Hypothesis for lateral ventricular dilatation in communicating hydrocephalus: new understanding of the Monro-Kellie hypothesis in the aspect of cardiac energy transfer through arterial blood flow.

Many theories have been postulated to date regarding mechanisms involved in non-enlargement of the subarachnoid space and enlargement of the ventricles in patients with communicating hydrocephalus, but none have been prove to be definite. Cerebrospinal fluid (CSF) movement is known not to bulk flow but rather pulsatile flow that develops from the energy of the blood flow ejected from the heart, in an isolated system of the intracranial cavity surrounded by a solid skull, as in the Monro-Kellie hypothesis. The authors attempt to explain the mechanisms involved in selective enlargement of the lateral ventricle in patients with communicating hydrocephalus by re-addressing the Monro-Kellie hypothesis with respect to cardiac energy transfer and dissipation by the Windkessel effect. The authors present a concept whereby the large energy of blood flow from the heart that is conveyed to the intracranial artery, arteriole, brain parenchyme, ventricle, and CSF within the confined cranial space as in the Monro-Kellie hypothesis, and which ultimately dissipates to maintain an intracranial energy equilibrium. In the same context, if, for some reason the intracranial equilibrium in the energy transfer and dissipation is changed or disrupted, then structural changes would have to occur to achieve and maintain a new intracranial equilibrium. We postulate that the above described mechanisms are those responsible for the development enlarged of lateral ventricles in patients with communicating hydrocephalus. Structural enlargement of the lateral ventricles in communicating hydrocephalus is a consequence of CSF pathway obstruction and resultantly increased CSF absorption function in the lateral ventricle which markedly increases the pulsatile CSF energy flow returning to the lateral ventricles, thus causing collision of pulsatile CSF flow with the brain parenchyme at the ventricular wall, which subsequently leads to structural enlargement of the lateral ventricles. Also, the collision between the CSF pulsation and brain parenchyme pulsation reduces the Windkessel effect of the brain parenchyme which increases the intracranial artery pulse pressure, which in turn is transmitted to the CSF and increases CSF pulse pressure. This vicious circle results in the high pulse pressure within the lateral ventricle structurally dilating the lateral ventricle. Our theory also explains the relationship between ventricle dilatation and idiopathic intracranial hypertension, venous sinus thrombosis, achondroplasia.