A case of congenital cerebellar tumor is reported. The tumor is composed of a few incomplete tubular structures analogous to the neural tube, and of neuroblastic, mature ganglionic, astrocytic, ependymal and undetermined neuroepithelial cells. A tentative diagnosis of congenital cerebellar neuroepithelial tumor with multiple divergent differentiations is made: the histogenesis is discussed. From a histogenetic point of view this tumor is given the provisional name of matrix cell tumor.
A congenital anaplastic infratentorial ependymoma, occurring in a female infant whose sister also died of brain tumor, is described. The tumor, located in the cerebellum and the fourth ventricle, is characterized by predominantly undifferentiated neuroepithelial cells associated with numerous mitoses, and partially of the cells demonstrating differentiation into ependymal cells and astrocytes. Of special interest is the fact that the elder sister of the patient had also died of a congenital glioma located in the cerebellum and the fourth ventricle, which leads to the discussion about the influences of genetic factors in the development of the familial gliomas as well as about the histogenesis of the tumor examined.
Unilateral transient cerebral ischemia was produced in Mongolian gerbils by clipping the left common carotid artery for 1 h. About 60% of the gerbils with neurological symptoms had post-ischemic seizures. The majority of those that had seizures died within a few days, and sections of their cerebral cortices contained many dark and shrunken neurons. However, the gerbils that did not have seizures survived without any severe complications. In the cerebral cortex of the latter, the neurons with diffuse or peripheral pallor of the perikarya were seen along with a small number of dark and shrunken neurons. Diffuse pallor occurred within a few hours following ischemia in layers III, V, and VI, and disappeared 1 or 2 days after recirculation. Electron microscopically, these neurons showed dispersion of ribosomes, simple and elongated profiles of rough endoplasmic reticulum (r-ER), clustered vacuoles, and mild to moderate mitochondrial swelling. Occasional net-like tubulomembranous structures, probably derived from r-ER, were observed. On the other hand, peripheral pallor became apparent after 5 days following ischemia, usually involving layer II first and gradually extending to the deeper layers. Concomitantly, the amount of neuropil decreased and the dendrites exhibited tortuosity and irregularity in layer II. Electron microscopically, these neurons showed marked swelling of peripheral perikarya and polyribosomes and organelles were located peripherally to the nuclei. In addition, numerous degenerated axon terminals and distended dendrites were observed around the neurons. These observations indicate that diffuse pallor represents damage directly induced by ischemia and subsequent recirculation, while peripheral pallor is the delayed and remote effect of ischemia, probably due to degeneration of neuronal processes.
Numerous investigations have so far been conducted in an attempt to explor the anatomical substratum of the blood-brain barrier phenomenon. With the introduction of electron microscopy, it has been confirmed that the cerebral capillaries have no perivascular spaces (DEMPSEY and WISLOCKI~), FARQUHAR and HARTMAN~), MAYNARD, SCHULTZ and P E A S E ~~~, AMBO and SHIMODA~)~), etc.). Recently, it has become a predominant opinion that the characteristics of the pericapillary fine structure is of considerable importance as a blood-brain barrier.Another problem as to the blood-brain barrier lies in the developing central nervous system. In fetuses and young mammals, the barrier is assumed to be more or less undeveloped. BEHENSEN (1927)Q established this assumption in the brain of the newborn mice by giving trypan blue.With an electron microscope, an attempt has been made to study certain morphological elements as to the developing blood-brain barrier. In addition, an experiment on the injured barrier in mature animals was carried out to clarify the morphological basis of the barrier. MATERIALS AND METHODSAlbino rats of Gifu-strain were used. The specimens for electron microscopy were obtained from the developing rats of 8 fetuses, older than the 14th gestation day, and 15 sucklings, younger than the 14th postnatal day. Seven adult rats were also examined. The gestation day of the fetus was started to be calculated from the night a t which time each female rat was kept in a cage together with a male rat.On the 14th, 16th, and 19th days of gestation, respectively laparotomy was carried out on the pregnant females under ether anesthesia. Every fetus in either side of the bicornic uterus was given a single injection of a tracer solution via amniotic circulation (As to the solution, it is mentioned below in detail). Fetuses in the other uterine horn were remained untreated. Leaving an interval of 30 minutes after giving the injection, the living fetuses were separated from their mother.In these sucklings, a single injection of the tracer solution was given to their femoral vein as well as in the adult rat. The cerebral tissues were examined 30 minutes after giving the injection in accordance to the case of fetus. The tissues were obtained not only from the cerebral cortex, or the cortical anlage of the fetal cerebrum, but also from the other organs such as t h e kidney and the heart muscle. An additional experiment of cerebral herniation was performed a s follows: Male adult rat received a trepanation of the skull, 3 m m in diameter, under ether anesthesia. At the Sucklings in the Znd, 8th. and 14th days of age were examined.
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