Modification of LowFrequency Spontaneous Oscillations in Blood Flow Velocity in Large‐ and Small‐Artery Disease

During a 30‐m mute period, the blood flow velocity of both middle cerebral arteries (MCAs) was measured bilaterally in 27 patients with obstructive carotid disease (n = 18, large‐artery disease) or subcortical vascular encephalopathy (n = 9, smallartery disease) and in control subjects of similar age and sex distribution (n = 14) To identify low‐frequency spontaneous oscillations (LFSOs), MCA envelope curves were Fourier transformed with filter application to select low‐frequency spectra (0.01–0.05, 0.05–0.15, 0.15–0.50 Hz) To measure the extent of LFSO amplitudes, a coefficient of variation (CoV) was calculated. In addition, a coefficient of correlation (CoC) was calculated to assess LFSO bilateral synchron1c1ty. Normal ranges for CoV (mean = 5.38 ± 1.82%) and CoC (mean = 0.91 ± 0.06) were established in control subjects. In patients with large‐artery disease, a significant CoV reduction was observed Ipsilateral to the carotid lesion (CoV mean = 3.91 ± 1.10%, p < 0.05, Wilcoxon's test) with a contralateral compensatory mcrease (CoV mean = 5.68 ± 1.79%) In addition, a significant desynchronlzation of LFSOs was found in patients w1th large‐artery disease (CoC = 0.39 ± 0.35, p < 0.05). This was less obvious in patients with small‐artery d1sease, who demonstrated a marked bilateral reduct1on of LFSO activity (CoV mean = 3.60 ± 0.71%, p < 0 05) and CoC values. Presuming that LFSOs reflect cerebral blood flow fluctuations caused by phasic arteriolar dilation and contraction, CoV and CoC values indicate integrity versus compromise and exhaustion of arteriolar regulation or compromised vascular reserve capacity in patients with extensive obstructive disease and, for the first time, in patients with small‐artery disease too. This is important as no other method is presently available to record vasomotor function in the arteriolar network.