More about NPH. A Pulse Wave Encephalopathy?

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

More about NPH. A Pulse Wave Encephalopathy?

Postby frodo » Thu Mar 12, 2015 4:42 pm

This time I have found the paper of the week faster than Cece and Cheer !!!!


Is There A Pulse Wave Encephalopathy Component To Multiple Sclerosis?
http://www.ncbi.nlm.nih.gov/pubmed/25760216

Abstract
The dominant hypothesis in multiple sclerosis is that it is an autoimmune disease; however, there is considerable evidence that the immune attack on myelin may be secondary to a cytodegenerative event.

Furthermore, the immune modulating therapies longest in clinical use, although modulating the frequency and severity of exacerbation, do not affect long-term progression towards disability. Clearly alternative perspectives on the etiology of multiple sclerosis are warranted. In this paper I outline the commonalities between idiopathic normal pressure hydrocephalus and multiple sclerosis.

These include decreased intracranial compliance as evidenced by increased cerebrospinal fluid volume and velocity of cerebrospinal fluid flow through the cerebral aqueduct; increased ventricular volume; periventricular demyelination lesions; increase in size of Virchow-Robin spaces; presence of Hakim's triad comprised of locomotory disabilities, cognitive problems and bladder control problems. Furthermore, multiple sclerosis is associated with decreased arterial compliance.

These are all suggestive that there is a pulse wave encephalopathy component to multiple sclerosis. There are enough resemblances between normal pressure hydrocephalus and multiple sclerosis to warrant further investigation. Whether decreases in intracranial compliance is a consequence of multiple sclerosis or is a causal factor is unknown. Effective therapies can only be developed when the etiology of the disease is understood.
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Re: More about NPH. A Pulse Wave Encephalopathy?

Postby 1eye » Sat Mar 14, 2015 6:46 pm

Pulses of arterial blood pressure may conduct via non-compliant tissue or liquid, into the CSF, where they may cause movement up and down the spinal column, for instance. Pulses of arterial blood pressure may also be conducted to veins. Veins may have the greatest compliance of any part of the brain, and may therefore be the most vulnerable to wave interference. These conducted pressure waves may interact with pulses in the normal direction of blood flow, and may periodically result in local nodes of zero pressure and flow. Pulses of refluxed blood may have similar results, in a different, or the same phase of the heartbeat.

Thinking more about this: except for refluxed blood, there is never any negative blood pressure, so conducted pressure cannot cancel, but must always at most add to the normal pressure and flow from the heart. So we may have instantaneously higher peaks, but never subtractions from blood flow. Superimposed on this always positive blood flow waveform, with pulses from conducted artery expansions, we may (if there is reflux) possibly have localized nodes of zero or negative blood pressure/flow, from refluxed blood.
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Re: More about NPH. A Pulse Wave Encephalopathy?

Postby ThisIsMA » Mon Mar 16, 2015 4:51 pm

Great find! I wish more research dollars would go toward figuring this out. It seems so logical. Here’s another (older) article by the same author. It even mentions CCSVI:

http://www.ncbi.nlm.nih.gov/pubmed/23691321

Mult Scler Int. 2013;2013:598093. doi: 10.1155/2013/598093. Epub 2013 Apr 4.

The evidence for hypoperfusion as a factor in multiple sclerosis lesion development.
Author: Juurlink BH

Author information
1Department of Anatomy & Cell Biology, University of Saskatchewan, Saskatoon, SK, Canada S7N 5E5 ; College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia.

Abstract
The evidence that hypoxia is a precipitating factor in causing early MS lesions includes increased protein levels of hypoxia-inducible factor-1 α ; presence of the D-110 hypoxia-inducible protein; increased expression of hypoxia-inducible genes in lesions as well as in adjacent normal-appearing white matter (NAWM); loss of myelin-associated glycoprotein in myelin of early MS lesions; a 50% reduction of blood flow through NAWM with areas of lowest blood flow having the greatest probability of lesion development. Why MS-like lesions develop following hypoxemic insults in some individuals but not in others is likely dependent upon the presence of immune predisposing factors that are governed genetically. Hypoperfusion may be due to decreased arterial supply, restricted venous return, or a combination of these. There are clinical trials ongoing or planned to treat chronic cerebrospinal venous insufficiency (CCSVI) through angioplasty. I suggest that it is important that clinical trials addressing vascular issues in MS should examine how the vascular intervention affects white matter perfusion and determine whether the extent of perfusion recovery and maintenance of this recovery is related to functional recovery and maintenance of functional recovery. Consideration should also be given to the possibility of arterial problems playing a role in hypoperfusion in some MS patients.

PMID: 23691321 [PubMed] PMCID: PMC3649777
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