Intracranial Collaterals in Acute Stroke and Clinical Outcome

Intracranial collaterals Assessment in acute ischemic stroke In clinical practice, infarct growth does not always progress to involve the full extent of the vascular territory, even if the affected intracranial artery fails to recanalize. The presence and recruitment of various collateral channels are believed to be responsible for this phenomenon in acute ischemic stroke (AIS). These collaterals may also play an important role in influencing the safety and efficacy of acute revascularization approaches. Although blood supply from the leptomeningeal collaterals may temporarily maintain the ischemic penumbra, the persistence and effectiveness of this alternative circulatory supply is erratic and unpredictable. Some collaterals may disappear over time (collateral failure); this is one of the mechanisms responsible for clinical deterioration following initial improvement.

Conversely, dramatic resolution of initial neurologic deficits may be seen though the occluded intracranial artery did not recanalize, often attributable to the rapid improvement of cerebral perfusion via effective collateral pathways (collateral recruitment). Therefore, the temporal behavior of intracranial collaterals may play an important role in determining the functional outcome in AIS patients.

CT angiography (CTA) of the brain is acutely performed in AIS patients before or immediately after administering IV tissue plasminogen activator (tPA) The Alberta Stroke Program Early CT (ASPECTS) leptomeningeal collaterals score on CT-angiography helps in prognosticating functional outcome in acute ischemic stroke (AIS) patients treated with intravenous thrombolysis. Leptomeningeal collaterals in AIS are dynamic, especially during the first few hours or days of AIS.

In animals, 3 different types of collaterals have been identified: transient collaterals that could be seen immediately after the stroke and last less than 90 minutes; impermanent collaterals that disappear after 90-150 minutes; and persistent collaterals, which can be seen for longer periods.

Patients with good collateral flow demonstrated less hypo perfused tissue and less infarct growth within the penumbra zone than those with poor collateral . A relationship is found between good early collaterals on pretreatment imaging and smaller infarct volume with better outcomes.

The initial state of the collateral circulation on the pretreatment CTA also has bearing on the clinical effect of the collateral recruitment on the day 2 CTA.

However, collateral recruitment with poor pretreatment collaterals was associated with poor functional outcome at 3 months and a higher risk of intracranial hemorrhage.

One plausible mechanism that delayed collateral recruitment lead to worse outcomes could be related to the maximal vasodilation in the ischemic area and how collateral recruitment in the adjacent regions may trigger a steal-like phenomenon with resultant expansion of the ischemic core. Another possible mechanism could be related to failed autoregulation in the affected vascular territory, leading to increased hyper perfusion damage with a higher chance of bleeding.

IInclusion Criteria:

• Patient presenting to the emergency department with symptoms consistent with ischemic stroke.
• Age > 18 yrs.
• Evidence of a visible and symptomatic intracranial occlusion on baseline CT-angiography (intracranial ICA, M1 MCA segment +/- intracranial ICA, proximal M2 MCA).
• Treatment with IV tPA.

Exclusion criteria

• Intracranial hemorrhage (ICH) identified on baseline CT.
• Previous moderate to large stroke in the ipsilesional hemisphere.
• Modified Rankin Scale > 2 at baseline.
• Unable to have CT-angio performed due to recent estimated creatinine clearance eCCr<60 ml/min, contrast allergy or other reasons.
• Any terminal illness (patient not expected to survive > 1 year).