Page:EB1911 - Volume 19.djvu/457

 of the superficial association fibres of the cerebral cortex affects especially the frontal and central convolutions, and is the earliest and most constant microscopical change in progressive paralytic dementia; it is accompanied usually by meningeal and vascular changes, atrophy of the nerve cells, and proliferation of the neuroglia (fig. 11); especially characteristic is the perivascular infiltration with lymphocytes and plasma cells (see Plate II., fig. 7). It was indeed thought that this condition of the vessels was pathognomonic of general paralysis; it certainly is not, for it is found throughout the central nervous system in sleeping sickness and cerebro-spinal syphilis (Plate II., figs. 8 and 9). It sometimes occurs in the neighbourhood of cerebral tumours but it is not found in uraemia or lead encephalitis. Possibly new methods may enable us to show changes of structure in diseases such as epilepsy and delusional insanity, in which hitherto no naked eye or microscopical structural defects accounting for the symptoms have been certainly demonstrated. In conditions of acute mania there is usually considerable vascular engorgement. We should, however, probably be more correct in assuming that insanity (especially those forms in which there is neither amentia or dementia) is due to alterations in the quality rather than the quantity of blood in the brain. The primary dementia of adolescence, which in 80% of the cases occurs before the age of 25, in which hereditary taint is most common, and which frequently is accompanied by, or terminates in, tuberculosis, can be explained by the effect of toxaemic conditions of the blood on cerebral neurones with an inborn low specific energy and metabolic activity. The histological changes found in the brain do not serve to explain the symptoms and we must look to bio-chemical changes in the body acting upon an innately unstable brain to explain the problems of the disordered mind in this disease.

Microscopical Changes in Degeneration of the Neurone.—About 1850, Waller demonstrated that a nerve fibre underwent degeneration to its termination when separated from its cell of origin; hence the term “Wallerian degeneration.” Embryological researches by Professor His showed that the axis-cylinder process (the essential conducting portion of the nerve fibre) is an outgrowth of the nerve cell. The cell, therefore, is the trophic and genetic centre of the nerve fibre. Acute alterations and death of the nerve cells may occur from toxic conditions of the blood; from high fever (107°-110° F.); arrest of the blood supply, as in thrombosis and embolism; or actual destruction by injury, haemorrhage or inflammation. These morbid processes produce, as a rule, bio-chemical as well as morphological changes in the nerve cell and its processes. Space will not allow of a full description, but some of these changes are indicated in figs. 18-22, with explanatory text. When a nerve cell dies, the nerve fibre undergoes secondary degeneration and death; that is to say, the whole neurone dies, and regeneration, at any rate in the higher vertebrates, does not take place. Restoration, or partial restoration, of function is due to other structures taking on the function, and the more specialized that function is, the less likely is restoration to take place. If, however, a peripheral nerve is divided, its component fibres are merely severed from their cells of origin. All that portion of the nerve which is in connexion with the nerve cells of origin practically undergoes no change. The peripheral portion undergoes degeneration, but from the central end of the nerve new axis cylinders again grow out and a new nerve is formed. With this regeneration comes restoration of function, which may be hastened by suturing the ends of the cut nerve. A similar regeneration, however, does not occur after section of fibres of the white matter of the central nervous system, and this may be due to the fact that the nerve fibres of the white matter of the cerebro-spinal axis possess no nucleated sheath of Schwann, which, by the light of recent investigations, is shown to play an important part in regeneration; in the writer’s opinion, the neurilemmal sheath of the old fibre forms a new protoplasmic basis, into which the axis-cylinder from above grows, the passage of stimulus determining its function. Fig. 17, Nos. 1-8, with explanatory text, shows the changes which occur in degeneration and regeneration of a peripheral nerve after section, with loss of function; and subsequent union, with restoration of function. The writer, in conjunction with Professor Halliburton, has shown that the characteristic microscopical changes in the myelin sheath which occur in the process of degeneration are due to a splitting up of the complex phosphoretted substance “protagon” into glycero-phosphoric acid, choline and-oleic acid by a process of hydration. The Marchi reaction, which has been found so useful for demonstrating degeneration of the central and peripheral nervous systems, is dependent upon the fact that the myelin sheath, after hardening in a solution of bichromate of potash, does not turn black when acted upon by osmic acid, whereas the simpler non-phosphoretted fatty product of degeneration is stained black. When the Marchi reaction of degeneration is fully developed, it has been ascertained that the nerve yields no phosphorus. The degeneration resulting from section of a nerve is termed secondary, to distinguish it from another, primary, due to slow