Abstract

Recent perfusion-weighted imaging studies have shown that two clinical pictures characterize multiple sclerosis: intermittent focal inflammatory demyelination and diffuse progressive axonal degeneration. Their etiopathogenesis is not known. We hypothesize that a chronic obstacle to the outflow of blood from the brain can cause these two clinical pictures. We had already shown angiographically that the stenosis of the internal jugular vein causes a systemic-cerebral shunt and a reversal of the venous circulation brain and gives rise to the new circuit that directly connects the superior vena cava system to the straight sinus. This new circuit can cause the BBB to break and new plaques to form. The introduction of near-infrared spectroscopy (NIRS) in cardiac surgery has made it possible to demonstrate that obstruction of the superior vena cava is capable of causing cerebral hypoperfusion, responsible for the progressive degeneration of axons. To confirm the relationship between superior vena cava syndrome and cerebral hypoperfusion, in 35 of the152 patients with multiple sclerosis (MS) and jugular vein stenosis, operated on the plastic of jugular vein enlargement, we measured oxygen saturation in the brain. Material and Methods To measure changes in the oxygen saturation of regional brain tissue (rctSO2) before, during and after clamping the jugular veins, we applied two sensors in the left and right frontal region, and we connected them to a biosignal recorder (Invos-5100 system). Results Closing or opening the IJV produced significant changes in the rctSO2 values. Before clamping, saturations varied between 77% - 78%, while during clamping they decreased reaching values between 48% - 58% (p <0, 05). After declamping, the rctSO2 returned to its starting values. These results confirmed that obstruction of the jugular veins causes a significant reduction in rctSO2 values and cerebral hypoperfusion. Conclusions In MS patients, chronic jugular veins stenosis generates two different clinical pictures: Diffuse cerebral hypoperfusion, documented by the lowering of rctSO2. Systemic-cerebral shunt and inversion of cerebral venous circulation capable of causing a breakdown of the blood-brain barrier (BBB)

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