Extending the hydrodynamic hypothesis in chronic hydrocephalus

Abstract

Dear Editor: I greatly enjoyed reading the review article and the theories put forward by Dr. Greitz [6] regarding the pathophysiology of hydrocephalus as well as the subsequent editorials and follow-up letter from Dr. Greitz [7]. Essentially, Dr. Greitz proposes a hydrodynamic theory for the pathophysiology of chronic hydrocephalus. This involves a reduction in the compliance of the arterial tree with, as a consequence, the subsequent failure of arterial pulse pressure dampening. This would cause an elevation in arteriolar and capillary pulse pressure and induce a hyperdynamic brain parenchymal pulsation, which in turn would compress the ventricular system, leading to hyperdynamic aqueduct flow and water-hammer dilatation of the ventricular system. I fully agree with this portion of the hypothesis but note, as the editorials did, that it does not go far enough in that it fails to answer the problems of the failure of bulk flow of CSF. I believe that the answer lies in what causes the reduction in arterial compliance and what other effects this reduction in compliance would have on the venous system and the CSF outflow through the arachnoid granulations. Dr. Greitz does not fully address where the reduction in compliance resides. If it were an intrinsic problem with the walls of the arterial tree (say, atherosclerosis or atheroma), then it is difficult to see why normal pressure hydrocephalus would not be a much more wide spread disease than it is. If, as I have argued, the reduction in compliance is in the walls delimiting the subarachnoid space [1] (the so-called walls of the container) then the result on the arterial tree would be the same as if the artery walls themselves were stiffer. This is because the arteries can only expand into the space made available by the shifting of CSF (water is incompressible), if the walls of the container are stiff and there is nowhere for the CSF to shift to, then the arteries also fail to expand. The benefit of moving the reduction in the compliance from the walls of the arteries to the walls of the container is that we can also begin to explain the other manifestations of chronic hydrocephalus. It has long been known that the compliance of the walls of the container has a direct effect on the apparent resistance to CSF resorption across the arachnoid granulations with, for example, experimentation on cats showing a significant reduction in CSF pressure from craniectomy [9]. In humans, craniectomy is performed for raised intracranial pressure and even in those with an obvious CSF resorption abnormality a percentage will go on to develop the “syndrome of the trephined”, which is a physiological state of reduced CSF pressure and low-pressure symptoms [5]. How can compliance affect the resistance to CSF flow across the arachnoid granulations? The answer is that it cannot affect resistance but can interact with impedance. I have argued that if the resistance to non-pulsatile flow across the arachnoid granulations were low but the walls of the granulations were rigid (a high percentage of collagen) then their impedance to pulsatile flow would be high [3]. A reduction in the CSF pulse pressure as occurs in craniectomy would reduce the overall “apparent” resistance to CSF outflow by minimising the effect of the high impedance and as a corollary an increase in CSF pulse pressure as is noted in hydrocephalus [4] (secondary to the reduction in dampening afforded by the walls of the container) would increase the apparent resistance to CSF flow by making the intrinsic high impedance of the granulations interact with a more pulsatile flow. It remains to be explained why CSF preferentially appears to be resorbed through the walls of the ventricular system into the deep brain parenchyma and not into the much larger capillary bed afforded by the cortex. The effect of a reduction in compliance does not just affect the arterial tree. The venous system also passes through the subarachG. A. Bateman (*) Department of Medical Imaging, John Hunter Hospital, Locked Bag 1, Newcastle Region Mail Centre, Newcastle 2310, Australia e-mail: grant.bateman@hnehealth.nsw.gov.au Tel.: +61-2-49213414 Fax: +61-2-49213428