静脈狭窄と多発性硬化症の間の物理的リンク

この論文は、内頸静脈（IJV）の下肢での狭窄または閉塞が、流体力学の物理学に従って、静脈内に立っている圧力波を引き起こすと仮定しています。この圧力波には、大きな圧力変動の領域と、比較的少ない変動の他の領域があり、ピーク圧力値も大幅に低くなります。仮説的な圧力波の波長が、閉塞から毛細血管床の静脈端までの距離に匹敵する場合、高圧変動の領域が静脈に存在します。閉塞の程度に応じて、毛細血管床の静脈の圧力変動は、遮るもののない静脈に存在するものよりもかなり大きくなります。局所高血圧に相当する毛細血管層のvenule端にあるこの血圧変動のこの増加は、ベッド全体の圧力低下を減らすと予測され、ダーシーに従ってベッドを通る血流を減少させる法。このような血流のベッドを通る流れの減少には、フィックの原理に従って、酸素、グルコース、およびその他の栄養素の脳組織への移動の減少が伴います。脳組織の酸素レベルの低下（すなわち、低酸素症）は、疲労の増加と被験者患者の精神的視力の低下と関連しています。また、脳組織における酸素の剥奪は、乏突起伸展細胞の死をもたらす可能性があり、それが脳の神経軸索を囲むミエリンの劣化をもたらす可能性があります。さらに、この論文は、極端な閉塞の場合、毛細血管床のvenule端での予測される局所高血圧が十分に高く、血液脳関門に局所的な破壊を引き起こす可能性があると予測しています。このような血液脳関門の破壊により、血液から脳組織への白血球（自動免疫攻撃細胞）の移動が可能になり、修復機能の減少が通常変性または劣化したミエリンを攻撃できるようになります。オリゴデンドロサイト細胞によって提供されます。ミエリンに対するこのような白血球攻撃は、長い間多発性硬化症と関連してきました。

This paper hypothesizes that a stenosis or obstruction at a lower extremity of an internal jugular vein (IJV) would, in accordance with the physics of fluid dynamics, cause a standing pressure wave within the vein. This pressure wave would possess regions of large pressure fluctuations and other regions of relatively little fluctuation which also have substantially lower peak pressure values. If the wavelength of the hypothesized pressure wave is comparable to the distance from the obstruction to the venule end of the capillary bed, then a region of high pressure fluctuation would exist at the venules. Depending on the degree of obstruction, the pressure fluctuations at the venules of the capillary bed would be substantially greater than those that would exist in a healthy unobstructed vein. This increase in blood pressure fluctuation located at the venule end of the capillary bed, which would be equivalent to local hypertension, is predicted to reduce the pressure drop across the bed which, in turn, would reduce blood flow through the bed in accordance with Darcy's Law. Such a reduction in blood flow through the bed would be accompanied by a reduction in the transfer of oxygen, glucose and other nutrients into the brain tissue in accordance with Fick's Principle. The reduction in oxygen levels in the brain tissue (i.e. hypoxia), would, in turn, be associated with increased fatigue and decreased mental acuity in the subject patient. Also the deprivation of oxygen in the brain tissue may result in the death of oligodendrocyte cells, which, in turn would result in the deterioration of the myelin surrounding the brain's neural axons. In addition, the paper also predicts that, in cases of extreme obstruction, the predicted localized hypertension at the venule end of the capillary bed may be sufficiently high to cause a localized disruption in the blood-brain barrier. Such a disruption of the blood-brain barrier could then allow the migration of leukocytes (auto-immune attack cells), from the blood into the brain tissue, enabling them to attack myelin, which has degenerated or deteriorated from the reduction in repair function normally provided by oligodendrocyte cells. Such leukocyte attack on myelin has long been associated with multiple sclerosis.