✓ Cerebral blood flow (CBF) was measured during the 1st week of subarachnoid hemorrhage in 46 patients who were in a good clinical grade and had a proven ruptured intracranial aneurysm. The mean initial CBF in patients who developed cerebral ischemia was 42 ml/min−1/l00 gm brain−1, which was significantly lower than in patients who did not develop cerebral ischemia (49 ml/min−1/l00 gm brain−1). This reduced CBF was not secondary to raised intracranial pressure or angiographic spasm. Patients with a reduced CBF (less than 50 ml/min−1/100 gm brain−1) and diffuse subarachnoid blood on computerized tomography had a very high incidence (78%) of cerebral ischemia, despite a good clinical grade at the time of measurement. Serial CBF measurements are of value in monitoring the evolution of cerebral vasospasm.
Neville W. Knuckey, Richard A. Fox, Ivor Surveyor and Bryant A. R. Stokes
Matthew R. Reynolds, Jon T. Willie, Gregory J. Zipfel and Ralph G. Dacey Jr.
orgasm lasts 20 to 60 seconds and is accompanied by more profound autonomic changes. 63 For these reasons, it would appear that women could actually be more susceptible to aneurysmal SAH than men. However, anecdotal evidence suggests that the risk of sexually related cerebral aneurysm rupture is greater in men than women. 54 , 73 , 88 While the exact reason for this finding is unclear, a number of factors may help to explain this observation. One explanation for the greater incidence of sexually induced aneurysmal SAH in men may be due to the greater overall
Laith M. Kadasi, Walter C. Dent and Adel M. Malek
: Hemodynamic patterns of anterior communicating artery aneurysms: a possible association with rupture . AJNR Am J Neuroradiol 30 : 297 – 302 , 2009 6 Cebral JR , Castro MA , Burgess JE , Pergolizzi RS , Sheridan MJ , Putman CM : Characterization of cerebral aneurysms for assessing risk of rupture by using patient-specific computational hemodynamics models . AJNR Am J Neuroradiol 26 : 2550 – 2559 , 2005 7 Cebral JR , Mut F , Weir J , Putman CM : Association of hemodynamic characteristics and cerebral aneurysm rupture . AJNR Am J
Brian L. Hoh, Koji Hosaka, Daniel P. Downes, Kamil W. Nowicki, Erin N. Wilmer, Gregory J. Velat and Edward W. Scott
aneurysm rupture can be devastating, with 30%–50% mortality and 50% significant morbidity. 20 , 29 , 36 , 49 Only a small percentage of unruptured cerebral aneurysms go on to rupture, however, and their management consists of either watchful waiting, surgical clipping, or endovascular coiling. If the pathophysiology of how unruptured aneurysms go on to rupture were better understood, then a drug could potentially be developed that could stabilize and protect an unruptured aneurysm from becoming prone to rupture. The same or similar type of drug could also stabilize
John W. Thompson, Omar Elwardany, David J. McCarthy, Dallas L. Sheinberg, Carlos M. Alvarez, Ahmed Nada, Brian M. Snelling, Stephanie H. Chen, Samir Sur and Robert M. Starke
Cerebral aneurysm rupture is a devastating event resulting in subarachnoid hemorrhage and is associated with significant morbidity and death. Up to 50% of individuals do not survive aneurysm rupture, with the majority of survivors suffering some degree of neurological deficit. Therefore, prior to aneurysm rupture, a large number of diagnosed patients are treated either microsurgically via clipping or endovascularly to prevent aneurysm filling. With the advancement of endovascular surgical techniques and devices, endovascular treatment of cerebral aneurysms is becoming the first-line therapy at many hospitals. Despite this fact, a large number of endovascularly treated patients will have aneurysm recanalization and progression and will require retreatment. The lack of approved pharmacological interventions for cerebral aneurysms and the need for retreatment have led to a growing interest in understanding the molecular, cellular, and physiological determinants of cerebral aneurysm pathogenesis, maturation, and rupture. To this end, the use of animal cerebral aneurysm models has contributed significantly to our current understanding of cerebral aneurysm biology and to the development of and training in endovascular devices. This review summarizes the small and large animal models of cerebral aneurysm that are being used to explore the pathophysiology of cerebral aneurysms, as well as the development of novel endovascular devices for aneurysm treatment.
Shivanand P. Lad, Raphael Guzman, Michael E. Kelly, Gordon Li, Michael Lim, Karl Lovbald and Gary K. Steinberg
✓Vasospasm following cerebral aneurysm rupture is one of the most devastating sequelae and the most common cause of delayed ischemic neurological deficit (DIND). Because vasospasm also is the most common cause of morbidity and mortality in patients who survive the initial bleeding episode, it is imperative not only to diagnose the condition but also to predict which patients are likely to become symptomatic. The exact pathophysiology of vasospasm is complex and incompletely elucidated. Early recognition of vasospasm is essential because the timely use of several therapeutic interventions can counteract this disease and prevent the occurrence of DIND. However, the prompt implementation of these therapies depends on the ability to predict impending vasospasm or to diagnose it at its early stages.
A number of techniques have been developed during the past several decades to evaluate cerebral perfusion, including positron emission tomography, xenon-enhanced computed tomography, single-photon emission computed tomography, perfusion- and diffusion-weighted magnetic resonance imaging, and perfusion computed tomography. In this article, the authors provide a general overview of the currently available perfusion imaging techniques and their applications in treating vasospasm after a patient has suffered a subarachnoid hemorrhage. The use of cerebral perfusion imaging techniques for the early detection of vasospasm is becoming more common and may provide opportunities for early therapeutic intervention to counteract vasospasm in its earliest stages and prevent the occurrence of DINDs.
Christopher D. Wilson, Sam Safavi-Abbasi, Hai Sun, M. Yashar S. Kalani, Yan D. Zhao, Michael R. Levitt, Ricardo A. Hanel, Eric Sauvageau, Timothy B. Mapstone, Felipe C. Albuquerque, Cameron G. McDougall, Peter Nakaji and Robert F. Spetzler
Aneurysmal subarachnoid hemorrhage (aSAH) may be complicated by hydrocephalus in 6.5%–67% of cases. Some patients with aSAH develop shunt dependency, which is often managed by ventriculoperitoneal shunt placement. The objectives of this study were to review published risk factors for shunt dependency in patients with aSAH, determine the level of evidence for each factor, and calculate the magnitude of each risk factor to better guide patient management.
The authors searched PubMed and MEDLINE databases for Level A and Level B articles published through December 31, 2014, that describe factors affecting shunt dependency after aSAH and performed a systematic review and meta-analysis, stratifying the existing data according to level of evidence.
On the basis of the results of the meta-analysis, risk factors for shunt dependency included high Fisher grade (OR 7.74, 95% CI 4.47–13.41), acute hydrocephalus (OR 5.67, 95% CI 3.96–8.12), in-hospital complications (OR 4.91, 95% CI 2.79–8.64), presence of intraventricular blood (OR 3.93, 95% CI 2.80–5.52), high Hunt and Hess Scale score (OR 3.25, 95% CI 2.51–4.21), rehemorrhage (OR 2.21, 95% CI 1.24–3.95), posterior circulation location of the aneurysm (OR 1.85, 95% CI 1.35–2.53), and age ≥ 60 years (OR 1.81, 95% CI 1.50–2.19). The only risk factor included in the meta-analysis that did not reach statistical significance was female sex (OR 1.13, 95% CI 0.77–1.65).
The authors identified several risk factors for shunt dependency in aSAH patients that help predict which patients are likely to require a permanent shunt. Although some of these risk factors are not independent of each other, this information assists clinicians in identifying at-risk patients and managing their treatment.
Michael S. Pepper
polymorphism, 27VNTR, occurs in intron 4 and has been associated with cerebral and aortic aneurysms and occlusive coronary artery disease. Although alterations in levels of eNOS protein expression and enzyme activity have been described in association with these polymorphisms, the challenge now will be to define clearly the role of eNOS in the pathophysiology of cerebral aneurysm rupture. Who knows, maybe this will allow us to move from a predictive parameter to a therapeutic target. See the corresponding article in this issue, pp 526–531.
ischemia after cerebral aneurysm rupture. J Neurosurg 62 : 850 – 855 , 1985 Knuckey NW, Fox RA, Surveyor I, et al: Early cerebral blood flow and computerized tomography in predicting ischemia after cerebral aneurysm rupture. J Neurosurg 62: 850–855, 1985 8. Mathew NT , Meyer JS , Hartmann A : Diagnosis and treatment of factors complicating subarachnoid hemorrhage. Neuroradiology 6 : 237 – 245 , 1974 Mathew NT, Meyer JS, Hartmann A: Diagnosis and treatment of factors complicating subarachnoid hemorrhage