The number of neurofilaments and microtubules present in nerve fibers was determined for sciatic nerves from adult mice and from rats of three different ages. More microtubules than neurofilaments were found in nonmyelinated fibers; the ratio of tubules/filaments was reversed in myelinated fibers and was found to change with axon caliber independent of the presence of a myelin sheath. A series of regression analyses indicated that axon caliber correlates best with the sum of the number of neurofilaments and microtubules per fiber. This correlation was only slightly better than that for neurofilaments alone. Axon caliber also correlated better with the filament-tubular material than with the thickness of the myelin sheath. The results were similar for both rats and mice, and age differences were not apparent in the samples of nerves analyzed.Microtubules are present in the cytoplasm of most cell types during interphase, and they may occur in great number during cell division and under a variety of experimental and pathologic conditions (Bloom and Fawcett, '68). These structures may play a major role in influencing cell shape by imparting a rigidity to various regions of the cell (Tilney, '65; Porter, '66; Tilney and Porter, '69). Recent studies have associated microtubules with the mechanism of cytoplasmic movements in simple organisms and in cultures of nervous system tissues (Allen, '64). It has been suggested, also, that the presence of microtubules and neurofilaments in neurons may in some way be related to the flow of protein in and out of neuronal processes (Weiss and Holland, '67; Ochs, Sabri and Johnson, '69; Sjostrand and Karlsson, '69; Karlsson and Sjostrand, '69).Previous studies from our laboratory have emphasized the importance of axon caliber in controlling myelin sheath thickness during growth of peripheral nerve fibers (Friede and Samorajski, '67, '68; Samorajski and Friede, '68b). Because of the possible participation of neurofilaments and microtubules in growth and axoplasmic transport, the concentration of these structures in relation to axon caliber might be of considerable importance. The present study was undertaken in an effort ANAT. REC., 167: 379-388.to relate filament and tubule concentration with axon caliber in sciatic nerves from young and adult rats and mice. MATERIALS AND METHODSThree adult mice, and 3 rats, 6 and 12 days old and 1 adult, were used for the morphologic comparisons of microtubuleneurofilament density in the fibers of sciatic nerves, In addition, osmotically shocked sciatic nerves from four adult rats were included for comparative purposes.For the first study, the animals were anesthetized with Nembutal (30 mg/kg, I.P.) and both sciatic nerves were exposed and covered with cold 4% glutaraldehyde in 0.2 M cacodylate buffer, pH 7.2, After preliminary fixation in situ for approximately ten minutes, small segments of the nerve were excised and placed in fixative for an additional ten hours at 4°C. After a rinse in buffer, the tissues were placed in cacodylate buffer...

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Wallerian degeneration was studied in the phrenic or sciatic nerves of mice following transplantation into Millipore diffusion chambers of 0.22 micron pore size which were implanted in the peritoneal cavity and kept for up to eight weeks. This method positively eliminates the access of nonresident cells to the tissue, at the same time providing proper conditions for tissue survival. Such nerves showed no proliferation of Schwann cells and no evidence for their active role in the removal or digestion of myelin. Schwann cells rejected their sheaths and the latter persisted for weeks, leading either to sheath distension (the sheath becoming wider and thinner) or to collapse (the sheath becoming thicker, collapsing upon the empty axis cylinder). The outer envelope of Schwann cytoplasm separated into pseudopodia rich in microtubules. Sheath rejection led to a slow decay of the myelin in the absence of active phagocytosis. There was profuse fibroblastic proliferation from the epineurium and perineurium, from which cells migrated into the chambers developing fatty change. No evidence was found to link the fatty change in fibroblasts to sheath decay. Diffusion chambers of 5.0 micron pore size were invaded by leukocytes and monocytes. Nerves kept in such chambers showed active phagocytosis of myelin leading to its removal, similar to Wallerian degeneration in situ. Phagocytes were shown to attack selectively the rejected myelin sheaths, distinguishing the latter from the surviving Schwann cells, even though both structures derive from the same cell. The activity of phagocytes in digesting myelin was mediated by a signal which diminished in intensity with time; there was very little active phagocytosis of myelin in nerves that had been predegenerated in 0.22 micron pore chambers. Various modifications of the experiment, including studies with co-cultured peritoneal macrophages or bone marrow, indicate a need for additional activating factors to induce myelin phagocytosis.

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SUMMARY Electron microscopic data on human bridging veins show thin walls of variable thickness, circumferential arrangement of collagen fibres and a lack of outer reinforcement by arachnoid trabecules, all contributory to the subdural portion of the vein being more fragile than its subarachnoid portion. These features explain the laceration of veins and the subdural location of resultant haematomas.Most subdural haematomas due to venous bleeding have been attributed to lacerations in bridging veins. These veins form short trunks passing directly from the brain to the dura mater, almost at right angles to both. Between these two points, bridging veins take a straight course with no tortuosity to allow for the possible displacement of brain.' Trotter2 speculated that subdural haematomas are invariably due to trauma tearing large veins, an interpretation elaborated by Krauland.3 According to Leary,4 the common sources of subdural haematomas are ruptured bridging veins, which tend to yield at the arachnoid junction, producing small openings. Yance5 reported two cases of subdural haematoma caused by rupture of bridging veins, and found that the torn veins were occluded by newly formed thrombotic clots. However, little attention has-been given to the laceration mechanism of bridging veins.The cranial ends of bridging veins are firmly fixed to the rigid dura mater, while the cerebral ends are attached to the movable hemisphere. The falx protects the brain from lateral displacement, but there is no protection against antero-posterior movement. Bearing this in mind, Trotter2 speculated that a sharp blow to the front or the back of the head could easily produce a substantial cerebral dislocation, causing the rupture of bridging veins. Leary4 assumed that bridging veins tear easily because their

The phylogeny of ependymal cells and astrocytes can be traced to a single primitive progenitor the ependymoglia or the tanycyte, respectively. Ependymoglia cells have ependymal perikarya having astrocyte-like processes that terminate subpially in primitive glial footplates. Such cells prevail in primitive nervous systems, but they also persist regionally in the mature mammalian brain. Their fine structure has been studied in many species. An electronmicroscopic study of 8 ependymomas reveals that the neoplastic cells possess features characteristic of primitive ependymoglia; in particular they possess cell processes filled with glial filaments, terminating submesenchymally in a primitive, piston-shaped footplate. The perivascular pseudorosettes of ependymomas are the equivalents of these cell poles. The dominant phenomenon of ependymoma structure appears to be a reversion of cellular organization to the stage of primitive ependymoglia cells. On reviewing 43 ependymomas and 71 astrocytomas 11 neoplasms were found having a tissue structure reminiscent of the evolution of piloid astrocytes from ependymoglia or tanycytes, respectively. These features correspond to transitional stages seen in normal primitive brains. Tumors of this type may be characterized as a tanycytic variant of ependymomas. They appear to be relatively common in the spinal cord and present a source of confusion with piloid astrocytomas.

The structure of macrocapillaries (also called 'sinusoids") in the outer membrane of chronic subdural hematomas was investigated by electron microscopy, with particular attention paid to vascular permeability. One characteristic of macrocapillaries is the frequent formation of gap junctions between adjacent endothelial cells. In endothelial gap junctions 0.6 to 8 microns in diameter, numerous blood components, including red blood cells and plasma, can be seen squeezing or spilling into the interstitial space of the outer membrane. Irregularly deformed erythrocytes are located around the macrocapillaries, and amorphous material is seen among scattered thin collagen fibers. It is suggested that endothelial gap junctions of macrocapillaries play an important role in the leakage of blood, causing enlargement of chronic subdural hematomas.

Nerve fiber populations of the vagus and sciatic nerves of mice were classified according to the number of myelin lamellae present in the sheaths. This method for classifying fiber populations was superior to others used previously since it provided a more sensitive procedure for the analysis of individual fibers and better control over the technical factors involved in tissue processing.The relationship of the number of myelin lamellae in the sheath to axon circumference was found to be linear. In fresh tissue there was one myelin lamella far every 0.24 p increase in axon circumference above a value of 2.32 p (the mean circumference of an average-sized nonmyelinated fiber). A formula was proposed which may be useful for understanding how axons control myelin development and interpreting developmental stages, as well as for evaluating pathologic conditions affecting the peripheral nervous system. The critical diameter above which fibers were found to be myelinated was about 0.8 p for fixed nerve and 1.1 p for fresh nerve. The ratio of axon diameter to fiber diameter ranged between 0.5 and 0.9 and was not related to fiber size.