Great news!

Dr. Bernhard Juurlink, Canadian Neurovascular Health Society board member, to present at ISNVD:

ABSTRACT

Arterial Pulse Pressure Waves Causing Endothelium And Myelin Damage May be A Causal Factor In Multiple Sclerosis

Bernhard H.J. Juurlink, Professor emeritus, Department of Anatomy & Cell Biology, University of Saskatchewan

Background: Mechanical deformation of myelin and endothelium can result in cell damage that initiates inflammation. Inflamed vessels release chemokines/cytokines that activate immune cells allowing CNS infiltration of immune cells. If such infiltrating cells recognize myelin antigens as foreign an immune response is initiated resulting in MS lesions.

Mechanical damage of microvessels and adjacent myelin can occur if arterial pulse pressure waves are not dissipated before reaching the microvasculature. This force dissipation results from the elastic expansion of the arterial walls absorbing some of the force and by the increased resistance of the branching arterial tree. The cranium being a rigid bony box can only allow expansion of arteries during systole if there is displacement of cerebrospinal fluid (CSF) and/or venous blood. A number of studies have shown that CSF flow through the cerebral aqueduct has a larger volume and greater velocity in MS patients than in healthy controls: this can only be due to more of the arterial pulse pressure force penetrating deeper than normal resulting in more of the force being exerted onto the ventricular CSF1, as well as onto myelin and endothelium.

Both the stiffness of the arteries and how readily venous blood is displaced influence the pulse pressure wave dissipation. Studies have shown that MS patients generally have stiffer arteries than matched controls2 and many have obstructed venous return3,4. Obstruction of the venous return reduces the ability of arteries to dissipate the pulse pressure force5 whereas venous angioplasty ameliorates MS symptoms6.

Conclusions: To treat MS it is critical to understand what causes the initial damage to endothelium and myelin. Are pulse pressure forces involved? It is important to know what proportion of MS patients have problems with arterial pulse pressure wave dissipation; and of those, which have obstructed venous return, increased stiffness of arteries or a combination7.


References

(1) Egnor, M. et al. 2002. A model of pulsations in communicating hydrocephalus. Pediatr Neurosurg 36: 281-303.

(2) Fjeldstad, C. et al. 2010. Arterial compliance in multiple sclerosis: a pilot study. Angiology 61: 31-6.

(3) Zamboni, P. et al. 2009. Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis. J Neurol Neurosurg Psychiatr 80: 392-399.

(4) Sethi, S. et al. 2015. Jugular venous flow abnormalities in multiple sclerosis patients compared to normal controls. J Neuroimaging 25: 600-607.

(5) Frydrycchowski et al. 2012. Influence of acute jugular compression on the cerebral blood flow velocity, pial artery pulsation and width of subarachnoid space in humans. PLoS One 7: e48245.

(I seem to be missing two references.)

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