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 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).

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).

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