Flynn T E, Martin J R
J Neurol Sci. 1983 Oct-Nov;61(3):327-39. doi: 10.1016/0022-510x(83)90166-1.
Six-week-old outbred mice were infected intracerebrally with a low dose of the MS strain of herpes simplex virus type 2. About 1% of neurologically abnormal survivors developed paralysis or severe leg weakness during the first three weeks of infection. Weakness persisted with little subsequent improvement. Five to 8 months later, 4 such mice were killed, and each spinal cord was examined in Epon sections in a series of transverse sections along their lengths. All cords had 2 or more major white matter lesions which were typically greatly elongated in the rostrocaudal dimension, as seen in multiple sequential sections. While a lesion's appearance frequently suggested some degree of tract association, its size, contour and position frequently varied from level to level in a manner which is not characteristic of tract degeneration. Further, axons were preserved in these lesions, and had been remyelinated. This was accomplished by a combination of oligodendrocytes and Schwann cells. The only evidence of Wallerian degeneration in these spinal cords was a modest reduction in the cross-sectional area of a white matter column associated with the most severe lesions. These pathological findings are consistent with previous ones in this model. Rostrocaudal elongation of spinal cord lesions may be seen in other animal models of virus-induced demyelination; this and other features reported here have been described in multiple sclerosis.
六周龄的远交系小鼠经脑内接种低剂量的2型单纯疱疹病毒MS株。在感染的前三周,约1%神经功能异常的存活小鼠出现瘫痪或严重腿部无力。无力症状持续存在,随后改善甚微。5至8个月后,处死4只此类小鼠,对每只脊髓沿其长度方向制作一系列横切片,用环氧树脂包埋后进行检查。所有脊髓均有2个或更多主要的白质病变,在多个连续切片中可见,这些病变在前后方向上通常明显拉长。虽然病变的外观常常提示一定程度的神经束关联,但其大小、轮廓和位置在不同水平上常常变化,这并非神经束变性的特征。此外,这些病变中的轴突得以保留,并已重新髓鞘化。这是由少突胶质细胞和施万细胞共同完成的。这些脊髓中沃勒变性的唯一证据是与最严重病变相关的白质柱横截面积略有减小。这些病理发现与该模型先前的发现一致。脊髓病变的前后拉长在病毒诱导的脱髓鞘其他动物模型中也可见到;本文报道的这一特征及其他特征在多发性硬化症中也有描述。