Cerebral blood flow response to neural activation after acute ischemic stroke: a failure of myogenic regulation?

We tested two hypotheses: (1) neurovascular coupling is impaired after acute ischemic stroke, (2) subcomponent analysis of cerebral blood flow velocity can reveal significant differences between acute ischemic stroke and healthy controls. This was explored through the comparison of nineteen acute ischemic stroke patients with healthy controls. Recordings of cerebral blood flow velocity, blood pressure and end-tidal CO₂ were obtained during 60s of passive elbow flexion. Cerebral blood flow velocity changes were decomposed into standardized subcomponents describing the contributions of blood pressure (V _BP), resistance area product (V _RAP) and critical closing pressure (V _CrCP). The passive paradigm led to a bilateral cerebral blood flow velocity increase in both groups, but in acute ischemic stroke the magnitude of change was significantly lower. Blood pressure increases were shown to be an important contributor to cerebral blood flow velocity response throughout the paradigm in both groups, with no significant difference between groups. The V _CrCP contribution was not different between groups or hemispheres; its continuous rise during activation indicating a vasodilatory effect. On the other hand, the V _RAP contribution showed significant differences (p = 0.03), thus suggesting myogenic impairment in acute ischemic stroke. Cerebral blood flow velocity responses to passive elbow flexion suggest an impairment of neurovascular coupling in acute ischemic stroke. Subcomponent analysis suggests an impairment of the myogenic pathways, giving a greater insight into the different mechanisms contributing to neurovascular coupling. Further research is needed to assess the clinical value of subcomponent analysis of neurovascular coupling and the natural history of such changes following acute ischemic stroke.