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.
 | |
| Fig. 17.—Diagram to illustrate various stages in degeneration and regeneration of medullated nerve fibres. | |
| 1, | Normal medullated nerve with node of Ranvier. |
| 2, | Degenerated nerve, ten days after section, showing degenerated myelin stained black; disappearance of axis-cylinder. |
| 3, | Central end of cut nerve, showing at the top an axis-cylinder budding out, proliferated neurilemmal cells, and still some degenerated myelin in sheath. |
| 4, | Peripheral cut end of same, showing proliferated neurilemmal cells, still some degenerated myelin. |
| 5, | Complete absorption of degenerated myelin, proto-plasmic basis of new fibre formed out of neurilemmal cells. |
| 6, | A new fibre, with axis-cylinder. |
| 7, | Central end of cut nerve at junction, showing an axis-cylinder sprouting and forming a number of axis-cylinder processes, which grow into the peripheral end to form new channels of conduction. |
| 8, | Is a new regenerated fibre resembling a sympathetic fibre in having as yet no myelin sheath; as the nerve becomes excitable and stimulus passes, a myelin sheath is formed. |
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,
Fig. 18.—Diagram drawn from photomicrograph to show different forms of neuroglia cells in a patch of sclerosis secondary to degeneration and disappearance of the neurones. Observe the large branched cells of Deiters.
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
