Mise B, Klarica M, Seiwerth S, Bulat M
Department of Pharmacology, School of Medicine, University of Zagreb, Croatia.
Acta Neurochir (Wien). 1996;138(7):862-8; discussion 868-9. doi: 10.1007/BF01411265.
One group of cats had an acrylic screw implanted into the adqueduct of Sylvius, while the other group of animals received a solution of kaolin into the cisterna magna. Three weeks later the dye phenolsulphonphthalein was instilled into the lateral ventricle to ascertain communication between CSF compartments, and thereafter the brain was perfused with formalin. As shown by planimetry of brain ventricles both groups of experimental animals developed hydrocephalus, i.e., coronal surface of brain ventricles was about 10 times larger in kaolin and about 3 times in aqueductal screw experiments than in the controls, respectively. In aqueductal screw experiments communication of CSF between lateral ventricle and subarachnoid spaces was not blocked but only restricted, i.e., an aqueductal stenosis was produced. In kaolin experiments communication of CSF between lateral ventricles and spinal subarachnoid space was blocked by thick meningeal adhesions in the upper cervical region, while the central spinal canal was dilated (hydromyelia) with enhanced CSF communication between it and the lumbar subarachnoid space. We assume that during systolic expansion of brain the CSF is displaced from the cranial cavity toward the spinal subarachnoid space which accommodates an additional volume of CSF primarily due to compliance of the spinal dural sac, while during diastole CSF recoils in the opposite direction. Thus, in case of aqueductal stenosis the undisplaced volume of CSF from the ventricles can be accommodated due to diminution of cerebral blood volume and brain parenchyma so that hydrocephalus develops over time. Since the cervical subarachnoid space is blocked in kaolin experiments the systolic brain expansion forces CSF from basal cisterns via the fourth ventricle into the aqueduct and central canal with consequent development of hydrocephalus and hydromyelia.
一组猫在中脑导水管植入丙烯酸螺钉，而另一组动物在小脑延髓池注入高岭土溶液。三周后，将酚磺酞染料注入侧脑室以确定脑脊液腔之间的连通性，此后用福尔马林灌注大脑。通过脑室平面测量显示，两组实验动物均出现脑积水，即高岭土实验中脑室冠状面比对照组大约大10倍，导水管螺钉实验中比对照组大约大3倍。在导水管螺钉实验中，侧脑室与蛛网膜下腔之间的脑脊液连通未被阻断，只是受到限制，即产生了导水管狭窄。在高岭土实验中，侧脑室与脊髓蛛网膜下腔之间的脑脊液连通被颈上部增厚的脑膜粘连阻断，而中央脊髓管扩张（积水性脊髓炎），其与腰段蛛网膜下腔之间的脑脊液连通增强。我们认为，在大脑收缩期扩张时，脑脊液从颅腔向脊髓蛛网膜下腔移位，脊髓蛛网膜下腔主要由于脊髓硬膜囊的顺应性而容纳额外的脑脊液量，而在舒张期脑脊液则向相反方向回缩。因此，在导水管狭窄的情况下，由于脑血容量和脑实质减少，脑室中未移位的脑脊液量可以得到容纳，从而随着时间的推移发展为脑积水。由于在高岭土实验中颈段蛛网膜下腔被阻断，大脑收缩期扩张迫使脑脊液从脑基底池经第四脑室进入导水管和中央管，从而导致脑积水和积水性脊髓炎的发生。
