Abstract
The aim of the study was to investigate the Internal Jugular Veins dynamics using contrast enhanced ultrasonography in Multiple Sclerosis patients, clinically isolated syndrome patients and healthy controls. Contrast enhanced ultrasonography imaging of the Internal Jugular Vein was performed in fifty-eight patients with Multiple Sclerosis, seven clinically isolated syndrome patients and in thirteen healthy controls. Time-intensity curves were quantified using a semi-automated method and compared with clinical disease outcomes. Wash-out parameters were calculated and six Time-intensity curves shapes were created. Significantly reduction of wash-out rate in Internal Jugular Veins was detected in Multiple Sclerosis patients compared to healthy controls [22.2% (2.7%–65.9%) vs. 33.4% (16.2%–76.8%); P<0.005]. Internal Jugular Vein enhancement was heterogeneous in patients with Multiple Sclerosis and consisted of slow wash-out Time-intensity curves shapes, compared with almost only one type of Time-intensity curves shape in control subjects that correspond to fast enhancement and fast wash-out. The vein wash-in parameters were similar in Multiple Sclerosis group compared with controls. A significant correlation was found between Internal Jugular Vein wash-out and level of disability (R = −0.402, p<0.05). Contrast enhanced ultrasonography of the Internal Jugular Vein with time intensity curve analysis revealed alterations of cerebral venous outflow in Multiple Sclerosis patients, however mechanisms that determine this condition remains unclear.
Highlights
The most widely accepted hypothesis is that MS is an inflammatory and degenerative autoimmune disease that leads to destruction of CNS myelin, with multifactorial pathogenesis [1]
Internal jugular vein wash-out rate and wash-out AUC were significantly increased in patients with MS compared with Clinically Isolated Syndrome (CIS) and HCs (Table 2)
Even after jugular veins with retrograde flow were excluded from the statistical analysis, washout rate values remained significantly lower in the MS group compared to HCs and CIS [in MS patients without retrograde flow WO rate was 24.7% CIS 29.2% and HCs 35.4% p,0.05]
Summary
The most widely accepted hypothesis is that MS is an inflammatory and degenerative autoimmune disease that leads to destruction of CNS myelin, with multifactorial pathogenesis [1]. Abnormalities of cerebral hemodynamics in MS have been investigated by using single photon emission tomography, PET and perfusion MR imaging [3,4,5] These studies have demonstrated widespread hypoperfusion in focal lesions, and in both the grey and white matter in patients with MS and all clinical phenotypes [4,5] and in the very early stage of the disease [6]. These findings are consistent with earlier histopathologic studies reporting vascular occlusive changes in MS, characterized by thrombosis of small veins and capillaries, vein wall hyalinization, and intravascular fibrin deposits [7,8]. MS patients showed a reduced visibility of cerebral veins that is inversely correlated with the periventricular and whole-brain T2lesion load [11], low cerebral venous blood flow, low cerebral blood volume and higher MTT compared with healthy controls [12,13]
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