Neocortical Capillary Flow Pulsatility is Not Elevated in Experimental Communicating Hydrocephalus

Abstract

While communicating hydrocephalus (CH) is often characterized by increased pulsatile flow of cerebrospinal fluid (CSF) in the cerebral aqueduct, a clear-cut explanation for this phenomenon is lacking. Increased pulsatility of the entire cerebral vasculature including the cortical capillaries has been suggested as a causative mechanism. To test this theory, we used two-photon microscopy to measure flow pulsatility in neocortical capillaries 40 to 500 μm below the pial surface in adult rats with CH at 5 to 7 days (acute, n=8) and 3 to 5 weeks (chronic, n=5) after induction compared with intact controls (n=9). Averaging over all cortical depths, no increase in capillary pulsatility occurred in acute (pulsatility index (PI): 0.15±0.06) or chronic (0.14±0.05) CH animals compared with controls (0.18±0.07; P=0.07). More specifically, PI increased significantly with cortical depth in controls (r=0.35, P<0.001), but no such increase occurred in acute (r=0.06, P=0.3) or chronic (r=0.05, P=0.5) CH. Pulsatile CSF aqueductal flow, in contrast, was elevated 10- to 500-fold compared with controls. We conclude that even in the presence of markedly elevated pulsatile CSF flow in the aqueduct, there is no concurrent increase in microvascular pulsatile flow.