Stahl W, Kaneda Y
Department of Infectious Diseases, Tokai University School of Medicine, Kanagawa, Japan.
Parasitology. 1997 Mar;114 ( Pt 3):219-29. doi: 10.1017/s0031182096008505.
The prevailing hypothesis concerning the pathogenesis of toxoplasmic hydrocephalus alleges that (a) parasites invade and destroy the ependymal lining of the lateral ventricles, followed by (b) the sloughing of masses of degenerating ependymal and inflammatory cells leading to obstruction of the ventricular foramina and aqueduct of Sylvius, thereby initiating the hydrocephalus. Our observations in chronically infected mice indicate otherwise. Parasite invasion of the ependyma was not detected; the intraventricular masses of cellular 'debris' contained neither ependymal nor inflammatory cells; and obstruction of the ventricular foramina and/or aqueduct was not seen. As an alternative hypothesis, we suggest the development of hydrocephalus in the infected mice was consequent to severe leptomeningeal inflammation blocking the subarachnoid space and impeding the resorption of cerebrospinal fluid by the arachnoid villi. Narrowing of the aqueduct of Sylvius, when present, was adjudged the result, not the cause of the hydrocephalus, due to compression of the midbrain by the enlarging lateral ventricles.
（a）寄生虫侵入并破坏侧脑室的室管膜内衬，随后（b）大量变性的室管膜和炎性细胞脱落，导致脑室孔和中脑导水管阻塞，从而引发脑积水。我们对慢性感染小鼠的观察结果却并非如此。未检测到寄生虫对室管膜的侵袭；脑室内的细胞“碎片”团块中既没有室管膜细胞也没有炎性细胞；也未发现脑室孔和/或中脑导水管阻塞。作为另一种假说，我们认为感染小鼠发生脑积水是由于严重的软脑膜炎阻塞了蛛网膜下腔，并阻碍了蛛网膜绒毛对脑脊液的吸收。当存在中脑导水管变窄时，这被判定为脑积水的结果而非原因，因为扩大的侧脑室对中脑产生了压迫。
