Is the ischemia found in normal pressure hydrocephalus secondary to venous compression or arterial constriction? A comment on Ohmura et al.

BACKGROUND

In a recent study of normal pressure hydrocephalus published by Ohmura et al., there was a progressive reduction in the cerebral blood volume within the cortex, as measured by near-infrared spectroscopy, following an increase in the intracranial pressure from an infusion study. The authors contend that this reduction in blood volume occurred due to the collapse of the venous structures, starting from the smallest veins adjacent to the capillaries and involving the entire venous outflow tract. We wish to outline some problems with this interpretation.

MAIN BODY

It has been previously shown that venous collapse secondary to an increase in intracranial pressure always starts at the most distal point in the veins. The critical buckling pressure for a tube depends on the cube of the ratio of the wall thickness and the internal diameter. The smallest veins have ratios which are larger than the distal cortical veins, so the latter are the ones to collapse first. The collapse of the distal venous outflow cuff always leads to an increase in the transmural pressure of the veins upstream from it, leading to venous dilatation and not a reduction in venous volume. Only a simultaneous arteriolar constriction of a greater volume than the venous volume increase can account for the progressive reduction in blood volume, which occurs once the ICP is greater than the sinus outflow pressure in normal pressure hydrocephalus.

CONCLUSIONS

The reduction in cerebral blood volume which occurs in the cortex in normal pressure hydrocephalus cannot be due to widespread venous collapse. Therefore, there must be a large component of arteriolar constriction accompanying this disease.