Trophic Disorders

TROPHIC DISORDERS, changes in the biochemical processes in tissues of a neurogenic nature. The regulatory influence of the nervous system on tissue nutrition is realized in two ways. On the one hand, the nervous system contains (according to the views of some researchers, which cannot be considered indisputable) central apparatuses for individual types of metabolism (carbohydrate, fat, salt, water, etc.); on the other hand, specific cellular groups of the animal and vegetative nervous systems are particularly closely connected with the metabolism in individual tissues and organs. The trophic influence of the central nervous system is transmitted to organs via general somatic and sympathetic nerves. According to Speransky, the neurotrophic function is not localized in the nervous system but is realized through morphological elements scattered throughout the entire nervous system, both animal and vegetative. The existence of special trophic centers and nerves has not been proven. The very assumption of them is hardly acceptable, since it separates the function of tissues from their nutrition. The nervous system, which regulates the functioning of other tissues, thereby also influences their nutrition (however, I. P. Pavlov admits and even assumes that trophic nerves may exist). Trophic disorders can apparently be caused both by the disconnection between tissues and central nerves and the resulting disappearance or weakening of nervous influence, and by those lesions of the nervous system that are caused by irritation of its peripheral apparatus or carry abnormal trophic excitation to the periphery. From here, the irritation is transmitted to the cellular groups of the nervous system and disrupts, among others, their trophic function. Disturbances of the vasomotor and reflex apparatuses have an auxiliary significance in the origin of trophic disorders. The most studied are trophic disorders of the musculature. They appear in a particularly sharp degree in diseases of the peripheral neuron. As a result of the interruption of the connection between the muscle and the cells of the anterior horn, it ceases to receive, on the one hand, innervation currents, which leads to paralysis, and simultaneously, on the other hand, the trophic influence regulating its metabolism does not reach the muscle. The clinical expression of this is flaccid paralysis with degenerative atrophy. Its morphological essence boils down to the narrowing of muscle fibers, the gradual disappearance of transverse striation, and fatty, and subsequently waxy, degeneration of the fibers. Muscle nuclei proliferate noticeably. Subsequently, connective or fatty tissue develops in place of the former fibers, and along with this, individual muscle fibers increase significantly in size. The chemical composition of the muscle changes; the amount of fat in it increases and the amount of water decreases. A noticeable increase in sodium salts and a decrease in potassium salts occurs. The change in salt content is caused by a violation of the cell membrane, by virtue of which its ionic permeability changes. These changes in chemical composition lie at the basis of the reaction of degeneration. The second form, reflex atrophy, occurs in diseases of the joints and posterior roots. In both cases, dynamic changes occur in the cellular apparatuses of the spinal cord, which entails, among other things, changes in their trophic functions. In joint afflictions, these apparatuses are under the influence of abnormal, excessive irritations coming from the membranes of the diseased joints; in lesions of the posterior roots, on the contrary, these apparatuses are deprived of the usual centripetal impulses flowing to them, which are necessary for normal activity. Proceeding from the idea of a close connection between the tone and nutrition of muscles, Bekhterev bases arthrogenic atrophy on reflex hypotonia caused by joint affliction; according to Bekhterev, reflex vascular spasm also plays a certain role in the origin of these atrophies. Reflex atrophies belong to the category of simple ones and are not accompanied by qualitative changes in electrical excitability. The contractile substance and transverse striation of the muscles are preserved. Muscle fibers only decrease in size; proliferation of muscle nuclei either does not occur at all or is weakly expressed. Amyotrophies are also not uncommon in lesions of the central motor neuron, in particular in hemiplegias. According to Roth, in hemiplegia, they are caused mainly by an insufficient influx of arterial blood due to a coexisting disturbance of the vascular apparatus (vasomotor atrophy). Charcot, to explain cerebral atrophies, assumed dynamic, and then secondary, atrophic processes in the cells of the anterior horns at the beginning of diseases. Diseases of the extrapyramidal system also sometimes cause atrophy of individual muscle groups and even the entire musculature of half of the body. The basic mechanism for extrapyramidal amyotrophies is conceived by analogy with pyramidal ones in the sense of Charcot. If, for the considered forms of amyotrophies, one should admit some participation of the vegetative nervous system in their pathogenesis, then for other forms it is especially significant. It has been experimentally proven that destruction of the boundary sympathetic trunk causes sharp changes in the chemistry of muscles. Carbohydrate metabolism, which plays a huge role in the nutrition and work of the musculature, suffers especially. Amyotrophy occurring in the area of trauma without gross damage to nervous apparatuses, as well as progressive hemiatrophy of the face, owe their origin to disturbances of vegetative innervation. Some forms of muscular atrophy, in which trophic disorders have a clear character of dystrophy, are also attributed to lesions of the vegetative nervous system (Shcherbak). Trophic disorders of muscles in the form of hypertrophy are significantly rarer than amyotrophies. Hypertrophies sometimes occur in hyperkineses of an extrapyramidal character; they are significantly rarer in lesions of peripheral nerves. The nervous system, mainly its vegetative division, takes significant part in the innervation of the skin and its glandular apparatus. The trophics of the skin are reflected both by the complete loss of trophic innervation, due to the interruption of the connection between the skin and the nervous system, and by pathological changes in the latter while maintaining the connection. In such cases, those irritants that act for a long time on the central end of the pathologically changed nerve are of particular importance. Weak but prolonged irritants of the nerve, such as, for example, minor mechanical or thermal trauma, light solutions of chemicals, or infections applied to the nerve, are especially prone to causing trophic disorders of the skin and its appendages. The epithelial covering of the skin shows the greatest trophic dependence on the nervous system. Reflex influences traveling along sensory and vasomotor pathways play a large role in maintaining the proper nutrition of the skin. Therefore, the simultaneous loss or change of trophic influences together with sensory-vascular lesions especially predispose to the appearance of trophic disorders of the skin. However, it is undoubted that the most severe trophic disorders of the skin can occur with complete preservation of sensitivity and vascular reflexes. The experience of the war showed that an acute bedsore in a spinal cord injury sometimes developed after 18 hours with complete preservation of sensitivity (Schlesinger), while the transection of a peripheral nerve or posterior root noticeably affects vascular reactions only on the seventh or eighth day (Breslauer). Also, in ordinary hemiplegia, neurogenic bedsores sometimes occur very quickly after a stroke on the paralyzed limb, which should be distinguished from ordinary ones (Popova). Skin deprived of normal trophic influences to a significant extent loses the ability to resist external irritants. Slight pressure, drying, or an increase in temperature can in these cases grossly disrupt the metabolism in the cells of the skin, lead to their death, and to the formation of necrotic areas as a result of this. Only by placing denervated skin in exceptionally favorable conditions in the sense of protecting it from external irritants is it sometimes possible to preserve its trophics. Upon the formation of necrosis and the loss of local immunity, microorganisms saprophytic in the skin acquire parasitic properties. Thus, in a number of diseases of both the central and peripheral nervous system, trophic ulcers and bedsores (see) arise, especially in those cases where a drop in sensitivity occurs together with the disturbance of trophics. Disturbances of the trophics of the skin and its appendages can also have a more subtle character; such is vitiligo (see). The combination of local atrophy of the skin with improper secretion of sebum and sweat causes the onset of the so-called "glossy skin." A particularly frequent trophic disorder of the skin is shingles (see Herpes, herpes zoster). Trophic disturbances in the water and fat balance of the skin and subcutaneous tissue have a diverse clinical reflection. Most cases of dystrophia adiposogenitalis (see Dystrophy) are attributed to the lesion of the central apparatuses of trophics located on the floor of the third ventricle.

To the same category of central dystrophies belong excessive obesity or weight loss in chronic stages of epidemic encephalitis, the melting away of fat and musculature in tuberculous meningitis. On the other hand, deposits of fatty streaks along the course of individual nerves are observed. The retention of water by the skin and subcutaneous tissue leads to the formation of edema. Combining sometimes with the induration of connective tissue, they produce a picture of firm, woody edema. Trophic disorders of the skeletal system are most often expressed by atrophy of the bones. The cortical layer thins, the trabeculae loosen, and the boundaries between the spongy and dense layers are blurred. As a result, the density of the bone tissue decreases and the susceptibility to its fractures increases. Atrophy of some parts is sometimes accompanied by hypertrophy of other parts of the bone. Such a process lies at the basis of neurogenic arthropathies in tabes and syringomyelia. Simple bone atrophies are observed in lesions of peripheral nerves or anterior horns (poliomyelitis). Traumatic injuries of the nervous system during wartime have especially expanded the range of trophic disorders occurring in lesions of the peripheral nervous system. In one part of them, trophic disorders are localized in the area of the direct nerve injury, in another, they extend far beyond its limits. Such are the atrophies of muscles and subcutaneous tissue in combination with hypertrichosis, hyperhidrosis, and decalcification of bones, occurring in places distant from the site of the wound and included in the reflex syndrome of Babinski and Froment. From this example, it is evident that trophic disorders, sometimes occurring in isolation in individual tissues, are frequently combined with one another. Trophic disorders are encountered as individual symptoms in a vast number of diseases of all parts of the nervous system. Grouping into regular combinations, in the absence of another primary disease, they constitute a large group of trophoneuroses and trophoneuropathies (see Amyotrophy, Angioneuroses, Angiotrophoneuroses, Trophoneuroses).

M. Neiding. Recently, a new view on the trophic function of the nervous system has appeared (A. D. Speransky and his school), which changes the understanding of the essence of trophic disorders. The neurotrophic function as such does not have a definite localization; the morphological elements corresponding to it are scattered throughout the entire nervous system, both central and peripheral (including the autonomic); each of the elements is connected with all nerve elements and together with them carries out its function; thanks to this, trophic disorders of any specific part of the organism are not independent, limited processes associated with a known localization in the nervous system, but the result of a series of processes, one of the manifestations of continuously changing combinations that form within the nervous system. From this, it is clear that any irritation of any part of the nervous system, by causing a reorganization of intraneural relations, can produce changes of a neurotrophic character not only in the immediate but also in distant regions of the organism. When very persistent changes arise, the matter is not limited only to the loss of any function, but a focus of new painful excitations is created, involving other healthy parts in the process. Every nerve irritation falling on the altered nerve tissue will primarily be reflected in the area of the affected sections, intensifying the painful irritation existing there, and then be transmitted to neighboring sections. In connection with such an understanding of the essence of trophic disorders, the proposed methods of treatment also stand. Since the pathological process develops as a result of occurring intraneural changes, treatment must also be directed toward disrupting the established combinations and creating new ones. Surgical interventions used until now for trophic disorders are too strong irritants and inflict severe trauma on the nervous system, which can cause a worsening of the process and relapse; if any benefit is obtained from surgical intervention, it depends only on the act of intervention itself, thanks to the rearrangement of the established intraneural combinations that occurs, but for this, it is better to use weaker irritants that are less traumatic to the nervous system. Over a number of years, A. D. Speransky studied various irritants not associated with anatomical damage to the nervous system but capable of creating at least a temporary reorganization of intraneural relations within it. Various methods were tested, and finally, he settled on the method of local anesthesia with novocaine. Prof. Vishnevsky created his own method of local anesthesia, known as the method of "creeping infiltration," which blocks that part of the nervous system that was usually subjected to transection. Since trophic disorders are not associated with a specific part of the nervous system, these measures can be directed not at the tissue process or the nearest nerve parts, but at any part of the nervous system; influences directed at the nervous system, by virtue of its special structure and operation, are never local, but invariably reflect on the work of many of its parts, which ensures a change in painful manifestations at the periphery as well. In gangrene, in trophic ulcers of the lower extremities, the nerve network of the lumbar region is blocked, and a continuous circular block of the entire limb above the affected parts is also used. The therapeutic effect was monitored over many months.