Neurology India, Vol. 58, No. 3, May-June, 2010, pp. 339-340
Another small step toward understanding hydrocephalus
Jogi V Pattisapu
University of Central Florida College of Medicine, Emeritus Medical Director, Pediatric Neurosciences, Arnold Palmer Hospital for Children, 83. W. Columbia St. Orlando, FL - 32806, USA
Date of Acceptance: 17-Jun-2010
Code Number: ni10094
I congratulate the authors on a well-executed study of the cerebrospinal fluid (CSF) absorption in a canine model of kaolin-induced hydrocephalus using tritiated H20 absorption into the bloodstream in acute and chronic phases of the condition.  It was refreshing to correlate newer findings with our age-old understanding of CSF circulation in mammals.
This experiment studied the presumed absorption of CSF via the arachnoid villi, while the major nasal output pathway was surgically blocked.  Magnetic resonance imaging confirmed hydrocephalus after suboccipital kaolin injection, and 1 ml tritiated H20 was injected into the subarachnoid spaces at 3 days, 2 weeks, and 12 weeks to assess its concentration in blood up to 48 h afterward. Interestingly, the chronic condition seemed to have the most effect, at least early (<16 h postinjection), whereas less CSF flow is suggested during the earlier stages. This interesting finding raises questions of primary CSF absorption via the arachnoid villi, in the acute conditions of increased intracranial pressure (ICP).  Perhaps similar mechanisms for normal pressure hydrocephalus should be considered based on these results. 
In many animal models after kaolin injection, ICP raise occurs over 1-2 weeks, where a delayed absorption defect occurs, presumably due to fibrosis causing increased resistance to flow.  Unfortunately, ICP measurements were not available, which might correlate with CSF flow rates suggested by this study. Other studies using kaolin have identified alterations/fibrosis around the superior sagittal sinus (after suboccipital injection), which might alter the findings in this experiment.  The reader is advised to consider these factors as additional sources for finding of tritiated H20 in this study.  Also, because many canine species develop syringomyelia with hydrocephalus (perhaps as a compensatory mechanism), evaluation of lumbar CSF for tritiated H20 concentration might offer interesting correlation with blood levels.  Transventricular CSF outflow may account for some of the findings (especially using this model of nasal pathway obstruction), and should be considered as an alternative source of blood tritiated H20.
The authors commented on multiple reasons that partially explain their findings, which should stimulate the readers' thinking into our current understanding of CSF circulation.  Several factors, including arachnoid villi fibrosis, hypoxia, lumbar CSF absorption, growth factors, and parenchymal fluid absorption via aquaporins were suggested. However, because aquaporins are upregulated in the subependymal and subpial regions in hydrocephalus, one should consider this avenue for CSF absorption more closely, especially involving transparenchymal route into the bloodstream. Several potential drug treatment options should be considered using these concepts.
Once again, this study  emphasizes the need to question our understanding of CSF circulation in view of acceptable data suggesting that multiple absorption pathways play key roles at various stages of the hydrocephalic condition.
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