Communicating hydrocephalus: the biomechanics of progressive ventricular enlargement revisited.
BACKGROUND
This article investigates the physical mechanisms involved in the chronic ventricular enlargement that accompanies communicating hydrocephalus (CH)--including its normal and low-pressure forms. In particular, it proposes that this phenomenon can be explained by the combined effect of: (a) a reversal of interstitial fluid flow in the parenchyma, and (b) a reduction in the elastic modulus of the cerebral mantle.


METHODS
To investigate this hypothesis, these changes have been incorporated into a finite element computer simulation of CH, in which brain tissue is idealized as a sponge-like material. The fluid pressure in the lateral ventricles and the subarachnoid space has been set to 10 mmHg, while the fluid pressure inside the parenchyma has been set to 7.5 mmHg. The elastic moduli of white and gray matter have been set to the reduced values of 1 and 5 kPa, respectively.


RESULTS
The simulation revealed a substantial ventricular distension (6.5 mm mean outward displacement), which was accompanied by the appearance of stress concentrations in the cerebral mantle.


CONCLUSIONS
These results support the notion that a relative reduction in intraparenchymal fluid pressure coupled with low tissue elasticity can produce both a significant ventricular enlargement and periventricular solid stress concentrations.
Peña
A
A
Academic Neurosurgery Unit, University of Cambridge, UK.
Harris
N G
NG
Bolton
M D
MD
Czosnyka
M
M
Pickard
J D
JD
D001696:Biomechanical Phenomena; D001921:Brain / Q000503:physiopathology; D002552:Cerebral Ventricles / Q000473:pathology* / Q000503:physiopathology*; D002555:Cerebrospinal Fluid / Q000502:physiology; D006801:Humans; D006849:Hydrocephalus / Q000145:classification / Q000473:pathology / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000502:physiology*