rebleeding (p = 0.07) or in-hospital mortality (p = 0.99). Secondary infarction was the only independent predictor of secondary increase of S100B (OR 9.9; 95% CI (3–35); p < 0.001). Secondary elevation of S100B protein serum levels is associated with secondary infarction in ruptured brain arteriovenous malformations.
ER  - 
TY  - JOUR
T1  - Vasospasm and cerebral infarction following isolated intraventricular hemorrhage
A1  - Gerard, Elizabeth
A1  - Frontera, Jennifer A.
A1  - Wright, Clinton B.
Y1  - 2007/11//
KW  - Arteriovenous malformation
KW  - Delayed cerebral ischemia Stroke
KW  - Fisher grade
KW  - Intraventricular hemorrhage
KW  - Vasospasm
JF  - Neurocritical Care
VL  - 7
IS  - 3
SP  - 257
EP  - 259
DO  - 10.1007/s12028-007-0057-1
UR  - http://link.springer.com/10.1007/s12028-007-0057-1
N2  - Introduction: Cerebral arterial vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is an important cause of delayed neurologic deterioration. Vasospasm following isolated intraventricular hemorrhage (IVH) is less common. Accepted predictors of vasospasm following SAH include poor Hunt-Hess grade, elevated transcranial Doppler velocities, and the thickness of cisternal blood on neuroimaging [1, 2]. The role of intraventricular hemorrhage in vasospasm is more controversial. Methods: Case report and review of the literature. Results: A 41-year-old woman developed symptomatic delayed vasospasm 10 days following isolated IVH due to the rupture of an arteriovenous malformation (AVM). Conclusion: Intraventricular hemorrhage can independently cause significant delayed vasospasm. Possible mechanisms are described. © Humana Press Inc. 2007.
ER  - 
TY  - JOUR
T1  - Severe vasospasm caused by repeated intraventricular haemorrhage from small arteriovenous malformation.
A1  - Kobayashi, M.
A1  - Takayama, H.
A1  - Mihara, B.
A1  - Kawase, T.
Y1  - 2002/04//
JF  - Acta neurochirurgica
VL  - 144
IS  - 4
SP  - 405
EP  - 6
DO  - 10.1007/s007010200059
UR  - http://www.ncbi.nlm.nih.gov/pubmed/12021892
N2  - A 26-year-old man was admitted due to intraventricular haemorrhage (IVH) in the right lateral ventricle, without apparent subarachnoid haemorrhage (SAH) in the basal cistern (Fig. 1a). He had no significant past history. He had severe headache, but was alert without any neurological deficit. Angiograms showed small abnormal vessels fed by the right anterior choroidal artery, without early venous drainage (Fig. 1b, c). The right posterior cerebral artery was hypoplastic and the posterior branch of the middle cerebral artery reached the occipital lobe. His headache improved within several days and angiograms at Day 20 showed no arterial narrowing. On Day 33, he developed a larger IVH again (Fig. 1d). At the onset he was alert, but fell into a confused state 17 days later. Angiograms revealed severe narrowing of middle and anterior cerebral arteries bilaterally (Fig. 1e, f). Despite endovascular intervention, he developed cerebral infarction in the right temporo-occipital region. CT cisternography demonstrated communicating hydrocephalus 28 days after rebleeding. Following a lumboperitoneal shunt procedure, the abnormal vessels were resected because of his repeated episodes and the same abnormal vessels demonstrated angiographically. The pathological diagnosis was that of an arteriovenous malformation (AVM). Postoperative angiograms demonstrated the arteries of normal caliber without abnormal vessels. The patient returned to his job 4 months later despite a left homonymous hemianopsia.
ER  - 
TY  - JOUR
T1  - Inflammation, Cerebral Vasospasm, and Brain Injury in Subarachnoid Hemorrhage—A Shifting Paradigm and a New Beginning*
A1  - Chou, Sherry Hsiang-Yi
Y1  - 2018/11//
KW  - determination
KW  - protein crystallography
KW  - protein data bank
KW  - r -factor
KW  - resolution
KW  - restraints
KW  - structure
KW  - structure interpretation
KW  - structure quality
KW  - structure refinement
KW  - structure validation
JF  - Critical Care Medicine
VL  - 46
IS  - 11
SP  - 1883
EP  - 1885
SN  - 2163684814
DO  - 10.1097/CCM.0000000000003373
UR  - http://journals.lww.com/00003246-201811000-00030
ER  - 
TY  - JOUR
T1  - Admission risk factors for cerebral vasospasm in ruptured brain arteriovenous malformations: An observational study
A1  - Chhor, Vibol
A1  - Le Manach, Yannick
A1  - Clarençon, Fréderic
A1  - Nouet, Aurélien
A1  - Daban, Jean-Louis
A1  - Abdennour, Lamine
A1  - Puybasset, Louis
A1  - Lescot, Thomas
Y1  - 2011///
JF  - Critical Care
VL  - 15
IS  - 4
SP  - R190
EP  - R190
DO  - 10.1186/cc10345
UR  - http://ccforum.biomedcentral.com/articles/10.1186/cc10345
N2  - Introduction: Cerebral vasospasm is a well-documented complication of aneurismal subarachnoid hemorrhage but has not been extensively studied in brain arteriovenous malformations (BAVMs). Here, our purpose was to identify risk factors for cerebral vasospasm after BAVM rupture in patients requiring intensive care unit (ICU) admission.Methods: Patients admitted to our ICU from January 2003 to May 2010 for BAVM rupture were included in this observational study. Clinical, laboratory and radiological features from admission to ICU discharge were recorded. The primary endpoint was cerebral vasospasm by transcranial Doppler (TCD-VS) or cerebral infarction (CI) associated with vasospasm. Secondary endpoints included the Glasgow Outcome Scale (GOS) at ICU discharge.Results: Of 2,734 patients admitted to our ICU during the study period, 72 (2.6%) with ruptured BAVM were included. TCD-VS occurred in 12 (17%) and CI in 6 (8%) patients. All patients with CI had a previous diagnosis of TCD-VS. A Glasgow Coma Scale score <8 was a risk factor for both TCD-VS (relative risk (RR), 4.7; 95% confidence interval (95% CI), 1.6 to 26) and CI (RR, 7.8; 95% CI, 0.1 to 63). Independent risk factors for TCD-VS by multivariate analysis were lower Glasgow Coma Scale score (odds ratio (OR) per unit decrease, 1.38; 95% CI, 1.13 to 1.80), female gender (OR, 4.86; 95% CI, 1.09 to 25.85), and younger age (OR per decade decrease, 1.39; 95% CI, 1.05 to 1.82). The risk of a poor outcome (GOS <4) at ICU discharge was non-significantly increased in the patients with TCD-VS (RR, 4.9; 95% CI, 0.7 to 35; P = 0.09). All six patients with CI had poor outcomes.Conclusions: This is the first cohort study describing the incidence and risk factors for cerebral vasospasm after BAVM rupture. Larger studies are needed to investigate the significance of TCD-vasospasm and CI in these patients. © 2011 Chhor et al.; licensee BioMed Central Ltd.
ER  - 
TY  - JOUR
T1  - Cerebral Vasospasms After Intraventricular Hemorrhage From an Arteriovenous Malformation -Case Report-
A1  - YOKOBORI, Shoji
A1  - WATANABE, Akihiro
A1  - NAKAE, Ryuta
A1  - ONDA, Hidetaka
A1  - FUSE, Akira
A1  - KUSHIMOTO, Shigeki
A1  - YOKOTA, Hiroyuki
Y1  - 2010///
KW  - Arteriovenous malformation
KW  - Cerebral infarction
KW  - Intraventricular hemorrhage
KW  - Vasospasm
JF  - Neurologia medico-chirurgica
VL  - 50
IS  - 4
SP  - 320
EP  - 323
DO  - 10.2176/nmc.50.320
UR  - http://www.jstage.jst.go.jp/article/nmc/50/4/50_4_320/_article
N2  - A 33-year-old female presented with a rare case of severe vasospasm following the rupture of an arteriovenous malformation (AVM) without subarachnoid hemorrhage. Initial computed tomography (CT) revealed a subcutaneous hematoma and cast formation of intraventricular clots without the deposition of subarachnoid blood in any basal cistern. Cerebral angiography revealed a small AVM located in the right parietal lobe without aneurysmal formations. Repeat CT demonstrated no evidence of subarachnoid clots expected with the presence of intraventricular clots and she was transferred to a general ward. She suffered sudden onset of motor aphasia and disturbance of consciousness on Day 17 after the hemorrhage. Magnetic resonance imaging indicated diffuse cortical infarction and subsequent magnetic resonance angiography revealed severe narrowing of the bilateral internal carotid arteries. Three-dimensional CT angiography on the same day indicated similar findings. She was transferred back to the intensive care unit for critical treatment. However, she suffered persistent mild right hemiparesis and motor aphasia. The characteristic features of vasospasm after intraventricular hemorrhage from AVMs are delayed onset, acute deterioration of consciousness, female predominance, and localization to the bilateral internal carotid arteries. Treatment of patients with AVM rupture should consider the risk of severe vasospasm, even if there is no subarachnoid clot.
ER  - 
TY  - JOUR
T1  - A systematic review of the frequency and prognosis of arteriovenous malformations of the brain in adults.
A1  - Al-Shahi, Rustam
A1  - Warlow, C
Y1  - 2001/10//
KW  - Diagnostic imaging
KW  - Epidemiologic measurements
KW  - Intracranial aneurysm
KW  - Intracranial arteriovenous malformations
KW  - Prognosis
JF  - Brain : a journal of neurology
VL  - 124
IS  - Pt 10
SP  - 1900
EP  - 26
DO  - 10.1093/brain/124.10.1900
UR  - https://academic.oup.com/brain/article-lookup/doi/10.1093/brain/124.10.1900
UR  - http://www.ncbi.nlm.nih.gov/pubmed/11571210
N2  - By systematically reviewing the literature, we have found that there is very little information about the frequency and clinical course of arteriovenous malformations (AVMs) of the brain in adults because the methods of most studies have been flawed, and AVMs tend to be treated once they are discovered. The incidence of AVMs is approximately 1 per 100 000 per year in unselected populations, and the point prevalence in adults is approximately 18 per 100 000. AVMs account for between 1 and 2% of all strokes, 3% of strokes in young adults, 9% of subarachnoid haemorrhages and, of all primary intracerebral haemorrhages, they are responsible for 4% overall, but for as much as one-third in young adults. AVMs are far less common causes of first presentations with unprovoked seizures (1%), and of people presenting with headaches in the absence of neurological signs (0.3%). At the time of detection, at least 15% of people affected by AVMs are asymptomatic, about one-fifth present with seizures and for approximately two-thirds of them the dominant mode of presentation is with intracranial haemorrhage. The limited high quality data available on prognosis suggest that long-term crude annual case fatality is 1-1.5%, the crude annual risk of first occurrence of haemorrhage from an unruptured AVM is approximately 2%, but the risk of recurrent haemorrhage may be as high as 18% in the first year, with uncertainty about the risk thereafter. For untreated AVMs, the annual risk of developing de novo seizures is 1%. There is a pressing need for large, prospective studies of the frequency and clinical course of AVMs in well-defined, stable populations, taking account of their prognostic heterogeneity.
ER  - 
TY  - JOUR
T1  - Cerebral Vasospasm: A Review
A1  - Findlay, J. Max
A1  - Nisar, Joshua
A1  - Darsaut, Tim
Y1  - 2016/01//
KW  - cerebral ischemia
KW  - cerebral vasospasm
KW  - intracranial aneurysm
KW  - subarachnoid hemorrhage
JF  - Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
VL  - 43
IS  - 1
SP  - 15
EP  - 32
DO  - 10.1017/cjn.2015.288
UR  - https://www.cambridge.org/core/product/identifier/S0317167115002887/type/journal_article
N2  - Cerebral vasospasm is a prolonged but reversible narrowing of cerebral arteries beginning days after subarachnoid hemorrhage. Progression to cerebral ischemia is tied mostly to vasospasm severity, and its pathogenesis lies in artery encasement by blood clot, although the complex interactions between hematoma and surrounding structures are not fully understood. The delayed onset of vasospasm provides a potential opportunity for its prevention. It is disappointing that recent randomized, controlled trials did not demonstrate that the endothelin antagonist clazosentan, the cholesterol-lowering agent simvastatin, and the vasodilator magnesium sulfate improve patient outcome. Minimizing ischemia by avoiding inadequate blood volume and pressure, administering the calcium antagonist nimodipine, and intervention with balloon angioplasty, when necessary, constitutes current best management. Over the past two decades, our ability to manage vasospasm has led to a significant decline in patient morbidity and mortality from vasospasm, yet it still remains an important determinant of outcome after aneurysm rupture.
ER  - 
TY  - JOUR
T1  - Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: Beyond Vasospasm and Towards a Multifactorial Pathophysiology
A1  - Geraghty, Joseph R.
A1  - Testai, Fernando D.
Y1  - 2017/12//
KW  - Cortical spreading depolarization
KW  - Delayed cerebral ischemia
KW  - Microthrombosis
KW  - Neuroinflammation
KW  - Subarachnoid hemorrhage
KW  - Vasospasm
JF  - Current Atherosclerosis Reports
VL  - 19
IS  - 12
SP  - 50
EP  - 50
DO  - 10.1007/s11883-017-0690-x
UR  - http://link.springer.com/10.1007/s11883-017-0690-x
N2  - Purpose of Review: Delayed cerebral ischemia (DCI) is common after subarachnoid hemorrhage (SAH) and represents a significant cause of poor functional outcome. DCI was mainly thought to be caused by cerebral vasospasm; however, recent clinical trials have been unable to confirm this hypothesis. Studies in humans and animal models have since supported the notion of a multifactorial pathophysiology of DCI. This review summarizes some of the main mechanisms under investigation including cerebral vascular dysregulation, microthrombosis, cortical spreading depolarizations, and neuroinflammation. Recent Findings: Recent guidelines have differentiated between DCI and angiographic vasospasm and have highlighted roles of the microvasculature, coagulation and fibrinolytic systems, cortical spreading depressions, and the contribution of the immune system to DCI. Many therapeutic interventions are underway in both preclinical and clinical studies to target these novel mechanisms as well as studies connecting these mechanisms to one another. Summary: Clinical trials to date have been largely unsuccessful at preventing or treating DCI after SAH. The only successful pharmacologic intervention is the calcium channel antagonist, nimodipine. Recent studies have provided evidence that cerebral vasospasm is not the sole contributor to DCI and that additional mechanisms may play equal if not more important roles.
ER  - 
TY  - JOUR
T1  - Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage
A1  - Suzuki, Hidenori
A1  - Kanamaru, Hideki
A1  - Kawakita, Fumihiro
A1  - Asada, Reona
A1  - Fujimoto, Masashi
A1  - Shiba, Masato
Y1  - 2021///
KW  - Cerebral vasospasm
KW  - Delayed cerebral ischemia
KW  - Early brain injury
KW  - Inflammation
KW  - Matricellular protein
KW  - Microcirculation
KW  - Subarachnoid hemorrhage
JF  - Histology and Histopathology
VL  - 36
IS  - 2
SP  - 143
EP  - 158
DO  - 10.14670/HH-18-253
N2  - Aneurysmal subarachnoid hemorrhage (SAH) remains a serious cerebrovascular disease. Even if SAH patients survive the initial insults, delayed cerebral ischemia (DCI) may occur at 4 days or later post-SAH. DCI is characteristics of SAH, and is considered to develop by blood breakdown products and inflammatory reactions, or secondary to early brain injury, acute pathophysiological events that occur in the brain within the first 72 hours of aneurysmal SAH. The pathology underlying DCI may involve large artery vasospasm and/or microcirculatory disturbances by microvasospasm, microthrombosis, dysfunction of venous outflow and compression of microvasculature by vasogenic or cytotoxic tissue edema. Recent clinical evidence has shown that large artery vasospasm is not the only cause of DCI, and that both large artery vasospasm-dependent and-independent cerebral infarction causes poor outcome. Animal studies suggest that mechanisms of vasospasm may differ between large artery and arterioles or capillaries, and that many kinds of cells in the vascular wall and brain parenchyma may be involved in the pathogenesis of microcirculatory disturbances. The impairment of the paravascular and glymphatic systems also may play important roles in the development of DCI. As pathological mediators for DCI, glutamate and several matricellular proteins have been investigated in addition to inflammatory molecules. Glutamate is involved in excitotoxicity contributing to cortical spreading ischemia and epileptic activity-related events. Microvascular dysfunction is an attractive mechanism to explain the cause of poor outcomes independently of large cerebral artery vasospasm, but needs more studies to clarify the pathophysiologies or mechanisms and to develop a novel therapeutic strategy.
ER  - 
TY  - JOUR
T1  - Del vasoespasmo a la lesión cerebral precoz: una nueva frontera en la investigación de la hemorragia subaracnoidea
A1  - Muñoz-Guillén, N.M.
A1  - León-López, R.
A1  - Túnez-Fiñana, I.
A1  - Cano-Sánchez, A.
Y1  - 2013/06//
KW  - Biomarkers
KW  - CT perfusion
KW  - Early brain injury
KW  - Subarachnoid haemorrhage
KW  - Vasospasm
JF  - Neurología
VL  - 28
IS  - 5
SP  - 309
EP  - 316
DO  - 10.1016/j.nrl.2011.10.015
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0213485311004464
N2  - Introduction: Delayed vasospasm has traditionally been considered the most important determinant of poor outcome after subarachnoid haemorrhage (SAH). Consequently, most of the research and therapies are directed towards reducing the incidence of vasospasm (VSP). To date, however, clinical trials based on this strategy have not delivered a definitive treatment for preventing or reducing brain injury after SAH. This fact has caused a paradigm shift in research, which now focuses on early brain injury (EBI) occurring in the first 72. hours after SAH. It has also changed the idea of VSP's role in brain damage, and suggests the need for re-evaluating the pathophysiological process of SAH. Development: This review examines the current state of knowledge on the pathophysiological mechanisms associated with EBI and summarises the diagnostic options currently available. Conclusion: It seems that the research approach needs to be changed so that investigators will focus on prevention of EBI, reduction of secondary brain complications and ultimately, the optimisation neurological outcome. © 2011 Sociedad Española de Neurología.
ER  - 
TY  - CHAP
T1  - Radiographic Vasospasm and Clinical (Symptomatic) Vasospasm
A1  - Singh, Jasmeet
A1  - Wicks, Robert T.
A1  - Wilson, John A.
A1  - Wolfe, Stacey Q.
A1  - Fargen, Kyle M.
Y1  - 2018///
KW  - Cerebral vasospasm
KW  - Cortical spreading depolarization
KW  - Cortical spreading depression
KW  - Delayed cerebral ischemia
KW  - Parametric color coding
KW  - Symptomatic vasospasm
PB  - Elsevier
JF  - Intracranial Aneurysms
SP  - 161
EP  - 178
SN  - 9780128117408
DO  - 10.1016/B978-0-12-811740-8.00011-3
UR  - https://linkinghub.elsevier.com/retrieve/pii/B9780128117408000113
N2  - Cerebral vasospasm is a focal or diffuse, temporary narrowing of cerebral arteries as evidenced by digital subtraction angiography, transcranial Doppler, magnetic resonance, or computed tomography angiography. Cerebral vasospasm often results when cerebral vessels are exposed to blood in the subarachnoid space (subarachnoid hemorrhage), but may also occur after traumatic brain injury or secondary to inflammatory conditions such as meningitis and vasculitis. Radiographic spasm may progress to clinical (symptomatic) vasospasm as evidenced by neurologic deterioration and eventual permanent neurologic defect secondary to infarction. Autoregulatory dysfunction, inflammation, microcirculatory failure, and spreading cortical depolarization are multiple facets of the disease process that must be addressed with multimodal treatment to achieve improved neurologic outcomes. Rapid identification of symptomatic vasospasm with urgent treatment is essential to prevent permanent neurologic deficit. Ultimately, symptomatic vasospasm is best managed with hypertension followed by endovascular treatment with intra-arterial spasmolytics and/or balloon angioplasty.
ER  - 
TY  - JOUR
T1  - Non-traumatic subarachnoid hemorrhage is associated with subnormal blood creatinine levels
A1  - Kralova, Ivana
A1  - Winsö, Ola
A1  - Olivecrona, Magnus
A1  - Naredi, Silvana
Y1  - 2010/10//
KW  - Central nervous system
KW  - Kidney
JF  - Scandinavian Journal of Clinical and Laboratory Investigation
VL  - 70
IS  - 6
SP  - 438
EP  - 446
DO  - 10.3109/00365513.2010.506925
UR  - http://www.tandfonline.com/doi/full/10.3109/00365513.2010.506925
N2  - Objective. The aim of this study was to examine the hypothesis that patients with non-traumatic subarachnoid hemorrhage (SAH) have statistically significant subnormal creatinine levels and that the creatinine levels are associated with severity of disease. Materials and methods. This was a retrospective observational study over 2 years (20052006) in which the SAH patients were divided into patients with severe symptoms and patients with mild/moderate symptoms, and were compared to patients with; traumatic brain injury, trauma without brain injury and patients undergoing elective knee surgery. Blood creatinine levels (day 13, and day 7) were recorded. Results. Compared to a normal distribution, SAH patients had statistically significant subnormal creatinine levels day one through seven. SAH patients with severe symptoms had statistically significant subnormal creatinine levels already on day one, in contrast to patients with mild/moderate symptoms. Women with severe symptoms had statistically significant subnormal creatinine levels throughout the study period in contrast to men with severe symptoms who had a normal distribution of creatinine at admission. Women with mild/moderate symptoms had a normal distribution of creatinine only at admission in contrast to men who had a normal distribution of creatinine throughout the study period. Male patients with traumatic brain injury, all trauma patients without brain injury and all patients undergoing elective knee surgery had a normal distribution of creatinine on all studied days. Conclusions. SAH is associated with subnormal serum creatinine levels. This finding is more pronounced in patients with severe symptoms and in women. © 2010 Informa Healthcare.
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TY  - JOUR
T1  - Cerebral vasospasm with subarachnoid hemorrhage from cerebral arteriovenous malformations
A1  - Sasaki, Tomio
A1  - Mayanagi, Yoshiaki
A1  - Yano, Hirohiko
A1  - Kim, Shi-in
Y1  - 1981/09//
JF  - Surgical Neurology
VL  - 16
IS  - 3
SP  - 183
EP  - 187
DO  - 10.1016/0090-3019(81)90004-5
UR  - https://linkinghub.elsevier.com/retrieve/pii/0090301981900045
ER  - 
TY  - JOUR
T1  - Long-term outcome in patients with aneurysmal subarachnoid hemorrhage requiring mechanical ventilation
A1  - Chalard, Kevin
A1  - Szabo, Vivien
A1  - Pavillard, Frederique
A1  - Djanikian, Flora
A1  - Dargazanli, Cyril
A1  - Molinari, Nicolas
A1  - Manna, Federico
A1  - Costalat, Vincent
A1  - Chanques, Gerald
A1  - Perrigault, Pierre-Francois
ED  - Ehrman, Robert
Y1  - 2021/03//
JF  - PLOS ONE
VL  - 16
IS  - 3
SP  - e0247942
EP  - e0247942
SN  - 1111111111
DO  - 10.1371/journal.pone.0247942
UR  - https://dx.plos.org/10.1371/journal.pone.0247942
N2  - Background Patients affected with aneurysmal subarachnoid hemorrhage (aSAH) often require intensive care, and then present distinctive outcome from less severe patients. We aimed to specify their long-term outcome and to identify factors associated with poor outcome. Methods We conducted a retrospective study in a French university hospital intensive care unit. Patients with aSAH requiring mechanical ventilation hospitalized between 2010 and 2015 were included. At least one year after initial bleeding, survival and degree of disability were assessed using the modified Rankin Scale (mRS) via telephone interviews. A multivariable logistic regression analysis was performed to determine independent factors associated with poor outcome defined as mRS≥3. Results Two-hundred thirty-six patients were included. Among them, 7 were lost to follow-up, and 229 were analyzed: 73 patients (32%) had a good outcome (mRS<3), and 156 (68%) had a poor outcome (mRS≥3). The estimated 1-year survival rate was 63%. One-hundred sixty-three patients patients (71%) suffered from early brain injuries (EBI), 33 (14%) from rebleeding, 80 (35%) from vasospasm and 63 (27%) from delayed cerebral ischemia (DCI). Multivariable logistic regression identified independent factors associated with poor outcome including delay between aSAH diagnosis and mRS assessment (OR, 0.96; 95% CI, 0.95-0.98; p<.0001), age (OR per 10 points, 1.57; 95% CI, 1.12-2.19; p = 0.008), WFNS V versus WFNS III (OR, 5.71; 95% CI 1.51-21.61; p = 0.004), subarachnoid rebleeding (OR, 6.47; 95% CI 1.16-36.06; p = 0.033), EBI (OR, 4.52; 95% CI 1.81-11.29; p = 0.001) and DCI (OR, 4.73; 95% CI, 1.66-13.49; p = 0.004). Conclusion Among aSAH patients requiring assisted ventilation, two-third of them survived at one year, and one-third showed good long-term outcome. As it appears as an independant factor associated with poor outcome, DCI shoud retain particular attention in future studies beyond angiographic vasospasm.
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TY  - JOUR
T1  - Brain arteriovenous malformations
A1  - Lawton, Michael T.
A1  - Rutledge, W. Caleb
A1  - Kim, Helen
A1  - Stapf, Christian
A1  - Whitehead, Kevin J.
A1  - Li, Dean Y.
A1  - Krings, Timo
A1  - TerBrugge, Karel
A1  - Kondziolka, Douglas
A1  - Morgan, Michael K.
A1  - Moon, Karam
A1  - Spetzler, Robert F.
Y1  - 2015/12//
JF  - Nature Reviews Disease Primers
VL  - 1
IS  - 1
SP  - 15008
EP  - 15008
DO  - 10.1038/nrdp.2015.8
UR  - http://www.nature.com/articles/nrdp20158
N2  - An arteriovenous malformation is a tangle of dysplastic vessels (nidus) fed by arteries and drained by veins without intervening capillaries, forming a high-flow, low-resistance shunt between the arterial and venous systems. Arteriovenous malformations in the brain have a low estimated prevalence but are an important cause of intracerebral haemorrhage in young adults. For previously unruptured malformations, bleeding rates are approximately 1% per year. Once ruptured, the subsequent risk increases fivefold, depending on associated aneurysms, deep locations, deep drainage and increasing age. Recent findings from novel animal models and genetic studies suggest that arteriovenous malformations, which were long considered congenital, arise from aberrant vasculogenesis, genetic mutations and/or angiogenesis after injury. The phenotypical characteristics of arteriovenous malformations differ among age groups, with fistulous lesions in children and nidal lesions in adults. Diagnosis mainly involves imaging techniques, including CT, MRI and angiography. Management includes observation, microsurgical resection, endovascular embolization and stereotactic radiosurgery, alone or in any combination. There is little consensus on how to manage patients with unruptured malformations; recent studies have shown that patients managed medically fared better than those with intervention at short-term follow-up. By contrast, interventional treatment is preferred following a ruptured malformation to prevent rehaemorrhage. Management continues to evolve as new mechanistic discoveries and reliable animal models raise the possibility of developing drugs that might prevent the formation of arteriovenous malformations, induce obliteration and/or stabilize vessels to reduce rupture risk. For an illustrated summary of this Primer, visit: http://go.nature.com/TMoAdn.
ER  - 
TY  - JOUR
T1  - Severe symptomatic vasospasm after rupture of an arteriovenous malformation.
A1  - Kothbauer, Karl
A1  - Schroth, Gerhard
A1  - Seiler, Rolf W
A1  - Do, D D
Y1  - 1995/05//
JF  - AJNR. American journal of neuroradiology
VL  - 16
IS  - 5
SP  - 1073
EP  - 5
UR  - http://www.ncbi.nlm.nih.gov/pubmed/7639129
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC8337792
N2  - A 31-year-old woman had intracerebral and intraventricular hemorrhage from an arteriovenous malformation. Vasospasm of the internal carotid arteries developed and was treated with angioplasty. On initial CT scans, only traces of blood were seen in the basal cisterns; thus, the development of symptomatic vasospasm was an unexpected complication.
ER  - 
TY  - JOUR
T1  - Transluminal angioplasty and intra-arterial papaverine for the treatment of cerebral vasospasm after ruptured arteriovenous malformations.
A1  - Zubkov, Alexander Y
A1  - Lewis, Adam I
A1  - Scalzo, David
Y1  - 1999/01//
JF  - Surgical neurology
VL  - 51
IS  - 1
SP  - 75
EP  - 9; discussion 80
DO  - 10.1016/s0090-3019(98)00031-7
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0090301998000317
UR  - http://www.ncbi.nlm.nih.gov/pubmed/9952127
N2  - BACKGROUND This is the first report on the use of intra-arterial papaverine and percutaneous transluminal angioplasty in two patients with severe, symptomatic cerebral vasospasm who suffered ruptured arteriovenous malformations (AVMs). CASE DESCRIPTIONS The source of hemorrhage was a venous aneurysm in the first case and a pedicular aneurysm of the distal posterior inferior cerebellar artery in the second case. In both cases, the AVMs were located in the superior vermis and there was minimal subarachnoid hemorrhage. The first patient underwent removal of the AVM before the period of cerebral vasospasm and the second patient underwent removal of the AVM after the cerebral vasospasm had resolved. The outcome was excellent in the first patient and poor in the second patient. CONCLUSION Arteriovenous malformation with ruptured aneurysms may be at high risk for cerebral vasospasm even when there is minimal subarachnoid hemorrhage. We recommend early treatment of AVMs with ruptured pedicular, intranidal, or venous aneurysms to avoid rebleeding and to allow for aggressive treatment of cerebral vasospasm. The management of cerebral vasospasm after AVM rupture is discussed.
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TY  - JOUR
T1  - Occurrence of severe vasospasm following intraventricular hemorrhage from an arteriovenous malformation
A1  - Maeda, Keiichiro
A1  - Kurita, Hiroki
A1  - Nakamura, Tsuneo
A1  - Usui, Masaaki
A1  - Tsutsumi, Kazuo
A1  - Morimoto, Tadashi
A1  - Kirino, Takaaki
Y1  - 1997/09//
KW  - Angiographically occult malformation
KW  - Arteriovenous malformation
KW  - Intraventricular hemorrhage
KW  - Vasospasm
JF  - Journal of Neurosurgery
VL  - 87
IS  - 3
SP  - 436
EP  - 439
DO  - 10.3171/jns.1997.87.3.0436
UR  - https://thejns.org/view/journals/j-neurosurg/87/3/article-p436.xml
N2  - ✓ The authors present two rare cases of severe cerebral vasospasm following the rupture of arteriovenous malformations (AVMs). Computerized tomography revealed intracerebral hemorrhage in the thalamus in one case and in the putamen in the other, both accompanied by cast formation of intraventricular clots without radiological evidence of subarachnoid hemorrhage. Initial angiograms showed arterial narrowing of the bilateral internal carotid arteries in the supraclinoid portion but failed to demonstrate an arteriovenous shunt. Subsequent angiograms clearly demonstrated the existence of an AVM. Radiological features and possible mechanisms are discussed.
ER  - 
TY  - JOUR
T1  - Subarachnoid Hemorrhage—Factors in Prognosis and Management
A1  - Stornelli, S. A.
A1  - French, J. D.
Y1  - 1964/09//
JF  - Journal of Neurosurgery
VL  - 21
IS  - 9
SP  - 769
EP  - 780
DO  - 10.3171/jns.1964.21.9.0769
UR  - https://thejns.org/view/journals/j-neurosurg/21/9/article-p769.xml
ER  - 
TY  - JOUR
T1  - Cerebral vasospasm with subarachnoid haemorrhage from arteriovenous malformations of the brain
A1  - Nishimura, K.
A1  - Hawkins, T. D.
Y1  - 1975///
JF  - Neuroradiology
VL  - 8
IS  - 4
SP  - 201
EP  - 207
DO  - 10.1007/BF00337652
UR  - http://link.springer.com/10.1007/BF00337652
N2  - The results of a retrospective review of the clinical and radiological records of 63 patients with proven cerebral arteriovenous malformation are reported. Patients with dural arteriovenous malformations, and malformations with atypical angiographic features were excluded from the study. Of these 63 patients, 52 had a proven or suspected subrachnoid haemorrhage and 8 patients showed angiographic evidence of cerebral arterial spasm. Two of these patients had an associated intracranial aneurysm and were excluded from the study. The other 6 patients were shown to have spasm between two to thirteen days after a subarachnoid haemorrhage. The incidence of vasospasm associated with subarachnoid haemorrhage in this series was at most 12%. The probable explanation for the relative rarity of vasospasm associated with arteriovenous malformations of the brain, reported by other authors and confirmed by this study, is that the majority of these malformations are peripherally or deeply situated and subarachnoid bleeding is less likely to reach the base of the brain where arterial spasm mainly occurs as compared with haemorrhage from an aneurysm arising from the circle of Willis. © 1975 Springer-Verlag.
ER  - 
TY  - JOUR
T1  - Vasospasm After Arteriovenous Malformation Rupture
A1  - Gross, Bradley A.
A1  - Du, Rose
Y1  - 2012/09//
KW  - AVM
KW  - Arteriovenous malformation
KW  - DIND
KW  - Hemorrhage
KW  - Natural history
KW  - Stroke
KW  - Vasospasm
JF  - World Neurosurgery
VL  - 78
IS  - 3-4
SP  - 300
EP  - 305
DO  - 10.1016/j.wneu.2011.12.090
UR  - https://linkinghub.elsevier.com/retrieve/pii/S1878875011016354
L1  - file:///Users/julianamayorga/Desktop/Vasospasm After Arteriovenous Malformation Rupture.pdf
N2  - Objective: Vasospasm and resultant clinical deterioration caused by delayed cerebral ischemia (CD-CDI) are a considerable source of morbidity after aneurysmal subarachnoid hemorrhage (SAH). Although they are a relatively common cause of spontaneous SAH, AVM rupture and ensuing vasospasm are rarely reported. Methods: We reviewed our own series of 122 patients with AVMs. Seventy-three patients sustaining 84 hemorrhages were analyzed. In addition, we performed a review of the literature of vasospasm after AVM rupture. Results: Seventy of 84 hemorrhages (83%) had an intraparenchymal component, 27 (32%) a subarachnoid component, and 51 (61%) had an intraventricular component. No patients experienced CD-DCI, and of the 84 hemorrhages reported, only one patient experienced mild angiographic vasospasm (1.1%). Alternatively, this finding represents 1 in 34 cases (2.9%) who underwent definitive angiography between the fourth and fifteenth day after the hemorrhage. Nineteen additional cases of angiographic vasospasm after AVM rupture are reported in the literature. The mean age of these patients was 33 years; there was a 1.25:1 female to male predominance in this group. One-half of these patients had an intraparenchymal hemorrhage, and only 56% of them had SAH. All patients had intraventricular hemorrhage when assessed. The median time to onset of vasospasm was nine days. Across four series, the rate of angiographic spasm after SAH from an AVM was 6.3% (9/142 cases). Conclusions: Even in cases of SAH from AVMs, angiographic vasospasm after AVM rupture is relatively rare. We thus do not recommend empiric delayed angiography to assess for vasospasm in these patients. Nevertheless, it does remain a rare possibility and should be considered in those with CD-DCI. © 2012 Elsevier Inc. All rights reserved.
ER  - 
TY  - JOUR
T1  - Arteriovenous malformations
A1  - Parkinson, Dwight
A1  - Bachers, Gary
Y1  - 1980/09//
JF  - Journal of Neurosurgery
VL  - 53
IS  - 3
SP  - 285
EP  - 299
DO  - 10.3171/jns.1980.53.3.0285
UR  - http://www.ncbi.nlm.nih.gov/pubmed/7420143
UR  - https://thejns.org/view/journals/j-neurosurg/53/3/article-p285.xml
N2  - ✓ One hundred cases of macroscopic supratentorial arteriovenous malformations are studied, along with the significant literature. On the basis of morphology, they are subdivided into straight-line, single-unit, multiple-unit, intra- and extracranial, venous-wall types, and one other of questionable type. The study does not confirm a relationship of pregnancy to bleeding. It does confirm the absence of vasospasm in association with these lesions, the increasing tendency of the lesion to bleed the smaller it is, the equal sex distribution, the peak incidence in the patient's fourth decade, the lack of significance of family history, and the lack of associated vascular lesions. The study stresses the advantages of preoperative three-dimensional angiography, surgical magnification, and intraoperative serial angiography. It is emphasized again that the fistula itself must be removed or obliterated.
ER  -