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Aneurysmal subarachnoid hemorrhage - Reply
... Subarachnoid hemorrhage (SAH) is a sub-type of stroke defined by bleeding in the subarachnoid space where cerebrospinal fluid (CSF) circulates (Suarez, Tarr, & Selman, 2006). It represents 5% of all strokes and 25% of hemorrhagic strokes, affecting more than 30,000 North Americans each year with an annual cost to the United States of more than 1.7 billion dollars (Bederson et al., 2009;Graf & Nibbelink, 1974;Singer, Ogilvy, & Rordorf, 2011a;Wiebers, Torner, & Meissner, 1992). ...
... hemiparesis, dysphasia, visual field impairment and abnormal pupillary reaction), and meningismus (neck stiffness, photophobia, and headache without actual inflammation or infection of the meninges). Atypical signs include seizure, thunderclap headache, confusion, trauma that result from the loss of consciousness after aneurysm rupture, ataxia, nystagmus, third nerve palsy, sixth nerve palsy, retinal hemorrhage, and papilledema (Edlow & Caplan, 2000;Suarez et al., 2006;Togha, Sahraian, Khorram, & Khashayar, 2009;Vindlacheruvu & Mendelow, 2002). For patients who present with these signs and symptoms, non-contrast computerized tomography (CT) scan -the gold standard for diagnosing SAH-is indicated to rule out/confirm bleeding. ...
... If the initial CT scan was negative for bleeding, a lumber puncture is required to test for blood in the cerebrospinal fluid (CSF). Elevated red blood cells or xanthochromia (yellowish appearance of the CSF) indicate bleeding in the subarachnoid space and thus CT/cerebral angiography will be needed to identify the source of bleeding (Suarez et al., 2006). ...
Background and Purpose: Delayed cerebral ischemia (DCI) and Hunt and Hess (HH) grade are known risk factors for poor outcomes after aneurysmal subarachnoid hemorrhage (aSAH). DCI is often attributed to focal perfusion deficit (vasospasm/infarction). Global perfusion deficit (e.g. inadequate cerebral perfusion pressure (CPP)) can impair cerebral blood flow (CBF). The relationship between CPP and DCI remains unclear. Further, the exact mechanism of how HH grade relates to poor outcomes is uncertain. This study aimed to describe the temporal profiles of CPP change and to investigate the relationship between CPP, DCI, HH, and post-aSAH outcomes. Method: DCI was defined as clinical deterioration due to impaired CBF. Growth curve analysis was used to examine temporal profiles of CPP change. Logistic regression was utilized to examine the association between DCI and percentages of CPP values >110, >100, <70, and <60 mmHg. The associations between minimum CPP (measured 12 hours prior to DCI), DCI, and DCI onset, were tested using logistic regression and accelerated failure time model. The mediation effect of DCI on the relationship between HH and outcomes was tested using bootstrap confidence interval. Outcomes were assessed at 3 and 12 months and included: mortality, neuropsychological, functional, and physical outcomes. Results: There was a significant linear increase in CPP over time (β =0.06, SE=0.006, p<0.001). The covariance (-0.52) between the initial CPP and the linear change parameter was negative indicating that subjects with high CPP had a slower rate of increase and those with low CPP had a faster rate (p<0.001). For every 10% increase in the proportion of CPP>100 or >110 mmHg, the odds of DCI increased by 1.21 and 1.43, respectively. For every 10 mmHg increase in CPP, the odds of DCI increased by 2.78 (95%CI 2.00-3.87). High CPP was associated with earlier onset of DCI (p<.001). DCI did not mediate the relationship between HH and outcomes. Conclusions: When used prophylactically, induced hypertension contributes to higher CPP values. Based on the CPP trends/correlations observed, induced hypertension may not confer expected benefits in patients with aSAH. Findings raise concerns about safety of induced hypertension and the need for determining limits for hypertension, which current guidelines lack.
... In approximately eighty percent of nontraumatic SAH cases, intracranial aneurysmal rupture is the cause (aSAH) [2]. Typically, SAH is associated with a 40-50% mortality rate [3,4], while outcomes and complications such as rebleeding, increased intracranial pressure (ICP), reduction of cerebral blood flow, brain edema, vasospasm, hydrocephalus, and seizures in survivors are correlated with level of consciousness on admission, age, and the amount of blood visible in the cranium by CT scan [5]. These morbidities lead to poor outcome profiles. ...
... SAH affects approximately 30,000 Americans annually and carries a mortality rate of 40-50% [1,4]. Over half of those whom survive the initial injury go on to face complications such as increased ICP, CV, cerebral edema, seizures or stroke [5]. These complications are characterized by poor outcome profiles, and less than half of aSAH survivors resume normal pre-hemorrhage function by the first year of recovery [17]. ...
... Aneurysmal SAH is more common among females with a peak incidence at 55 years of age on average [5]. Further risk factors for the development of aSAH are: the African-American race [5,23], cigarette smoking [24][25][26][27], hypertension [28], heavy alcohol use [4,28,29], and cocaine use [5]. ...
Background: Haptoglobin (Hp) binds hemoglobin (Hgb), thereby inhibiting free radical production. It is presumed that Hp 2-2 genotype is associated with worse functional outcome after aneurysmal subarachnoid hemorrhage (aSAH) related to the weaker affinity for Hgb binding, decreased clearance of hemoglobin from the site of hemorrhage, and an associated increase in secondary injury with the alpha-2 allele.Objective: The objective is to describe the relationship between Hp genotype and mortality and gross functional outcome after aSAH.Methods: A total sample of 268 subjects was narrowed down to a sample of 193 Caucasian subjects (due to differences in allele frequency distribution among races), age 18-75 with a diagnosis of aSAH, Fisher Grade greater than or equal to 2, DNA and outcome data available and without pre-existing chronic neurologic disease/deficit were enrolled into an ongoing study (NR004339). Demographic and medical condition variables were extracted from medical records. Modified Rankin Score (MRS) and Glasgow Outcome Score (GOS) were assessed at 3, 6, 12, and 24 months after aSAH. Data analysis included univariate analysis as well as multivariate logistic regression analysis, controlling for covariates including age, sex, and severity of hemorrhage (Fisher grade).Results: The sample was primarily female (n=138; 71.5%) and Caucasian (n=237; 88.4%) with a mean age of 54.45 years. This sample was further narrowed down to include only subjects of Caucasian race due to differences in allele frequency distribution among other races previously published in literature. Haptoglobin 2-2 genotype was significantly correlated with MRS at 3 months post aSAH during univariate analysis (p=.04) and at 3 months after controlling for covariates in the multivariate logistic regression analysis (p=.05). Univariate analysis produced a significant (p=.02) relationship between subjects whose genotypes yielded at least one alpha-2 allele and development of cerebral vasospasm (CV). Subjects whose genotypes had only one alpha-2 allele were significantly (p=.01) associated with Fisher grade. Fisher grade and Hunt and Hess score were both significantly associated with poor outcomes on MRS at all four time periods. Age was significantly (p=.01) correlated with Hp 1-1 and Hp 1-2 genotypes; specifically, these patients were younger than those with Hp 2-2 genotype. After controlling for covariates, Fisher grade was the only covariate that maintained significance in predicting outcomes after aSAH at all four time periods.Conclusions: Subjects whose genotypes contain at least one alpha-2 allele more often had poor outcomes on MRS at 3 months post aSAH and were more likely to develop CV. Additionally, haptoglobin genotype can be used as predictor of gross functional outcome when measured using MRS at 3 months after aSAH. The Fisher grading scale and Hunt and Hess scoring system are both significantly useful for predicting outcomes (GOS, MRS, mortality) at all four time periods after aSAH.
... It is a medical emergency and can lead to death or severe disability. Up to half of all cases of SAH are fatal and 10-15% die before reaching a hospital, and those who survive often have neurological or cognitive impairment [3] . ...
... After a subarachnoid hemorrhage is confirmed, its origin needs to be determined, the choice is between cerebral angiography and CT angiography [1,3] . ...
... Aneurysmal subarachnoid hemorrhage (aSAH) accounts for less than 5% of all strokes (1,2). However, it affects patients at a younger age than other types of stroke and has very high morbidity and mortality rates (1,3). ...
... Aneurysmal subarachnoid hemorrhage (aSAH) accounts for less than 5% of all strokes (1,2). However, it affects patients at a younger age than other types of stroke and has very high morbidity and mortality rates (1,3). The incidence of aSAH has not changed, but medical advances have decreased mortality over the last few decades (2,4). ...
Objectives: Aneurysmal subarachnoid hemorrhage (aSAH) accounts for less than 5% of strokes but is associated with significant morbidity and mortality. Amongst survivors, neurocognitive complaints are common, often despite normal imaging. We used magnetoencephalography (MEG) to investigate neurophysiological function during a visual working memory task in aSAH survivors with good recovery and normal structural imaging.
Methods: Patients with aSAH treated with coiling and exhibiting good outcome measured by Glasgow Outcome Scale (GOS) and without related parenchymal structural lesions in post-treatment MRI, were recruited and compared to age- and sex-matched controls. All participants underwent intelligence and cognitive screening, structural MRI, and MEG testing in conjunction with a 1-back visual working memory task. Sensor-level global field power and virtual electrode source analysis of neuronal activity and connectivity in aSAH were assessed.
Results: Thirteen patients and 13 matched controls were enrolled (age: 56 ± 11 years, 19 female). The 1-back task was completed with similar accuracy despite a trend for a longer reaction time in aSAH patients (p = 0.054). During encoding and recognition phases, aSAH patients showed significantly increased neuronal activation and hyperconnectivity in periventricular areas, specifically the anterior and posterior cingulate gyri.
Conclusions: Increased posterior and anterior cingulate gyri neuronal activity is demonstrated in aSAH patients during visual working memory tasks, in the absence of structural lesions. These areas work mainly as a hub to “organize” memory storage and retrieval. Increased activity in these areas might be compensatory due to injury and consequently loss of neuronal response in connected areas in the working memory networks.
... Subarachnoid hemorrhage (SAH) is a neurologic emergency associated with significant morbidity and mortality representing the deadliest type of acute stroke (Suarez et al., 2006). The hallmarks of SAH include increased intracranial pressure (ICP), hypoperfusion, and delayed cerebral ischemia (with or without vasospasm ) (Eide and Sorteberg, 2006; Ansar and Edvinsson, 2009; Westermaier et al., 2011; Kelly et al., 2013; Danura et al., 2015). ...
... Vasospasm: Vasospasm is often thought to be the prime mechanism of delayed cerebral ischemia after aneurysmal SAH (Suarez et al., 2006). Vasospasm was detected immediately after SAH (30 min) but not thereafter , indicating that vasospasm is transient in this mild SAH model. ...
Subarachnoid hemorrhage (SAH) is associated with significant morbidity and mortality. We implemented an in-scanner rat model of mild SAH in which blood or vehicle was injected into the cistern magna, and applied multimodal MRI to study the brain prior to, immediately after (5min to 4h), and upto 7days after SAH. Vehicle injection did not change arterial lumen diameter, apparent diffusion coefficient (ADC), T2, venous signal, vascular reactivity to hypercapnia, or foot-fault scores, but mildly reduce cerebral blood flow (CBF) up to 4h, and open-field activity up to 7days post injection. By contrast, blood injection caused: (i) vasospasm 30min after SAH but not thereafter, (ii) venous abnormalities at 3h and 2days, delayed relative to vasospasm, (iii) reduced basal CBF and to hypercapnia 1-4h but not thereafter, (iv) reduced ADC immediately after SAH but no ADC and T2 changes on days 2 and 7, and (v) reduced open-field activities in both SAH and vehicle animals, but no significant differences in open-field activities and foot-fault tests between groups. Mild SAH exhibited transient and mild hemodynamic disturbances and diffusion changes, but did not show apparent ischemic brain injury nor functional deficits.
... Although women have historically been considered more likely than men to suffer from SAH (de Rooij et al., 2007), newer epidemiologic research reveals that this difference occurs only after the sixth decade of life (de Rooij et al., 2007). The most common cause of SAH is trauma as the corticomeningeal vessels are ruptured (Suarez, Tarr, & Selman, 2006). Most spontaneous causes of SAH are related to aneurysm rupture, which is the focus of this section (Suarez et al., 2006). ...
... The most common cause of SAH is trauma as the corticomeningeal vessels are ruptured (Suarez, Tarr, & Selman, 2006). Most spontaneous causes of SAH are related to aneurysm rupture, which is the focus of this section (Suarez et al., 2006). ...
Subarachnoid hemorrhage (SAH) causes 5% of all strokes and is responsible for about 18,000 deaths per year in the United States (Aneurysmal Subarachnoid Hemorrhage, 2008). The incidence of SAH has been estimated at 6 to 8 per 100,000 persons per year (Linn, Rinkel, Algra, & van Gijn, 1996). In nearly 15% (range 5–34%) of patients with SAH, no source of hemorrhage can be identified via four-vessel cerebral angiography (Alen et al., 2003; Gupta et al., 2009), resulting in two major types of SAH: aneurysmal (ASAH) and nonaneurysmal (NASAH). Anecdotal evidence and contradictory research suggest that patients with NASAH experience some of the same health-related quality of life (HRQOL) issues as patients with ASAH. The purpose of this quantitative survey design study was to compare health-related quality of life (HRQOL) 1 to 3 years post-hemorrhage in patients who have experienced a NASAH to those who have experienced an ASAH. This is the first US study to specifically investigate HRQOL in NASAH and the second study comparing HRQOL outcomes between aneurysmal and nonaneurysmal subarachnoid hemorrhage patients. Our results are comparable to the first study by Hutter and Gilsbach, (1995), which also found that the two groups are much more similar than different. There were no significant differences between 28 of the 36 demographic and clinical characteristics examined in this study. Our study confirms previous findings that there is a significant impact on employment for both hemorrhage groups and an even greater inability to return to work for the NASAH patients. The nonaneurysmal group had more physical symptom complaints while the aneurysmal group had more emotional symptoms. Lastly, both groups had low levels of PTSD, and these levels did not differ significantly between groups. However, PTSD and social support were shown by regression analysis to impact HRQOL for both groups. We recommend that clinicians assess for PTSD in all subarachnoid hemorrhage patients and institute treatment early, which will decrease the negative effects on HRQOL. This may include offering psychological services or social work early in the hospital course to all SAH patients. Further research and policy changes are needed to assist in interventions that improve vocational reintegration after SAH. NASAH patients should no longer be referred to as having suffered a “benign hemorrhage.” They have had a life changing hemorrhage that may forever change their lives and impact their HRQOL.
... Ендоваскулярна нейрорентгенохірургія • Артериальные аневризмы (АА) головного мозга представляют собой одну из наиболее сложных нейрохирургических патологий. Разрывы аневризмы сопровождаются высокой летальностью -от 30 до 40 % по данным разных авторов [1][2][3][4]. Высокая вероятность повторных кровотечений из разорвавшейся аневризмы заставляет нейрохирургов спешить с проведением операции, чтобы избежать этого. Большинство авторов утверждают, что операцию при разрыве аневризмы следует проводить как можно раньше -в острый период (в первые часы или сутки после разрыва) [5][6][7][8]. ...
Objective – to find out the causes of adverse effects of microsurgical exclusion of arterial aneurysms during the acute rupture period.
Materials and methods. The results of 41 microsurgical exclusions of arterial aneurysms in the first two days after the rupture were analyzed. There were 17 men and 24 women. The age of patients was from 32 to 78 years, the average age was 50 years. Neurological status, the severity of the Hunt–Hess condition, and the level of consciousness on the Glasgow com scale were assessed. The Glasgow Scale was used to evaluate the quality of life of surviving patients.
Results. After surgery, 12 (29.2 %) patients died. A statistically significant dependence of mortality have been established by the Hunt–Hess scale, the level of consciousness on the Glasgow scale, the prevalence of angiospasm according to cerebral angiography and the presence of ischemia according to spiral computed tomography. The severity of subarachnoid hemorrhage according to Fisher and angiospasm according to transcranial dopplerography, although they affect the mortality and outcome of surgery, but not statistically significant.
Conclusion. Given the high mortality rate after microsurgical operations in the acute period of arterial aneurysms rupture the indications for their conduct should be more balanced. It should be taken into account the presence of adverse predictors.
... A neurysmal subarachnoid hemorrhage (SAH) is a common neurological condition that accounts for 80% of nontraumatic SAH. 1 The incidence of aneurysmal SAH in the United States exceeds 30 000 individuals annually, and this appears to have remained steady over the past few decades. 2 It is still associated with significant morbidity and mortality, 1,3 despite recent advances in diagnostic imaging, endovascular and microsurgical techniques, as well as perioperative intensive care unit management that has increased the survival rate by ≈17%. [4][5][6][7] The clinical outcome of patients who survive an aneurysmal SAH ranges between complete independence and permanent disability. ...
Background and Purpose—
Predicting long-term functional outcomes after intracranial aneurysmal rupture can be challenging. We developed and validated a scoring system—the Southwestern Aneurysm Severity Index—that would predict functional outcomes at 1 year after clipping of ruptured aneurysms.
Methods—
Ruptured aneurysms treated microsurgically between 2000 and 2014 were included. Outcome was defined as Glasgow Outcome Score (ranging from 1, death, to 5, good recovery) at 1 year. The Southwestern Aneurysm Severity Index is composed of multiple prospectively recorded patient demographic, clinical, radiographic, and aneurysm-specific variables. Multivariable analyses were used to construct the best predictive models for patient outcomes in a random 50% of the cohort and validated in the remaining 50%. A scoring system was created using the best model.
Results—
We identified 527 eligible patients. The Glasgow Outcome Score at 1 year was 4 to 5 in 375 patients (71.2%). In the multivariable logistic regression, the best predictive model for unfavorable outcome included intracerebral hemorrhage (odds ratio [OR], 2.53; 95% CI, 1.55−4.13), aneurysmal size ≥20 mm (OR, 6.07; 95% CI, 1.92−19.2), intraventricular hemorrhage (OR, 2.56; 95% CI, 1.15−5.67), age >64 (OR, 3.53; 95% CI, 1.70−7.35), location (OR, 1.82; 95% CI, 1.10−3.03), and hydrocephalus (OR, 2.39; 95% CI, 1.07−5.35). The Southwestern Aneurysm Severity Index predicts Glasgow Outcome Score at 1 year with good discrimination (area under the receiver operating characteristic curve, derivation: 0.816, 95% CI, 0.759−0.873; validation: 0.803, 95% CI, 0.746−0.861) and accurate calibration ( R ² =0.939).
Conclusions—
The Southwestern Aneurysm Severity Index has been internally validated to predict 1 year Glasgow Outcome Scores at initial presentation, thus optimizing patient or family counseling and possibly guiding therapeutic efforts.
... ubarachnoid hemorrhage caused by spontaneous aneurysm rupture is a common and complicated neurological disorder [1]. Cerebral aneurysm is congenital in most cases, in which one part of the artery wall is dilated like a balloon and highly prone to spontaneous rupture. ...
Background and Aim: This study aimed to present the results of early and delayed operation on patients with ruptured brain aneurysms. In addition to comparing the results and rates of morbidity and mortality in the surgical procedure and identifying the effective factors, this study aimed to provide methods to improve the treatment of brain aneurysm.
Methods and Materials/Patients: This was a retrospective study on 60 patients with a definitive diagnosis of brain aneurysm admitted to Neurosurgery Ward of Poursina Hospital, Rasht, Iran from 2009 to 2013.
Results: 7(11.7%) patients on the first 3 days and 37(61.7%) patients on the days 4-14 and 16(26.7%) after 2 weeks and selectively underwent surgery. In total, 11.7% of patients died and 15% developed severe complications. In the group underwent surgery on the first 3 days, 2(28.5%) patients died and 2 experienced severe complications. In the second group (in 4-14 days), 4(10.8%) patients died and 5(13.5%) suffered from severe complications, and in the group (16 patients) with delayed surgeries, 1(6.2%) patient died and 2(12.5%) suffered from severe complications. Neurological grading and operation time were important factors in complications and mortality of patients.
Conclusion: This study showed that Hunt and Hess neurological grading score has a direct relationship with increased morbidity and mortality rates, while delayed operation is associated with a reduction in morbidity and mortality. Given the complications of early aneurysm surgery (during the first 3 days) compared with delayed surgery, and also most of these patients die due to vasospasm or recurrent hemorrhage before the onset of a delayed phase, performing early surgery in these patients requires further evaluation. According to this study, the reduction of each episode of occlusion with temporary clipping will result in fewer complications.
... У дослідженні, прове- деному в Кореї, чинниками ризику були молодший вік, оклюзійна гідроцефалія, низький показник за шкалами Hunt-Hess, Fisher та повторний крововилив до оперативного втручання [4] (Табл. 2) Тяжкий неврологічний дефіцит більшою мірою пов`язаний з ризиком розвитку постінсультної епілеп- сії (28% -протягом першого року та 47% -у наступні 4 роки) порівняно з легким чи відсутнім фокальним неврологічним дефіцитом (12% -протягом першого року і 15% -у наступні 4 роки) [23,24]. ...
Судоми – досить часте явище при субарахноїдальному крововиливі (САК) аневризматичного генезу. На їх частку припадає від 6 до 24% від усіх нетравматичних САК. Вони можуть бути “ранні” (в перші 2 тиж) або “пізні”, тобто переходити у симптоматичну епілепсію. Досить часто (13–24%) судомний напад може бути першим клінічним симптомом захворювання з/без “громоподібного” головного болю. Якщо вплив інших чинників (низькі значення за шкалами Hunt–Hess, WFNS, GCS в дебюті захворювання, наявність внутрішньомозкової гематоми, оклюзійної гідроцефалії, симптомного вазоспазму) асоціюється з несприятливим прогнозом при САК, то вплив судом, які виникли в дебюті САК, є найбільш дискутабельним і найменш вивченим питанням. Відсутні чіткі рекомендації щодо призначення протисудомної терапії для первинної та вторинної профілактики, поліпшення прогнозу для пацієнта із САК і якості його життя. Наведено огляд даних літератури та досліджень, проведених останніми роками, для з`ясування значення судомного нападу в перебігу САК.
... [23,31,32]. Some experts proposed the role of female hormones in female preference for non-traumatic intracranial hemorrhage but there is a controversy about this [33,34]. The results of this study were compatible with most other studies. ...
Background and Aim: This study aimed at analyzing the demographic characteristics of the patients with non-traumatic intracranial hemorrhage, their angiographic results and the correlation between computed tomography (CT) scan and angiography findings.
Methods and Materials/Patients: In a descriptive study, we retrospectively reviewed the records of the patients with non-traumatic intracranial hemorrhage based on their brain CT or lumbar puncture findings from 2011 to 2017. For all patients, four vessel catheter angiography via the femoral approach was performed in the Medical Imaging Center of Kermanshah University of Medical Sciences, Iran.
Results: We investigated 143 cases with non-traumatic intracranial hemorrhage which was indicated in CT findings (91.61%) or lumbar puncture (8.39%). Of 143 patients, 64 (44.8%) were men and 79 (55.2%) women (mean age 53.7±12.1 years old). Moreover, 104(72.7%) patients had Subarachnoid Hemorrhage (SAH), 19(13.3%) of them had Intracranial Hemorrhage (ICH), 8(5.6%) ones had Intraventricular Hemorrhage (IVH) and 12(8.4%) patients had normal brain CT. There were 100 cases of aneurysm (69.93%), 13 cases of Arteriovenous Malformations (AVM) (9.09%), 28 cases with negative angiograms (19.58%), and 2 cases with other pathologies (1.4%). Seven (4.89%) cases of multiple aneurysms were also recorded. Of 13 patients with AVM, 8(61.5%) patients had AVM in parieto-occipital region, 2(15.4%) in temporal, 1(7.7%) in frontal region and 2(15.4%) had deep AVM. Two (1.4%) patients with SAH had dural AVF. Twenty-eight (19.6%) patients had negative angiogram, 22 cases of them had second angiography after one to two weeks. The most common positive finding in the second angiogram was Acom aneurysm (18.18%).
Conclusion: Aneurysms and AVMs are the most common causes of non-traumatic intracranial hemorrhage. The most common site of intracranial aneurysms is the circle of Willis. A second angiogram after one to two weeks is necessary in most patients with negative results in first angiography after non-traumatic intracranial hemorrhage.
... Although most intracranial aneurysms remain asymptomatic, aSAH is a devastating condition with high rates of case fatalities and permanent disabilities [9][10][11][12][13]. The ISUIA suggested that the morbidity and mortality associated with aneurysm treatment exceeds the mid-term rupture risk of small aneurysms [4]. ...
Purpose:
There is a controversy concerning the risk of rupture of small intracranial aneurysms. We sought to determine the size and morphological features of ruptured intracranial aneurysms.
Material and methods:
The hospital files and images from all patients referred during one decade (2007-2016) to a specialized neurovascular center were retrospectively reviewed. Neck diameter, fundus depth and width as well as neck width based on catheter angiography were measured. Aneurysm morphology was classified as either regular, lobulated, irregular or fusiform.
Results:
A total of 694 consecutive patients with aneurysmal subarachnoid hemorrhage (aSAH) were identified (65.9% female, median age 54.3 years). The anterior communicating artery (AcomA) was the most frequent location of ruptured aneurysms. The medians for aneurysm depth, width and neck diameter were 5 mm, 4.5 mm and 3 mm, respectively. A regular contour of the aneurysm sac was found in 19%.
Conclusion:
The majority of aSAH are caused by small intracranial aneurysms. There is no safety margin in terms of small aneurysm size of regular shape without daughter aneurysms. Treatment should also be offered to patients with small, regularly shaped intracranial aneurysms, together with an empirical risk-benefit assessment.
... patients admitted to hospital in good clinical status for the treatment of ruptured Acommm aneurysm, about 80% have achieved favourable outcome.[3]About 46% of survivors after SAH may have cognitive impairment.[2,4]Endovascular coiling has increasingly become an alternative procedure for surgical clipping in both ruptured and unruptured aneurysms in last few decades.[5,6]However, ...
Aneurysmal Subarachnoid Hemorrhage (aSAH) remains a devastating and often fatal form of stroke. The aneurysm is targeted for obliteration to prevent re-bleeding and to manage the possible complications from the event. Endovascular coiling has emerged as a less invasive alternative to conventional surgical clipping to treat aneurysms.
: This study was done in 50 cases of anterior communicating (Acommm) aneurysm presented in the department of neurosurgery, SMS medical college, Jaipur from November 2015 to August 2016 to evaluate the outcome of both modalities used in the treatment of ruptured Acommm aneurysm. 50 patients with Hunt and Hess (H&H) grade I, II or III were classified into two groups of microsurgical clipping and endovascular coiling.
: Mortality rate was comparable in both groups that were 21. 21% in the clipping group and 23. 52% in the coiling group. Good Glasgow outcome score (GOS) were found in 60. 60% of clipping and 58. 58% of coiling group. All the complications found to be more in clipping group but that were not statistically significant except for hyponatremia which was significantly higher in clipping group(P=0. 007).
: There was no statistically significant difference in GOS at 6 month of follow up between the two groups. We recommend further interventional studies with larger sample sizes and longer follow up for better evaluation of the modalities.
... In general, subarachnoid hemorrhages are associated with extremely high rates of mortality of about 45-50%, significant morbidity exists among survivors (van Gijn et al., 2007;Bederson et al., 2009) and chronic disabilities are common (Kantor et al., 2014). It should be noted that subarachnoid hemorrhage associated with TBI accounts for about half of all cases, and subsequent cerebral vasospasm following both aneurysmal and traumatic subarachnoid hemorrhages is among the leading causes of morbidity and mortality with no proven effective treatment (Suarez et al., 2006;Amyot et al., 2015). Thus, identifying the mechanisms underlying TBI pathologies and intrinsic, potentially protective responses involving acute reactants, such as Hp (Vejda et al., 2002;Campbell et al., 2005), will provide new insights into the development of novel strategies for TBI treatment. ...
Neurodegeneration is characterized by the progressive loss of neural tissue that result in various neurodegeneration-initiated cerebral failures and complex diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease. All these medical conditions are accompanied by the disruption of blood-brain barrier (BBB). The BBB is an interface, separating the brain from the circulatory system and protecting the central nervous system from potentially harmful chemicals while regulating transport of essential molecules and maintaining a stable environment. Owing to the inability of the neurons to regenerate on their own after neurodegeneration or severe damage to the neural tissue, neurodegenerative disorders do not have natural cures on their own. Neuroregeneration is a viable way to curb neurodegeneration. One of the current approaches is stem cell-based therapy that has been shown to be potentially helpful for the application of neuronal cell replacement for neuroregeneration.
... e l s e v i e r . c o m / l o c a t e / m g e n e the brain (Suarez et al., 2006).SAH is mainly caused by three reasons, rupture of a cerebral arterial aneurysm, an arterial-venous malformation , or head trauma (Ruigrok et al., 2005). An aneurysm is a localized bulge in the wall of an artery (Raya and Diringer, 2014). ...
Subarachnoid haemorrhage (SAH) is characterised by bleeding in the subarachnoid space in the brain. There are various polymorphisms in genes which are associated with this disease. We performed a systematic meta- analysis to investigate the relationship of APOE polymorphism on aSAH. A comprehensive literature search was done in the Pubmed database, Science Direct, Cochrane library and Google Scholar. The OR and 95% CI were evaluated for the gene and aSAH association using fixed and random effect models. Publication bias was assessed using Begg's funnel plot and Egger's regression test. All statistical evaluations were done using the software Review Manager 5.0 and Comprehensive Meta Analysis v2.2.023. A total of 9 studies were assessed on APOE polymorphism (1100 Cases, 2732 Control). Meta analysis results showed significant association in ε2/ ε2 versus ε3/ε3, ε2 versus ε3 genetic models and ε2 allele frequency. In subgroup analysis statistically significant association was observed in Asians in the genetic models ε2/ ε2 versus ε3/ε3, ε2/ε3 versus ε3/ε3, ε2 versus ε3 and also in ε2 allele frequency. However, in Caucasian population only ε2/ε2 versus ε3/ε3 genetic model showed significant association between APOE and risk of aSAH. In this meta-analysis study, the ε2/ε2 genotype is associated with increased risk of aSAH.
... The 6-month mortality rate ranges from 40 to 50 %, and 30 % of survivors harbor permanent neurological impairment [2]. In recent years, research has focused on neuropsychological sequels of aSAH patients [3][4][5][6][7]and on factors related to diminished quality of life in patients with good neurological recovery [8]. Several reports over the last decade have explored the relationship between Susanna Bacigaluppi and Nicola Bragazzi have contributed equally to this work. ...
Purpose
Pituitary dysfunction is reported to be a common complication following aneurysmal subarachnoid hemorrhage (aSAH). The aim of this meta-analysis is to analyze the literature on clinical prevalence, risk factors and outcome impact of pituitary dysfunction after aSAH, and to assess the possible need for pituitary screening in aSAH patients.
Methods
We performed a systematic review with meta-analysis based on a comprehensive search of four databases (PubMed/MEDLINE, ISI/Web of Science, Scopus and Google Scholar).
Results
A total of 20 papers met criteria for inclusion. The prevalence of pituitary dysfunction in the acute phase (within the first 6 months after aSAH) was 49.30 % (95 % CI 41.6–56.9), decreasing in the chronic phase (after 6 months from aSAH) to 25.6 % (95 % CI 18.0–35.1). Abnormalities in basal hormonal levels were more frequent when compared to induction tests, and the prevalence of a single pituitary hormone dysregulation was more frequent than multiple pituitary hormone dysregulation. Increasing age was associated with a lower prevalence of endocrine dysfunction in the acute phase, and surgical treatment of the aneurysm (clipping) was related to a higher prevalence of single hormone dysfunction. The prevalence of pituitary dysfunction did not correlate with the outcome of the patient.
Conclusions
Neuroendocrine dysfunction is common after aSAH, but these abnormalities have not been shown to consistently impact outcome in the data available. There is a need for well-designed prospective studies to more precisely assess the incidence, clinical course, and outcome impact of pituitary dysfunction after aSAH.
... Aneurysmal subarachnoid hemorrhage (SAH) is a neurological emergency with an incidence of 2-22 per 100,000 per year ( Van Gijn and Rinkel, 2001 ). Among survivors, approximately one third to one half suffer from long term neurologic disability ( Suarez et al., 2006 ;AlTamimi et al., 2010 ). Delayed cerebral ischemia (DCI) is one of the most significant complications in the days that ensue after an acute aneurysmal SAH, occurring in up to 30% of patients ( Roos et al., 2000 ). ...
Background:
Thirty percent of patients with subarachnoid hemorrhage experience delayed cerebral ischemia or delayed ischemic neurologic decline (DIND). Variability in the definitions of delayed ischemia makes outcome studies difficult to compare. A recent consensus statement advocates standardized definitions for delayed ischemia in clinical trials of subarachnoid hemorrhage. We sought to evaluate the interrater agreement of these definitions.
Methods:
Based on consensus definitions, we assessed for: (1) delayed cerebral infarction, defined as radiographic cerebral infarction; (2) DIND type 1 (DIND1), defined as focal neurologic decline; and (3) DIND2, defined as a global decline in arousal. Five neurologists retrospectively reviewed electronic records of 58 patients with subarachnoid hemorrhage. Three reviewers had access to and reviewed neuroradiology imaging. We assessed interrater agreement using the Gwet kappa statistic.
Results:
Interrater agreement statistics were excellent (95.83%) for overall agreement on the presence or absence of any delayed ischemic event (DIND1, DIND2, or delayed cerebral infarction). Agreement was "moderate" for specifically identifying DIND1 (56.58%) and DIND2 (48.66%) events. We observed greater agreement for DIND1 when there was a significant focal motor decline of at least 1 point in the motor score. There was fair agreement (39.20%) for identifying delayed cerebral infarction; CT imaging was the predominant modality.
Conclusions:
Consensus definitions for delayed cerebral ischemia yielded near-perfect overall agreement and can thus be applied in future large-scale studies. However, a strict process of adjudication, explicit thresholds for determining focal neurologic decline, and MRI techniques that better discriminate edema from infarction seem critical for reproducibility of determination of specific outcome phenotypes, and will be important for successful clinical trials.
... is may occur spontaneously, usually from a ruptured cerebral aneurysm or may result from head injury. 1 It is a form of stroke and comprises 1 to 7 % of all strokes 2 and a ects about 6/100,000 of the population and women are a ected more commonly than men, usually present before the age of 65. 3 Up to half of all cases are fatal and 10-15% dies before reaching to the hospital 4 and those who survive often have neurological or cognitive impairment. 5 Cerebral aneurysms are the most common cause of non traumatic subarachnoid hemorrhage and is responsible for 70 to 75% of spontaneous SAH, 5% of which is caused by AVM (arterio-venous malformation) and in 20% cases no causes are found. 6 Ruptured "berry" aneurysm is the most common among the aneurysmal SAH and is responsible for 85% of cases. ...
The present study was undertaken to evaluate the morphological anatomy of cerebral vessels in patients of aneurysmal subarachnoid hemorrhage. The cross-sectional observational study was carried out in the Department of Neurology, Dhaka Medical College Hospital, Dhaka from January 2013 to June 2013. Adult patients of spontaneous subarachnoid haemorrhage (SAH), diagnosed clinically and confirmed by CT scan of the head were included in the study. However, patients who are not capable financially of undergoing Digital Subtraction Angiography (DSA), traumatic subarachnoid haemorrhage, intracerebral haemorrhage and patients taking antiplatelet and anticoagulant drugs and with comorbidities were excluded. A total of 30 subjects meeting the above eligibility criteria were selected consecutively from the study population. The present study demonstrated that 80% of the patients were 50 or younger than 50 years old (mean age 45.0 ± 9.4 years) with a male preponderance (60%). Sudden headache accompanied by vomiting was invariably complained by the patients at onset of Athe disease. On admission two-thirds (66.7%) of the patients were unconscious. 4 out of 30(16.65%) patients exhibited neurological deficit. Of the risk factors, hypertension and smoking demonstrated their significant presence (around 45%) among the patients studied. Based on Glasgow Coma Scale, 7(23.3%) patients out of 30 in the present study were in grade-v. Our data showed that the common site of aneurysm was anterior communication artery (36.7%) followed by middle cerebral artery (26.7%) and posterior communicating artery (23.3%). Saccular aneurysms formed the main bulk (93%) of the cases irrespective of anatomical distribution of aneurysm. In aneurysmal subarachnoid haemorrhage, aneurysms are mainly located in anterior communicating and middle cerebral arteries and of medium-sized. Majority are saccular type and narrow-necked.Bangladesh Med J. 2015 Sep; 44 (3): 125-129
... I ntracranial aneurysm (IAs) is a common disease with an estimated overall prevalence of 3.2% in the general population. 1 Rupture of IA is the most common cause of subarachnoid hemorrhages (SAH), accounting for about 85% of all nontraumatic SAH. 2 SAH is a catastrophic neurological condition, with a case fatality of $50% and as many as 46% of survivors may have long-term cognitive impairment. 3 Although the pathogenesis of the IA remains unclear, modifiable factors such as hypertension, active smoking, and excessive alcohol consumption have been associated with the risk of IA. 4 In addition, accumulating evidence has indicated an important role of genetic component in pathogenesis of IA. First-degree relatives in familial IA families have a relative risk of up to 4.2 when compared with the general population. ...
The therapy of inflammatory bowel disease, particularly with tumor necrosis factor (TNF) blockers, may be associated with a number of cutaneous adverse effects, including psoriasis-like, eczema-like, and lichenoid eruptions. Other rare skin complications are neutrophilic dermatoses such as amicrobial pustulosis of the folds (APF), which is a chronic relapsing pustular disorder classified in this spectrum.
The authors analyzed clinical, histopathologic, and cytokine expression profiles of 3 inflammatory bowel disease patients with APF triggered by adalimumab (patient 1) and infliximab (patients 2 and 3).
All 3 patients presented with sterile pustules involving the cutaneous folds, genital regions, and scalp 6 months after starting adalimumab (patient 1) and 9 months after starting infliximab (patients 2 and 3). Histology was characterized by epidermal spongiform pustules with a dermal neutrophilic and lymphocytic infiltrate. Tumor necrosis factor blocker withdrawal associated with topical and systemic corticosteroids induced complete remission of APF in all 3 patients. The expressions of interleukin (IL)-1 beta and its receptors as well as TNF alpha and its receptors were significantly higher in APF than in controls. Also IL-17, leukocyte selectin, and chemokines, such as IL-8, [C-X-C motif] chemokine ligand 1/2/3 (C = cysteine, X = any amino acid), [C-X-C motif] chemokine ligand 16 (C = cysteine, X = any amino acid), and RANTES (regulated on activation, normal T cell expressed and secreted) were significantly overexpressed. Finally, the authors found significant overexpression of both metalloproteinases 2/9 and their inhibitors 1/2.
The observation of 3 patients with APF following anti-TNF therapy expands not only the clinical context of APF but also the spectrum of anti-TNF side effects. Overexpression of cytokines/chemokines and molecules amplifying the inflammatory network supports the view that APF is autoinflammatory in origin.
... Los aneurismas cerebrales son dilataciones anormales en la pared de las arterias responsables de aproximadamente 80% de las HSA no traumáticas 1-3 . Los aneurismas localizados en la circulación anterior constituyen aproximadamente 90% de los aneurismas cerebrales, de ellos la mayoría se encuentra en la arteria comunicante anterior [1][2][3][4][5] . El tratamiento etiológico definitivo de la hemorragia subaracnoidea por ruptura aneurismática consiste en la coloca-ción de clips metálicos en el cuello del aneurisma con técnica microquirúrgica, para su oclusión. ...
La hemorragia subaracnoidea espontánea se debe a la ruptura de un aneurisma cerebral, su tratamiento definitivo consiste en la colocación de clips metálicos en el cuello de dicho aneurisma con técnica microquirúrgico o en la colocación mediante técnica endovascular de coils que provocan la trombosis intraluminal del aneurisma. Si bien la técnica endovascular es aceptada como la terapia de elección en los aneurismas de circulación posterior, muchos aneurismas de circulación anterior con cuello ancho y anatomía compleja constituyen un reto para el procedimiento endovascular. Sin embargo, en las últimas décadas, el desarrollo de nuevas técnicas y dispositivos para el manejo endovascular ha permitido el tratamiento adecuado de estas lesiones. Estas técnicas incluyen la embolización con remodelación, el uso de stent más coils y el uso de stents diversores de flujo; las mismas que tienen por objetivo mejorar el empaquetamiento de los coils dentro del aneurisma y además, la reconstrucción de la anatomía del vaso portador así como del flujo sanguíneo del mismo, constituyendo no sólo un manejo anatómico del aneurisma sino también un manejo funcional de la arteria portadora.
... angioplasty or directed application of vasodilating agents (37). Due to the emergence of the more rigorous principles of evidence-based medicine, the need has arisen for a review of the available evidence on which to base the prevention and treatment of vasospasm in patients suffering from aneurysmal SAH. ...
Aim:
Delayed cerebral ischemia (DIND) and cerebral vasospasm (CV) remain the most common and debilitating neurological complications following aneurysmal subarachnoidal hemorrhage (SAH). Many reports demonstrate the importance of proanthocyanidines (PR) on the vascular system, including endothelium-dependent relaxation of blood vessels. These effects of PR to cerebral vascular system was examined in this study.
Material and methods:
Fifty-two adult Sprague-Dawley male rats were used to experimental double hemorrhage model. They were divided to control, sham, pre- and post-interventional treatment groups. 100mg/kg PR was administrated for the treatment for respect to groups. Basilar artery diameter (BAD) and arterial wall thickness were measured and apoptosis ratio of the endothelial cells was calculated. Arterial walls were examined electron microscopically (EM).
Results:
There were significant differences between the groups except control and pre-SAH (p=0.37) and post-SAH and pre-SAH groups (p=0.15) respect to BAD. According to arterial wall thickness, apoptosis ratio and grading there were significant differences between the groups except control and pre-SAH (p=0.85, p=0.49 and p=0.18 respectively) and SAH and post SAH (p=0.08, p=0.21 and p=0.24 respectively) groups. EM findings revealed that pro-apoptotic and pro-necrotic degenerated endothelial cells with seldom vacuolization in post-SAH treatment group which were more serious in SAH group.
Conclusion:
We demonstrated that pre-SAH administration of PR induces better vasodilatation and protection of basillar artery (BA) from vasospasm (VS), which could yield neuroprotective and vasodilatator effects. In addition, PR appears to be involved in relieving oxidative damage, with antioxidant-antiapoptotic-antinecrotic effect that may contribute to vascular dilation.
... Conversely , mean levels of IL-6 peaked in the corresponding time frame, particularly in patients with poor outcome. This timeline coincides with the onset of vasospasm[10], although this relationship was not explored in the current study. The ambitious follow-up period of 6 months is also conceptually one of the strengths, as compared with 3 months in most studies[11]. ...
Inflammation is purported to play an important role in the clinical course of subarachnoid hemorrhage. The current study by Höllig et al. entails using dehydroepiandrosterone sulfate, a hormone that inhibits key inflammatory pathways, as a predictor of functional outcome in these patients.
... The most common cause of SAH is trauma. During a traumatic injury, the corticomeningeal vessels are ruptured as opposed to spontaneous causes of SAH that are related to aneurysm rupture (Suarez, Tarr, & Selman, 2006). Rupture of an aneurysm releases blood directly into the cerebrospinal fluid (CSF) under arterial pressure (Greenberg, 2005). ...
Subarachnoid hemorrhage (SAH) is divided into two major types (aneurysmal [ASAH] and nonaneurysmal [NASAH]) because, in approximately 15% of the patients who experience SAH, no source of hemorrhage can be identified. Anecdotal evidence and contradictory research suggest that patients with NASAH experience some of the same health-related quality of life (HRQOL) issues as patients with ASAH. This quantitative survey design study compared 1-3 years after hemorrhage the HRQOL in patients who had experienced an NASAH with those who had experienced an ASAH. This is the first U.S. study to specifically investigate HRQOL in NASAH and the second to compare HRQOL outcomes between patients with ASAH and NASAH. These study results corroborate those of the first-that the two groups are much more similar than different. It confirms that the impact on employment for both hemorrhage groups is significant, and it also finds an even greater inability to return to work for the patients with NASAH. Physical symptom complaints were more common in the group with NASAH, whereas the group with ASAH experienced more emotional symptoms. Both groups had low levels of posttraumatic stress disorder (PTSD), with those levels not differing significantly between groups. However, PTSD and social support were shown to impact HRQOL for both groups. The authors recommend that clinicians assess all patients with SAH for PTSD and institute treatment early. This may include offering psychological services or social work early in the hospital course. Further research and policy changes are needed to assist in interventions that improve vocational reintegration after SAH. Patients with NASAH should no longer be described as having experienced a "benign hemorrhage." They have had a life-changing hemorrhage that may forever change their lives and impact their HRQOL.
... 1,2 With an overall mortality of $ 45%, aSAH is a major contributor to the stroke-related loss of productive life years because it occurs at younger ages than ischemic stroke or intracerebral hemorrhage (ICH). [3][4][5][6] In addition to the primary bleeding event and delayed ischemic neurologic deficits, early rebleeding from ruptured intracranial aneurysms is a devastating complication associated with high mortality and morbidity. 7 The prevention of rebleeding and its associated complications is the main rationale of early surgical or interventional aneurysm treatment. ...
Objective To assess clinical and radiographic risk factors for intraoperative aneurysm rupture (ioAR) during surgical clipping after aneurysmal subarachnoid hemorrhage (aSAH) and to analyze its influence on patient outcome. Methods Patient selection was based on a retrospective analysis of our prospective subarachnoid hemorrhage patient database including consecutive patients between January 2008 and August 2012 with aSAH undergoing microsurgical clipping. Demographic data, cardiovascular risk factors, preoperative radiologic aneurysm characteristics, as well as timing of surgery and preoperative severity grades (Hunt and Hess [HH], Fisher, World Federation of Neurological Societies [WFNS]), were collected from hospital charts and surgery videos and compared between patients with and without ioAR. Results Of 100 patients (38 men, 62 women) with a median age of 57.4 years (range: 23-85 years), ioAR occurred in 34 cases (34%). Univariate analyses showed that severity grades were significantly higher in the ioAR group (Fisher p = 0.012; HH p = 0.002; WFNS p = 0.023). IoAR was significantly associated with intracerebral hemorrhage (ICH) (23% versus 47%; p = 0.013) and the spot sign as an indicator of active bleeding within the ICH (0% vs 44%; p = 0.007). Multivariate analysis showed that HH was the only significant predictor of ioAR (p = 0.03; odds ratio: 2.3; 95% confidence interval, 1.1-5.0). With a mean follow-up of 17.6 months ( ± 16.6), Glasgow Outcome Scale score, mortality rate (12% versus 15%; p = 0.82), delayed cerebral ischemia (36% versus 38%; p = 0.51), and shunt dependency (32% versus 44%; p = 0.23) were comparable between the non-ioAR and ioAR group. Conclusions Initial clinical status and spot sign were associated with ioAR during microsurgical clipping of ruptured aneurysms. However, there was no difference regarding clinical outcome and complications of the two groups.
Georg Thieme Verlag KG Stuttgart · New York.
... SAH from the rupture of an intracranial aneurysm is a neurologic emergency. The fatality rate of SAH is decreasing, but about one quarter of patients succumb in the first 24 hours and of those surviving, almost half will have long term cognitive impairment123. The immediate recognition of SAH in the ED is crucial for the right choice of therapy. ...
We discuss a patient with an aneurysmal subarachnoid hemorrhage (SAH) presenting with chest pain, electrocardiogram changes compatible with myocardial infarction, and headache. SAH is a medical emergency but an initial misdiagnosis is common, and diagnosis can be delayed due to atypical presentations. The delay of diagnosis of SAH may endanger the life of the patient. Electrocardiogram abnormalities have been described previously in aneurysmal SAH, and can obscure the correct diagnosis.
Copyright © 2015 Elsevier Ltd. All rights reserved.
... More than 80% of patients who died due to subarachnoid haemorrhage scored 4–5 on the Hunt & Hess Scale, while a further 10% scored 3. This also confirms the high severity on admission, and hence a high expected mortality [26, 27]. Furthermore, the majority (89%) of patients who died due to stroke had a National Institutes of Health Stroke Scale score of ≥ 15, which predicts severe neurological deficit and high mortality [28]. ...
We conducted a multicentre study of 1844 patients from 42 Spanish intensive care units, and analysed the clinical characteristics of brain death, the use of ancillary testing, and the clinical decisions taken after the diagnosis of brain death. The main cause of brain death was intracerebral haemorrhage (769/1844, 42%), followed by traumatic brain injury (343/1844, 19%) and subarachnoid haemorrhage (257/1844, 14%). The diagnosis of brain death was made rapidly (50% in the first 24 h). Of those patients who went on to die, the Glasgow Coma Scale on admission was ≤ 8/15 in 1146/1261 (91%) of patients with intracerebral haemorrhage, traumatic brain injury or anoxic encephalopathy; the Hunt and Hess Scale was 4-5 in 207/251 (83%) of patients following subarachnoid haemorrhage; and the National Institutes of Health Stroke Scale was ≥ 15 in 114/129 (89%) of patients with strokes. Brain death was diagnosed exclusively by clinical examination in 92/1844 (5%) of cases. Electroencephalography was the most frequently used ancillary test (1303/1752, 70.7%), followed by transcranial Doppler (652/1752, 37%). Organ donation took place in 70% of patients (1291/1844), with medical unsuitability (267/553, 48%) and family refusal (244/553, 13%) the main reasons for loss of potential donors. All life-sustaining measures were withdrawn in 413/553 of non-donors (75%).
© 2015 The Association of Anaesthetists of Great Britain and Ireland.
To investigate the diagnostic performance of 64-section computed tomographic (CT) angiography in the detection of intracranial aneurysms.
This study was approved by the institutional review board; written informed consent was obtained. One hundred eight consecutive patients suspected of having intracranial aneurysms were recruited. All patients underwent both 64-detector CT angiography and digital subtraction angiography (DSA) for the detection of intracranial aneurysms. CT angiograms were reviewed by two independent blinded readers. Sensitivity, specificity, and positive and negative predictive values for aneurysm detection with CT angiography were calculated by using DSA and surgical findings as the reference standard.
One hundred seven aneurysms were seen in 96 patients. Of those, DSA helped detect 106. On a per-aneurysm basis, the sensitivity, specificity, and positive and negative predictive values for CT angiography were 99%, 100%, and 100% and 92.3%, respectively. For aneurysms smaller than 3 mm, sensitivity was 93.7% for reader 1 and 96.8% for reader 2. However, the sensitivity and specificity were both 100% for aneurysms larger than 3 mm. Therapeutic decisions could be made on the basis of information provided by CT angiography.
Sixty-four-detector CT angiography is an accurate imaging method for the detection of aneurysms. It may be used as the initial imaging technique in the diagnostic work-up of patients suspected of having intracranial aneurysms.
Automatic detection of intracranial aneurysm based on Digital Subtraction Angiography (DSA) images is a challenging task for the following reasons: 1) effectively leverage the temporal information of the DSA sequence; 2) effectively extract features by avoiding unnecessary interference in the raw DSA images of large resolution; 3) effectively distinguish the vascular overlap from intracranial aneurysm in DSA images. To better identify intracranial aneurysm from DSA images, this paper proposed an automatic detection framework with cascade networks. This framework is consisted of a region localization stage (RLS) and an intracranial aneurysm detection stage (IADS). The RLS stage can significantly reduce the interference from unrelated regions and determine the coarse effective region. The IADS stage fully employed the spatial and temporal features to accurately detect aneurysm from DSA sequence. This method was verified in the posterior communicating artery (PCoA) region of internal carotid artery (ICA). In clinical trials, the accuracy of the baseline method was 62.5% with area under curve (AUC) of 0.650, and the time cost of the detection was approximately 62.546s. However, the accuracy of this method was 85.5% with AUC of 0.918, and the time cost of detection was about 3.664s. The experimental results showed that the proposed method significantly improved the accuracy and speed of intracranial aneurysm automatic detection.
High mobility group box 1 (HMGB1) is a classic damage-associated molecular pattern that has an important role in the pathological inflammatory response. In vitro studies have demonstrated that the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in the regulation of HMGB1 expression, mediating the inflammatory response. Therefore, the purpose of the present study was to evaluate JAK2/STAT3 pathway involvement in the subarachnoid hemorrhage (SAH)-dependent regulation of HMGB1, using an in vivo rat model. A SAH model was established by endovascular perforation. Western blotting, immunohistochemistry and immunofluorescence were used to analyze HMGB1 expression after SAH. In addition, the effects of AG490 after SAH on JAK2/STAT3 phosphorylation, HMGB1 expression and brain damage were evaluated. The results of the present study demonstrated that JAK2/STAT3 was significantly phosphorylated (P<0.05) and the total HMGB1 protein level was significantly increased (P<0.05) after SAH. In addition, the cytosolic HMGB1 level after SAH demonstrated an initial increase followed by a decrease to the control level, while the nuclear HMGB1 level after SAH demonstrated the opposite trend, with an initial decrease and subsequent increase. AG490 administration after SAH significantly inhibited JAK2/STAT3 phosphorylation (P<0.05), suppressed the expression and translocation of HMGB1, reduced cortical apoptosis, brain edema and neurological deficits. These results demonstrated the involvement of the JAK2/STAT3 pathway in HMGB1 regulation after SAH.
Objective
The cause of severe clinical vasospasm after aneurysmal subarachnoid hemorrhage remains unknown, despite extensive research over the past 30 years. However, the intra-arterial administration of vasodilating agents and balloon angioplasty have been successfully used in severe refractory cerebral vasospasm.
Materials and Methods
We retrospectively analyzed the data of 233 patients admitted to our institute with aneurysmal subarachnoid hemorrhage (SAH) over the past 3 years.
Results
Of these, 27 (10.6%) developed severe symptomatic vasospasm, requiring endovascular therapy. Vasospasm occurred at an average of 5.3 days after SAH. A total of 46 endovascular procedures were performed in 27 patients. Endovascular therapy was performed once in 18 (66.7%) patients, 2 times in 4 (14.8%) patients, 3 or more times in 5 (18.5%) patients. Intra-arterial vasodilating agents were used in 44 procedures (27 with nimodipine infusion, 17 with nicardipine infusion). Balloon angioplasty was performed in only 2 (7.4%) patients. The Average nimodipine infusion volume was 2.47 mg, and nicardipine was 3.78 mg. Most patients recovered after the initial emergency room visit. Two patients (7.4%) worsened, but there were no deaths.
Conclusion
With advances in endovascular techniques, administration of vasodilating agents and balloon angioplasty reduces the morbidity and mortality of vasospasm after aneurysmal SAH.
Background:
Only a minority of intracranial aneurysms rupture to cause subarachnoid hemorrhage.
Objective:
To test the hypothesis that unruptured aneurysms have different characteristics and risk factor profiles compared to ruptured aneurysms.
Methods:
We recruited patients with unruptured aneurysms or aneurysmal subarachnoid hemorrhages at 22 UK hospitals between 2011 and 2014. Demographic, clinical, and imaging data were collected using standardized case report forms. We compared risk factors using multivariable logistic regression.
Results:
A total of 2334 patients (1729 with aneurysmal subarachnoid hemorrhage, 605 with unruptured aneurysms) were included (mean age 54.22 yr). In multivariable analyses, the following variables were independently associated with rupture status: black ethnicity (odds ratio [OR] 2.42; 95% confidence interval [CI] 1.29-4.56, compared to white) and aneurysm location (anterior cerebral artery/anterior communicating artery [OR 3.21; 95% CI 2.34-4.40], posterior communicating artery [OR 3.92; 95% CI 2.67-5.74], or posterior circulation [OR 3.12; 95% CI 2.08-4.70], compared to middle cerebral artery). The following variables were inversely associated with rupture status: antihypertensive medication (OR 0.65; 95% CI 0.49-0.84), hypercholesterolemia (0.64 OR; 95% CI 0.48-0.85), aspirin use (OR 0.28; 95% CI 0.20-0.40), internal carotid artery location (OR 0.53; 95% CI 0.38-0.75), and aneurysm size (per mm increase; OR 0.76; 95% CI 0.69-0.84).
Conclusion:
We show substantial differences in patient and aneurysm characteristics between ruptured and unruptured aneurysms. These findings support the hypothesis that different pathological mechanisms are involved in the formation of ruptured aneurysms and incidentally detected unruptured aneurysms. The potential protective effect of aspirin might justify randomized prevention trials in patients with unruptured aneurysms.
Objective:
The aim of this study was to evaluate the prevalence of hypopituitarism in the acute stage after aneurysmal subarachnoid hemorrhage (SAH) as well at the chronic stage, at least 1 year after bleeding, to assess its implications and correlation with clinical features of the studied population.
Patients and methods:
This was a prospective cohort study that evaluated patients admitted between December 2009 and May 2011 with a diagnosis of SAH secondary to cerebral aneurysm rupture. Clinical and endocrine assessment was performed during the acute stage after hospital admission and before treatment at a mean of 7.5 days (SD ± 3.8) following SAH, and also at the follow-up visit at a mean of 25.5 months (range: 12-55 months) after the bleeding.
Results:
Out of the 119 patients initially assessed, 92 were enrolled for acute stage, 82 underwent hormonal levels analysis, and 68 (82.9%) were followed up in both acute and chronic phases. The mean age and median age were lower among patients with dysfunction in the acute phase compared to those without dysfunction (P < .05). The prevalence of dysfunction in the acute phase was higher among patients with hydrocephalus on admission computed tomography (57.9%) than among those without it (P < .05). At chronic phase, there was an association between dysfunction and Hunt & Hess scale score greater than 2 (P < .05).
Conclusions:
We believe that there is not enough literature evidence to incorporate routine endocrinological evaluation for patient victims of SAH, but we should always keep this differential diagnosis in mind when conducting long-term assessments of this population.
The aim of the current study was to observe the effects of simvastatin and taurine on delayed cerebral vasospasm (DCVS) following experimental subarachnoid hemorrhage (SAH) in rabbits. A total of 48 New Zealand white rabbits were allocated at random into four groups (control, SAH, SAH + simvastatin and SAH + taurine groups; n=12 each). The rabbit model of DCVS was established using a double hemorrhage method, which involved injecting autologous arterial blood into the cisterna magna in the SAH groups. The SAH + simvastatin group was administered oral simvastatin (5 mg/kg) daily between days 0-6. The SAH + taurine group was administered oral taurine (50 mg/kg) daily between days 0-6. Starch (50 mg/kg) was administered orally to the animals in the other two groups (control and SAH groups). The control group were not subjected to any other injections or treatment. The internal diameter and internal diameter/wall thickness of the basilar artery (BA) were measured. The expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were determined using immunohistochemical and quantitative polymerase chain reaction methods following the sacrifice of all animals on day 7. The activity of nuclear factor (NF)-κB in the BA was also measured using an electrophoretic mobility shift assay. The BA walls in the SAH + simvastatin and SAH + taurine groups exhibited reduced narrowing and corrugation of the tunica elastica interna compared with the SAH group. At the protein and cDNA levels, it was found that cerebral vasospasm of the BA in the SAH + simvastatin and SAH + taurine groups was alleviated, as indicated by the reduced expression of TNF-α, IL-1β, IL-6 and NF-κB compared with the SAH group (P<0.05). In conclusion, simvastatin and taurine reduced DCVS following SAH in rabbits, which suggests that these compounds may exert anti-inflammatory effects.
Intracranial hypotension (IH) can occur following lumbar drainage for clipping of an intracranial aneurysm. We observed 3 cases of IH, which were all successfully treated by epidural blood patch (EBP). Herein, the authors report our cases.
Se revisa la iconografía de los hallazgos por tomografía computada (TC) y resonancia magnética (RM) de la cefalea, según nuestra experiencia. De acuerdo con la base MESH, esta entidad se define como un dolor craneano, que puede ser de ocurrencia benigna o la manifestación de una amplia gama de desórdenes.
Las cefaleas se clasifican por su evolución temporal (aguda o crónica), presentación (en estallido, gravativa, etc.) o coexistencia de síntomas asociados, como auras, convulsiones o déficits focales. También se dividen en primarias o secundarias, según la existencia o no de una patología subyacente. Las primarias pueden tener manifestaciones clínicas definidas, pero en las secundarias ciertos signos y síntomas deben alertar sobre la presencia de una patología estructural. En este caso, las neuroimágenes tienen un rol esencial al detectar las causantes del cuadro.
Nuestros hallazgos correspondieron a cefaleas primarias (p. ej: infarto migrañoso) y a etiologías orgánicas, entre las que se destacaron causas vasculares, como patología venosa (trombosis), vasoespasmo y leucoencefalopatía posterior reversible; hemorragias intraparenquimatosas y extraaxiales; cefaleas postraumáticas y posquirúrgicas; y causas infecciosas y tumorales (apoplejía hipofisaria e hipertensión endocraneana). Además, hubo malformaciones (Arnold-Chiari, p.ej.) y otras como hipotensión endocraneana.
En algunos casos inicialmente se realizó una TC y luego una RM, mientras que en otros la RM fue el método de elección.
Las neuroimágenes facilitan el estudio de la cefalea, caracterizando la afección en primaria o secundaria. En el segundo caso permiten, a su vez, clasificar los hallazgos.
Objective: To determine if risk factors such as advanced age, history of hypertension or diabetes, initial neurologic status, radiological grade of the subarachnoid hemorrhage, therapeutic hypertension, presence of fever, vasospasm and symptomatic vasospasm are associated with the presence of cerebral infarction in aneurismatic subarachnoid hemorrhage (ASAH) treated with endovascular therapy. Material and methods: we conduct a case-control study in the Christus Muguerza Alta Especialidad Hospital in Monterrey, Nuevo Leon, from medical records of the patients, in a period from January 2007 to May 2012. Results: during the period from January 2007 to May 2012 were reviewed 200 cases, and were identified 12 cases with infarction and 22 controls without infarction, both with ASAH and treated with endovascular therapy (relationship cases - controls 1: 1.8), in the population of Christus Muguerza AltaEspecialidad Hospital in Monterrey, Nuevo Leon. We found that for the cases 66.6% were male and 33.3% were female, for the controls 77.2% female and 22.7% were male. With an average age of 54 years for cases and 50 years for controls. Risk factors associated with cerebral infarction in ASAH are the presence of hypertension (OR: 6.3 1.035-43.02 95% p=0.016), male sex (OR: 6.8 95% CI 1.14-45.52 p=0.02), presence of intraventricular hemorrhage (OR: 8.7 95% CI 1.25-77.1 p=0.011). The most important risk factor was the presence of vasospasm, which increases 17 times the probability of infarction (OR: 17, 95% CI: 2.23-168.25, P = 0.001), and symptomatic vasospasm increases 29 times the risk of stroke (OR: 29.4, 95% CI 2.45-809.79, p = 0.001). Also, a binary logistic regression analysis for risk factors was conducted, in which only one variable was significant: symptomatic vasospasm (OR: 16.75 95% CI 0.74 - 375.72, p = 0.0001). Conclusion: symptomatic vasospasm is the most important risk factor for the presence of cerebral infarction in ASAH.
Endoglin is an essential molecule during angiogenesis, vascular development, and integrity. Till now, many studies have investigated the association between endoglin polymorphisms and intracranial aneurysm (IA) risk, with the results remained inconclusive. Therefore, we performed a meta-analysis to summarize the possible association.
We searched PubMed and Embase until June 2015 to identify studies addressing the association between endoglin polymorphisms and IA risk. The summary odds ratios (ORs) and their corresponding 95% confidence interval (CI) were calculated to assess the strength of the association.
Eleven studies with a total of 1501 cases and 2012 controls were finally included in this meta-analysis, with 10 studies investigating endoglin 6-bp insertion (6bINS) polymorphism and 4 studies investigating 1800956 polymorphism. No significant association between endoglin 6bINS polymorphism and IA risk was detected in overall estimation (I/I vs wt/I + wt/wt: OR = 1.21, 95% CI = 0.87–1.69) or in the subgroup analysis by ethnicity, control source, or ruptured status. However, we observed an association with borderline significance of 6bINS with IA occurrence (I/I vs wt/I + wt/wt: OR = 1.49, 95% CI = 0.99–2.25, P = 0.058) in studies applying matched controls. Furthermore, we detected a significant association for 6bINS polymorphism of endoglin with increased risk of familial IA (I vs wt, OR = 1.64, 95% CI = 1.10–2.42) but not sporadic IA (I vs wt, OR = 1.09, 95% CI = 0.68–1.45). With regard to rs1800956, our pooled results indicated a significantly decreased IA risk in individuals carrying C allele (C/C vs G/C + G/G: OR = 0.65; 95% CI = 0.45–0.94).
This meta-analysis provided no evidence for the association between 6bINS polymorphism with overall IA risk. However, we detected a significant association of 6bINS allele with increased risk of familial IA. Also, we found that rs1800956 was significantly related to IA occurrence. Further, well-designed studies with large sample size are warranted and updated meta-analysis is needed to verify our findings.
Objective:
The aim of this study was to investigate the image quality of cerebral dual-energy computed tomography (CT) angiography using a nonlinear image blending technique as compared with the conventional linear blending method in patients with spontaneous subarachnoid hemorrhage (SAH).
Methods:
A retrospective review of 30 consecutive spontaneous SAH patients who underwent a dual-source, dual-energy (80 kV and Sn140 kV mode) cerebral CT angiography was performed with permission from hospital ethical committee. Optimized images using nonlinear blending method were generated and compared with the 0.6 linear blending images by evaluating cerebral artery enhancement, attenuation of SAH, image noise, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR), respectively. Two neuroradiologists independently assessed subjective vessel visualization per segment using a 5-point scale.
Results:
The nonlinear blending images showed higher cerebral artery enhancement (307.24 ± 58.04 Hounsfield unit [HU]), lower attenuation of SAH (67.07 ± 6.79 HU), and image noise (7.18 ± 1.20 HU), thus achieving better SNR (43.92 ± 11.14) and CNR (34.34 ± 10.25), compared with those of linear blending images (235.47 ± 46.45 HU for cerebral artery enhancement, 70.00 ± 6.41 HU for attenuation of SAH, 8.39 ± 1.25 HU for image noise, 28.86 ± 8.43 for SNR, and 20.37 ± 7.74 for CNR) (all P < 0.01). The segmental scorings of the nonlinear blending image (31.6% segments with a score of 5, 57.4% segments with a score of 4, 11% segments with a score of 3) ranged significantly higher than those of linear blending images (11.5% segments with a score of 5, 77.5% segments with a score of 4, 11% segments with a score of 3) (P < 0.01). The interobserver agreement was good (κ = 0.762), and intraobserver agreement was excellent for both observers (κ = 0.844 and 0.858, respectively).
Conclusions:
The nonlinear image blending technique improved vessel visualization of cerebral dual-energy CT angiography by optimizing contrast enhancement in spontaneous SAH patients.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share thework provided it is properly cited. The work cannot be changed in any way or used commercially.
PURPOSE:
To demonstrate the relationship between of sphingosine-1-phosphate (S1P) expression and subarachnoid hemorrhage (SAH).
METHODS:
The basilar arteries from a "double-hemorrhage" rabbit model of SAH were used to investigate the relation between S1P expression and SAH. Various symptoms, including blood clots, basilar artery cross-sectional area, and S1P phosphatase expression were measured at day 3, 5, 7, 9.
RESULTS:
The expression of S1P was enhanced in the cerebral vasospasm after subarachnoid hemorrhage in the rabbits. And S1P expression was consistent with the basilar artery cross-sectional area changes at day 3, 5, 7, 9.
CONCLUSION:
Sphingosine-1-phosphate expression in the cerebral arterial may be a new indicator in the development of cerebral vasospasm after subarachnoid hemorrhage and provide a new therapeutic method for SAH.
OBJECT
Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes brain edema and blood-brain barrier (BBB) disruption following experimental SAH.
METHODS
C57BL/6 wild-type (WT) or TNC knockout (TNKO) mice were subjected to SAH by endovascular puncture. Ninety-seven mice were randomly allocated to WT sham-operated (n = 16), TNKO sham-operated (n = 16), WT SAH (n = 34), and TNKO SAH (n = 31) groups. Mice were examined by means of neuroscore and brain water content 24–48 hours post-SAH; and Evans blue dye extravasation and Western blotting of TNC, matrix metalloproteinase (MMP)-9, and zona occludens (ZO)-1 at 24 hours post-SAH. As a separate study, 16 mice were randomized to WT sham-operated, TNKO sham-operated, WT SAH, and TNKO SAH groups (n = 4 in each group), and activation of mitogen-activated protein kinases (MAPKs) was immunohistochemically evaluated at 24 hours post-SAH. Moreover, 40 TNKO mice randomly received an intracerebroventricular injection of TNC or phosphate-buffered saline, and effects of exogenous TNC on brain edema and BBB disruption following SAH were studied.
RESULTS
Deficiency of endogenous TNC prevented neurological impairments, brain edema formation, and BBB disruption following SAH; it was also associated with the inhibition of both MMP-9 induction and ZO-1 degradation. Endogenous TNC deficiency also inhibited post-SAH MAPK activation in brain capillary endothelial cells. Exogenous TNC treatment abolished the neuroprotective effects shown in TNKO mice with SAH.
CONCLUSIONS
Tenascin-C may be an important mediator in the development of brain edema and BBB disruption following SAH, mechanisms for which may involve MAPK-mediated MMP-9 induction and ZO-1 degradation. TNC could be a molecular target against which to develop new therapies for SAH-induced brain injuries.
Introduction:
Early identification of delayed cerebral ischemia (DCI) in patients with aneurysmal subarachnoid hemorrhage (aSAH) is a major challenge. The aim of this study was to investigate whether quantitative EEG (qEEG) features can detect DCI prior to clinical or radiographic findings.
Methods:
A prospective cohort study was performed in aSAH patients in whom continuous EEG (cEEG) was recorded. We studied 12 qEEG features. We compared the time point at which qEEG changed with the time point that clinical deterioration occurred or new ischemia was noted on CT scan.
Results:
Twenty aSAH patients were included of whom 11 developed DCI. The alpha/delta ratio (ADR) was the most promising feature that showed a significant difference in change over time in the DCI group (median -62 % with IQR -87 to -39 %) compared to the control group (median +27 % with IQR -32 to +104 %, p = 0.013). Based on the ROC curve, a threshold was chosen for a combined measure of ADR and alpha variability (AUC: 91.7, 95 % CI 74.2-100). The median time that elapsed between change of qEEG and clinical DCI diagnosis was seven hours (IQR -11-25). Delay between qEEG and CT scan changes was 44 h (median, IQR 14-117).
Conclusion:
In this study, ADR and alpha variability could detect DCI development before ischemic changes on CT scan was apparent and before clinical deterioration was noted. Implementation of cEEG in aSAH patients can probably improve early detection of DCI.
Background:
Haptoglobin (Hp) genotype has been shown to be a predictor of clinical outcomes in subarachnoid hemorrhage. Cerebral salt wasting (CSW) has been suggested to precede the development of symptomatic vasospasm.
Objective:
To determine if Hp genotype was associated with CSW and subsequent vasospasm after aneurysmal subarachnoid hemorrhage.
Methods:
Hp genotypic determination was done for patients admitted with a diagnosis of subarachnoid hemorrhage. Outcome measures included CSW, delayed cerebral infarction, and Glasgow Outcome Score of 4 to 5 at 30 days. Criteria for CSW included hyponatremia <135 mEq/L, and urine output >4 L in 12 hours with urine sodium >40 mEq/L.
Results:
A total of 133 patients were included in the study. The 3 Hp subgroups did not differ in terms of baseline characteristics. CSW occurred in 1 patient (3.4%) with Hp 1-1, 8 (14.0%) patients with Hp 2-1, and 15 (31.9%) patients with Hp 2-2 (P = .004). In the multivariate regression model, Hp 2-2 was associated with CSW (odds ratio [OR]: 4.94; CI: 1.78-17.43; P = .01), but Hp 2-1 was not (OR: 2.92; CI: 0.56-4.95; P = .15) compared with Hp 1-1. There were no associations between Hp genotypes and functional outcome or delayed cerebral infarction. CSW was associated with delayed cerebral infarction (OR: 7.46; 95% CI: 2.54-21.9; P < .001).
Conclusion:
Hp 2-2 genotype was an independent predictor of CSW after subarachnoid hemorrhage. Because CSW is strongly associated with delayed cerebral infarction, the use of Hp genotype testing requires more investigation, and larger prospective confirmation is warranted. Additionally, a more objective definition of CSW needs to be delineated.
Abbreviations:
CSW, cerebral salt wastingDCI, delayed cerebral ischemiaGOS, Glasgow Outcome ScaleHp, HaptoglobinmRS, modified Rankin ScaleSAH, subarachnoid hemorrhageTCD, transcranial Doppler.
Objective:
Studies show that phosphodiesterase-V (PDE-V) inhibition reduces cerebral vasospasm (CVS) and improves outcomes after experimental subarachnoid hemorrhage (SAH). This study was performed to investigate the safety and effect of sildenafil (an FDA-approved PDE-V inhibitor) on angiographic CVS in SAH patients.
Methods:
A2-phase, prospective, nonrandomized, human trial was implemented. Subarachnoid hemorrhage patients underwent angiography on Day 7 to assess for CVS. Those with CVS were given 10 mg of intravenous sildenafil in the first phase of the study and 30 mg in the second phase. In both, angiography was repeated 30 minutes after infusion. Safety was assessed by monitoring neurological examination findings and vital signs and for the development of adverse reactions. For angiographic assessment, in a blinded fashion, pre- and post-sildenafil images were graded as "improvement" or "no improvement" in CVS. Unblinded measurements were made between pre- and post-sildenafil angiograms.
Results:
Twelve patients received sildenafil; 5 patients received 10 mg and 7 received 30 mg. There were no adverse reactions. There was no adverse effect on heart rate or intracranial pressure. Sildenafil resulted in a transient decline in mean arterial pressure, an average of 17% with a return to baseline in an average of 18 minutes. Eight patients (67%) were found to have a positive angiographic response to sildenafil, 3 (60%) in the low-dose group and 5 (71%) in the high-dose group. The largest degree of vessel dilation was an average of 0.8 mm (range 0-2.1 mm). This corresponded to an average percentage increase in vessel diameter of 62% (range 0%-200%).
Conclusions:
The results from this Phase I safety and proof-of-concept trial assessing the use of intravenous sildenafil in patients with CVS show that sildenafil is safe and well tolerated in the setting of SAH. Furthermore, the angiographic data suggest that sildenafil has a positive impact on human CVS.
Intracranial pressure (ICP) control is a therapeutic target in patients with aneurysmal subarachnoid hemorrhage, although only a limited number of studies assessed its course and effect on outcome. Pressure-time dose (PTDICP) is a method to quantify the burden and the time spent above a defined threshold of ICP. PTDICP or its relationship with outcome has never been evaluated in aneurysmal subarachnoid hemorrhage.
Analysis of data prospectively collected from aneurysmal subarachnoid hemorrhage patients admitted to Neurointensive Care Unit. Monitored data, including intraparenchymal ICP, were digitally recorded minute-by-minute in the first 7 days. PTDICP (mm Hg h) was computed using 4 predefined thresholds (15, 20, 25, and 30 mm Hg). Outcome was assessed through Extended Glasgow Outcome Scale at hospital discharge and at 6 months.
Fifty-five patients were enrolled. Forty-two patients (76%) presented with a poor clinical grade. Overall, mortality was 17% at hospital discharge and 34% at 6 months. Half of patients required extensive therapy to control high ICP during day 1. Median ICP was 10 mm Hg (4-75), whereas median PTDICP15, PTDICP20, PTDICP25, PTDICP30 were, respectively, 13, 4, 2, and 1 mm Hg h. We observed an association between mortality at hospital discharge and higher level of PTDICP using 20, 25, and 30 mm Hg as thresholds and between exposure to a moderate-level PTDICP30 and unfavorable long-term outcome.
PTDICP may better define one of the insults that the brain suffers after aneurysmal rupture, and exposure to moderate PTDICP30 was significant prognostic factor of 6-month unfavorable outcome.
© 2015 American Heart Association, Inc.
The incidence of traumatic brain injury (TBI) in the United States was 3.5 million cases in 2009, according to the Centers for Disease Control and Prevention.1 It is a contributing factor in 30.5% of injury-related deaths among civilians.2 Additionally, since 2000, over 260,000 service members were diagnosed with TBI, with the vast majority classified as mild or concussive (76 percent). The objective assessment of TBI via imaging is a critical research gap, both in the military and civilian communities. In 2011, the Department of Defense (DoD) prepared a congressional report summarizing the effectiveness of seven neuroimaging modalities (computed tomography [CT], magnetic resonance imaging [MRI], transcranial Doppler [TCD], positron emission tomography [PET], single photon emission computed tomography [SPECT], electrophysiologic techniques (magnetoencephalography and electroencephalography), and functional near-infrared spectroscopy [fNIRS]) to assess the spectrum of TBI from concussion to coma. For this report, neuroimaging experts identified the most relevant peer-reviewed publications and assessed the quality of the literature for each imaging technique in the clinical and research settings. Although CT, MRI, and TCD were determined to be the most useful modalities in the clinical setting, no single imaging modality proved sufficient for all patients due to the heterogeneity of TBI. All imaging modalities reviewed demonstrated the potential to emerge as part of future clinical care. This paper describes and updates the results of the DoD report and also expands on the use of angiography in patients with TBI.
The great majority of acute brain injury results from trauma or from disorders of the cerebrovasculature, i.e. ischaemic stroke or haemorrhage. These injuries are characterized by an initial insult that triggers a cascade of injurious cellular processes. The nature of these processes in spontaneous intracranial haemorrhage is poorly understood. Subarachnoid haemorrhage, a particularly deadly form of intracranial haemorrhage, shares key pathophysiological features with traumatic brain injury including exposure to a sudden pressure pulse. Here we provide evidence that axonal injury, a signature characteristic of traumatic brain injury, is also a prominent feature of experimental subarachnoid haemorrhage. Using histological markers of membrane disruption and cytoskeletal injury validated in analyses of traumatic brain injury, we show that axonal injury also occurs following subarachnoid haemorrhage in an animal model. Consistent with the higher prevalence of global as opposed to focal deficits after subarachnoid haemorrhage and traumatic brain injury in humans, axonal injury in this model is observed in a multifocal pattern not limited to the immediate vicinity of the ruptured artery. Ultrastructural analysis further reveals characteristic axonal membrane and cytoskeletal changes similar to those associated with traumatic axonal injury. Diffusion tensor imaging, a translational imaging technique previously validated in traumatic axonal injury, from these same specimens demonstrates decrements in anisotropy that correlate with histological axonal injury and functional outcomes. These radiological indicators identify a fibre orientation-dependent gradient of axonal injury consistent with a barotraumatic mechanism. Although traumatic and haemorrhagic acute brain injury are generally considered separately, these data suggest that a signature pathology of traumatic brain injury-axonal injury-is also a functionally significant feature of subarachnoid haemorrhage, raising the prospect of common diagnostic, prognostic, and therapeutic approaches to these conditions.
© The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
Intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) account for about 10–20% of strokes. Compared with ischemic stroke, neurological impairment tends to be more severe and outcomes are generally worse. An improved understanding of the pathophysiology of these conditions has increased the therapeutic options. With ICH, efforts focus on reducing early hematoma expansion and attenuating perihematomal edema. With SAH, clinicians must seek to prevent aneurysm rebleeding and limit both early and delayed ischemic injury. Prevention and timely recognition and treatment of potential causes of secondary brain injury, such as hydrocephalus, nonconvulsive seizures, intracranial hypertension, fever, anemia, hypoxemia, hypotension and hypo- or hyperglycemia, is crucial in maximizing the chance of a favorable recovery. Systemic complications, such as neurogenic stunned myocardium and pulmonary edema, must be recognized and treated appropriately. For patients with stupor and coma, physicians should communicate regularly with surrogate decision makers. Assessment of patients' prognosis should be transparent, based on best available evidence, and neither unrealistically optimistic nor pessimistic.
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