Every year in the US there are approximately 30,000 reported cases of aneurysmal subarachnoid hemorrhage (SAH), accounting for 5% of all strokes.^1–3 Mortality has been documented in the range of 20–40% and over 40% experience long-term deficits.^2,4,5 Although SAH is less common than diseases such as ischemic stroke and heart attack, it affects a younger population and contributes to a disproportionately high ratio of long-term disability after stroke. SAH is responsible for 27% of all strokerelated potential life-years lost before 65 years of age.⁶ Long-term neurological injuries in SAH arise from the acute injuries due to sudden aneurysm rupture and, in a significant fraction of SAH patients, secondary neurological injuries due to delayed cerebral vasospasm. Past literature has often referred to this secondary neurological insult as delayed cerebral ischemia (DCI). Recent studies on vasospasm have demonstrated that DCI, defined differently in various studies, likely includes both reversible states of cerebral ischemia and completed strokes. As a result, current literature has moved away from using the term DCI in studying SAH and vasospasm.

The definition of vasospasm is variable in the literature. Guidelines from the American Heart Association (AHA) in 2009 defined cerebral vasospasm as “the delayed narrowing of large-capacitance arteries at the base of the brain.”³ Onset of vasospasm has been reported to occur somewhere between days four and 15 post-SAH.^5,7 There are various diagnostic criteria for cerebral vasospasm following SAH. Symptomatic or clinical vasospasm is often defined as neurological deterioration of greater than 2 points in the Glasgow Coma Scale without apparent etiology other than cerebral ischemia.⁸ In these cases, delayed symptomatic vasospasm has also been referred to as DCI and is reported to occur in 15–40% of patients after aneurysmal SAH.^3,9 Vasospasm can be defined by transcranial Doppler ultrasonography (TCD) criteria; most centers use a Lindegaard ratio of >3–4.5 to indicate mild, 4.5–6 to indicate moderate, and >6 to indicate severe vasospasm in the anterior circulation. Vasospasm as recorded by TCD is reported to occur in 46–70% of patients after SAH, and is defined by either peak or mean flow velocity.^4,7 Four-vessel diagnostic cerebral angiography is currently the gold standard for radiographic detection of vasospasm, and angiographic vasospasm has been documented to occur in 30–70% of patients after aneurysmal SAH (see Figures 1 and 2).³ Other radiographic diagnostic modalities such as computed tomography angiography (CTA) and perfusion magnetic resonance imaging (MRI) with angiography are also used to detect vasospasm.

To View full article : register here