Internal Jugular Vein Entrapment in a Multiple Sclerosis Patient

Abstract

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.

The omohyoid muscle entrapment of the internal jugular vein. A still unclear pathogenetic mechanism

“…In addition, in our patient we documented collateral circles activation, not yet observed in the Simka's case. 5 Different from previous reports, the ultrasound finding was confirmed by MRV ( Figure 1). …”

Chronic cerebrospinal venous insufficiency: current perspectives

“…Consequently, such a vein may appear venographically unchanged. 34 Further, decreased venous flow in the IJVs resulting from poor inflow from cerebral veins cannot be revealed by catheter venography. Similarly, unless an intracranial venogram is performed, atypical anatomy of the cerebral sinuses cannot be demonstrated.…”

“…In a case of pathological venous outflow from the brain, some patients present with diminished inflow to the IJV resulting from decreased cerebral venous flow, primarily caused by neurologic disease (eg, reduced cerebral metabolism, brain atrophy), from atypical anatomy of the cerebral sinuses (such as hypoplasia of one or both of transversal and/or sigmoid sinuses), 110,111 or a combination of these. In some individuals, one or both IJVs are found to be externally compressed, usually by aberrant adjacent muscles (Figure 6), 34,112 arteries, 113 or bony structures. 30,32,37,40,[46][47][48] Such compression may also result Chronic cerebrospinal venous insufficiency from reduced rigidity of the venous wall that, for reasons not presently well understood, perhaps altered composition of collagen fibers, is seen in some patients with multiple sclerosis.…”

An overview of randomized controlled trials on endovascular treatment for chronic cerebrospinal venous insufficiency in multiple sclerosis patients

“…This analysis, which involved also secondary progressive MS patients who participated in this study, utilized the venographic classification of CCSVI lesions suggested by Giaquinta [20] and focused at MRI findings after 12-month follow-up, demonstrated significantly less new MS plaques revealed by MRI in the treatment arm of the study. Moreover, patients with favorable morphology of CCSVI lesions, such as focal or segmental defects were significantly more likely to be free from new MS lesions in comparison with patients presenting with less favorable morphology of venous abnormalities, such as long intraluminal defects, hypoplasia of the internal jugular vein or external compression of this vein by adjacent muscles [28,29].…”