Questioning the classical flow of CSF

Data has already been adding up which clarifies the classic model of CSF flow that experts rely on, is not correct.  In almost all modern neuroscience literature, since the original work on hydrocephalus by Dr. Dandy, Dr. Blackfin, and Dr. Cushing, CSF is made by the choroid plexus.   Then CSF flows through the lateral ventricles into the foramen of Monroe, into the third ventricle, through the aqueduct of Sylvius, and into the fourth ventricle where it exits the ventricular system through the foramen of Magendie or Lushka into the cerebral subarachnoid space.  Then the CSF bathes the brain or spinal cord but eventually gets absorbed mostly in the arachnoid granulations, which was originally questioned by Dr. Dandy (2-Dandy) or a small amount through the olfactory lymphatic pathway. (1-Oreskovic)

This is the classical pathway which is still used today to formulate theories on how acute hydrocephalus, NPH, low-pressure hydrocephalus (3-Smalley), pseduotumor cerebri, and other CSF flow abnormalities happen.

However, a lab group in Croatia is strongly questioning the classical pathway, and for good reason.(1-Oreskovic). There group has found:

  1. Upright position creates a sub-atmospheric pressure environment intracranially, and a significantly increased pressure region in the lumbar cistern.  Given the physics of fluid dynamics, shouldn’t normal flow go from the lumbar cistern to the head? (4-Klarica)
  2. Acute hydrocephalus created by sudden blockage of the aqueduct of Sylvius or kaolin injection into the cisterna magna does not lead to increased pressure after 21 days.  How does ventriculomegaly form? (5-Mise)
  3. Heavy water in the ventricles never makes it out of the ventricular system, but is found in the blood stream. While marked-insulin does travel from the ventricles to the subarachnoid space, it probably travels from the subarachnoid space to the ventricles.  This suggests that water and thus CSF is not traveling in a unidirectional fashion as Dr. Dandy described, and macromolecules probably travel in both directions due to diffusion. (6-Bulat)

These experimental findings along with the recent discoveries of the brain lymphatic system, the glymphatic system, MRI phase contrast and time-SLIP studies of CSF flow in-vivo, and anecdotal evidence of patients with complete aqueduct blockages (by pineal region tumors) without acute hydrocephalus, brings a person to wonder, do we really have any understanding of CSF flow dynamics?

References:
1.Orešković D, Radoš M, Klarica M: New Concepts of Cerebrospinal Fluid Physiology and Development of Hydrocephalus. Pediatr Neurosurg:2016
2.Dandy WE: Experimental hydrocephalus. Ann Surg 2:345–351, 1919
3.Smalley ZS, Venable GT, Einhaus S: Low-Pressure Hydrocephalus in Children: a Case Series and Review of the Literature. Neurosurgery, 2017, pp 439–447
4.Klarica M, Radoš M, Erceg G, Petošić A, Jurjević I, Orešković D: The influence of body position on cerebrospinal fluid pressure gradient and movement in cats with normal and impaired craniospinal communication. PLoS ONE 9:e95229, 2014
5.Mise B, Klarica M, Seiwerth S, Bulat M: Experimental hydrocephalus and hydromyelia: a new insight in mechanism of their development. Acta Neurochir (Wien) 138:862–8– discussion 868–9, 1996
6.Bulat M, Lupret V, Orehković D, Klarica M: Transventricular and transpial absorption of cerebrospinal fluid into cerebral microvessels. Coll Antropol 32 Suppl 1:43–50, 2008

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