Development of cerebral collaterals is a dynamic process and cannot be described with a snapshot imaging. Furthermore in hyperacute stroke presence of collaterals harbors potential for the penumbral preservation until chemical or mechanical revascularization and the absence of collateral pathways can increase risk of hemodynamic compromise in patients with stroke.
This interesting retrospective analysis evaluated 68 patients with symptomatic ICA occlusion. Risk factors for recurrent ipsiateral ischemic event and TCD flow patterns were evaluated. 14 (20.6 %) patients at a median time of 29.5 days (IQR 8 – 89) during the median follow up of 6 months (IQR 4 – 24) had ipsilateral ischemic event.
TIA and DM were as expected predictive of recurrent event, as described in ABCD2 score. Interestingly, Stroke was not. Also usual suspects such as smoking, A-Fib, HTN etc. were not associated with ischemic event. Shockingly, use of statin and antiplatelets was associated with ischemic events.
Presence all four collateral pathways (ACoA, PCoA, LM, OA) was associated with ischemia. What does this mean? Maybe population with ischemic events has baseline more atherosclerosis and previously established collaterals. It is hard to find explanation. Increase in P2 velocities may be predictive of presence of secondary collateral pathways, but wouldn’t we expect increase in velocities of contralateral MCA and contralateral or both A2 segments as well?
It is hard to make conclusions from this retrospective study with small number of patients, but I command investigators for raising awareness of potential use of neurosonology in the management of patients with stroke. Application of neurosonology (Carotid duplex, TCD, TCI) can be challenging in the community because this methodology is operator dependent, however it can be invaluable in established and accredited laboratories.
In my opinion this article highlights one thing, TIA is a neurologic emergency and our opportunity to change long-term outcomes.