代償性水頭症とシャント手術の意義

―HRPと電顕による脳室上衣細胞の実験的観察―

抄録

The author defined the term “compensated hydrocephalus” as follows: It demonstrates normal cerebrospinal fluid pressure but has enlarged ventricles in its chronic stage after the impaired cerebrospinal fluid (CSF) circulation being restored through a pathological subsidiary pathway. A series of animal experiments was performed to reveal a part of the pathophysiological conditions and the effects of shunting procedures as a treatment of hydrocephalus.
Adult mongrel dogs were the choice as experimental animals. Kaolin suspension (20 mg/kg. 0.7 ml of artificial CSF) was introduced into the cisterna magna and dogs were observed for more than two months. Using Pudenz's shunt system, ventriculo-peritoneal shunt operations were performed for a group of the compensated hydrocephalus and these dogs were observed for an additional three weeks thereafter.
After the injection of 30 mg of Horseradish Peroxidase (HRP) as a tracer, the perfusion of the 2% glutaraldehyde and 2.5% paraformaldehyde fixative solution was made at 30 min., 60 min., 2 hrs. and 3 hrs. for electron microscopical study of the ependymal and subependymal layers of the ventricular system in these three groups.
There was neither interruption nor deficit of the ependyma of the lateral ventricle of the compensated hydrocephalus as it might be observed in the specimen from acute hydrocephalus, but there were some spindle shaped separations of the ependymal intercellular spaces. The organelles such as endoplasmic reticulum were reduced in number considerably and this indicated the trace of the so-called CSF edema. In shunted hydrocephalic dogs, these organelles restored its normal figure. The injected HRP was absorbed quickly through the ependymal intercellular space in hydrocephalic dogs. The most marked difference in these three groups became prominent 2 hrs. after the injection. Although in hydrocephalic dogs, the HRP already disappeared from the ependymal intercellular spaces, in shunted dogs, it remained markedly in the ependymal intercellular space as well as in the depth of the myeline sheath. The latter demonstrated a close similarity to the picture seen in normal dogs. The author considered that the movement of the HRP in the ependymal and subependymal layers indicated newly established transependymal pathological pathways in the hydrocephalic dogs and this is improved in the dogs in which shunting procedures were added.
This investigation showed that the compensated hydrocephalus, which was reached at the heavy cost of the brain parenchyma, was not following the process to cure in spite of its normal CSF pressure. The ependymal and subependymal layers returned to its normal morphological conditions after the shunt operation.