JOURNAL ARTICLE
Add like
Add dislike
Add to saved papers

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.

Medical Hypotheses 2009 Februrary
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.

Full text links

For the best experience, use the Read mobile app

Group 7SearchHeart failure treatmentPapersTopicsCollectionsEffects of Sodium-Glucose Cotransporter 2 Inhibitors for the Treatment of Patients With Heart Failure Importance: Only 1 class of glucose-lowering agents-sodium-glucose cotransporter 2 (SGLT2) inhibitors-has been reported to decrease the risk of cardiovascular events primarily by reducingSeptember 1, 2017: JAMA CardiologyAssociations of albuminuria in patients with chronic heart failure: findings in the ALiskiren Observation of heart Failure Treatment study.CONCLUSIONS: Increased UACR is common in patients with heart failure, including non-diabetics. Urinary albumin creatininineJul, 2011: European Journal of Heart FailureRandomized Controlled TrialEffects of Liraglutide on Clinical Stability Among Patients With Advanced Heart Failure and Reduced Ejection Fraction: A Randomized Clinical Trial.Review

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

Read by QxMD is copyright © 2021 QxMD Software Inc. All rights reserved. By using this service, you agree to our terms of use and privacy policy.

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app