To sleep, perchance to oxygenate

September 30, 2010 at 9:12am

One of the most profound, although seemingly minor, changes for my husband, now 18 months since his venoplasty for jugular and dural sinus stenosis--has been the return of dreaming.  After his procedure, he would wake up in the morning and recount for me his vivid dream from the night before.  It was so strange to us...he realized that for several years, he couldn't remember his dreams. 

He was now sleeping soundly, no longer spasming or waking up gasping for air.  And in this deep sleep, his dreams had returned. 

When I went to the CCSVI international symposium in Bologna last year, Dr. Salvi got up and spoke about the changes in his patients after angioplasty.  And one of the global differences his patients noted was deeper, more restful sleep, and the return of dreams.  He had a wonderful illustration that came on the screen during his power-point-- a cartoon of a person deeply sleeping, smiling, with a colorful dream bubble over their head.  I almost leapt out of my seat.  "That's happened to Jeff!"  I whisper/exclaimed to Dr. Dake, seated on my left.  "He's dreaming again."

Now, I read time and time again from patients and their caregivers about the return of deep, restful sleep and dreaming.  I realize that dreaming might not seem important in the grand scheme of recovery from MS....but I believe it is.  I believe it is proof of a brain that is healing.  A brain that does not have REM (rapid eye movement) sleep, does not dream.   There is research that links dreams, REM sleep and oxygenation.

"REM sleep time is strongly reduced by hypoxic and increased by hyperoxic atmosphere, in accordance with the existence of an O2 diffusion limitation. Any pathological decrease in arterial PO2 and/or O2 delivery creates a specific risk in REM sleep."

http://www.ncbi.nlm.nih.gov/pubmed/11382905

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During REM sleep, there is an increase in blood flow to the limbic system and the brain stem, with circulation to these structures decreasing during non-REM sleep.  As brain activity increases during REM sleep, the cerebral requirements for glucose and oxygen both increase....

Fundamentals of Sleep Technology--Butkov, Lee-Choing  2007

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Harvard professor visits Dr. Zamboni in Italy-- The More Iron, The More Severe the Disease

September 28, 2010 at 7:30am

From the Italian press---Professor Rohit Bakshi of Harvard University came to Ferrara University to discuss how his decade long study of iron deposition in MS brains has now intertwined with Dr. Zamboni's research:

Here is a Google translation of the press release:

Too much iron, more severe disease

New Ferrara - September 24, 2010 page 19 Section: Commentary

"It 's another piece of the puzzle that is made," says the researcher Paolo Zamboni.To place a new tile on the mosaic of research on multiple sclerosis was yesterday Professor Rohit Bakshi, Harvard University, came to Ferrara to explain the outcome of a decade of study during which he analyzed the role of iron as a contributory cause of the disease. His line of research was independent from that beaten by Ferrara Zamboni, but its conclusions have been come to intertwine with the results of tests carried out by the researcher and neurologist Bologna Ferrara Fabrizio Salvi on Ccsvi, which have established a hypothetical link between stenosis of the venous vessels in the brain iron accumulation and the onset of multiple sclerosis.

"The current therapies - said the scientist in the main hall of the university - are not effective in stopping the neurodegeneration. Bakshi was able, with a common magnetic resonance imaging to measure the actual concentration of iron in the brain, an operation in the past only run during the autopsy. Plaques and iron stores were associated, but especially "the greater the presence of iron - Bakshi said - the more you exacerbate the effects of the disease." Studies have revealed that the abnormal presence of iron affects the white matter and gray and tends to cause atrophy of certain areas of the brain.

http://ricerca.gelocal.it/lanuovaferrara/archivio/lanuovaferrara/2010/09/24/UCNPO_UCN06.html?ref=search

http://lanuovaferrara.gelocal.it/cronaca/2010/09/23/news/sclerosi-multipla-oggi-la-lezione-di-bakshi-2406157

Please note that Dr. Bakshi is confirming that current pharmaceuticals DO NOT stop the neurodegeneration of the MS disease process.

Here is an article on Dr. Bakshi's studies of MS and iron deposition from 2003:

http://www.webmd.com/multiple-sclerosis/news/20031022/multiple-sclerosis-tied-to-iron-in-brain

Venous Malformations

September 6, 2010 at 7:46pm

Dr. Zamboni--the vascular researcher who discovered CCSVI and has spent years developing a diagnostic and treatment protocol), has found many different types of venous malformations in those with MS.    It is very important to understand that CCSVI can be caused by several issues.  The doctors researching CCSVI are finding many defects.  And each individual has unique issues.

Dr. Zamboni has described CCSVI as created by truncular venous malformations, mostly "intraluminal defects", meaning problems inside the walls of the jugular and azygos veins.  

The types of malformations found by Dr. Zamboni and included in his published research are:

• Annulus --refers to significant circumferential stenosis of the whole venous wall; 
• Septum/valve malformation --refers to anomalous valve apparatuscausing significant flow obstacles at the level of the junction of the IJVs with the brachiocephalic/anonymous trunk; 
• Hypoplasia --refers to under-developed long venous segments; 
• Twisting-- refers to severe stenosies in consequence of a twisted venous segment; 
• Membranous obstruction--  (web) refers to a membrane almost occluding a vein; 
• Agenesis-- refers to the complete anatomical absence of a venous segment. 

Annulus, septum, membranous obstruction, hypoplasia and agenesis are truncular malformations previously described in other venous segments (cava, iliac, deep veins of the lower limbs).13 In Figure 7 there are some examples of venous stenosing lesions morphologically quite similar to those described in the IJVs/AZ in course of CCSVI. In contrast, twisting of the AZ is a truncular malformation never been described so far (Figure 8). In Table 1the distribution of the different truncular lesions in the extracranial and extravertebral cerebrospinal veins aregiven, and the more typical malformations are shown in the figures.

Here is the full paper:

http://phleb.rsmjournals.com/cgi/content/full/25/6/269

This research is very important to understand, because there is no one size-fits all approach to treating CCSVI.  And the IRs are working hard to develop a standard protocol.  That's what the convening meetings and conferences are all about.    

It is very understandable to want to believe that your doctor knows everything about CCSVI....it's a natural response, especially before undergoing a medical treatment, and perhaps paying for it.    But we need to be honest and upfront.  We are at the beginning stages.  Read Dr. Zamboni's paper, and note that there are many underlying issues creating Chronic Cerebrospinal Venous Insufficiency.  It's different in everyone.

Joan