FIG. 58.
Motor and trophic centres and fibres in spinal cord
Diagram of the Arrangement and Connection of Motor and Trophic Centres and Fibres in the Spinal Cord and Motor Nerve (after Erb):a, motor fibre of spinal cord from the brain tod, the motor cell, which is joined to the musclemby the motor nerve;b, trophic cell in the spinal cord for the muscle, to which it is joined by the trophic fibrebʹ;c, trophic cell in the spinal cord for the motor nerve, to which it is joined by the trophic fibrecʹ;s, a fibre bringing sensory (reflex) impulses to the cell.Ifdis destroyed, the fibres frombandcperish with it, and the result is paralysis and atrophy of the muscle and degeneration in the motor nerve—e.g.poliomyelitis anterior. Ifbis destroyed, the muscle atrophies, and paralysis is a secondary result—e.g.progressive muscular atrophy. Ifcis destroyed, the nerve degenerates, and paralysis and atrophy of the muscle are secondary results—e.g.neuritis with reaction of degeneration. Ifais destroyed, voluntary power is lost, but reflex power remains, and no atrophic changes occur—e.g.lateral sclerosis. If the motor nerve is cut betweendandm, the result is the same beyond the division as when the motor cell is destroyed.
HYPERTROPHY.—Trophic changes are not limited to the process of atrophy. There are conditions of hypertrophy of supposed nervous origin. Samuel considers the hypertrophy of one testicle which attends atrophy of the other from section of its nerve as an example of this. It has been ascertained that one kidney hypertrophies when the other is atrophied or extirpated. When the spleen is removed the lymphatic glands increase in size. But these facts are capable of another explanation—viz. that increased demand upon the organ leads to its increased growth. Hypertrophy of the skin and of the tongue is seen in cretins in contrast with the deformity of the body and atrophy of the limbs. A hemihypertrophy of the face has been noticed in several cases, the counterpart of hemiatrophy; and in one case a unilateral hypertrophy of the entire body was observed.85The local thickening of the skin known as ichthyosis hystrix, and other hypertrophies of the skin, certain deposits of pigment, and vitiligo, have been ascribed to nervous causes. Mitchell has recorded cases of abnormal growth of the nails and hair after injuries to the nerves, and similar phenomena have followed central lesions. He has also described a thickening of the skin of the first three fingers and of the back of the hand following a wound of the brachial plexus. These conditions of the skin and its appendages indicate an abnormal activity in the cells of the affected part, a rapid metabolism and reproduction, resulting in an undue production of tissue, apparently dependent on nervous impulses reaching the cells from a distance. The insane ear may be mentioned in this connection as a trophic disturbance due to central lesion.
85Ziel,Virchow's Archiv, xci., S. 92.
MYXŒDEMA(cachexie pachydermique) is a disturbance of nutritive processes characterized by a production of mucin, which is deposited in all the tissues of the body, but especially in the subdermal connective tissue.86It is considered by the majority of authors a trophic neurosis, and is therefore considered here.
86Sir William W. Gull, “On a Cretinoid State supervening in Adult Life,”Trans. Clin. Soc. London, 1874, vol. vii. p. 170; Ord, “On Myxœdema,”Med.-Chir. Trans., 1878, vol. lxi. p. 57; Mahomed,Lancet, 1881, ii. No. 26; Hadden,Brain, 1882; W. A. Hammond,Neurological Contributions, 1881, i. p. 36; Ballet,Archives de Neurologie, 1881, vol. iii. p. 30;Schmidt's Jahrbucher, vol. clxxxix. p. 30, and cxcviii. 264; “The Brown Lectures,” Victor Horseley,Lancet, Jan., 1886.
PATHOLOGY.—In the few autopsies which have been made an increase in the connective tissue of all the organs has been found, in the meshes of which a thick, transparent, slimy substance (called animal gum), consisting of mucin, is present. This may compress and destroy the parenchyma of the organs involved. There is also found a thickening of the coats (adventitia and media) of the vessels. An atrophy of the thyroid gland has occurred in every case, and experimental extirpation of the thyroid in animals produces symptoms so nearly identical with those of myxœdema that this is considered the chief pathological feature of the disease. Whether this atrophy is due to a compression by the mucin deposited, or is due to a disease of the trophic centres of the thyroid in the medulla, or is a primary affection of the gland, remains to be determined.
ETIOLOGY.—The actual causation is unknown. Cold and mental shock have been considered exciting causes in some cases. Women are much more liable to the disease than men, and it develops after the age of forty in the majority of cases. It may occur in childhood and result in acretinoid state. Syphilis and tuberculosis do not appear to be etiological factors.
SYMPTOMS.—The disease begins gradually, and the nervous symptoms or the local œdema may appear together or in succession. The patient notices a thickening of the skin, which becomes dry, rough, and scaly. The thickening is uniform and involves the entire body. It is most marked where the subdermal connective tissue is loose, as in the cheeks, lips, eyelids, and in all parts where the skin is thrown into folds. The hands and feet do not escape. The thickened skin is hard, and does not pit on pressure, thus differing from ordinary œdematous swelling. It appears of a waxy color, and is free from perspiration, the sweat-glands becoming atrophied from pressure. The hair may fall out or become woolly and brittle, and may change its color. In a few cases spots of pigment have appeared on various regions.87The nails are brittle. The teeth are carious. The mucous membranes show similar changes, and the mouth and tongue, rectum and vagina, may be so swollen as to impair their respective functions. Digestive disturbances, constipation alternating with diarrhœa, and uterine hemorrhages, which occur, are ascribed to this cause. Albumen is occasionally found in the urine, but is not a constant symptom. The nervous symptoms are constant. The patients complain of paræsthesiæ and anæsthesia of the extremities or over the entire body, and the special senses may be impaired, as well as the tactile sense. They are very liable to severe attacks of neuralgia. They suffer from subjective sensations of cold, and are easily affected by changes of temperature. Motion is interfered with; tremors occur early; movements become slow and awkward; the gait is unsteady; the voice is rough and nasal; but no true paralysis or muscular atrophy has been observed. The patella-tendon reflex is occasionally lost, but not in all cases.
87Allan McLane Hamilton,Journ. Nerv. and Ment. Dis., 1885, April, p. 180.
These symptoms have been ascribed to the pressure of the mucin upon the terminal filaments of the nerves, and also to changes in the central nervous system. That the latter theory is probably correct is shown by the occurrence of mental symptoms in the majority of cases. The patients become apathetic and all mental action is slowly performed. Indifference to surroundings, loss of memory, and inability to concentrate the attention may be succeeded by transient delirium, hallucinations, and occasionally by delusions of persecution, and the patient finally lapses into a state of imbecility. If the disease develops in early life, education is impossible, and the patient remains in an infantile condition.
Whether the changes in the nervous system are due to pressure by deposit of mucin (Hadden), or are due to an altered nutrition of the most delicate tissues of the body consequent upon the general metabolic derangement (Horseley), is undetermined. In experimental myxœdema the degenerative processes have been found in the nerve-cells.
There are no symptoms referable to the heart or lungs, and if cirrhosis of the kidney and liver develop, their symptoms supervene upon and are secondary to those of myxœdema. High arterial tension has been noticed in the majority of the cases.
TheCOURSEof the disease is a chronic one, and is progressive. There are, however, intermissions in the severity of the symptoms in some cases. Recovery does not occur.
DIAGNOSIS.—The diagnosis from the accumulation of fat is made by observing the thickening of the nose, lips, fingers, and tongue, and the changes in the skin and its appendages. Scleroderma is not universal like myxœdema. In scleroderma the skin is harder and more adherent to subjacent parts, is not transparent and waxy, and the nervous symptoms are wanting. Cretinism seems to be closely allied to myxœdema, but is only observed before the age of seven and is accompanied by hypertrophy of the thyroid gland.
TREATMENT.—The treatment is only palliative. Simple nutritious diet, especially milk diet, with the use of such tonics as iron and quinine, has been found useful. The progress of the disease is hastened by exposure to cold, and in a very warm climate the symptoms may remain stationary for several years. Jaborandi or pilocarpine has been used in some cases with a moderate degree of success. Nitro-glycerin, gr.1/100, has also been of benefit. For the paræsthesiæ and anæsthesia of the early stage the faradic brush has been applied, and for the motor weakness the faradic current, with the effect of relieving but not curing these symptoms. During the attacks of neuralgia morphine may be employed.
Inflammation.—The most important trophic disturbances are those which consist of an actual disintegration of tissue. These are very numerous. Herpes zoster, certain forms of eczema and pemphigus, lepra anæsthetica, scleroderma, acute ulceration of the fingers, perforating ulcer of the foot, acute bed-sores, keratitis with anæsthesia of the cornea, sympathetic ophthalmia, and various forms of joint disease, are examples of such trophic diseases.88For the discussion of the skin and eye diseases mentioned the reader is referred to special articles on those subjects. In regard to lepra anæsthetica, it may be mentioned that in this disease lesions have been found both in the sensory nerves and in the posterior cornua of the spinal cord.89
88Leloir, “Tropho-neuroses,”Nouveau Dictionnaire de Médecine et Chirurgie practiques, 1885.
89Virchow, “Nerven Lepra,”Geschwülste, ii. 521; Tschirijew,Travaux du Laboratoire de Vulpian, 1879.
I have reported90a case of acute ulceration of the ends of the fingers and toes occurring in an anæmic girl aged twelve, and persisting for more than a year, associated with cyanosis of the hands and feet, and with a tendency to rapid ulceration of any part of the body which happened to be exposed to pressure. The hair of the eyebrows, eyelids, and to a less extent that of the scalp, fell out during the disease. There was no local asphyxia and no appearance of gangrene; hence the case was not one of Raynaud's disease. Its symmetrical distribution, the lack of any constitutional organic disease or of any local cause for the production of the ulceration, and the anæmic and nervous condition present, all pointed to a disturbance of the central nervous system. It did not yield to treatment, either local or general or electrical. Mills has seen a similar case.91
90Journal Nerv. and Ment. Disease, Feb., 1886, clinical cases.
91Mills,Amer. Journ. Med. Sci., Oct., 1878.
Perforating ulcer of the foot begins on the sole, beneath any of the metatarso-phalangeal articulations, preferably the first or the fifth, or under the heel, as a small pustule under the epidermis. This ruptures, and the ulcer which results begins to extend in a direction vertical to the surface, involving the deeper tissues or even opening into the joint and destroying the bone. It appears rather like a sinus than an ulcer, and isremarkable from the fact that it is not painful and is insensitive to touch, although it may prevent the patient from walking on account of extreme tenderness. The epidermis around the sinus is thickened and insensitive, and there may be anæsthesia of the entire sole of the foot, and even of the leg, although this is due to the neuritis present, which is also the cause of the ulcer, rather than to the ulceration. The circulation is sluggish in the affected extremity; it becomes cyanotic on exposure to cold, and seems peculiarly liable to become œdematous. The œdema may go on to suppuration, and involve the articulations, and ankylosis of the smaller joints may follow. This, too, is to be traced to the neuritis. The skin of the foot becomes pigmented, and may be dry or covered with offensive sweat. As the patient cannot walk while the ulcer remains, the condition demands treatment. Rest, moist warm applications, antiseptic lotions, scraping out the sinus, and other surgical means appropriate to the treatment of ulcers and sinuses do not often prove of benefit, and in obstinate cases recourse has been had to amputation of the foot. Electrical treatment has been tried in vain.
Such perforating ulcers may occur symmetrically on both feet, and may be numerous. They also occur rarely on the hands. They have been observed not infrequently in locomotor ataxia, occurring either early or late in the disease,92and have appeared in patients suffering from dementia paralytica. The only constant lesion found is a degeneration of the peripheral nerve supplying the affected part.
92For bibliography see Ross,Diseases of Nervous System, 2d ed., i. p. 256, and Blum,Berliner klin. Wochen., 1875, Nos. 13-15.
Acute bed-sores (decubitus) develop in many cases of spinal and cerebral disease, but not in all. It is argued that anæsthesia of a part or simple pressure upon a part or irritation of an anæsthetic part will not explain their occurrence, and that they must be traced to a destruction of trophic centres in the cord or brain. No amount of attention to the position and cleanliness of the patient is thought to be sufficient to prevent them in some cases, and their progress is often so rapid as to remove them from the category of simple ulceration. Their most frequent seat is upon the buttocks, over the sacrum, on the heels, and over the scapulæ; but it is believed that in the conditions in which they appear in these places pressure on any part may cause one. They begin within a few hours after the occurrence of the lesion as irregular mottled patches of redness, in which there soon appear small or large vesicles filled with dark serum. These rupture, leaving little areas of ulcerated surface, which soon unite to form a large ulcer with softened, infiltrated, and bloody base and ragged edges. The tissues around and within the ulcer have a tendency to slough and to become gangrenous, and the process goes on rapidly until a considerable area of the surface is completely destroyed, together with the deeper structures, fat, muscles, and fasciæ, down to the bone, which may become necrosed. Acute cystitis is so frequently associated with acute bed-sore that it is traced to the same nervous cause, though here, again, another explanation is possible. The constitutional disturbance produced by these two affections may be increased by a true septicæmia, to which the patient succumbs; or metastatic abscesses may be formed, and pyæmia cause death; or, lastly, the ulcer on the back may lay bare the vertebræ and erode their ligaments, thus opening a way for the extension of suppuration tothe meninges of the spinal cord. The duration may be from a few days to two weeks, and the prognosis is very grave.
Chronic bed-sores develop in a similar manner, although all the processes described occur more slowly and are much less severe. They do not show the tendency to extend so widely or so deeply, nor to become gangrenous. They remain stationary after attaining a certain size, and the tissues seem to lack all tendency to reproduction and repair. When the central lesion which they follow begins to pass away they heal; sometimes local treatment is successful; but in many cases they persist for years, always threatening the life of the patient from the possibility of their sudden aggravation or from the occurrence of the complications already mentioned in connection with the acute process.
Since neither form of decubitus occurs after lesion of the anterior cornua of the spinal cord, nor in sclerosis of the posterior or lateral columns, nor in those cases of locomotor ataxia in which extensive invasion of the posterior cornua is present, while they are particularly frequent as a complication of general myelitis, hemorrhage in the cord, and syringo-myelitis, it is argued that the trophic centres whose destruction is the cause of these bed-sores lie in the central gray matter of the cord, near to the central canal. In unilateral lesion of the cord the bed-sore occurs on the anæsthetic side of the body—i.e.on the side opposite to the seat of the lesion—a fact which may indicate a decussation of the trophic nerve-fibres in the cord,93but which has also been urged in proof of the theory that the sore is always due to irritation of an insensitive surface.
93Recklinghausen believes that these cases of disturbance of nutrition can be explained by injury of anæsthetic parts in which vaso-motor disturbances of central origin exist (Handbuch d. Path. d. Ernahrung, pp. 236, 237).
The treatment of bed-sores belongs to the domain of surgery, the same methods being pursued as in the case of any large ulcer. The application of electricity to the sore has been tried, but the results are not sufficiently encouraging to warrant its recommendation.
Joint affections of neurotic origin are discussed in the articles upon Locomotor Ataxia, Hemiplegia, and Hysteria.
It is evident from this review that the nervous centres have some influence upon the activity of the cells of which the body is made up, and that they control the processes of growth, function, repair, and reproduction. The facts are too numerous, too varied, and too positive to admit of any other explanation. Trophic disturbances must therefore be considered as a set of symptoms referable to various lesions of the nervous system. It is evident from the preceding discussion that they may be produced by disease of the peripheral nerves; by disease of the ganglionic cells, which nourish those nerves; by disease of the spinal cord, especially in the region of the central gray matter; and, finally, by disease of the brain. Whether in the last condition the effect is a direct one, or is produced secondarily by an irritation of the spinal centres, cannot yet be determined. There are no trophic centres as yet localized in the cerebrum, but the pathological facts already mentioned warrant the conclusion that such centres will not long elude search. Certain facts observed in cases of infantile hemiplegia point to the motor area of the cortex as the seat of trophic centres for the motor mechanisms; since it is found that when the motor cortex is destroyed in early life the bones and muscleswhich it controls fail to develop properly. Trophic centres for sensory mechanisms are not yet discovered. Certain investigations of Luciani recently published94point to the cerebellum as the part of the brain which governs the general nutrition of the body, but these need confirmation.
94Alienist and Neurologist, July, 1885.
CONCLUSION.—While an attempt has been made here to consider vaso-motor and trophic neuroses separately, it must be admitted that in very many conditions the two are coincident. This follows inevitably from what has been stated regarding the localization of the vaso-motor and trophic centres in the spinal cord, and regarding the course of the vaso-motor and trophic nerves from the spinal centres to the periphery. These two classes of centres and nerves lie side by side in the central and peripheral organs, and it is less surprising that they should be jointly affected than that one should ever be involved alone. In any case of lesion of the peripheral nerves or of the central nervous system they may be expected. In all cases they are to be regarded as symptoms of such lesions rather than as distinct diseases.
A.
A.
Abdomen, state of, in lead colic,
684
in tubercular meningitis,
726
,
727
Abscess of the brain,
791
,
792
of the spinal cord,
808
Achromatopsia, hysterical,
247
Aconite and aconitia, use of, in neuralgia,
1224
,
1227
hypodermically in exacerbations of cerebral syphilis,
1015
Acoustic sensory disturbances in nervous diseases,
40
,
41
Acrodynia,
1254
Acute affections produced by heat,
387
alcoholism,
586
cerebral anæmia,
776
encephalitis,
791
myelitis, spinal,
810
poisoning by alcohol in lethal doses,
596
simple meningitis,
716
spinal meningitis,
749
pachymeningitis,
747
Æsthesodic system of encephalon, localization of lesions in,
81
of spinal cord, localization of lesions in,
69
Affective mental disease,
153
Age, influence on causation of acute spinal meningitis,
750
of catalepsy,
315
of cerebral anæmia,
777
of chorea,
441
of chronic lead-poisoning,
680
,
686
,
688
of disseminated sclerosis,
883
of embolism and thrombosis of cerebral veins,
951
of epilepsy,
470
of family form of tabes dorsalis,
871
of general paralysis of the insane,
77
of hæmatoma of the dura mater,
707
of hysteria,
216
of hystero-epilepsy,
293
of insanity,
116
,
117
of intracranial hemorrhage and apoplexy,
927
of labio-glosso-laryngeal paralysis,
1173
of migraine,
406
,
1230
of myxœdema,
1271
of neuralgia,
1217
of paralysis agitans,
433
of progressive unilateral facial atrophy,
694
of syphilitic affections of nerve-centres,
1000
of tabes dorsalis,
856
of the opium habit,
650
of thrombosis of cerebral veins and sinuses,
983
of tubercular meningitis,
725
of tumors of the brain,
1029
spinal cord,
1090
of writers' cramp,
512
relation of, to limitation of the myelitis in infantile paralysis,
1147
Agraphia in hemiplegia,
957
Akinesis in nervous diseases, definition of,
42-44
Alalia (see
Speech, Disorders of
).
Alexia in nervous diseases,
31
Albuminuria in chronic lead-poisoning,
682
,
689