Elsevier

Medical Hypotheses

Volume 77, Issue 6, December 2011, Pages 1074-1078
Medical Hypotheses

A physics link between venous stenosis and multiple sclerosis

https://doi.org/10.1016/j.mehy.2011.09.006Get rights and content

Abstract

This paper hypothesizes that a stenosis or obstruction at a lower extremity of an internal jugular vein (IJV) would, in accordance with the physics of fluid dynamics, cause a standing pressure wave within the vein. This pressure wave would possess regions of large pressure fluctuations and other regions of relatively little fluctuation which also have substantially lower peak pressure values. If the wavelength of the hypothesized pressure wave is comparable to the distance from the obstruction to the venule end of the capillary bed, then a region of high pressure fluctuation would exist at the venules. Depending on the degree of obstruction, the pressure fluctuations at the venules of the capillary bed would be substantially greater than those that would exist in a healthy unobstructed vein. This increase in blood pressure fluctuation located at the venule end of the capillary bed, which would be equivalent to local hypertension, is predicted to reduce the pressure drop across the bed which, in turn, would reduce blood flow through the bed in accordance with Darcy’s Law. Such a reduction in blood flow through the bed would be accompanied by a reduction in the transfer of oxygen, glucose and other nutrients into the brain tissue in accordance with Fick’s Principle. The reduction in oxygen levels in the brain tissue (i.e. hypoxia), would, in turn, be associated with increased fatigue and decreased mental acuity in the subject patient. Also the deprivation of oxygen in the brain tissue may result in the death of oligodendrocyte cells, which, in turn would result in the deterioration of the myelin surrounding the brain’s neural axons.

In addition, the paper also predicts that, in cases of extreme obstruction, the predicted localized hypertension at the venule end of the capillary bed may be sufficiently high to cause a localized disruption in the blood–brain barrier. Such a disruption of the blood–brain barrier could then allow the migration of leukocytes (auto-immune attack cells), from the blood into the brain tissue, enabling them to attack myelin, which has degenerated or deteriorated from the reduction in repair function normally provided by oligodendrocyte cells. Such leukocyte attack on myelin has long been associated with multiple sclerosis.

Introduction

The positive correlation between cerebrospinal venous stenosis and multiple sclerosis as reported initially by Zamboni et al. [1], [2] and subsequently by other medical research teams [3], [4], has received considerable attention and also criticism [5], [6] within the community of MS researchers and patients. Since Zamboni’s initial publications appeared, blocked veins and venous blood reflux have been observed in thousands of MS patients. Endovascular angioplasty techniques have been used to clear vein blockages in many patients in many facilities around the world. The scientific and popular presses, and many internet sites, offer myriad anecdotal results of the angioplasty procedure that describe substantial changes in symptoms such as reductions in chronic fatigue and improvement in mental clarity. To date no adequate description of any cause and effect relationship between venous stenosis, brain functions and multiple sclerosis is yet available.

Section snippets

The hypothesis

This paper applies the physics of fluid dynamics to address a potential relationship between internal jugular vein (IJV) obstructions, brain functions, chronic fatigue and multiple sclerosis. To illustrate the basic principle, the condition is modeled, using the physics of fluid dynamics, as a pressure wave in a fluid-filled tube that has a blockage at one end. The fluid dynamics model is then extended to address blood pressure pulsation in an internal jugular vein when the vein is obstructed

Fluid pressure superposition

If a fluid is contained within a tube, and if pressure pulses or waves are introduced simultaneously into opposite ends of the tube, then these pressure waves propagate in opposite directions along the tube. As they pass through one another the pressures are additive. Hence, the total pressure at a particular time and point in the tube is the sum of the two individual pulse pressures at that time and point. In fluid mechanics this is referred to as the Principle of Superposition. Graphic

Standing pressure waves in open and blocked tubes

If a periodic pulsatile fluid pressure wave is introduced into the open end of a tube that has a blockage at the other end, it propagates down the tube, and when that wave strikes the blocked end it must propagate back toward the input end in order to preserve mass continuity. If the time between peaks in the pressure wave is equal to the time taken for the wave to propagate from the input end to the blocked end, then the condition known as “resonance” occurs. Such resonance implies that a

Pulses in internal jugular veins

Consider the case of a blood pulse entering an internal jugular vein from the venule end of the capillary bed. Typically an internal jugular vein is about 15 cm long and the rate of blood flow is typically about 15 cm/s. Hence, it takes about one second for the blood pulse to travel the length of the vein from the venules to the valve end of the IJV (at its junction with the subclavian vein). A fairly typical condition found in MS patients is a thickened or incompetent IJV valve which does not

Predicted effects from standing pressure waves in the internal jugular vein

The hypothesized obstruction-induced increase in blood pressure fluctuations at the venule end of the cerebral capillary bed, which might be referred to as local hypertension, could cause a sequence of events that, ultimately, could impact chronic fatigue, mental acuity and even, potentially, multiple sclerosis. This predicted sequence of effects is discussed below.

Effect of local hypertension on capillary bed pressure drop and rate of blood flow

With a standing pressure wave, as discussed above, an obstruction near the valve end of the IJV could increase the pressure at the venule end of the capillary bed, and this in turn would decrease the amount of pressure drop between the entry points (arteriolar end) of the cerebral capillary bed and the exit points (venule end) of the bed.

In accordance with Darcy’s Law ([11], p. 8), which says simply that the rate of blood flow in a length of vessel is proportional to the pressure difference

Effect of local hypertension on the blood brain barrier

Disruption of the blood brain barrier has been reported [23], [24], [25] as being associated with, or as a precursor to, the onset of multiple sclerosis. It has also been reported [26] that one of the potential causes of blood–brain barrier disruption is sufficiently high or acute hypertension. It has further been reported [27] that if there is a failure in the blood brain barrier it would occur at the cerebral venules, not capillaries or arterioles. Such venules are particularly vulnerable to

Effect on secondary stenoses

Finally, some MS research [30] indicates that, with a blockage (stenosis) at or near an IJV valve, there may be a secondary stenosis a few centimeters above that of the valve blockage. Such a secondary stenosis could be explained through the existence of a relatively non-fluctuating standing-wave node at that position. If the hydrostatic pressure within the vein at that node is less than that of the surrounding muscle and tissue, then the vein would, in principle, collapse. If the valve end

A last comment

There seems to be a growing perception in the multiple sclerosis research community that there are a number of contributing factors that underlie the etiology of multiple sclerosis. Factors such as genetics, geographic distribution, gender, diet, viral infection and others have all had some association with multiple sclerosis. This paper hypothesizes that the physics of fluid dynamics may also have an association because many of the predicted characteristics that arise, even from the

Conflict of interest statement

Dr. Tucker has no competing or conflicting interests. No grants or other funding for this commentary was required or received. Dr. Tucker’s reading of the sciences associated with vein stenosis and chronic fatigue have been stimulated by his son’s multiple sclerosis.

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