![]() |
Multiple Sclerosis and Hyperbaric Oxygen Therapy
|
||
|
MULTIPLE SCLEROSIS DISEASE MODELS |
THE VASCULAR THEORY OF MULTIPLE SCLEROSIS A 2005 study at the University of Dundee in Scotland showed that MS inflammation severely restricts oxygen transport. Whether the cause of this inflammation is a direct autoimmune response or the result of faulty blood filtration is uncertain. In the vascular theory, MS is seen as a cerebrovascular-ischemic disease, caused by a defect in the blood vessels serving central nervous system. Injury to the blood vessels would lead to swelling, which would restrict critical oxygen delivery. When the oxygen supply is slowed or cut off, tissue damage occurs, including demyelination, destruction of the myelin sheaths protecting the nerves. The body's attempt to "clean up" the injured areas could lead to further damage from the immune system. The lining of the bloods vessels where capillaries rejoin the veins is the weakest part of the vascular system. Blood vessels become more permeable (leaky) with inflammation and increased capillary pressure, allowing migration of fluid and white blood cells into the surrounding tissues. These vascular abnormalities are not confined to the central nervous system. MS patients often have rather curious pinpoint-sized red dots on the skin called skin petechiae, caused by the leakage from capillaries below the skin. Swank found these small hemorrhages in 77.4% of female MS patients. The vascular hypothesis raises the question why MS is not more widely distributed. The roles of genetics, myelin weaknesses, and the existence of redundant neuronal pathways may affect prevalence, but further study is required. Some theorists believe that apparently normal blood pressure may be pathologic in the MS population, causing dilation of the arteries, the formation of dangerous free radicals, injury to the blood vessels, and swelling. The body's response would be to produce TxA2, a strong venous constrictor. The resultant narrowing of the veins would again trap fat emboli, closing off the thin-walled venules. The alternating arteriole (small artery) swelling and venule (small vein) constriction would explain the “spotty” nature of multiple sclerosis lesions . MRI Support for the Vascular Theory Magnetic resonance imaging has shown that microembolic debris is common even in the healthy population. Although the damage is silent, with the offending particulate matter usually engulfed by specialized cells within the lung (phagocytosis)—a failure of this mechanism would result in the potential for damage. Studies of diver decompression have shown that lung microfiltration is extremely important in the protection of the nervous system. Brooks et al. reported that oxygen utilization and blood flow were significantly reduced in the white brain matter and grey cortical matter of MS patients as compared with the general population. Additionally, the lowest level of oxygenation corresponded with the greatest amount of brain atrophy, and the greatest IQ deterioration was tied to the lowest levels of oxygen utilization.Although five times more fat emboli pass through the brain's gray matter (neuron cells) than through the white matter, these tissues are protected by more concentrated, redundant capillary blood supply. The white matter, the fibers (axons) which carry electrical signals from the neuron's cell body to its connecting nerves, has no areas supplied by more than one blood source. If one supply is obstructed there is no “back-up.” In other areas of the brain with two arteries flowing in opposite directions, the brain tissue between may be supplied by neither. For these reasons, lesions are often quite predictable, affecting the optic nerve, certain motor pathways, and bowel and bladder function. MS lesions create damage equivalent to mini-strokes for the affected neurons. In 1992, McDonald noted damage to the blood brain barrier in enhanced MRI scans. The sudden symptom onset, dissemination in time, affected sites, blood-brain barrier dysfunction, and the fact that MS patients have identical immune markers at the same level as stroke patients support the vascular theory. |
||