Welcome! This blog contains research, information on lifestyle, nutrition, dietary supplements and health for those with MS, as well as continuing information on the understanding of CCSVI and cerebral hypoperfusion. This blog is informative only--all medical decisions should be discussed with your own physicians.The posts are searchable---simply type in your topic of interest in the search box at the top left.Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the immune paradigm of MS, and continues the 15 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.To learn how this journey began, read my first post from August, 2009. Be well! Joan
Wednesday, December 30, 2009
Vascular white matter lesions are 50-500 times more likely than MS
December 30, 2009 at 2:57pm
Neurologists refer to the "unique" presentation of MS as an autoimmune disease- with oligoclonal banding in CSF showing myelin degradation and perivenous (or around the veins) white matter lesions on MRI.
But these features are not unique to MS. Most of these signs are also found as result of hypoxic injuries to the brain: including (but not limited to) stroke, diffuse cerebral hypoxia, dementia and vascular insufficiency- in which the immune system is similarly activated. What makes MS unique are the perivenous lesions, shown on MRI. MS is diagnosed as MS because of the location of the lesions, age of the patient and their symptoms.
Here is research from a radiology web site, authored by Dr. Barkhof, on white matter lesions in MRI.
MS vs. Vascular findings
Consequently, it is not wise to put MS in the differential diagnosis, if the clinician does not suspect the patient of having MS and on the MR incidental white matter lesions (WML) are found. The odds are against the diagnosis of MS, because vascular WMLs are 50-500 times more likely than MS plaques.
MS is a diagnosis of exclusion. It can be 500 times more likely that someone has a vascular disorder. Diagnosticians can also exclude those patients who are old, who have had a stroke, who have been poisoned by carbon monoxide, who have high blood pressure- even though these patients may have MRIs that look strikingly similar to an MS patient. When the mode of brain injury is apparent, the diagnosis is easier. MS researchers have here-to-fore not had an explanation for injury, and so the autoimmune theory was employed. Even though the main issues for these lesions are predominantly vascular.
Dr. Zamboni is now showing us that there is a mode of brain injury in MS patient- chronic cerebrospinal venous insufficiency created by venous stenosis and reflux, which is directly linked to the slowed perfusion and hypoxic-like lesions found in the MS brain-as well as the degradation of gray matter due to iron deposition.
Please consider the following research:
Hypoxia-like tissue injury as a component of multiple sclerosis lesions.
Recent studies have looked at lesion load in a fashion analogous to that seen with multiple sclerosis. A particularly relevant clinical model for white matter disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) which combines the potential components of small vessel disease, resulting in progressive neurological deficit, with a common association with migraine which can also be associated with white matter lesions. However, the most common pathogenic factor associated with the microangiopathy, which appears to be at the heart of ischemic demyelination, continues to be hypertension.
Multiple Sclerosis: The Role of MR Imaging
Y. Ge From Department of Radiology/Center for Biomedical Imaging, New York University Medical Center, New York, NY
commentary on this research:
Ischemia and Multiple Sclerosis: Perfusion MR Imaging Provides Insight into an Underexplored Pathophysiology
Jack Simon, Guest Editorialist
a University of Colorado Health Sciences Center
Deep white matter ischemia