either locally as the result of an ischaemia, or generally as from some impairment of the blood, such as that prevailing in pernicious anaemia, tend to suffer from fatty degeneration; and at first sight it seems somewhat remarkable that under-nourished tissues should develop fat in their substance (figs. 26 and 27, Pl. II.). The fatty matter, however, it must be borne in mind, is the expression of dissimulation of the actual substance of the proteids of the tissues, not of the splitting up of proteids or other carbonaceous nourishment supplied to them.
A part deprived of its natural nerve-supply sooner or later suffers from the effects of malnutrition. When the trigeminus nerve is divided (Majendie), or when its root is compressed injuriously, say by a tubercular tumour, the cornea begins to show points of ulceration, which, increasing in area, may bring about total disintegration of the eyeball. The earliest interpretation put upon this experiment was that the trophic influence of the nerve having been withdrawn, the tissue failed to nourish itself, and that degeneration ensued as a consequence. The subsequent experiments of Snellen, Senftleben, and, more lately, of Turner, seem to show that if the eyeball be protected from the impingement of foreign particles, an accident to which it is liable owing to its state of anaesthesia, the ulceration may be warded off indefinitely. If the eyeball be kept perfectly clean and no organism be admitted from the outside then ulceration will not follow. If, on the other hand, any pathogenic organisms be present the results are disastrous because the tissue, deprived of its nervous trophic supply, has greatly lessened resistance. The bed-sores which follow paralysis of the limbs are often quoted as proof of the direct trophic action of the nerve-supply upon the tissues, yet even here the evidence is somewhat contradictory. Still, there are facts which, for want of a better explanation, we are almost bound to conclude are to be accounted for on the direct nerve-control theory. The common variety of bed-sore is the result of continuous pressure on and irritation of the skin, the vitality and resisting power of which are lowered by a lesion of the cord cutting off the trophic supply to the skin affected. The acute bed-sore is, in some cases, a true trophic lesion occurring, as it may, on parts not subjected to continuous pressure or irritation. Trophic disturbance in the nutrition of the skin may be so great that a slight degree of external pressure or irritation is sufficient to excite even a gangrenous inflammation. Again, a fractured bone in a paralysed limb often fails to unite, while another in the opposite sound limb unites readily, and an ulcerated surface on a paralysed limb shows little healing reaction. A salivary gland degenerates when its nerve-supply is cut off; and the nerves leading up to the symmetrical sloughs in Raynaud's disease have been found in an advanced state of degeneration (Affleck and Wiglesworth). It is just a question, however, whether, even in instances such as these, the nutritional failure may not be explained upon the assumption of withdrawal of the local vasomotor control. There seems to be little doubt, notwithstanding, that one of the chief functions of the nerve cell is that of the propagation of a trophic influence along its axon. When a nerve-trunk is separated from its central connexion, the distal portion falls into a state of fatty degeneration (Wallerian or secondary degeneration). That special trophic nerves, however, exist throughout the body, seems to be a myth. It is much more likely, as Verworn alleges, that the nerves which influence the characteristic function of any tissue regulate thereby the metabolism of the cells in question—in other words, that every nerve serves as a trophic nerve for the tissues it supplies. It is a significant fact that neoplasms contain very few nerve-fibres, even although growing luxuriantly, and there is a doubt whether the few twigs contained in them may not merely have been dragged into their midst as the tumour mass expanded (Young).
Overwork.—The effect of overwork upon an organ or tissue varies in accordance with (a) the particular organ or tissue concerned, (b) the amount of nourishment conveyed to it, and (c) the power of assimilation possessed by its cells. In the case of muscle, if the available nourishment be sufficient, and if the power of assimilation of the muscle cells remain unimpaired, its bulk increases, that is to say, it becomes hypertrophied.
It may be advisable to define exactly what is meant by “hypertrophy,” as the term is often used in a loose and insignificant sense. Mere enlargement of an organ does not imply that it is in a state of hypertrophy, for some of the largest organs met with in morbid anatomy are in a condition of extreme atrophy. Some organs are subject to enlargement from deposition within them of a foreign substance (amyloid, fat, &c.). This, it need hardly be said, has nothing to do with hypertrophy. The term hypertrophy is used when the individual tissue elements become bigger to meet the demands of greater functional activity; hyperplasia, if there is an increase in the number of these elements; and pseudo-hypertrophy, when the specific tissue element is largely replaced by another tissue.
There are conditions in which we have an abnormal increase in the tissue elements but which strictly should not be defined as hypertrophies, such as new-growths, abnormal enlargements of bones and organs due to syphilis, tuberculosis, osteitis deformans, acromegaly, myxoedema, &c. The enormously long teeth sometimes found in rodents also are not due to hypertrophy, as they are normally endowed with rapid growth to compensate for the constant and rapid attrition which takes place from the opposed teeth. Should one of these teeth be destroyed the opposed one loses its natural means of attrition and becomes a remarkable, curved tusk-like elongation. The nails of the fingers, or the hair of the scalp may grow to an enormous length if not trimmed.
True hypertrophy is commonly found in the hollow muscular organs such as the heart, bladder and alimentary canal. As any obstruction to the outflow of the contents throws an increased amount of work on the walls, in order to overcome the resistance, the intermittent strain, acting on the muscle cells, stimulates them to enlarge and proliferate, fig. 28, Pl. II., and gives rise to adaptive hypertrophy. Should there be much loss of tissue of an organ, the cells of the remaining part will enlarge and undergo an active proliferation (hyperplasia) so that it may be made up to the original amount. Or again, in the case of paired organs, if one be removed by operation, or destroyed by disease, the other at once undertakes to carry on the functions of both. To do so a general enlargement takes place until it may reach the size and weight equal to the original pair. This is known as compensatory hypertrophy.
Examples of physiological hypertrophy are found in the ovaries, uterus and mammary glands, where there is an increased functional activity required at the period of gestation. Local hypertrophy may also be due to stimulation resulting from friction or intermittent pressure, as one may see in the thickenings on the skin of the artisan's hands. The extreme development of the muscles in the weightlifting athlete and in the arm of the blacksmith is the result of increased functional activity with a corresponding increase in the vascular supply; this exercise may produce an over-development so excessive as to be classed as abnormal.
In atrophy we have a series of retrograde processes in organs and tissues, which are usually characterized by a progressive diminution in size which may even end in their complete disappearance (fig. 29, Pl. II.). This wasting may be general or local—continuously from the embryonic period there is this natural process of displacement and decay of tissues going on in the growing organism. The functions of the thymus gland begin to cease after the second year from birth. The gland then slowly shrinks and undergoes absorption. From atrophy of their roots, caused by the pressure of the growing permanent teeth, the “milk teeth” in children become loose and are cast off. The ovaries show atrophic changes after the menopause. In old age there is a natural wearing out of the elements of the various tissues. Their physiological activities gradually fail owing to the constructive processes having become so exhausted from long use that the destructive ones are able to overtake them. As the cell fails and shrinks, so does it become more and more unable to make good the waste due to metabolism. This physiological wasting is termed senile atrophy.
General atrophy or emaciation is brought about by the tissues being entirely or partially deprived of nutriment, as in starvation, or in malignant, tubercular, and other diseases of the alimentary system which interfere with the proper ingestion, digestion or absorption of food material. The toxic actions produced in continued fevers, in certain chronic diseases, and by intestinal parasites largely aid in producing degeneration, emaciation and atrophy.
Atrophy may follow primary arrest of function—disuse atrophy. The loss of an eye will be followed by atrophy of the optic nerve; the tissues in a stump of an amputated limb show atrophic changes; a paralysed limb from long disuse shows much wasting; and one finds at great depths of the sea fishes and marine animals, which have almost completely lost the organs
