Some tumours are highly vascular and a large thin-walled vessel may suddenly rupture and cause an apoplectic fit. If the growth is situated in a portion of the cortex having some special localizing function, e.g. the motor area (vide fig. 7), it may give rise to epileptiform convulsions, starting in a limb or definite group of muscles; but the irritation usually spreads to the whole motor area of the same side, and even extends to the opposite hemisphere, by an overflow of the discharge through the corpus callosum. In such case there is loss of consciousness. If, however, the tumour destroys the cerebral cortex of a particular region, it may give rise to a paralytic lesion, e.g. paralysis of the arm (vide Plate I., fig. 4).
Organic diseases of the blood-vessels, or of supporting and enclosing tissues, produce secondary degenerations of the nervous system. The symptoms, like the lesion, are obvious, coarse and obtrusive; frequently arising suddenly, they may in a short time terminate fatally, or tend towards partial or complete recovery. Various forms of motor and sensory loss and disturbance of function may arise, indicating destruction or disturbance of particular regions of the central nervous system; and degenerations in certain tracts and systems of fibres arise, corresponding in histological character with those observed when a nerve fibre is separated from its cell of origin by section (secondary degeneration of Waller and Türck) (vide fig. 8, with explanation). This form of degeneration must be distinguished from primary degeneration, which is due to an inherent nutritional defect of the nerve cell and all its processes (the neurone), in which a regressive metamorphosis occurs; it starts in the structures of the neurones latest developed (namely, the myelin sheath and the fine terminal twigs of the axis cylinder and dendrons), and proceeds back to the main branches and trunk, eventually destroying the trophic and genetic centre itself, the nerve cell. These primary degeneration processes are insidious in origin, progressive in character, and nearly always fatal in termination; they affect definite systems, groups and communities of neurones in a progressive manner, and, therefore, are associated with a progressive evolution of symptoms, related to the structures affected (vide figs. 9 and 10).
To cite some examples: (1) Locomotor ataxy, on the one hand, is a primary degeneration affecting the afferent system of neurones; it is characterized by muscular incoordination without wasting, inability to stand with the eyes shut, lightning pains in the limbs, absent knee-jerks, Argyll-Robertson pupils, and other symptoms pointing to a morbid process affecting especially the afferent sensory system-of neurones. (2) Progressive muscular atrophy, on the other hand, is a disease of the efferent motor system of neurones of the brain and spinal cord, characterized by progressive wasting of groups of muscles innervated by groups of neurones which are undergoing degeneration. A fatal termination to this disease frequently arises from affection of the medulla oblongata, causing what is known as bulbar paralysis. Infantile paralysis is an acute inflammation of the anterior horns of the spinal cord, causing destruction of the spinal motor neurones of the anterior horn. It differs from the above chronic disease in its sudden onset and non-progressive character; it resembles it in producing paralysis of muscles without sensory disturbance. (3) General paralysis of the insane is a degeneration which begins in the association system of neurones of the cerebral cortex, but which may be, and frequently is, associated with degeneration of the afferent or efferent systems (fig. 9).
Neuroses and psychoses have not hitherto been satisfactorily explained by definite morphological changes in the brain (Plate I., fig. 1). We know little or nothing accurately about the morbid histology of insanity, except as regards the morphological changes met with in cases of amentia and dementia. The conditions of amentia, namely, idiocy and imbecility, are associated with arrest of development of the brain, as a whole or in part, the naked-eye evidence of which may be afforded by small size and simplicity of convolutions of the brain as a whole or in part (Plate I., figs. 2, 8 and 10); and the microscopical evidence by arrest of development, or imperfect development, of structures connected with the higher functions of the mind. namely, the association neurones in the superficial layers of the cerebral cortex (fig. 11). Conditions of dementia, primary or secondary, are associated with progressive decay and atrophy of the superficial layers of the grey matter of the cortex, and nakedeye evidence thereof is afforded by partial or general wasting of the cerebral hemispheres, accompanied with thickening of the pia-arachnoid membrane, atrophy of the convolutions, and with deepening and widening of the intervening sulci (Plate I., fig. 7).
Motor Cells, drawn from Microphotographs of Preparations stained by Nissl method to show Microchemical Changes produced by various diseases. Fig. 12.—Normal motor cell from cerebral cortex, showing a mosaic pattern of the cytoplasm due to a substance stainable by basic aniline dyes; this stainable substance exists also on the dendrons. By comparing the appearances of this cell with the other figures a just idea can be obtained of the morbid changes which result in various pathological conditions. Fig. 13.—Cell from a case of hyper-pyrexia—disappearance of the mosaic pattern, substance uniformly stained; absence of the chromatic elements on the dendrons, due to a precipitation of cell-globulin by the heat. Fig. 14.—Cell in an advanced stage of coagulation necrosis, complete absence of mosaic pattern; diffuse fine dust-like stain; breaking off of the processes; all caused by softening of the brain from vascular obstruction. Fig. 15.—Another specimen from the same brain in a still more advanced stage of destruction, and showing a phagocyte attached to the cell and devouring the decayed structure. Fig. 16.—A cell with enormously swollen nucleus, the result of hydration clue to absorption of fluid after ligature of cerebral vessels. Such a cell will probably recover. |
The cerebro-spinal fluid fills up the space in the cranial cavity caused by the atrophy of the brain; consequently there is a great excess of this fluid. Before general paralysis was recognized as a disease some of the cases which died suddenly in a fit were doubtless termed serous apoplexy. This wasting so characteristic of general paralysis is especially due to atrophy of the cells and fibres of the superficial grey matter of the cortex, sections of which, examined microscopically, after suitable methods of staining have been employed, show great poverty, or complete loss, of three sets of delicate myelinated fibres, namely, tangential, super-radial and the inter-radial corresponding to the line of Baillarger. This degeneration
