Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage

Polin, Richard S.; Coenen, Volker A.; Hansen, Carolyn Apperson; Shin, Peter; Başkaya, Mustafa K.; Nanda, Anil; Kassell, Neal F.

doi:10.3171/jns.2000.92.2.0284

Cited by 159 publications

(63 citation statements)

References 30 publications

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“…However, a recent large randomized trial investigating the effect of prophylactic endovascular treatment showed a nonsignificant reduction of DCI without a beneficial effect on outcome (Zwienenberg- Lee et al, 2008). Thus, although transluminal angioplasty and intraarterial drug administration reduce vasospasm, improvement in clinical outcome is less obvious (Polin et al, 2000). Some patients show direct clinical improvement after angioplasty, but this effect is often not sustained.…”

Section: Introductionmentioning

confidence: 99%

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Vergouwen

Vermeulen

Coert

et al. 2008

J Cereb Blood Flow Metab

289

195

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Patients with aneurysmal subarachnoid hemorrhage (SAH) who experience delayed cerebral ischemia (DCI) have an increased risk of poor outcome. Delayed cerebral ischemia is considered to be caused by vasospasm. However, not all patients with DCI have vasospasm. Inversely, not all patients with vasospasm develop clinical symptoms and signs of DCI. In the past, treatments aiming at vasospasm were not successful in preventing ischemia. The purpose of this review is to give an overview of clinical data showing that DCI cannot always be attributed to vasospasm, and to present an in-depth analysis of clinical and autopsy studies on the role of microthrombosis in the pathogenesis of DCI. Clinical studies show that DCI is associated with an activation of the coagulation cascade within a few days after SAH, preceding the time window during which vasospasm occurs. Furthermore, impaired fibrinolytic activity, and inflammatory and endotheliumrelated processes, lead to the formation of microthrombi, which ultimately result in DCI. The presence of microthrombi is confirmed by autopsy studies. Insight in the pathophysiology of DCI is crucial for the development of effective therapies against this complication. Because multiple pathways are involved, future research should focus on drugs with pleiotropic effects.

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Section: Introductionmentioning

confidence: 99%

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Vergouwen

Vermeulen

Coert

et al. 2008

J Cereb Blood Flow Metab

289

195

View full text Add to dashboard Cite

show abstract

“…In addition, it demands an experienced endovascular surgeon and is associated with significant risk. 19,20 Intraarterial papaverine has been shown to reverse angiographic vasospasm and to reduce the velocities as detected by transcranial Doppler (TCD). 17,21 However, clinical trials have failed to demonstrate the effectiveness of intra-arterial papaverine on outcome.…”

mentioning

confidence: 99%

Intra-Arterial Nimodipine for Severe Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Influence on Clinical Course and Cerebral Perfusion

Hänggi¹,

Turowski²,

Beseoglu³

et al. 2008

AJNR Am J Neuroradiol

118

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“…Nonetheless, there was no definite connection with angiographic alleviation and functional improvement (Laskowitz & Kolls, 2010). Moreover, radiographic vasospasm improvement lacks evidence to declare its neural functional amelioration in CV (Polin et al., 2000). It should be pointed out that EBI may be the primary cause of mortality in SAH patients (Cahill & Zhang, 2009).…”

Section: Discussionmentioning

confidence: 99%

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

Cai

Bai

et al. 2017

Brain and Behavior

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Background and PurposeSubarachnoid hemorrhage (SAH)‐induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory cytokines and inhibit oxidative stress, inhibits SAH‐induced inflammation and oxidative stress are largely unknown.MethodsAdult male rats underwent autologous blood injection into prechiasmatic cistern to induce SAH. Curcumin (150 mg/kg) was administered at 0.5, 24 and 48 hr post‐SAH. Mortality calculation and neurological outcomes as well as morphological vasospasm of anterior cerebral artery were studied. Superoxide dismutase, lipid peroxidation, and inflammatory cytokines (MCP‐1 and TNF‐α) expression in prefrontal region were quantified. Furthermore, p65 and phosphor‐p65 were quantitatively analyzed.ResultsCurcumin remarkedly reduced mortality and ameliorated neurological deficits after SAH induction (p < .05); morphological results showed that cerebral vasospasm in curcumin‐treated group was mitigated (p < .05). SAH‐induced MCP‐1 and TNF‐α overexpression were inhibited in curcumin‐treated group (p < .05). Importantly, phosphor‐p65 was significantly inhibited after curcumin treatment (p < .05).ConclusionsCurcumin can inhibit SAH‐induced inflammatory response via restricting NF‐κB activation to alleviate cerebral vasospasm and early brain injury.

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Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage

Cited by 159 publications

References 30 publications

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Intra-Arterial Nimodipine for Severe Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Influence on Clinical Course and Cerebral Perfusion

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

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