There Is No Transmantle Pressure Gradient in Communicating or Noncommunicating Hydrocephalus

Abstract

This study demonstrates no factual support for existence of a transmantle pressure gradient in nonacute communicating or noncommunicating hydrocephalus.

New experimental model of acute aqueductal blockage in cats: Effects on cerebrospinal fluid pressure and the size of brain ventricles

“…3) in the isolated brain ventricles in our model cannot be easily incorporated into the classical hypothesis, but are rather consistent with our recently established observations which indicate that the CSF volume accumulation does not take place inside the brain ventricles under physiological pressure (Orešković et al, 2001;Orešković et al, 2002). Thus, the results observed in this study, as well as the results of some clinical and experimental studies (Holtzer and de Lange, 1973;Stephensen et al, 2002;Orešković et al, 1991) suggest that CSF volume under physiological pressure is constant within isolated ventricles, i.e. that the CSF formation and absorption in the ventricles are in balance.…”

Development of hydrocephalus and classical hypothesis of cerebrospinal fluid hydrodynamics: Facts and illusions

“…This consideration is supported by the observations that in patients with communicative and non-communicative hydrocephalus, transmantle pressure is absent (Stephensen et al, 2002). All of the evidence supports the idea that the transmantle pressure gradient may not be necessary or instrumental for the development of hydrocephalus, and that some other factors such as an increase in the ventricular CSF pulse pressure without affecting the CSF pressure (Di Rocco et al, 1978), an impairment of systolic-diastolic displacement of the CSF with the development of periventricular ischemia (Miše et al 1996), changes in the arterial pulsations (Greitz, 2004 and, an increase in ventricular CSF osmolarity without affecting the CSF pressure (Krishnamuthy et al, 2009), and venous compliance (Bateman, 2000 and2003) may play an important role in the development of that pathological process (see Section 8.…”

“…It is equally unclear if the pressure gradient can really be the fundamental mechanism of hydrocephalus development, regardless of whether it is low (Conner et al, 1984;Hakim and Hakim, 1984;Levine, 2008;Penn et al, 2005) or high (Kaczmarek et al, 1997;Nagashima et al, 1987;Smillic et al, 2005). There are, nevertheless, some other authors who believe that a CSF pressure gradient is not possible within the cranium firmly enclosed by bones, mostly because they did not observe such a gradient neither in experiments involving animals (Shapiro et al, 1987) nor in patients with communicating or non-communicating hydrocephalus (Stephensen et al, 2002).…”

The formation of cerebrospinal fluid: Nearly a hundred years of interpretations and misinterpretations

“…However, during a prolonged occlusion or stenosis of the aqueduct, the development of a ventricular dilatation probably without an increase in the ventricular pressure should be expected. This idea is supported by the observation that in patients with communicative and non-communicative hydrocephalus the transmantle pressure is absent (Stephensen et al, 2002). Furthermore, Holtzer and de Lange (1973) observed in some children with communicative and noncommunicative hydrocephalus that after the shunt obstruction the hydrocephalus did not progress suggesting that this pathological process was compensated.…”

“…There are, nevertheless, some other authors who believe that CSF pressure gradient is not possible within the cranium firmly enclosed by bones, mostly because they did not observe such a gradient neither in experiments involving animals (Shapiro et al, 1987) nor in patients with communicating or non-communicating hydrocephalus (Stephensen et al, 2002).…”