Rethinking the Collateral Vasculature Assessment in Acute Ischemic Stroke

Abstract

Occlusion of a cervical or cerebral artery results in disruption of blood flow to the brain and may result in irreversible infarction. Intracranial pial collaterals are a network of arteries that may preserve blood flow to otherwise critically hypoperfused brain areas until vessel recanalization is achieved. The robustness of these arterial collaterals is pivotal for the survivability of ischemic brain tissue and is associated with treatment success and long-term clinical outcome. More recently, the importance of venous outflow from ischemic brain tissue has been appreciated. Arterial collaterals and venous outflow are evaluated by neuroimaging parameters, and recent imaging advances have enabled a more comprehensive assessment of the entire collateral cascade in patients with acute ischemic stroke. Here we review novel imaging biomarkers for the assessment of arterial collaterals, tissue-level collateral blood flow, and venous outflow. We also summarize how a more comprehensive assessment of the cerebral blood flow leads to a better prediction of treatment efficacy and improved clinical outcomes.

Favourable arterial, tissue-level and venous collaterals correlate with early neurological improvement after successful thrombectomy treatment of acute ischaemic stroke

“…Our findings may also have practical implications for the future assessment of patients with AIS-LVO undergoing thrombectomy triage. Although the specific mechanisms of how each of the three collateral parameters impact procedural and clinical outcomes need further investigation, our findings imply that arterial, tissue-level and venous collaterals may influence clinical recovery after thrombectomy treatment in different manners 28. Our results suggest that PAC predominantly influence whether the ischaemic tissue will be able to recover significantly.…”

Hyperacute Perfusion Imaging Before Pediatric Thrombectomy

“…Because HIR interrogates the ischemic region itself, it is considered a tissue-level marker of cerebral collateral microcirculation and may be more important to tissue fate than the visible filling of angiographic collaterals postocclusion on CTA. 25,26 While over half of our cohort (8/15) had poor angiographic collaterals, by contrast, HIR was favorable in most patients; of interest, when HIR was defined as the ratio of Tmax>10/Tmax>4, all patients then qualified as favorable, suggesting that this ratio may not be an optimal marker of intrinsic collateral integrity. Reasons for the discrepancy between arterial and tissue-level collateral status in our cohort are unclear.…”

Severe hypocalcemia as a cause of transient ischemic attack? A debatable case and evidence from literature

“…Low blood flow in the brain below [10][11][12][13][14][15] Case Report mL/100gr/min will provoke ischemia [20]. If the blood flow to the brain is reduced to 6-8 mL/100gr/min, there will be a disturbance in the adenosine triphosphate (ATP) pump causing an increase in extracellular potassium, intracellular calcium, and cellular acidosis leading to histologic cell necrosis [21]. The accumulation of intracellular calcium may cause neuronal damage by initiating cytotoxic processes that lead to cell death [18,22].…”