Phlebology. 2014 Jul 31. pii: 0268355514544782. [Epub ahead of print]
OBJECTIVES:To evaluate the relationship between chronic cerebrospinal venous insufficiency (CCSVI) and the presence of a Chronic Venous Disorder (CVD).
METHOD:We included 55 subjects with CCSVI aged >18 years, and 186 controls without CCSVI. Each subject was evaluated with color Doppler sonography in accordance with Zamboni’s five criteria, examined by two neurologists and interviewed with an ad-hoc designed form. The neurologists and the sonographers were mutually blinded. CVD were classified according to CEAP.
RESULTS:Mean age was 42 years (SD = 9) in cases and 43 years (10) in controls (p = ns). The odds ratios in subjects CCSVI were 0.6 (0.2-2.2) for CEAP 1, 0.9 (0.2-4.5) for CEAP 2, and 1.0 (0.6-1.9) for family history of varicose veins. The prevalence of CVD and, family history of varicose veins, was similar between cases and controls for each Zamboni criterion.
CONCLUSIONS:We found no association of CCSVI with the presence of CVD or family history of varicose veins
Müller K, Kuchling J, Dörr J, Harms L, Ruprecht K, Niendorf T, Wuerfel J, Paul F, Sinnecker T. Detailing intra-lesional venous lumen shrinking in multiple sclerosis investigated by sFLAIR MRI at 7-T.J Neurol. 2014 Aug 14. [Epub ahead of print]
Intra-lesional venous lumen shrinking detectable by MRI was suggested as an in vivo marker of inflammation in multiple sclerosis (MS). In our study mean diameters of pre-, post- and intra-lesional venous sections were determined in 49 patients with MS or clinically isolated syndrome (CIS) using a pixel-wise analysis on susceptibility-weighted fluid-attenuated inversion recovery (sFLAIR) images and T2*-weighted (T2*w) imaging at 7 Tesla (T). We observed post-to-intra-lesional venous lumen shrinking on T2*w images (p = 0.036) in an analysis of 338 venous sections. Pre-to-intra-lesional venous lumen reduction was only detectable in less than 50 % of lesions and failed statistical significance when analysing T2*w (p = 0.325) and sFLAIR images (p = 0.258). In conclusion, thinning of intra-lesional veins in MS is-if detectable at all-probably less severe than previously reported, and affects only a minority of MS lesions.
Marshall O, Lu H, Brisset JC, Xu F, Liu P, Herbert J, Grossman RI, Ge Y.Impaired Cerebrovascular Reactivity in Multiple Sclerosis.
JAMA Neurol. 2014 Aug doi: 10.1001/jamaneurol.2014.1668. [Epub ahead of print]
IMPORTANCE:Cerebrovascular reactivity (CVR) is an inherent indicator of the dilatory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a spontaneous and instant increase of cerebral blood flow (CBF) in response to neural activation. The integrity of this mechanism is essential to preserving healthy neurovascular coupling; however, to our knowledge, no studies have investigated whether there are CVR abnormalities in multiple sclerosis (MS).
OBJECTIVE: To use hypercapnic perfusion magnetic resonance imaging to assess CVR impairment in patients with MS.
DESIGN, SETTING, AND PARTICIPANTS:A total of 19 healthy volunteers and 19 patients with MS underwent perfusion magnetic resonance imaging based on pseudocontinuous arterial spin labeling to measure CBF at normocapnia (ie, breathing room air) and hypercapnia. The hypercapnia condition is achieved by breathing 5% carbon dioxide gas mixture, which is a potent vasodilator causing an increase of CBF.
MAIN OUTCOMES AND MEASURES:Cerebrovascular reactivity was calculated as the percent increase of normocapnic to hypercapnic CBF normalized by the change in end-tidal carbon dioxide, which was recorded during both conditions. Group analysis was performed for regional and global CVR comparison between patients and controls. Regression analysis was also performed between CVR values, lesion load, and brain atrophy measures in patients with MS.
RESULTS:A significant decrease of mean (SD) global gray matter CVR was found in patients with MS (3.56 [0.81]) compared with healthy controls (5.08 [1.56]; P = .001). Voxel-by-voxel analysis showed diffuse reduction of CVR in multiple regions of patients with MS. There was a significant negative correlation between gray matter CVR and lesion volume (R = 0.6, P = .004) and a significant positive correlation between global gray matter CVR and gray matter atrophy index (R = 0.5, P = .03).
CONCLUSIONS AND RELEVANCE: Our quantitative imaging findings suggest impairment in functional cerebrovascular pathophysiology, by measuring a diffuse decrease in CVR, which may be the underlying cause of neurodegeneration in MS.