Abstract

Starting in 1984, the technique of angioplasty was no longer confined to only the treatment of peripheral and coronary arteries. In the original paper investigating the technique of angioplasty in cerebral arteries after cerebral vasospasm from aneurysmal subarachnoid hemorrhage (aSAH) , Zubkov et al. found an overall decrease in headaches and focal neurological deficits after the procedure (Zubkov et al, 1984). Despite advances in both medical and endovascular treatment of cerebral vasospasm since then, vasospasm remains a prominent source of morbidity and mortality for patients in the Neuro-Intensive Care Unit. At an estimated incidence rate of 10-28/100000 people, aSAH is associated with a 20% to 40% risk of development of symptomatic, cerebral vasospasm. Of these patients experiencing symptomatic vasospasm, an estimated 10-15% will die before medical therapy while the other 85-90% will have an overall mortality rate of 32-67% (Weant et al, 2010; Frontera et al, 2009). In a review of the literature investigating endovascular treatment of cerebral vasospasm, an absence of standardization is present across these studies. Starting from the basics, the literature has not produced a “gold standard” definition of vasospasm. While some groups define vasospasm by a clinical ,neurological deterioration (Andaluz et al, 2002), others use a variety of diagnostic modalities, such as Transcranial Doppler Velocities (Oskouian et al, 2002), digital subtraction angiography (Frontera et al, 2009), and narrowing of vessel diameter via CT angiography (Coenen et al, 1998), to make the same diagnosis. Therefore, assessing the overall efficacy of angioplasty for cerebral vasospasm is difficult when the literature provides different indications for the same treatment. Once a diagnosis of cerebral vasospasm is confirmed, a lack of standardization continues throughout its treatment. While some groups have associated a good neurological grade

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