Objective

Neurovascular coupling enables rapid adaptation of cerebral blood flow (CBF) to support neuronal activity. Modern techniques enable the simultaneous recording of neuronal activities and hemodynamic parameters. However, the causal relationship between electrical brain activity and CBF is still unclarified. In this study, we investigated the causal relationship between surface electroencephalogram (EEG) and cerebral blood flow velocity (FV) from transcranial Doppler using Granger causality (GC) analysis.

Approach

Twenty simultaneous recordings of EEG and FV from 17 acute ischemic stroke patients were studied. Each patient had simultaneous, continuous monitoring of EEG and bilateral FVs in either the middle cerebral arteries or posterior cerebral arteries. The causal interactions between FV (0.006-0.4 Hz) and EEG (delta, theta, alpha, beta and gamma bands) were investigated through GC index (GCI). In order to make the GCIs comparable, the proportion of GCI (PGCI) values where G-causality is statistically significant were calculated. Scores on the NIH Stroke Scale (NIHSS) and the modified Rankin Scale (mRS) for neurologic disability were recorded respectively at discharge. Patients were divided into a deceased (mRS = 6) and a survival group (mRS = 1 to 5), and a favorable (mRS: 1 to 2) and unfavorable outcome group (mRS: 3 ~ 6).

Main results

This study identified a causal relationship from EEG→FV, indicating EEG contained information that can be used for FV prediction. PGCI was negatively related with mRS (p < 0.05), indicating that stronger causalities between EEG and FV exist in patients with better outcome. The NIHSS was negatively related with the asymmetry of the two-side PGCI, calculated as the difference between the lesional side and non-lesional side PGCI.

Significance

A causal relationship from EEG→FV may exist in patients with ischemic stroke. The strength of G-causality may be related to stroke severity at discharge.

PURPOSE: Current studies on endovascular intervention for intracranial atherosclerosis select patients based on luminal stenosis. Coronary studies demonstrated that fractional flow measurements assess ischemia better than anatomical stenosis and can guide patient selection for intervention. We similarly postulated that fractional flow can be used to assess ischemic stroke risk. METHODS: This was a feasibility study to assess the technical use and safety of applying a pressure guidewire to measure fractional flow across intracranial stenoses. Twenty patients with severe intracranial stenosis were recruited. The percentage of luminal stenosis, distal to proximal pressure ratios (fractional flow) and the fractional flow gradients across the stenosis were measured. Procedural success rate and safety outcomes were documented. RESULTS: All 20 patients had successful crossing of stenosis by the pressure guidewire. Ten patients underwent angioplasty, and 5 had stenting performed. There was one perforator stroke, but not related to the use of the pressure wire. For the 13 patients with complete pre- and postintervention data, the mean preintervention stenosis, fractional flow and translesional pressure gradient were 76.2%, 0.66 and 29.9 mm Hg, whilst the corresponding postintervention measurements were 24.7%, 0.88 and 10.9 mm Hg, respectively. Fractional flow (r = -0.530, p = 0.001) and the translesional pressure gradient (r = 0.501, p = 0.002) only had a modest correlation with the luminal stenosis. CONCLUSION: Fractional flow measurement by floating a pressure guidewire across the intracranial stenosis was technically feasible and safe in this study. Further studies are needed to validate its use for ischemic stroke risk assessment.