Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

Abstract

<jats:p>The second leading cause of death and disability in patients with aneurysmal subarachnoid hemorrhage (SAH) is delayed cerebral ischemia due to vasospasm. Although up to 70% of patients have been shown to have angiographic evidence of vasospasm, only 20–30% will present with clinical changes, including mental status changes and neurological deficits that necessitate acute management. Endovascular capabilities have progressed to become viable options in the treatment of cerebral vasospasm. The rationale for intraarterial therapy includes the fact that morbidity and mortality rates have not changed in recent years despite optimized noninvasive medical care. In this report, the authors discuss the most common endovascular options—namely intraarterial vasodilators and transluminal balloon angioplasty—from the standpoint of mechanism, efficacy, limitations, and complications as well as the treatment algorithms for cerebral vasospasm used at our institution.</jats:p>

Arachnoid cell involvement in the mechanism of coagulation-initiated inflammation in the subarachnoid space after subarachnoid hemorrhage

“…Thrombin, TGF-β, and granulocyte-macrophage colony-stimulating factor can promote leptomeninggeal cell proliferation (Motohashi et al, 1995a;Takizawa et al, 2001;Jin et al, 2006). Additionally, clinical DCI usually happens on Day 3, peaks 1-2 weeks after SAH, and then subsides gradually (Claassen et al, 2001;Todo et al, 2008;Eddleman et al, 2009). The results of the present study are consistent with the time of DCI.…”

“…Subarachnoid hemorrhage (SAH) is a frequent occurrence in cerebrovascular accidents, and cerebral vasospasm, especially delayed cerebral ischemia (DCI), is a serious complication after SAH (Kubota et al, 1993;Raymackers et al, 2000;Claassen et al, 2001;Gomis et al, 2005;Todo et al, 2008;Eddleman et al, 2009). The aetiology and pathophysiology of SAH-related vasospasm remain controversial (Chrapusta et al, 2000;Wada et al, 2002;Hendryk et al, 2004;Aydin et al, 2005;Wang et al, 2005;Nekludov et al, 2007).…”

The Effect of Intraventricular Administration of Nicardipine on Mean Cerebral Blood Flow Velocity Measured by Transcranial Doppler in the Treatment of Vasospasm Following Aneurysmal Subarachnoid Hemorrhage

“…1 Mean maximum intracranial pressure before and during intrathecal nicardipine administration than repeated intraarterial therapies, which are sometimes necessary [25,26]. Our present study attempts to investigate the effects of intraventricular administration of nicardipine on mean cerebral blood flow velocity (Vm) as measured by TCD, a surrogate marker for cerebral vasospasm.…”

Factors associated with outcomes in ruptured aneurysmal patients: Clinical Study of 80 Patients

“…However, early treatment (particularly of poor-grade patients) may increase the periprocedural complications beyond the rates reported in the International Cooperative Trial [3][15] [16], and the acutely swollen, soft, hyperemic, poorly autoregulating brain was considered more prone to laceration, contusion, and infarction secondary to retraction [14] [17]. The risk of intra-operative rupture is higher with early surgery, and possible increase incidence of vasospasm following early surgery from mechanotrauma to vessels, thus delayed ischemic neurological deficits can be started promptly [18][19] [20].…”