This Is MS Multiple Sclerosis Community: Knowledge & Support

Here's a copy of a post from the LDN thread about alcohol. It refers to a web page where they have some scans of blood flow in brains of people wo have different issues. Just wondering if this could be a diagnostic tool for before/after CCSVI interventions...

I recall a study that referred to alcoholics as being x times more likely to develop MS. Sure it's on here somewhere.

Mark.

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RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap

It might be interesting to use SPECT scanning to investigate MS brain circulation before and after CCSVI treatment. Here are some random questions that come to mind. Should we expect low blood flow due to blockage and impaired drainage? Or, might there be higher levels of perfusion due to increased pressure on the distal side of the stenosis? Would the technique be able to distinguish between healthy oxygenated blood and hypoxic refluxed blood? My hypothesis is leaning towards the idea of abnormally high blood flow due to imparied drainage and an accumulation of the tracer in the brain.

On another note, I have read a couple of Dr. Amen's books and was hoping to find some discussion of MS. Unfortunately, the two books I've read, while indeed interesting and informative, have not mentioned MS. However, I recently came across the following journal article which seems related. This study measured blood flow in MS patients using MRI and found decreased perfusion. Note that the full paper is freely available.

Abnormalities of cerebral perfusion in multiple sclerosis.
J Neurol Neurosurg Psychiatry. 2004 Sep;75(9):1288-93.

BACKGROUND: Measuring perfusion provides a potential indication of metabolic activity in brain tissue. Studies in multiple sclerosis (MS) have identified areas of decreased perfusion in grey matter (GM) and white matter (WM), but the pattern in clinical subgroups is unclear. OBJECTIVES: This study investigated perfusion changes in differing MS clinical subgroups on or off beta-interferon therapy using a non-invasive MRI technique (continuous arterial spin labelling) to investigate whether different clinical MS subtypes displayed perfusion changes and whether this could give a further insight into the pathological mechanisms involved. METHODS: Sixty patients (21 relapsing remitting, 14 secondary progressive, 12 primary progressive, 13 benign) and 34 healthy controls were compared. Statistical parametric mapping (SPM '99) was used to investigate regional variations in perfusion in both GM and WM. Global WM perfusion was derived by segmenting WM from images using T(1) relaxation times. RESULTS: Regions of lower perfusion in predominantly GM were observed in the primary and secondary progressive cohorts, particularly in the thalamus. Increased WM perfusion was seen in relapsing remitting and secondary progressive cohorts. CONCLUSIONS: Low GM perfusion could reflect decreased metabolism secondary to neuronal and axonal loss or dysfunction with a predilection for progressive forms of MS. Increased WM perfusion may indicate increased metabolic activity possibly due to increased cellularity and inflammation. Improved methodology and longitudinal studies may enable further investigation of regional and temporal changes, and their relationship with physical and cognitive impairment.

NHE