Perfusion measures of cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) were analyzed in 75 lesions from 17 patients with the NAWM (normal appearing white matter) of 17 MR imaging negative control subjects as reference.
MTT values were found to be significantly prolonged for the enhancing and nonenhancing MS lesions and importantly for the NAWM in MS patients compared with normal control white matter.
There is a significantly prolonged time it takes for cerebral blood to get in and out of the brain in MS patients, even in normal appearing white matter...compared to controls. There is cerebral blood flow irregularity even prior to lesion formation.
This perfusion-based differentiation would not be apparent by conventional T2-weighted imaging. The magnitude of the prolonged MTT and reduced CBF indicating perfusion deficits for all these focal lesion clusters and the NAWM is provocative in itself and especially so in view of the new pathology literature and the direction it is leading us in determining factors in MS relevant to the microcirculation and ischemia. The authors interpret their findings as a primary vascular pathology rather than reflecting decreased metabolic demand.
Future studies will determine how perfusion measures will be used in demyelinating disease in the reading room. For now there is the opportunity with high-resolution perfusion MR imaging, diffusion MR imaging, and cellular and molecular imaging to look specifically at the normal and abnormal processes occurring at the endothelial level in MS. This will bring us closer to understanding the effects of intervention, including treatments targeting cellular migration and CNS surveillance, vasoreactivity, and the specific "good" and "bad" components of the inflammatory events in MS. This work by Ge et al provokes us to look at the microscopic pathology of MS by MR imaging in new ways. Whether perfusion abnormalities are cause or effect, we are delivered to a fork in the road of considerable interest.
To me, this study is further proof of venous insufficiency in MS.