ABSTRACT
OBJECTIVE: Multiple sclerosis (MS) is an inflammatory disease characterized by demyelinating plaques in the white matter. Chronic cerebrospinal venous insufficiency (CCSVI) has been proposed as a new hypothesis for the etiopathogenesis of MS disease. MS-CCSVI includes a significant decrease of cerebrospinal fluid (CSF) flow through the cerebral aqueduct secondary to an impaired venous outflow from the central nervous system. This study aimed to determine whether CSF flow dynamics are affected in MS patients and the contributions to differential diagnosis in active and chronic disease using phase-contrast magnetic resonance imaging (PC-MRI). MATERIALS AND METHODS: We studied 16 MS patients with chronic plaques (group 1), 16 MS patients with active plaques-enhanced on MRI (group 2), and 16 healthy controls (group 3). Quantitatively evaluation of the CSF flow was performed from the level of the cerebral aqueduct by PC-MRI. According to heart rates, 14–30 images were obtained in a cardiac cycle. Cardiac triggering was performed prospectively using finger plethysmography. RESULTS: No statistically significant difference was found between the groups regarding average velocity, net forward volume and the average flow (p > 0.05). Compared with the controls, group 1 and group 2, showed a higher peak velocity (5.5 ± 1.4, 4.9 ± 1.0, and 4.3 ± 1.3 cm/sec, respectively; p = 0.040), aqueductal area (5.0 ± 1.3, 4.1 ± 1.5, and 3.1 ± 1.2 mm2, respectively; p = 0.002), forward volume (0.039 ± 0.016, 0.031 ± 0.013, and 0.021 ± 0.010 mL, respectively; p = 0.002) and reverse volume (0.027 ± 0.016, 0.018 ± 0.009, and 0.012 ± 0.006 mL, respectively; p = 0.000). There were no statistical significance between the MS patients with chronic plaques and active plaques except for reverse volume. The MS patients with chronic plaques showed a significantly higher reverse volume (p = 0.000). CONCLUSION: This study indicated that CSF flow is affected in MS patients, contrary to the hypothesis that CCSVI-induced CSF flow decreases in MS patients. These findings may be explained by atrophy-dependent ventricular dilatation, which may occur at every stage of MS.