Short term change in blood flow causes lesions...
Posted: Mon Jan 07, 2013 2:40 pm
Another random goody found today.
http://brain.oxfordjournals.org/content/127/1/111.full
http://brain.oxfordjournals.org/content/127/1/111.full
In fact, a steep regional increase of CBV and CBF compared with the contralateral side could be detected up to 3 weeks prior to the breakdown of the BBB and subsequent contrast enhancement, indicating a dominant role of the vasculature preceding the inflammation of white matter tissue.
So...to me...this kind of takes ccsvi out as a cause for MS lesions. The blood flow issues related to the creation of ms lesions are short-lived. CCSVI is a constant issue. Am I thinking wrong here?In multiple sclerosis, vasogenic oedema and an increase of extracellular space in combination with myelin breakdown and tissue structure disruption were reported to result in increased ADC values in both, NAWM (Rocca et al., 2000; Werring et al., 2000; Cercignani et al., 2001; Caramia et al., 2002), and acute and chronic lesions (Tievsky et al., 1999; Filippi et al., 2000). Interestingly, a prominent perfusion increase was found prior to a significant increase in ADC in the present study. The peak of the CBV was followed by a gradual decline over 20 weeks, before it decreased more rapidly, and, in case of development of T1‐hypointensity (‘black hole’), remained below baseline. The initial elevation can presumably be explained by inflammation‐related vasodilation in the acute stage, whereas the decreased perfusion in later stages of the lesion might be due to the development of a (hypometabolic) gliotic scar, which is indicated by reduced N‐acetyl‐aspartate (NAA)/creatine ratios in magnetic resonance spectroscopy in T1‐hypointense lesions (van Walderveen et al., 1998; Li et al., 2003).