The major determinant of clinical recovery in acute ischaemic stroke is early reperfusion of the ischaemic penumbra. To this end, the advent of thrombolytic therapy is driving major reorganisations in acute stroke services with many more patients presenting to hospital earlier. This, coupled with major advances in brain imaging techniques, means that opportunities to improve understanding of the pathophysiology of acute stroke in the clinical setting now exist. Both CT and MR based structural and perfusion imaging are increasingly used in treatment decisions and have been used to demonstrate the contribution of indices such as age, hyperglycaemia, haematocrit and oxygen to penumbral tissue fate.1

A unique insight into the possible role of the cerebral collateral circulation in this process is provided in this issue of J Neurol Neurosurg Psychiatry (see page 625).2 Here, an analysis of collateral flow grade was made using a standardised scale on angiograms performed within 6 h of acute middle cerebral artery (MCA) territory stroke in patients recruited to the MERCI acute stroke trial.3 The penumbra and final volume of infarction were determined with MR imaging parameters. Not surprisingly, the greatest infarct growth occurred in patients who both failed to recanalise and had the poorest pretreatment collateral flow. The pretreatment collateral grade however was an independent predictor of infarct growth after multiple regression analysis and an important addition to the list.

In general, the role of collateral flow in response to ischaemia will depend on the location of the occluded vessel, the original “set up” determined developmentally and any physiologically relevant collateral supply to the penumbral zone.4 It is well known that cerebral vascular anatomy is variable with frequent asymmetry. Cerebral collaterals are either long and thin leptomenigeal vessels (pial) or shorter “bypass” segments across the circle of Willis, making responses to vascular occlusion complex.5 It is very unlikely that collaterals play any significant role in cortical branch or lacunar infarctions as these sites are too distal. With more proximal occlusions (eg, proximal MCA), flow is generally diverted retrogradely via collaterals to supply adjacent ischaemic tissue—changes driven mainly by the major haemodynamic shifts precipitated by the immediate collapse in perfusion distal to the occlusion. It is likely that angiogenic factors play an additional secondary signalling role. In the context of an acute occlusion given the length and tortuosity of these vessels and the supply of progressively deoxygenated blood from retrograde flow, it is likely that any effect on cerebral perfusion and penumbral tissue survival will be brief. In effect, good collaterals buy more time for successful recanalisation. Whether “collateral therapies” are worth pursuing is debatable but in current clinical practice simple measures that may assist any collateral supply such as oxygenation, intravenous fluid replacement, blood pressure control and head positioning should not be forgotten. In future acute stroke trials, non-invasive imaging of the vascular anatomy to assess both occlusion site/recanalisation and pretreatment collaterals (eg, with CT perfusion source images) in addition to regions of cortical mismatch would be informative additions.