The examinations undertaken indicate a possible connection between MS and CCSVI. The widely accessible and highly sensitive and specific Doppler ultrasound test may be useful for revealing, and preliminary analysis of, CCSVI pathologies.

This article discusses the biophysical aspects of venous outflow from the brain in healthy individuals and in patients with chronic cerebrospinal venous insufficiency. Blood flows out of the brain differently, depending on body position. In the supine position it flows out mainly through internal jugular veins, while in the upright position it uses the vertebral veins. This phenomenon is probably not due to the active regulation of the flow but instead results from the collapse of jugular veins when the head is elevated. Such a collapse is associated with a significant increase in flow resistance, which leads to redirection of the flow towards the vertebral pathway. Theoretical calculations respecting the rules of fluid mechanics indicate that the pressure gradients necessary for moving blood from the brain toward the heart differ significantly between the supine and upright positions. The occlusion of internal jugular veins, according to fluid mechanics, should result in significant increase in the flow resistance and the restriction of cerebral flow, which is in line with clinical observations. Importantly, the biophysical analysis of cerebral venous outflow implies that the brain cannot easily compensate for increased peripheral venous resistance (namely, an occlusion of the large extracranial veins draining this organ), either by elevating the pressure gradient or by decreasing the vascular resistance through the recruitment of additional drainage pathways. This may mean that chronic cerebrospinal venous insufficiency may cause the destruction of the delicate nervous tissue of the central nervous system.

Purpose We performed a retrospective cohort study in patients who underwent endovascular aneurysm repair (EVAR) to determine the incidence and predictors of myocardial injury and acute kidney injury (AKI). Methods We included 267 consecutive patients who underwent EVAR at two tertiary centres in Canada and Poland. The primary outcome was myocardial injury during hospital stay after EVAR defined as a troponin elevation (ultra-sensitivity troponin I Vidas C 19 ngÁL-1 , non-high-sensitivity troponin I Vidas C 0.01 lgÁL-1 , highsensitivity troponin T C 20 ngÁL-1 , non-high-sensitivity troponin T C 0.03 ngÁmL-1). The secondary outcome was AKI defined using the stage 1 of the Acute Kidney Injury Network criteria. Results Myocardial injury occurred in 78/267 patients (29%; 95% confidence interval [CI], 24.1 to 34.9) and with AKI occurring in 25/267 (9.4%; 95% CI, 6.4 to 13.5). In a multivariable analysis, the following variables were associated with an increased risk of myocardial injury: age (adjusted odds ratio [aOR], 1.65 per ten-year increase; 95% CI, 1.09 to 2.49), Revised Cardiac Risk Index score C3 (aOR, 2.85; 95% CI, 1.26 to 6.41), The American Society of Anesthesiology physical status score 4 (aOR, 2.24; 95% CI, 1.12 to 4.47), duration of surgery (aOR, 1.27 per each hour; 95% CI, 1.00 to 1.61), and perioperative drop in hemoglobin (aOR, 3.35 per 10 gÁdL-1 decrease; 95% CI, 1.00 to 11.3). Predictors of AKI were duration of surgery (aOR, 1.72 per hour; 95% CI, 1.36 to 2.17), a preoperative estimated glomerular filtration rate (eGFR) of 30-59 mLÁmin-1 (aOR, 3.82; 95% CI, 1.42 to 10.3), and an eGFR \30 mLÁmin-1 (aOR, 37.0; 95% CI, 7.1 to 193.8). Conclusion Myocardial injury and AKI are frequent during hospital stay after EVAR and warrant further investigation in prospective studies. Résumé Objectif Nous avons réalisé une étude de cohorte rétrospective auprès de patients ayant subi une Electronic supplementary material The online version of this article (

Multiple sclerosis patients examined with perfusion magnetic resonance (MR) imaging techniques have been found to have patterns of abnormal blood flow. These include prolonged mean transit time, a trend toward decreased cerebral blood flow in the area of plaques, and decreased cerebral blood flow and prolonged mean transit time within normal-appearing white matter. Increased cerebral blood flow and volume and decreased mean transit time (compared with the baseline values before the relapse) were found to precede the development of plaques. In addition, susceptibility-weighted imaging utilizing deoxyhemoglobin as the contrast has revealed that venous blood in cerebral veins of multiple sclerosis patients is less deoxygenated compared with healthy controls. All these findings were traditionally interpreted as a sign of local flow disturbances mediated by inflammatory and neurodegenerative processes. However, recent findings of significant stenoses in the extracranial veins that drain the brain and spinal cord shed new light on these MR results. With the assumption that a majority, if not all, of multiple sclerosis patients exhibit such extracranial venous obstacles, the perfusion MR images of multiple sclerosis patients should be reinterpreted. Perhaps ongoing MR studies with respect to extracranial venous hemodynamics may decipher some of the unsolved puzzles related to this neurologic disease.

We describe a multiple sclerosis patient presenting with compression of the internal jugular vein caused by aberrant omohyoid muscle. Previously this patient underwent balloon angioplasty of the same internal jugular vein. Ten months after this endovascular procedure, Doppler sonography revealed totally collapsed middle part of the treated vein with no outflow detected. Still, the vein widened and the flow was restored when the patient's mouth opened. Thus, the abnormality was likely to be caused by muscular compression. Surgical exploration confirmed that an atypical omohyoid muscle was squeezing the vein. Consequently, pathological muscle was transected. Sonographic control three weeks after surgical procedure revealed a decompressed vein with fully restored venous outflow. Although such a muscular compression can be successfully managed surgically, future research has to establish its clinical relevance.