Schwyzer R U, Henzi H
Incella, CH 6614 Brissago, Switzerland.
Med Hypotheses. 1988 Nov;27(3):167-79. doi: 10.1016/0306-9877(88)90137-5.
The conditions which lead to a plaque of demyelination in the retrobulbar optic nerve are discussed. Growth of the plaque occurs along venules as small fingerlike sleeves which develop outwards from the contour of the plaque. This occurs slowly and at intervals; the very gradually expanding lesion remain for a long time clinically silent. It is here postulated that the change to clinical disease is induced if cells digesting myelin debris settle in a more distal part of the perivascular space of a vein, than during the subclinical phase. In sufficient numbers these cells will impede the movement of molecules from extra-cellular fluid surrounding nodes of Ranvier into cerebrospinal fluid. A restriction in this vital drainage pathway results in oedema causing disturbed signal transmission in neurons passing through the veins drainage territory. Depending on intensity this can induce the characteristics symptom of blurred vision. These concepts have been used to speculate on sequential changes in neurons and to relate them to various phases of the disease. This seems to be justified as the pattern evolved corresponds well with the clinical symptomatology.
本文讨论了导致球后视神经脱髓鞘斑块的相关情况。斑块沿着小静脉生长,呈细小的指状袖套样,从斑块轮廓向外延伸。这种生长过程缓慢且不连续;病变逐渐扩大,在临床上长期无症状。本文推测,如果消化髓鞘碎片的细胞在静脉血管周围间隙的更远端聚集,相较于亚临床阶段,就会引发临床疾病。当这些细胞数量足够多时,会阻碍分子从郎飞结周围的细胞外液进入脑脊液。这一重要引流途径的受阻会导致水肿,进而干扰通过静脉引流区域的神经元的信号传递。根据其严重程度,这可能会引发视力模糊这一典型症状。这些概念已被用于推测神经元的相继变化,并将其与疾病的各个阶段联系起来。鉴于所提出的模式与临床症状学高度吻合,这似乎是合理的。