Treatment Options for Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Athar, Mohammad; Levine, Joshua M.

doi:10.1007/s13311-011-0098-1

Cited by 43 publications

(47 citation statements)

References 116 publications

(104 reference statements)

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“…By careful and controlled isolation of each vessel we can also exclude that vessel dysfunction happens due to mechanical damage by bleeding. Although mechanical irritation of vessels or brain damage are considered as possible contributing factors 4,8,24,25 to clinical vasospasm, in our study we intended to separate the mechanical effects from the effects of blood clot presence and ageing.…”

Section: Discussionmentioning

confidence: 99%

“…There is nowadays no specific therapy or prophylaxis for vasospasm 2,4,5 . The low success of current treatment strategies for vasospasm may be due to insufficient knowledge about the pathophysiology of vasospasm, despite a large number of in vitro and in vivo studies done to discover spastic mechanisms and to find an adequate treatment for cerebral vasospasm 6 .…”

Section: Cerebral Delayed Vasospasm Is a Severe Complication Followinmentioning

confidence: 99%

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Effects of iodinated contrast media in a novel model for cerebral vasospasm

Nikitina

Zavaritskaya

Semenyutin

et al. 2015

Arq. Neuro-Psiquiatr.

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Objective: We developed an in vitro model for vasospasm post subarachnoid hemorrhage that was suitable for investigating brain vessel autoregulation. We further investigated the effects of iodinated contrast medium on the vascular tone and the myogenic response of spastic cerebral vessels. Method: We isolated and perfused the superior cerebellar arteries of rats. The vessels were pressurized and studied under isobaric conditions. Coagulated blood was used to simulate subarachnoid hemorrhage. The contrast medium iodixanol was applied intraluminally. Results: Vessels exposed to blood developed significantly stronger myogenic tone (65.7 ± 2.0% vs 77.1 ± 1.2% of the maximum diameter, for the blood and the control group, respectively) and significantly decreased myogenic response, compared with the control groups. The contrast medium did not worsen the myogenic tone or the myogenic response in any group. Conclusion: Our results show that deranged myogenic response may contribute to cerebral blood flow disturbances subsequent to subarachnoid hemorrhage. The contrast medium did not have any negative influence on vessel tone or myogenic response in this experimental setting.Keywords: brain ischemia, cerebral angiography, contrast media, hemodynamics, intracranial aneurysm, intracranial vasospasm, subarachnoid hemorrhage. RESUMOObjetivo: Desenvolvemos um modelo in vitro para vasoespasmo subsequente à hemorragia subaracnóide que foi adequado para investigar a autorregularão dos vasos cerebrais. Em seguida investigamos os efeitos o meio de contraste iodado no tônus vascular e na resposta miogênica dos vasos cerebrais espásticos. Método: Isolamos e perfundimos as artérias cerebelares superiores de ratos. Os vasos foram pressurizados e estudados em condições isobáricas. Sangue coagulado foi utilizado para simular hemorragia subaracnóide. O meio de contraste iodixanol foi aplicado intraluminarmente. Resultados: Os vasos expostos ao sangue desenvolveram aumento significativo do tônus miogênico (65.7 ± 2.0% vs 77.1 ± 1.2% do maior diâmetro, para o grupo de sangue e o grupo controle, respectivamente) com resposta miogênica significativamente menor do que aquela dos controles. O meio de contraste iodado não piorou o tônus miogênico ou a resposta miogênica em nenhum dos grupos. Conclusão: Nossos resultados mostram que uma resposta miogênica pode contribuir para as alterações de fluxo sanguíneo cerebral subsequentes à hemorragia subaracnóide. O meio de contraste iodado não teve nenhuma influência negativa no tônus vascular ou na resposta miogênica neste modelo experimental.Palavras-chave: isquemia cerebral, angiografia cerebral, meio de contraste, hemodinâmica, aneurisma intracraniano, vasoespasmo intracraniano, hemorragia subaracnóide.Cerebral delayed vasospasm is a severe complication following spontaneous subarachnoid hemorrhage (SAH). Vasospasm is an important cause of death and contributes 10-12% to the overall mortality after SAH, which reaches approximately 50% within the first month 1,2,3 .There is nowadays no speci...

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Section: Discussionmentioning

confidence: 99%

Section: Cerebral Delayed Vasospasm Is a Severe Complication Followinmentioning

confidence: 99%

Effects of iodinated contrast media in a novel model for cerebral vasospasm

Nikitina

Zavaritskaya

Semenyutin

et al. 2015

Arq. Neuro-Psiquiatr.

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“…In general, there is a revised recommendation for the use of euvolemicinduced hypertension rather than triple-H therapy as the initial method for treatment of most patients with cerebral vasospasm. 15,22,48 …”

Section: Summary Of Triple-h Therapy Recommendationsmentioning

confidence: 99%

Cerebral Vasospasm in Critically III Patients with Aneurysmal Subarachnoid Hemorrhage: Does the Evidence Support the Ever-Growing List of Potential Pharmacotherapy Interventions?

Kiser

2014

Hosp Pharm

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The occurrence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is a significant event resulting in decreased cerebral blood flow and oxygen delivery. Prevention and treatment of cerebral vasospasm is vital to avert neurological damage and reduced functional outcomes. A variety of pharmacotherapy interventions for the prevention and treatment of cerebral vasospasm have been evaluated. Unfortunately, very few large randomized trials exist to date, making it difficult to make clear recommendations regarding the efficacy and safety of most pharmacologic interventions. Considerable debate exists regarding the efficacy and safety of hypervolemia, hemodilution, and hypertension (triple-H therapy), and the implementation of each component varies substantially amongst institutions. There is a new focus on euvolemic-induced hypertension as a potentially preferred mechanism of hemodynamic augmentation. Nimodipine is the one pharmacologic intervention that has demonstrated favorable effects on patient outcomes and should be routinely administered unless contraindications are present. Intravenous nicardipine may offer an alternative to oral nimodipine. The addition of high-dose magnesium or statin therapy has shown promise, but results of ongoing large prospective studies are needed before they can be routinely recommended. Tirilazad and clazosentan offer new pharmacologic mechanisms, but clinical outcome results from prospective randomized studies have largely been unfavorable. Locally administered pharmacotherapy provides a targeted approach to the treatment of cerebral vasospasm. However, the paucity of data makes it challenging to determine the most appropriate therapy and implementation strategy. Further studies are needed for most pharmacologic therapies to determine whether meaningful efficacy exists.

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“…Cerebral vasospasm can occur after subarachnoidian hemorrhage and is one of the leading causes of morbidity and mortality in this type of pathology (1)(2)(3). Subarachnoidian hemorrhage represent the bleeding in the subarachnoidian space and the most frequent pathology that can determine that bleeding are the ruptured aneurysms (4).…”

Section: Introductionmentioning

confidence: 99%

Drotaverinum – a new modality of prevention and treatment in cerebral vasospasm after subarachoidian hemorrhage?

Kakucs¹,

Berce²,

Tamas-Szora³

et al. 2016

Romanian Neurosurgery

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Aim: This study want to demonstrate the efficaciousness of drotaverinum as a replacer of papaverine in the prevention and treatment of vasospasm. Material and method: In this study were used 20 albino Wistar male rats. Rats were divided in two groups and vasospasm was induced to the both femoral artery and after that irrigation of the femoral arteries with drotaverinum was performed to demonstrate the vasodilatation that can appear (group A). In the group B after the obtaining of vasospasm irrigation of the femoral arteries with saline solution was performed and this group was used as witness. The length of the vessels was measured when was achieved the vasospasm and also before and after the administration of the solutions. Pictures were taken at every step of dissection and solutions administration to can measure the length of arteries before and after the administration of drotaverinum and the saline solution. Results: In all rats was obtained vasospasm at the femoral artery after clipping the artery and after we irrigate with adrenaline. In the group with drotaverinum we obtained the vasodilatation and in the witness group the caliber of the vessels remain the same. The statistical analysis of the data demonstrate a significant differences between the group were was used drotaverinum and the witness group were was used the saline solution (p<0,001). Conclusions: Drotaverinum has a good vasodilatative effect on arteries and he can prevent the apparition of vasospasm and it can even treat vasospasm if occur by producing local vasodilatation and a good circulation in the area where is administrated. This study showed quantitatively that drotaverinum can treat the experimental peripheral vasospasm in rats.

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Treatment Options for Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Abstract: Cerebral vasospasm occurs frequently after aneurysmal subarachnoid and contributes to delayed cerebral ischemia. In this article we address systematic problems with the literature on vasospasm and then review both established and experimental treatment options.

Cited by 43 publications

References 116 publications

Effects of iodinated contrast media in a novel model for cerebral vasospasm

Effects of iodinated contrast media in a novel model for cerebral vasospasm

Cerebral Vasospasm in Critically III Patients with Aneurysmal Subarachnoid Hemorrhage: Does the Evidence Support the Ever-Growing List of Potential Pharmacotherapy Interventions?

Drotaverinum – a new modality of prevention and treatment in cerebral vasospasm after subarachoidian hemorrhage?

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