Dr. Christopher Gottschalk was featured in the NY Times CCSVI story today, stating that there was no science behind his brother Adam's improvements after venoplasty. I strongly disagree, and will use his own published research to show why.

Hypoperfusion---means decreased blood flow through an organ.  

If prolonged, it may result in permanent cellular dysfunction and death.

One of the first things noted in the MS brain, after clinically isolated syndrome (CIS) is diagnosed, is hypoperfusion.  

This simply means less blood is going through brain tissue in people with MS. 

It is a measurable, quantifiable, scientific fact.  People with MS have hypoperfused brains.  

In fact, this lowered cerebral blood flow shows up in normal appearing white matter (NAWM)--which is brain tissue that does not have any lesions or immune activation.  That's right.  Hypoperfusion comes first, before lesions, before MS symptoms.  Here are some papers on this:

link   link   link   link

Dr. Zamboni's study was the first to find a correlation in the severity of extracranial venous malformations and slowed cerebral bloodflow. 

This pilot study is the first to report a significant relationship between the severity of CCSVI and hypoperfusion in the brain parenchyma. These preliminary findings should be confirmed in a larger cohort of MS patients to ensure that they generalize to the MS population as a whole. Reduced perfusion could contribute to the known mechanisms of virtual hypoxia in degenerated axons.

link

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Adam Gottschalk's brother, the neurologist Dr. Christopher Gottschalk from Yale University, has studied hypoperfusion in the brains of cocaine addicts. 

Here's some information about this research, in a press release from Yale University in 2003.

A diuretic commonly used to treat hypertension and congestive heart failure may improve brain blood flow in cocaine addicts, according to a study by Yale researchers in the June issue of the journal Drug and Alcohol Dependence.

Chronic cocaine use is associated with decreases in blood flow to the brain, but the mechanism for this decrease is not fully understood. Researchers theorize cocaine-induced constriction of the arteries in the brain and/or increased blood clotting may be involved.

The problems associated with decreased brain blood flow in some cocaine abusers are like the results of major strokes such as paralysis, loss of ability to speak, severe cognitive impairment and, in the worst cases, death, said Thomas Kosten, M.D., professor of psychiatry at Yale School of Medicine and lead author of the study.

"The patients in these studies with reduced blood flow to the brain had significant impairment in thinking, concentrating, reading and remembering things," Kosten said. "They also had significant depressive symptoms that may have been related to these deficiencies in brain functioning due to a lack of sufficient blood flow to the neurons."

He said increasing blood flow back to normal can reverse these cognitive impairments and make these patients more responsive to behavioral treatments, which require learning of new skills to refuse drugs. "These improvements in cognition can also enable these patients to return to productive employment and be active members of society," Kosten said.

To gauge the effects of the diuretic amiloride on cocaine dependent subjects, Kosten and his colleagues administered amiloride, aspirin or placebo to 49 patients for one month while they resided on a research unit. Blood flow in the brain was measured on admission to the unit and at the end of treatment.

At the time they were enrolled in the study, cocaine-dependent subjects showed decreased cerebral blood flow compared to 18 control subjects. After four weeks of treatment, the researchers found that the amiloride, but not aspirin or placebo, improved blood flow in the brain. None of the treatments affected blood clotting.

The authors speculate that the improvement by amiloride may be due to the medication's ability to dilate the arteries in the brain. The authors also pointed out that amiloride may be used in combination with other medications that also increase cerebral blood flow to treat cocaine dependent patients.

Co-authors included Christopher Gottschalk, M.D., Karen Tucker, Christine Rinder, M.D., Holly Dey, M.D., and Henry Rinder, M.D.

http://news.yale.edu/2003/07/07/diuretic-may-help-increase-brain-blood-flow-cocaine-addicts

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I sent the link to Dr. Gottschalk's research on hypoperfusion yesterday as part of a comment to the NY Times, but it was not published.

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In fact, the brains of people who are addicted to cocaine show white matter hyperintensities on MRI, due to vasoconstrictive ischemia and hypoperfusion.

The cocaine-dependent group had greater severity of white matter hyperintensities (WMH)  than the opiate-dependent group, which in turn had greater severity of WMH than the healthy comparison group (odds ratios=2.54 and 2.90, respectively). The cocaine-dependent group had greater lesion severity of deep and insular WMH than the opiate-dependent group and the healthy comparison group (odds ratio>3.25 for deep WMH; odds ratio>4.38 for insular WMH). For periventricular WMH, there were no significant differences between the three groups. The frontal lobes were the predominant locations of WMH in both substance-dependent groups. The greater prevalence and severity of WMH in cocaine-dependent subjects than in opiate-dependent subjects may reflect the fact that cocaine induces more ischemia via vasoconstriction than opiates. 

http://www.ncbi.nlm.nih.gov/pubmed/15313520 

Why is it scientifically acceptable for Dr. Christopher Gottschalk to give a variety of medications to cocaine addicts to increase their cerebral perfusion, yet it is not acceptable for his brother to have his venous malformations treated to increase his cerebral perfusion? 

And why, when these cocaine addicts feel better after in increase in cerebral bloodflow is it not called placebo?

Why do neurologists keep saying that we are not thinking scientifically, while they disregard the science of hypoperfusion in MS?

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Here is BNAC on the correlation of better perfusion in those treated with venoplasty:

...we noticed that the majority of the treated patients reported immediate temporary improvements in subjective complaints of fatigue and cognitive impairment post- intervention [82]. In another recent study, the re-establishment of cerebral venous return reduced chronic fatigue perception in a group of 31 MS patients with CCSVI who underwent the endovascular procedure, suggesting that fatigue could probably be associated with CCSVI. 

These data may suggest that reduced cerebral perfusion in MS patients is related to the presence and severity of venous out- flow blockages characterizing CCSVI. To test this hypothesis, a recent pilot study of 16 patients with MS and eight healthy subjects [81] investigated whether hypoperfusion of brain parenchyma is related to impaired venous outflow. It was found that hypoperfusion of the brain parenchyma in MS, but not in healthy controls, was associated with the presence and severity of CCSVI. Decreased CBF GM and WM regions of the brain parenchyma showed a strong relationship with increased severity of CCSVI. These preliminary findings are from a small group of subjects and should be confirmed in a larger cohort of MS patients [84]. 

http://www.expert-reviews.com/doi/abs/10.1586/ern.11.117 

I know this is dense, and not as "sexy" as a narrative of conflict between brothers.  But CCSVI science is important.

I hope a journalist or professional writer will pick up these ideas.  

We need independent research into cerebral perfusion before and after venoplasty. 

Because perfusion matters,

Joan

http://www.facebook.com/notes/ccsvi-in-multiple-sclerosis/hypoperfusion-and-published-research-by-dr-christopher-gottschalk/10151196624242211