study shows PTA helps head-ache long-term in MS

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

study shows PTA helps head-ache long-term in MS

Postby 1eye » Fri Jan 26, 2018 8:35 am

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Re: study shows PTA helps head-ache long-term in MS

Postby MarkW » Fri Jan 26, 2018 1:45 pm

Thanks for posting 1eye, I signed on again to post the same info.....
My 3 CCSVI procedures (2 with Dr S) definitely helped my brain fatigue and this improvement has lasted for four years, so far. Unfortunately my physical symptoms are progressive.
Mark Walker - Oxfordshire, England. Retired Pharmacist. 16 years of study about MS.
CCSVI Comments:
http://www.telegraph.co.uk/news/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: study shows PTA helps head-ache long-term in MS

Postby vesta » Sat Jan 27, 2018 9:43 am



Greetings:

Thanks much for posting this (Mark W too,) See also Frodo's post copy below of Jan 24 2018 about Hans Lassman. Slowly, glacial pace the old orthodoxy "auto-immune disease, suppress myelin inflammation" is crumbling.

frodo wrote:Hans Lassman is one of the leaders in MS research. He does not say the word "autoimmune" anymore, nor speaks too much about myelin.

Multiple Sclerosis Pathology.

https://www.ncbi.nlm.nih.gov/pubmed/29358320

Abstract

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS), which gives rise to focal lesions in the gray and white matter and to diffuse neurodegeneration in the entire brain. In this review, the spectrum of MS lesions and their relation to the inflammatory process is described.

Pathology suggests that inflammation drives tissue injury at all stages of the disease. Focal inflammatory infiltrates in the meninges and the perivascular spaces appear to produce soluble factors, which induce demyelination or neurodegeneration either directly or indirectly through microglia activation. The nature of these soluble factors, which are responsible for demyelinating activity in sera and cerebrospinal fluid of the patients, is currently undefined. Demyelination and neurodegeneration is finally accomplished by oxidative injury and mitochondrial damage leading to a state of "virtual hypoxia."


Best regards, Vesta
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