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Journal articles on the topic 'Subarachnoid Hemorrhage Subarachnoid Hemorrhage Vasospasm'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Hui, Ferdinand K., Albert J. Schuette, Shaye I. Moskowitz, Rishi Gupta, Alejandro M. Spiotta, Nancy A. Obuchowski, and C. Michael Cawley. "Antithrombotic States and Outcomes in Patients With Angiographically Negative Subarachnoid Hemorrhage." Neurosurgery 68, no. 1 (January 1, 2011): 125–31. http://dx.doi.org/10.1227/neu.0b013e3181fd82b6.

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Abstract BACKGROUND: Antithrombotic states are encountered frequently, either because of medical therapy or by preexistent pathological states, and may affect the severity of hemorrhagic strokes such as angiographically negative subarachnoid hemorrhages. OBJECTIVE: To determine the effects of antithrombotic states on the outcomes of patients with angiographically negative subarachnoid hemorrhage by examining data pooled from 2 institutions. METHODS: This is a retrospective review of patients who experienced angiographically negative subarachnoid hemorrhage at 2 institutions over the past 5 years. The patients were grouped into those with and those without an antithrombotic state at time of hemorrhage and were stratified according to presentation, clinical grades, outcomes, need for cerebrospinal fluid diversion, and development of vasospasm. Computed tomography of the head was assessed for bleed pattern and modified Fisher grade. Patients were excluded if a causative lesion was subsequently discovered. RESULTS: There is a statistically significant association between antithrombotic states and poorer presentation, higher Hunt and Hess score, increased amount of subarachnoid hemorrhage, higher modified Fisher grade, increased incidence of vasospasm, hydrocephalus, and poor outcomes as assessed by modified Rankin scale (P < .001). Patients with an antithrombotic state experience worse outcomes even with adjustment for the amount of hemorrhage as assessed by modified Fisher grade (P < .001). CONCLUSION: Patients in an antithrombotic state presenting with angiographically negative subarachnoid hemorrhage present with inferior clinical scores, diffuse hemorrhage patterns, and worse modified Fisher grades and have worse outcomes.

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2

Condette-Auliac, S., S. Bracard, R. Anxionnat, E. Schmitt, J. C. Lacour, M. Braun, J. Meloneto, A. Cordebar, L. Yin, and L. Picard. "Vasospasm After Subarachnoid Hemorrhage." Stroke 32, no. 8 (August 2001): 1818–24. http://dx.doi.org/10.1161/01.str.32.8.1818.

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3

Balanzar, Gerardo Guinto, and Yoshiaki Guinto-Nishimura. "Vasospasm in Subarachnoid Hemorrhage." World Neurosurgery 82, no. 6 (December 2014): e677-e678. http://dx.doi.org/10.1016/j.wneu.2013.09.003.

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4

Aires, Rogério, Márcio Francisco Lehmann, Renata Simm, Miguel Melgar, Carlos Alexandre Martins Zicarelli, and Paulo Henrique Pires De Aguiar. "Magnesium in subarachnoid hemorrhage." JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 21, no. 3 (March 19, 2018): 158–61. http://dx.doi.org/10.22290/jbnc.v21i3.845.

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Cerebral vasospasm is responsible for a great number of deaths and morbidity after acute subarachnoid hemorrhage. Beyond any doubt, it is related to physiopathology of endothelial cell contraction and relaxation. It has been proved as a therapeutic agent when administrated intravenously in patients after subarachnoid hemorrhage. A critical review of literature was accomplished by the authors in order to analyse all actions of vasospasm in SAH. The intravenous administration of magnesium is imperative and should be done immediately after the onset of SAH, as reccomended in the most important guidelines for the treatment of cerebral vasospasm.

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5

Burns, Shannon K., Kacie J. Brewer, Courtney Jenkins, and Sally Miller. "Aneurysmal Subarachnoid Hemorrhage and Vasospasm." AACN Advanced Critical Care 29, no. 2 (June 15, 2018): 163–74. http://dx.doi.org/10.4037/aacnacc2018491.

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Aneurysmal subarachnoid hemorrhage is potentially fatal and is associated with poor outcomes in many patients. Advances in neurosurgical and medical management of ruptured aneurysms have improved mortality rates in patients with aneurysmal subarachnoid hemorrhage. Surgical and endovascular interventions, such as external ventricular drain placement, aneurysm clipping, and endovascular coiling, have been developed over the past few decades. Patients with aneurysmal subarachnoid hemorrhage are also at risk for cerebral vasospasm and delayed cerebral ischemia. This article describes the diagnosis and treatment of aneurysmal subarachnoid hemorrhage, vasospasm, and cerebral ischemia. Concurrent medical considerations and ideas for future neuroinflammatory vasospasm research are also discussed.

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Milojevic, T. M., B. V. Baljozovic, M. Lj Rakic, B. D. Nestorovic, M. M. Dostanic, B. D. Milakovic, Z. Kojic, N. R. Repac, and I. S. Cvrkota. "Cerebral vasospasm after subarachnoid hemorrhage." Acta chirurgica Iugoslavica 55, no. 2 (2008): 55–60. http://dx.doi.org/10.2298/aci0802055m.

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Cerebral vasospasm causes permanent neurolological deficit or death occurrence in 13% of clinical cases. Peak frequency is from 8-10th day after SAH. The purpose of this study is factor analysis that may have influence on vasospasm development , as well as predictor determination. The study is prospective and analysis 192 patients treated in Institute of Neurosurgery, Clinical Centre of Serbia, Belgrade. The majority of patients were admitted in hospital in first four days after SAH, and 184 had GCS over 7. Univariate methods of factor analysis were used, and for significance of predictors influence testing multivariante regression analysis was used . Vasospasm occurred in 22,40% of all cases. No relationships have been found between sex, age, previous hypertension, timing of surgery, appearance of hydrocephalus and intracerebral hematoma, hypertermia or mean arterial blood pressure, with occurrence of cerebral vasospasm. Factors with significantly associated with the occurrence of vasospasm were: hearth disease, hypernatriemia, Hct, clinical grade on admission as well as preoperative clinical grade and Fisher CT scan grade. In the first four days after SAH, Fisher scan grade, preoperative clinical grade and Hct, appeared as predictors. After four days, clinical grade on admission and hypernatiemia, showed as predictors.

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7

Oyama, Katie, and Laura Criddle. "Vasospasm After Aneurysmal Subarachnoid Hemorrhage." Critical Care Nurse 24, no. 5 (October 1, 2004): 58–67. http://dx.doi.org/10.4037/ccn2004.24.5.58.

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8

Mohindra, Sandeep, Amey Savardekar, and Ankur Kapoor. "Vasospasm after iatrogenic subarachnoid hemorrhage." Neurology India 64, no. 7 (2016): 126. http://dx.doi.org/10.4103/0028-3886.178057.

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9

Macdonald, R. Loch. "Predicting Vasospasm After Subarachnoid Hemorrhage." World Neurosurgery 75, no. 1 (January 2011): 25–26. http://dx.doi.org/10.1016/j.wneu.2010.07.018.

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10

Roberts, Debra, and Emad Nourollah-Zadeh. "Cerebral vasospasm after subarachnoid hemorrhage." Neurology 93, no. 5 (July 5, 2019): 192–93. http://dx.doi.org/10.1212/wnl.0000000000007854.

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11

Billingsley, Joshua T., and Brian L. Hoh. "Vasospasm in Aneurysmal Subarachnoid Hemorrhage." World Neurosurgery 82, no. 3-4 (September 2014): 250–52. http://dx.doi.org/10.1016/j.wneu.2014.06.048.

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12

Janjua, Nazli, and Stephan A. Mayer. "Cerebral vasospasm after subarachnoid hemorrhage." Current Opinion in Critical Care 9, no. 2 (April 2003): 113–19. http://dx.doi.org/10.1097/00075198-200304000-00006.

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13

Frontera, Jennifer A., Andres Fernandez, J. Michael Schmidt, Jan Claassen, Katja E. Wartenberg, Neeraj Badjatia, E. Sander Connolly, and Stephan A. Mayer. "Defining Vasospasm After Subarachnoid Hemorrhage." Stroke 40, no. 6 (June 2009): 1963–68. http://dx.doi.org/10.1161/strokeaha.108.544700.

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14

Kosty, Toni. "Cerebral Vasospasm After Subarachnoid Hemorrhage." Critical Care Nursing Quarterly 28, no. 2 (April 2005): 122–34. http://dx.doi.org/10.1097/00002727-200504000-00005.

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15

Rabinstein, Alejandro A., and Eelco F. M. Wijdicks. "Cerebral vasospasm in subarachnoid hemorrhage." Current Treatment Options in Neurology 7, no. 2 (April 2005): 99–107. http://dx.doi.org/10.1007/s11940-005-0019-x.

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16

Topcuoglu, M. Akif, Johnny C. Pryor, Christopher S. Ogilvy, and J. Philip Kistler. "Cerebral vasospasm following subarachnoid hemorrhage." Current Treatment Options in Cardiovascular Medicine 4, no. 5 (October 2002): 373–84. http://dx.doi.org/10.1007/s11936-002-0017-1.

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17

Kiwak, Kevin J., and Roberto C. Heros. "Cerebral vasospasm after subarachnoid hemorrhage." Trends in Neurosciences 10, no. 2 (February 1987): 89–92. http://dx.doi.org/10.1016/0166-2236(87)90032-4.

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18

Shehabeldin, Mohamed, and Yazan Alderazi. "Management of cerebral vasospasm following aneurysmal subarachnoid hemorrhage." Southwest Respiratory and Critical Care Chronicles 5, no. 20 (July 19, 2017): 33. http://dx.doi.org/10.12746/swrccc.v5i20.410.

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Cerebral vasospasm is a serious complication following aneurysmal subarachnoidhemorrhage (SAH); it causes delayed cerebral ischemia (DCI) or infarction. Arterial vasospasmis considered the most common cause of disability and mortality among survivors of aneurysmalSAH. Monitoring for vasospasm is extremely important starting from the first day following ahemorrhage. The mechanism of vasospasm is not completely understood, but most data andstudies link the incidence of vasospasm to inflammatory responses secondary to extravasationof blood into the subarachnoid space. It is essential for critical care teams and health careproviders caring for patients with aneurysmal SAH to understand the clinical presentation andmanagement of cerebral vasospasm. In our review, we focus on the guidelines for monitoringand basic management of vasospasm and DCI which include monitoring options, hemodynamicand endovascular therapy, triggers for intervention, and triggers for treatment de-escalation.

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19

Kim, Joong-Goo, Chul-Hoo Kang, Jay Chol Choi, and Jong-Kook Rhim. "Unrecognized Ruptured Intracranial Aneurysm Presenting as Cerebral Vasospasm-Induced Ischemic Stroke: A Case Report." Neurointervention 16, no. 2 (July 1, 2021): 180–84. http://dx.doi.org/10.5469/neuroint.2021.00017.

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A 44-year-old woman presented with acute confusion, apparently due to a clinically silent subarachnoid hemorrhage followed by vasospasm, which in turn led to an ischemic stroke. During the initial evaluation, an acute ischemic stroke in the left middle cerebral artery territory was observed. Magnetic resonance imaging revealed a late subacute hemorrhage in the left basal cistern. Digital subtraction angiography indicated the presence of a small saccular aneurysm that had recently ruptured, as well as vasospasm in the left circle of Willis. Balloon angioplasty and balloon-assisted coil embolization were performed for the vasospasm and saccular aneurysm, respectively. This case demonstrates that clinically silent subarachnoid hemorrhages resulting in ipsilateral vasospasm and infarction can occur as complications of a ruptured aneurysm.

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20

D'Abbondanza, Josephine A., Jinglu Ai, Elliot Lass, Hoyee Wan, Shakira Brathwaite, Michael K. Tso, Charles Lee, Philip A. Marsden, and R. Loch Macdonald. "Robust effects of genetic background on responses to subarachnoid hemorrhage in mice." Journal of Cerebral Blood Flow & Metabolism 36, no. 11 (July 22, 2016): 1942–54. http://dx.doi.org/10.1177/0271678x15612489.

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Outcome varies among patients with subarachnoid hemorrhage but known prognostic factors explain only a small portion of the variation in outcome. We hypothesized that individual genetic variations influence brain and vascular responses to subarachnoid hemorrhage and investigated this using inbred strains of mice. Subarachnoid hemorrhage was induced in seven inbred and a chromosome 7 substitution strain of mouse. Cerebral blood flow, vasospasm of the middle cerebral artery, and brain injury were assessed. After 48 h of subarachnoid hemorrhage, mice showed significant middle cerebral artery vasospasm that correlated positively with reduction in cerebral blood flow at 45 min. Mice also had increased neuronal injury compared to sham controls; A/J and C57BL/6 J strains represented the most and least severe, respectively. However, brain injury did not correlate with cerebral blood flow reduction at 45 min or with vasospasm at 48 h. Chromosome 7 substitution did not influence the degree of vasospasm or brain injury. Our data suggested that mouse genetic background influences outcome of subarachnoid hemorrhage. Investigations into the genetic factors causing these inter-strain differences may provide insight into the etiology of the brain damage following subarachnoid hemorrhage. These findings also have implications for animal modeling of disease and suggest that genetic differences may also modulate outcome in other cardiovascular diseases.

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21

Luigi, Pellettieri, Nilsson Bo, Carlsson Carl-Axel, and Nilsson Ulf. "Serum Immunocomplexes in Patients with Subarachnoid Hemorrhage." Neurosurgery 19, no. 5 (November 1, 1986): 767–71. http://dx.doi.org/10.1227/00006123-198611000-00008.

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Abstract Immunocomplexes (IC) in serum were analyzed in 54 patients with subarachnoid hemorrhage (SAH) from ruptured arterial aneurysms. A previous study had shown that patients with SAH and vasospasm had a significantly higher incidence of ICs in the blood than patients without vasospasm. The aim of the present study was to study how the IC content varied with time and compare this pattern with the clinical picture. Forty-two patients presented clinical or radiological signs of cerebral vasospasm during their hospital stays, whereas 12 patients showed no such signs. The patients with vasospasm had a significantly higher amount of ICs in serum than those without vasospasm. In 37 patients with vasospasm, the changes of IC content during the 1st weeks after SAH correlated well with the clinical course. Data indicated that a high IC content preceded the onset of vasospasm and a low content preceded clinical improvement. This observation supports the idea that the presence of ICs might be the cause and not the result of vasospasm.

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22

Amuluru, Krishna, Fawaz Al-Mufti, Charles E. Romero, and Chirag D. Gandhi. "Isolated Intraventricular Hemorrhage Associated with Cerebral Vasospasm and Delayed Cerebral Ischemia following Arteriovenous Malformation Rupture." Interventional Neurology 7, no. 6 (2018): 479–89. http://dx.doi.org/10.1159/000490583.

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Background: Although it is well characterized in aneurysmal subarachnoid hemorrhage, vasospasm is exceedingly rare following cerebral arteriovenous malformation (AVM) rupture. Subsequently, this complication is poorly characterized with regard to delayed cerebral ischemia (DCI). We review cases of ruptured AVM to assess the frequency and severity of vasospasm on cerebral angiography, and DCI. Summary: We reviewed our institutional database of acute intracranial hemorrhages between 2005 and 2014. We identified patients with cerebral AVM rupture and evidence of vasospasm, which was confirmed with digital subtraction angiography (DSA). Cerebral angiograms were evaluated by 2 blinded neurointerventionalists for vasospasm. Statistical analyses were conducted on the angiographic results and variables of interest to determine predictors and associations of vasospasm and DCI. Thirty-six patients with acute intracranial hemorrhage due to ruptured cerebral AVM subsequently underwent cerebral angiography. The interrater reliability for vasospasm was 0.81. The incidence of vasospasm was 13.9% and the incidence of subsequent DCI was 11.1%. A significant relationship existed between isolated intraventricular hemorrhage and vasospasm (p = 0.001) and subsequent DCI (p = 0.006). Radiographic vasospasm was associated with DCI in 80% of the patients (p < 0.0001). No statistical significance existed between subarachnoid hemorrhage and the development of vasospasm or DCI (p = 1.000 and p = 0.626, respectively). All differences were significant at a 99% level of significance. Key Message: In cases of ruptured AVM, isolated intraventricular hemorrhage appears to be an independent risk factor for vasospasm and DCI. Vasospasm must be considered during late neurological deterioration following AVM hemorrhage, especially in the setting of isolated intraventricular hemorrhage.

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23

Gules, Ilker, Motoyoshi Satoh, Ben R. Clower, Anil Nanda, and John H. Zhang. "Comparison of three rat models of cerebral vasospasm." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2551—H2559. http://dx.doi.org/10.1152/ajpheart.00616.2002.

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A substantial number of rat models have been used to research subarachnoid hemorrhage-induced cerebral vasospasm; however, controversy exists regarding which method of selection is appropriate for this species. This study was designed to provide extensive information about the three most popular subarachnoid hemorrhage rat models: the endovascular puncture model, the single-hemorrhage model, and the double-hemorrhage model. In this study, the basilar artery and posterior communicating artery were chosen for histopathological examination and morphometric analysis. Both the endovascular puncture model and single-hemorrhage model developed significant degrees of vasospasm, which were less severe when compared with the double-hemorrhage model. The endovascular puncture model and double-hemorrhage model both developed more vasospasms in the posterior communicating artery than in the basilar artery. The endovascular puncture model has a markedly high mortality rate and high variability in bleeding volume. Overall, the present study showed that the double-hemorrhage model in rats is a more suitable tool with which to investigate mechanism and therapeutic approaches because it accurately correlates with the time courses for vasospasm in humans.

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24

Ryttlefors, Mats, Per Enblad, Elisabeth Ronne-Engström, Lennart Persson, Don Ilodigwe, and R. Loch Macdonald. "Patient Age and Vasospasm After Subarachnoid Hemorrhage." Neurosurgery 67, no. 4 (October 1, 2010): 911–17. http://dx.doi.org/10.1227/neu.0b013e3181ed11ab.

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Abstract BACKGROUND: Subarachnoid hemorrhage (SAH) from a ruptured intracranial aneurysm is a devastating disease with high mortality and morbidity. The incidence of SAH increases with advancing age. OBJECTIVE: To determine whether age is an independent predictor of angiographic vasospasm, delayed ischemic neurological deficits (DINDs), or abnormal transcranial Doppler (TCD) measurements in patients with aneurysmal subarachnoid hemorrhage. METHODS: Data from CONSCIOUS-1 (Clazosentan to Overcome Neurological Ischemia and Infarct Occurring After Subarachnoid Hemorrhage study), a dose-finding study of clazosentan, were used. Data on angiographic vasospasm, DINDs, and TCD abnormalities were prospectively recorded as well as baseline characteristics and treatment data. Patient age was considered in 3 ways: as a continuous variable, dichotomized at age 65 years, and categorized by decade. Age was investigated as the main variable, whereas other possible confounding variables were adjusted for in the multiple logistic regression modeling with each of 3 dichotomized vasospasm outcome measures, presence or absence of angiographic vasospasm, DINDs, and TCD abnormalities as the dependent variable. RESULTS: The proportions of patients with angiographic vasospasm, DINDs, and TCD abnormalities were 45%, 19%, and 81%, respectively. Age, whether considered as a continuous, dichotomous, or a categorical variable, was not significantly associated with angiographic vasospasm, DINDs, or abnormal TCD measurements. CONCLUSION: Age does not seem to be a significant predictor for cerebral vasospasm after subarachnoid hemorrhage.

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Filipce, Venko, and Aleksandar Caparoski. "The Effects of Vasospasm and Re-Bleeding on the Outcome of Patients with Subarachnoid Hemorrhage from Ruptured Intracranial Aneurysm." PRILOZI 36, no. 3 (December 1, 2015): 77–82. http://dx.doi.org/10.1515/prilozi-2015-0081.

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Abstract Vasospasm and re-bleeding after subarachnoid hemorrhage from ruptured intracranial aneurysm are devastating complication that can severely affect the outcome of the patients. We are presenting a series of total number of 224 patients treated and operated at our Department due to subarachnoid hemorrhage, out of which certain number developed vasospasm and re-bleeding. We are evaluating the effect of these complications on the outcome of the patients according to the Glasgow Outcome Scale at the day of discharge. In our experience both vasospasm and ReSAH can significantly influence the outcome of patients with subarachnoid hemorrhage from ruptured intracranial aneurysm.

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26

Sharma, BhawaniShanker, and DattarajParamanand Sawarkar. "Vasospasm: The enigma of subarachnoid hemorrhage." Neurology India 63, no. 4 (2015): 483. http://dx.doi.org/10.4103/0028-3886.161982.

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27

Tulamo, Riikka, Mika Niemelä, and Juha Hernesniemi. "Delayed Vasospasm in Aneurysmal Subarachnoid Hemorrhage." World Neurosurgery 77, no. 1 (January 2012): 39–41. http://dx.doi.org/10.1016/j.wneu.2010.01.028.

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28

De Aguiar, Paulo Henrique Pires, Antônio Santos De Araújo Júnior, Mirella Martins Fazzito, Renata Simms, Miguel Melgar, and Andrea Kleindienst. "Cerebral vasospasm following subarachnoid hemorrhage (SAH):." JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 20, no. 3 (March 19, 2018): 365–77. http://dx.doi.org/10.22290/jbnc.v20i3.873.

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Cerebral vasospasm and the delayed cerebral ischemia remain a source of substantial morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Hemodynamic manipulation better known as ‘triple H’ therapy is routinely used in the management of patients with acute vasospasmfollowing SAH. The rationale of inducing hypertension, hypervolemia and hemodilution is to improve blood flow to the injured brain and to prevent secondary ischemia. While the Ca2+ antagonist Nimodipine is still the only drug with proven benefit on neurologic outcome following SAH, several alternatives are under research. Tirilazad is not effective, and studies of hemodynamic maneuvers, magnesium, statin medications, endothelin antagonists, steroid drugs, anticoagulant/antiplatelet agents, and intrathecal fibrinolytic drugs have yielded inconclusive and controversial results. Steroids drugs and anticoagulant/antiplatelet agents have been abandoned so far, because of the lack of efficacy. The purpose of the present paper is to provide a systematic review of the existing literature on the treatment of cerebral vasospasm.

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Ritzenthaler, Thomas, Florent Gobert, and Fréderic Dailler. "“Vasospasm Mimic” After Aneurysmal Subarachnoid Hemorrhage." World Neurosurgery 124 (April 2019): 295–97. http://dx.doi.org/10.1016/j.wneu.2019.01.034.

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30

Kassell, N. F., T. Sasaki, A. R. Colohan, and G. Nazar. "Cerebral vasospasm following aneurysmal subarachnoid hemorrhage." Stroke 16, no. 4 (July 1985): 562–72. http://dx.doi.org/10.1161/01.str.16.4.562.

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31

Bar, B., L. MacKenzie, R. W. Hurst, R. Grant, J. Weigele, P. K. Bhalla, M. A. Kumar, M. F. Stiefel, and J. M. Levine. "Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage." Neurocritical Care 24, no. 2 (July 22, 2015): 180–88. http://dx.doi.org/10.1007/s12028-015-0177-y.

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32

Gump, William, and Daniel T. Laskowitz. "Management of post-subarachnoid hemorrhage vasospasm." Current Atherosclerosis Reports 10, no. 4 (August 2008): 354–60. http://dx.doi.org/10.1007/s11883-008-0054-7.

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33

Wilson, Craig D., and Jai Jai Shiva Shankar. "Diagnosing Vasospasm After Subarachnoid Hemorrhage: CTA and CTP." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 3 (May 2014): 314–19. http://dx.doi.org/10.1017/s031716710001725x.

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Cerebral vasospasm is a potentially devastating complication in patients with aneurysmal subarachnoid hemorrhage. The purpose of this article is to review the use of computed tomogram (CT) angiography and CT perfusion in the diagnosis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage and also assess their use in guiding treatment decisions. Both techniques are widely used for other indications but their use in cerebral vasospasm has not been well defined. Computed tomogram angiography can directly visualize arterial narrowing and CT perfusion is able to evaluate differences in perfusion parameters after aneurysmal subarachnoid hemorrhage with high sensitivity and specificity. CT perfusion is better at predicting which patients require endovascular treatment.

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Lee, Young, Scott L. Zuckerman, and J. Mocco. "Current Controversies in the Prediction, Diagnosis, and Management of Cerebral Vasospasm: Where Do We Stand?" Neurology Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/373458.

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Aneurysmal subarachnoid hemorrhage occurs in approximately 30,000 persons in the United States each year. Around 30 percent of patients with aneurysmal subarachnoid hemorrhage suffer from cerebral ischemia and infarction due to cerebral vasospasm, a leading cause of treatable death and disability following aneurysmal subarachnoid hemorrhage. Methods used to predict, diagnose, and manage vasospasm are the topic of recent active research. This paper utilizes a comprehensive review of the recent literature to address controversies surrounding these topics. Evidence regarding the effect of age, smoking, and cocaine use on the incidence and outcome of vasospasm is reviewed. The abilities of different computed tomography grading schemes to predict vasospasm in the aftermath of subarachnoid hemorrhage are presented. Additionally, the utility of different diagnostic methods for the detection and visualization of vasospasm, including transcranial Doppler ultrasonography, CT angiography, digital subtraction angiography, and CT perfusion imaging is discussed. Finally, the recent literature regarding interventions for the prophylaxis and treatment of vasospasm, including hyperdynamic therapy, albumin, calcium channel agonists, statins, magnesium sulfate, and endothelin antagonists is summarized. Recent studies regarding each topic were reviewed for consensus recommendations from the literature, which were then presented.

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35

Juvela, Seppo. "Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage." Journal of Neurosurgery 92, no. 3 (March 2000): 390–400. http://dx.doi.org/10.3171/jns.2000.92.3.0390.

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Object. The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH.Methods. Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique.On the whole, mean plasma ET concentrations in patients with SAH (mean ± standard error of mean, 2.1 ± 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 ± 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml compared with 2.1 ± 0.2 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml compared with 1.9 ± 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0–5, 3.2 ± 0.8 pg/ml; post-SAH Days 6–14, 2.7 ± 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 ± 0.3 compared with 1.9 ± 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others.Conclusions. Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

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Carpenter, David A., Robert L. Grubb, Lee W. Tempel, and William J. Powers. "Cerebral Oxygen Metabolism after Aneurysmal Subarachnoid Hemorrhage." Journal of Cerebral Blood Flow & Metabolism 11, no. 5 (September 1991): 837–44. http://dx.doi.org/10.1038/jcbfm.1991.143.

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Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1–4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.

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McConnell, Evan D., Helen S. Wei, Katherine M. Reitz, Hongyi Kang, Takahiro Takano, G. Edward Vates, and Maiken Nedergaard. "Cerebral microcirculatory failure after subarachnoid hemorrhage is reversed by hyaluronidase." Journal of Cerebral Blood Flow & Metabolism 36, no. 9 (July 22, 2016): 1537–52. http://dx.doi.org/10.1177/0271678x15608389.

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Aneurysmal subarachnoid hemorrhage remains one of the more devastating forms of stroke due in large part to delayed cerebral ischemia that appears days to weeks following the initial hemorrhage. Therapies exclusively targeting large caliber arterial vasospasm have fallen short, and thus we asked whether capillary dysfunction contributes to delayed cerebral ischemia after subarachnoid hemorrhage. Using a mouse model of subarachnoid hemorrhage and two-photon microscopy we showed capillary dysfunction unrelated to upstream arterial constriction. Subarachnoid hemorrhage decreased RBC velocity by 30%, decreased capillary pulsatility by 50%, and increased length of non-perfusing capillaries by 15%. This was accompanied by severe brain hypoxia and neuronal loss. Hyaluronidase, an enzyme that alters capillary blood flow by removing the luminal glycocalyx, returned RBC velocity and pulsatility to normal. Hyaluronidase also reversed brain hypoxia and prevented neuron loss typically seen after subarachnoid hemorrhage. Thus, subarachnoid hemorrhage causes specific changes in capillary RBC flow independent of arterial spasm, and hyaluronidase treatment that normalizes capillary blood flow can prevent brain hypoxia and injury after subarachnoid hemorrhage. Prevention or treatment of capillary dysfunction after subarachnoid hemorrhage may reduce the incidence or severity of subarachnoid hemorrhage-induced delayed cerebral ischemia.

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Schebesch, Karl-Michael, Christian Doenitz, Roland Zoephel, Thomas Finkenzeller, and Alexander T. Brawanski. "RECURRENT SUBARACHNOID HEMORRHAGE CAUSED BY A DE NOVO BASILAR TIP ANEURYSM DEVELOPING WITHIN 8 WEEKS AFTER CLIPPING OF A RUPTURED ANTERIOR COMMUNICATING ARTERY ANEURYSM." Neurosurgery 62, no. 1 (January 1, 2008): E259—E260. http://dx.doi.org/10.1227/01.neu.0000311087.19261.0a.

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Abstract OBJECTIVE Well-documented case reports of the rapid formation and rupture of de novo aneurysms of the posterior circulation are rare. CLINICAL PRESENTATION We report a patient with subarachnoid hemorrhage caused by an aneurysm of the anterior communicating artery that was clipped consecutively. Forty-four days after the initial subarachnoid hemorrhage, the patient experienced a second subarachnoid hemorrhage after the rupture of a newly grown aneurysm of the basilar tip. Between the two hemorrhages, transcranial Doppler sonography and neuroimaging revealed a fulminant generalized vasospasm. INTERVENTION To our knowledge, this is the first report of the rapid development and rupture of a de novo aneurysm of the posterior circulation after the rupture of an initial aneurysm of the anterior circulation. CONCLUSION We review the pertinent literature and discuss possible reasons for the development and rupture of this second aneurysm.

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Badger, Clint A., Brian T. Jankowitz, and Hamza A. Shaikh. "Treatment of cerebral vasospasm secondary to subarachnoid hemorrhage utilizing the Comaneci device." Interventional Neuroradiology 26, no. 5 (July 28, 2020): 582–85. http://dx.doi.org/10.1177/1591019920945554.

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Delayed cerebral ischemia due to vasospasm following subarachnoid hemorrhage continues to have high morbidity and mortality despite current treatments. This report highlights the use of the Comaneci (Rapid Medical, Yokneam, Israel), a device FDA approved for temporary coil embolization assistance, for the treatment of symptomatic vasospasm. Ten days post subarachnoid hemorrhage, a patient developed acute left-sided hemiparesis with angiographic vasospasm. Through a Headway 17 microcatheter, a Comaneci 17 was deployed in the right ICA terminus, M1, M2, A1, and, A2 segments resulting in improvement of angiographic vasospasm and the patient’s left-sided hemiparesis. On the following day, a repeat angiogram demonstrated no recurrence of vasospasm. The patient had complete return on neurologic function by post bleed day 18 continuing to her four-week follow-up appointment. This case demonstrates the feasibility of the Comaneci device as an effective tool in the treatment of vasospasm following subarachnoid hemorrhage.

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Sharma, Mohan R., Gerald A. Grant, Heather A. Nicoletto, Colleen M. Douville, and David W. Newell. "Spontaneous Nonaneurysmal Subarachnoid Hemorrhage: Review of 75 Cases." Nepal Journal of Neuroscience 2, no. 1 (January 31, 2005): 59–66. http://dx.doi.org/10.3126/njn.v2i1.19996.

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The primary objective of this study was to describe the clinical, radiological, and transcranial Doppler (TCD) ultrasonography characteristics of patients with spontaneous, nonaneurysmal subarachnoid hemorrhage (SNSAH), and analyze their short- term outcome at discharge. The secondary objective was to determine their risk factors for the development of vasospasm.Seventy-five patients with SNSAH were analyzed in terms of clinical, radiological, and TCD parameters, as well as Glasgow Outcome Scale (GOS) at discharge. The patients were then divided into two groups based on whether or not they developed vasospasm by TCD ultrasonography. Twenty of 75 patients (26.7%) had vasospasm by TCD criteria. Age, sex, cigarette smoking, hypertension, clinical Hunt and Hess and World Federation of Neurological Surgeons (WFNS) grading, Fisher’s grade on computerized tomography (CT) scan, or discharge GOS score did not correlate with the development of vasospasm. Hydrocephalus, identified in 11 (14.7%) patients upon admission, was significantly more common in patients with vasospasm (p< 0.0001). Patients with vasospasm stayed in the hospital significantly longer than those without vasospasm (P<0.001). Vasospasm in SNSAH is more prevalent than previously thought. There is no statistical correlation between the incidence of vasospasm in patients with SNSAH and age, sex, smoking, hypertension, and different admission clinical and Fisher’s grades. However, the presence of hydrocephalus at admission correlated significantly with the development of vasospasm. Despite the high incidence of vasospasm, there is no difference in short-term clinical outcome at discharge between the patients with and without vasospasm. Nepal Journal of Neuroscience, Volume 2, Number 1, 2005, page: 59-66

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Hara, Hideaki, Michael Nosko, and Bryce Weir. "Cerebral perivascular nerves in subarachnoid hemorrhage." Journal of Neurosurgery 65, no. 4 (October 1986): 531–39. http://dx.doi.org/10.3171/jns.1986.65.4.0531.

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✓ The authors have studied the changes induced by subarachnoid hemorrhage (SAH) in the density and distribution of cerebral perivascular nerves in monkeys and rats. The SAH was induced in monkeys by placement of an autologous blood clot after opening the basal cisterns over the arteries of the circle of Willis on one side. In the rat study, SAH was induced by injection of autologous arterial blood into the cisterna magna. The nerves examined were adrenergic nerves, acetylcholinesterase (AChE)-containing nerves, vasoactive intestinal polypeptide (VIP)-like immunoreactive nerves, and substance P-like immunoreactive nerves. In the monkey study, all animals underwent baseline cerebral angiography, then had repeat angiography just before sacrifice on Day 2, 7, 28, or 70 after SAH. Two sham-operated monkeys underwent the surgical procedure without clot placement and were sacrificed on postoperative Day 7, after repeat angiography. Clot placement in monkeys reduced staining of all middle cerebral artery (MCA) perivascular nerves for between 2 and 28 days post-SAH. The number of stained nerve fibers of MCA's on the non-operated side was slightly reduced on Days 2 and 7 after SAH. Sham-operated monkeys showed a mild reduction of staining in all nerves, but only on the operated side. Cerebral vasospasm was observed on all angiograms taken on Days 2 and 7 following SAH. No vasospasm was found in normal or sham-operated monkeys. The disappearance of nerve staining without associated vasospasm was found on the operated side of the sham-operated monkeys and on the clot side of the animal sacrificed on Day 28 after SAH. Rats sacrificed on Days 2 and 7 post-SAH showed reduction in adrenergic and VIP-like immunoreactive staining around basilar arteries, while nerves containing AChE were not affected. Saline-injected rats exhibited no change in the appearance of perivascular innervation. These results suggest that SAH as well as surgical manipulation of the vessel wall caused a reduction of the studied substances in cerebral perivascular nerves. This reduction in immunoreactive staining of perivascular nerves did not correlate with the development of angiographic vasospasm after SAH.

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Paoletti, Pietro, Paolo Gaetani, Guido Grignani, Lucia Pacchiarini, Vittorio Silvani, and Riccardo Rodriguez y Baena. "CSF leukotriene C4 following subarachnoid hemorrhage." Journal of Neurosurgery 69, no. 4 (October 1988): 488–93. http://dx.doi.org/10.3171/jns.1988.69.4.0488.

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✓ Leukotrienes derive from arachidonic acid metabolism via the lipoxygenase pathway and modulate several cellular events. In the central nervous system, leukotrienes are mainly synthesized in the gray matter and in vascular tissues. Their production is enhanced in ischemic conditions and in experimental subarachnoid hemorrhage (SAH). Previous studies have indicated the ability of the leukotrienes C4 and D4 to constrict arterial vessels in vivo and in vitro and have suggested their involvement in the pathogenesis of cerebral arterial spasm. In the present study, the authors measured lumbar and cisternal cerebrospinal fluid (CSF) levels of leukotriene C4 in 48 patients who had suffered aneurysmal SAH. In 12 of the cases, symptomatic and radiological spasm was evident. The mean lumbar CSF level of immunoreactive-like activity of leukotriene C4 (i-LTC4) was significantly higher (p < 0.005) than in control cases, while the cisternal CSF level was higher than the lumbar mean concentration (p < 0.005). Patients presenting with vasospasm had significantly higher levels of i-LTC4 compared to patients without symptomatic vasospasm. This is the first report concerning monitoring of i-LTC4 levels in the CSF after SAH. The results of this study suggest that: 1) metabolism of arachidonic acid via the lipoxygenase pathway is enhanced after SAH; 2) the higher cisternal CSF levels of i-LTC4 may be part of the biological response in the perianeurysmal subarachnoid cisterns after the hemorrhage; and 3) the higher CSF levels of i-LTC4 in patients presenting with vasospasm suggest that a relationship exists between this compound and arterial spasm and/or reflect the development of cerebral ischemic damage.

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Terada, Tomoaki, Norihiko Komai, Seiji Hayashi, Hiroshi Moriwaki, Genhachi Hyoutani, Yuji Uematsu, Jun Karasawa, and Haruhiko Kikuchi. "Hemorrhagic Infarction after Vasospasm Due to Ruptured Cerebral Aneurysm." Neurosurgery 18, no. 4 (April 1, 1986): 415–18. http://dx.doi.org/10.1227/00006123-198604000-00004.

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Abstract Hemorrhagic infarction after vasospasm is a rare condition in patients with aneurysmal subarachnoid hemorrhage (SAH). Induced hypertensive therapy is used for patients with vasospasm, but this treatment has a risk of inducing hemorrhagic infarction. A total of 221 patients whose first computed tomographic (CT) scans were examined within 2 weeks after SAH were investigated for this study. There was symptomatic vasospasm in 99 (45%), cerebral infarction in 37 (17%), and hemorrhagic infarction in 13 (6%). Hemorrhagic infarction usually occurred 20 to 30 days after aneurysmal rupture; this period corresponds with the remission stage of the vasospasm. On CT scans, the hemorrhagic infarction was revealed as a leaky hemorrhage in a low density area in 11 cases, and a massive hemorrhage with mass effect was seen in 2 cases. These findings suggest that hemorrhagic infarction after vasospasm may sometimes be fatal. Cerebral blood flow autoregulation in patients with vasospasm was normal or of a hypertensive type during the remission stage of vasospasm, when hemorrhagic infarction usually appeared. This finding shows that induced hypertension therapy is ineffective during this stage; it should be stopped by this stage because it is ineffective and also may aggravate hemorrhagic infarction.

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Kamali, Alireza, Reza Mansubi, and Mohsen Dalvandi. "The Effect of Milrinone on the Cerebral Vasospasm in Patients with Subarachnoid Hemorrhage." NeuroQuantology 17, no. 8 (August 25, 2019): ———. http://dx.doi.org/10.14704/nq.2019.17.8.2549.

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Blissitt, Patricia A., Pamela H. Mitchell, David W. Newell, Susan L. Woods, and Basia Belza. "Cerebrovascular Dynamics With Head-of-Bed Elevation in Patients With Mild or Moderate Vasospasm After Aneurysmal Subarachnoid Hemorrhage." American Journal of Critical Care 15, no. 2 (March 1, 2006): 206–16. http://dx.doi.org/10.4037/ajcc2006.15.2.206.

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• Background In patients with aneurysmal subarachnoid hemorrhage, elevation of the head of the bed during vasospasm has been limited in an attempt to minimize vasospasm or its sequelae or both. Consequently, some patients have remained on bed rest for weeks. • Objectives To determine how elevations of the head of the bed of 20° and 45° affect cerebrovascular dynamics in adult patients with mild or moderate vasospasm after aneurysmal subarachnoid hemorrhage and to describe the response of mild or moderate vasospasm to head-of-bed elevations of 20° and 45° with respect to variables such as grade of subarachnoid hemorrhage and degree of vasospasm. • Methods A within-patient repeated-measures design was used. The head of the bed was positioned in the sequence of 0°-20°-45°-0° in 20 patients with mild or moderate vasospasm between days 3 and 14 after aneurysmal subarachnoid hemorrhage. Continuous transcranial Doppler recordings were obtained for 2 to 5 minutes after allowing approximately 2 minutes for stabilization in each position. • ResultsNo patterns or trends indicated that having the head of the bed elevated increases vasospasm. As a group, there were no significant differences within patients at the different positions of the head of the bed. Utilizing repeated-measures analysis of variance, P values ranged from .34 to .97, well beyond .05. No neurological deterioration occurred. • Conclusions In general, elevation of the head of the bed did not cause harmful changes in cerebral blood flow related to vasospasm.

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Cecon, Angelo Daros, Eberval Gadelha Figueiredo, Edson Bor-Seng-Shu, Milberto Scaff, and Manoel Jacobsen Teixeira. "Extremely delayed cerebral vasospasm after subarachnoid hemorrhage." Arquivos de Neuro-Psiquiatria 66, no. 3a (September 2008): 554–56. http://dx.doi.org/10.1590/s0004-282x2008000400024.

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Pradilla, Gustavo, Kaisorn L. Chaichana, Stanley Hoang, Judy Huang, and Rafael J. Tamargo. "Inflammation and Cerebral Vasospasm After Subarachnoid Hemorrhage." Neurosurgery Clinics of North America 21, no. 2 (April 2010): 365–79. http://dx.doi.org/10.1016/j.nec.2009.10.008.

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Jordan, J. Dedrick, and Paul Nyquist. "Biomarkers and Vasospasm After Aneurysmal Subarachnoid Hemorrhage." Neurosurgery Clinics of North America 21, no. 2 (April 2010): 381–91. http://dx.doi.org/10.1016/j.nec.2009.10.009.

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Kale, Sushant P., Randall C. Edgell, Amer Alshekhlee, Afshin Borhani Haghighi, Justin Sweeny, Jason Felton, Jacob Kitchener, et al. "Age-Associated Vasospasm in Aneurysmal Subarachnoid Hemorrhage." Journal of Stroke and Cerebrovascular Diseases 22, no. 1 (January 2013): 22–27. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2011.05.024.

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Tallarico, Roberta T., Michael A. Pizzi, and William D. Freeman. "Investigational drugs for vasospasm after subarachnoid hemorrhage." Expert Opinion on Investigational Drugs 27, no. 4 (April 3, 2018): 313–24. http://dx.doi.org/10.1080/13543784.2018.1460353.

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