Schauf C L, Davis F A
J Neurol Neurosurg Psychiatry. 1974 Feb;37(2):152-61. doi: 10.1136/jnnp.37.2.152.
The simplest model for explaining conduction defects in multiple sclerosis (MS) and other demyelinating diseases assumes that the only abnormality present is loss of myelin. The consequences of such an assumption have been investigated by numerical solution of a well-known set of differential equations describing conduction in a model demyelinated axon. In agreement with clinical findings, we show that this model predicts that the temperature at which conduction block occurs is a steep function of the extent of demyelination, so that small temperature increases may block large numbers of conducting fibres. Decreasing calcium concentration (or increasing pH) is calculated markedly to improve the conduction velocity of conducting demyelinated fibres and will, in addition, restore conduction in blocked fibres. The effects of other pharmacological agents have also been computed. The presence of a demyelinating lesion in a nerve fibre is shown greatly to impair the ability of the fibre to conduct repetitive impulses, conduction failing at much lower frequencies than in normal fibres. These calculations provide some insight into the nature of conduction defects in demyelinated nerve, demonstrate that many clinical features of MS are the expected consequence of loss of myelin and do not require the presence of other defects for their explanation, and provide a useful approach to the search for a symptomatic therapy.
用于解释多发性硬化症（MS）及其他脱髓鞘疾病传导缺陷的最简单模型假定，唯一存在的异常是髓鞘缺失。通过对一组描述模型脱髓鞘轴突传导的著名微分方程进行数值求解，研究了这一假设的后果。与临床发现一致，我们表明该模型预测传导阻滞发生时的温度是脱髓鞘程度的陡峭函数，因此温度小幅升高可能会阻断大量传导纤维。计算表明，降低钙浓度（或提高pH值）可显著提高脱髓鞘传导纤维的传导速度，此外，还能恢复被阻断纤维的传导。还计算了其他药理剂的作用。结果显示神经纤维中脱髓鞘病变的存在会极大地损害纤维传导重复冲动的能力，传导失败的频率远低于正常纤维。这些计算为脱髓鞘神经传导缺陷的本质提供了一些见解，表明MS的许多临床特征是髓鞘缺失的预期后果，无需其他缺陷来解释，并且为寻找对症治疗提供了一种有用的方法。
