Abstract W P370: Is Local Hypoperfusion the Basis of Transient Neurological Deficits After STA-MCA Bypass in Moyamoya Disease?

Abstract

Object: Hyperperfusion is believed to be the cause of transient neurological deficits in patients who have undergone an STA-MCA bypass for Moyamoya disease (MMD). We evaluated this on the basis of cerebral blood flow data from thermal diffusion probes used at our center. Methods: We studied postoperative cerebral perfusion in 31 patients with MMD who underwent a direct STA-MCA bypass. A Hemedex Q500 flow probe (Hemedex, Inc, Cambridge, MA) with a Bowman cerebral perfusion monitor was placed in the frontal lobe adjacent to the bypass, and flow data was analysed using JMP 8.0.2 (SAS Inc., Cary, NC). Seven patients experienced a transient neurological event (TNE) after the left-sided operation, manifesting as dysphasia around 24 hours postoperative and improving by 48 hours. The patterns of median cerebral blood flows with respect to time were plotted for the 3 groups (left side with TNE, the left side with no TNE and the right side) with smoothing by the moving average method. Observations were divided into time blocks (1 = 0-8 hours, 2 = 8-16 hours, 3 = 16-24 hours, 4 = 24-32 hours, 5 = > 32 hours). Differences in median blood flow between various time blocks and between groups were also analysed to evaluate any significant differences. These were correlated with the clinical picture. Results: An average of 20 hours (IQR 10-32 hours) of postoperative flow data was available for each patient. A detailed analysis of 64980 minute-by-minute flow observations shows that the initial post-bypass flow was higher on the left side where TNEs occurred, followed by a widely fluctuating pattern and a sharp drop in the perfusion corresponding with a deficit (p < 0.001, mean difference of flow, t-test) when compared to the other groups where deficits were not observed. Conclusion: Based on our observations we demonstrate a pattern of blood flow that suggests local hypoperfusion as the cause of the deficit on the backdrop of impaired autoregulation and a fluctuating blood flow, contrary to the traditional view that attributes these to hyperperfusion.