Chapter LXXXII: Introduction: This disease remained unnoticed until twenty years ago, (6)

The origin of the vaso-dilators is also to be traced to the dorsal cord. The vaso-dilators of the bucco-facial region come from the second to the fifth dorsal nerves, whence they pass to the first thoracic ganglion, and thence by the annulus of Vieussens into the cervical sympathetic cord. Those of the eye, head, and ear come from the same ganglion, but have their spinal origin in the eighth cervical and first dorsal nerves. Those of the arm are traced into the upper thoracic sympathetic cord, which they reach from the five upper dorsal and last cervical nerves. Those of the leg are traced to the first and second lumbar ganglia and the lumbar sympathetic cord, which they reach from all the dorsal nerves from the sixth downward. Gaskell holds, however, that the vaso-dilators of the extremities pass out of the cord in the cervical and lumbar plexuses and accompany the cerebro-spinal nerves. The vaso-dilators of the thorax and {1248} abdomen are supposed to pass in the pulmonary plexus and splanchnic nerves, but this is not yet fully determined.

Gaskell[10] believes that vaso-motor nerves can be distinguished from motor and sensory nerves in the spinal nerve-roots by the smallness of their calibre. He finds such fine fibres only in the spinal nerve-roots between the second dorsal and second lumbar segments of the cord (in the dog), and in the three upper roots of the spinal accessory nerve. According to his account, the vaso-constrictors issue from the spinal cord in both anterior and posterior nerve-roots as medullated fibres, and pass to the sympathetic ganglia lying on the vertebræ (proximal or lateral ganglia); there they lose their medullary sheath, and either end in cells whence new fibres issue, or more probably pass directly onward as non-medullated fibres, having a connection with the unipolar cells of the ganglia only for purposes of nutrition. The number of fibres issuing from any one ganglion is much greater than the number entering it from the cord; hence it is supposed that each medullated fibre splits up into a group of non-medullated fibres; which is possible, as the researches of Ranvier have shown that each axis-cylinder is made up of numerous fibrils. Leaving these ganglia, the nerves pass either to the second series of ganglia (distal or collateral ganglia), whence they issue in plexuses to enter the vessels, or to the vessels directly, where they divide in plexuses. It is in the meshes of the plexus that the local ganglia of the vessel-walls are found. The vaso-dilators are thought to differ from the vaso-constrictors in passing directly to the distal ganglia as medullated fibres, not being connected in any way with the proximal ganglia. Gaskell makes no statement regarding their limits of origin from the cord, except to state that the nervi erigentes issue with the sacral nerves. He agrees with the view that the vaso-dilators act as inhibitory nerves upon the local ganglia.

[Footnote 10: _Journal of Physiology_, Jan., 1886.]

Vaso-motor Reflexes.—Thus far, reference has been made only to fibres whose direction of transmission is centrifugal, and whose exit from the spinal cord is by the anterior nerve-roots. There are other fibres, however, through which centripetal impulses pass, and these enter the spinal cord with the posterior nerve-roots. The function of these fibres is to transmit sensory impulses inward to reflex centres, and thus set in action motor mechanisms of a vaso-constrictor or dilator kind whose effects are produced at the periphery. There are, therefore, vaso-motor reflexes, as well as skin and tendon reflexes, whose centres are in the spinal cord. These reflex acts may be excited by impulses reaching the centre not only through the vaso-motor centripetal nerves, but also through the sensory nerves of the cerebro-spinal system. The effect of changes of temperature on the circulation in the skin (if the right hand be plunged in cold water there is a fall of temperature in the left hand), the effect of pain upon the color of the face and the size of the pupil, the red cheek on the affected side in pneumonia, the occurrence of glycosuria during sciatica,—are all instances of such reflex acts. Many vaso-motor affections are produced by irritation causing reflex effects at a distance from the seat of irritation—a fact always to be kept in mind. The utility of counter-irritation to the surface in diseases of the internal organs is explained by supposing that vascular changes are produced in those {1249} organs through reflex mechanisms set in action by the local irritation. While some of these reflexes may have their central mechanism in the local ganglia, it is probable that the majority are to be traced to the spinal cord. It is believed that the sympathetic ganglia are not the seat of reflex centres.

Since the vaso-motor nerves are connected almost exclusively with the dorsal portion of the spinal cord, it is very natural to conclude that the vaso-motor reflex centres are situated in this region; and the hypothesis has been advanced by Jacubovitch, and strongly urged by Gaskell,[11] that the cells of the vesicular columns of Clarke, which are peculiar to this region, are the seat of these reflex mechanisms. This hypothesis gains some support from the pathology of syringo-myelia. In this disease the gray matter surrounding the central canal and the vesicular columns are destroyed. The characteristic symptoms are vaso-motor and trophic disturbances, consisting of changes in the vascular tone, changes of local temperature, and various eruptions, in some cases going on to ulceration in the skin and mucous membranes. It is, however, undecided whether the vaso-motor centres of the cord are limited to the columns of Clarke, or are situated in the gray matter surrounding the central canal, since both these parts are destroyed in this disease.[12] That they are not located in the anterior or posterior gray cornua is determined by the fact that diseases limited exclusively to these areas do not cause vaso-motor disturbances. The situation of the various reflex centres for the various parts of the body is at different levels of the cord, as has been determined by the experiments already cited to establish the level of origin of the vaso-motor nerves. The exact location of the vaso-constrictor and vaso-dilator reflex centres for definite parts is yet to be ascertained.

[Footnote 11: _Loc. cit._]

[Footnote 12: See Fürstner, _Arch. für Psych._, xiv. 422.]

Vaso-motor Tracts.—These reflex centres are connected with the medulla by tracts which lie in the lateral columns of the spinal cord,[13] although it is not determined in which part of these columns. It is not possible as yet to separate the constrictors from the dilators in this tract, nor to determine whether it transmits impulses in both directions or only from above downward. Nor is the course of associating fibres between reflex centres at different levels known. In cases of transverse myelitis the control of the medulla is removed from the vascular centres below the lesion, and the lack of vascular tone seen in the paralyzed limbs, together with the susceptibility to local irritation, is the result of this division of the vaso-motor tracts.

[Footnote 13: “Owsjanikow and Tschirijew,” _Bull. de l'Acad. de St. Petersbourg_, xviii. 18.]

{1250} Medullary Centres.—It has been stated already that a general vaso-motor centre with both constrictor and dilator powers is situated in the medulla. This lies in two divisions on each side of the middle line, in or just beneath the floor of the fourth ventricle, from the calamus scriptorius up to the level of the sixth nerve-nucleus. Each division governs the vascular tone of its own side of the body,[14] and lesions in its region in man produce unilateral vaso-motor symptoms.[15] This centre can be excited to reflex action by strong irritation locally or through the blood, in which case a general constriction or dilatation of the vessels of the entire body will ensue. It seems probable, however, that the general centre in the medulla is made up of a number of special centres, each of which governs a definite set of organs. The vascular tone of the thoracic and abdominal viscera is certainly regulated by a series of such centres. Brown-Séquard and Schiff have produced hemorrhages in the lungs, pleura, stomach, intestines, and kidneys at different times by destructive lesions of the medulla, and the well-known experiments of Bernard, in which by puncture of the medulla local hyperæmia of the liver or kidneys was caused, producing glycosuria or polyuria, confirm this view. Lesions of these parts in man produce similar effects. Charcot has shown that in cerebral hemorrhage ecchymoses may be found in the stomach, pleura, and endocardium, and that pneumonia is especially frequent upon the paralyzed side. De Jonge[16] has been able to collect thirteen cases of diabetes mellitus in which a lesion of the medulla (hemorrhage or tumor) was found after death; and Flatten[17] has proven the existence of similar lesions in diabetes insipidus. The connection of these centres with the liver and kidneys has been traced elsewhere.[18] The medulla contains a special centre for the vaso-motor nerves of the abdomen, which are in the domain of the splanchnic nerves. This centre is excited reflexly by impulses reaching it through the depressor nerve of Cyon from the heart; so that when that organ is overburdened it may be relieved by a fall of arterial pressure produced by dilatation of the abdominal vessels. Whether the connection of the medulla with the centres in the semilunar ganglion which preside directly over these vessels is made by way of the spinal cord or by way of the pneumogastric nerve is still undetermined, though the researches of Gaskell favor the former view. Gastric and intestinal disturbances are certainly produced by nervous lesions in the medulla, but whether they are due to vascular changes is uncertain. The vomiting of mucus and blood, and the large watery evacuations which accompany mental shock or anxiety, as well as the polyuria associated with mental effort, have been ascribed to irritation of local centres in the medulla governing the gastro-intestinal and urinary organs by impulses received from the cortex above. The spleen is under the control of vaso-motor centres, since section of the splenic branches of the semilunar ganglia will produce a great enlargement of the organ, and irritation of the cut end of these branches will produce {1251} contraction.[19] The medulla also contains a vaso-dilator centre for the erectile tissues of the genital organs, irritation of which by mental action or local disease causes impulses to pass to the nervi erigentes by way of the spinal cord, resulting in a flow of blood to the parts. Although a centre has been thought to exist controlling the circulation in the lungs, whose paralysis has been supposed to explain the occurrence of sudden pulmonary œdema without other known cause, no definite facts regarding it are known. That the action of the heart is under the control of the medulla is a fact too well known to require more than a mention. The physiology of the nervous control of the heart cannot be discussed here.

[Footnote 14: Owsjanikow, _Arbeiten aus d. Physiol. Instit. zu Leipzig_, 1871.]

[Footnote 15: M. A. Starr, “Sensory Tract in Central Nervous System,” _Journ. Nerv. and Ment. Dis._, July, 1884, pp. 396-398.]

[Footnote 16: _Arch. f. Psych._, xiii.]

[Footnote 17: _Ibid._]

[Footnote 18: See Tyson, “Diabetes Mellitus,” _Pepper's System of Medicine_, Vol. I. p. 195; Edes, “Diabetes Insipidus,” _ibid._, Vol. IV. p. 30.]

[Footnote 19: Tarchanoff, _Pflüger's Arch._, viii. p. 97; Ross, _Diseases of the Nervous System_, vol. i. p. 225.]

While these medullary centres are certainly influenced by impulses reaching them from the cerebral hemispheres, as is evident from the vaso-motor symptoms produced by mental action—_e.g._ pallor from fright, blushing, etc.—it is impossible to state in what portion of the hemispheres in man the higher vaso-motor centres lie. Eulenburg and Landois locate them in the motor area in animals.[20] They are certainly beyond control of the will, and are wholly reflex in their action, a purely mental act in this case being the excitant of a purely physical result.[21]

[Footnote 20: _Arch. f. Path. Anat._, Bd. lxviii. p. 245.]

[Footnote 21: In addition to the articles already cited the reader is referred to Landois's _Physiology_, to Duval's article, “Vaso-moteurs,” in the _Dictionnaire de Médecine et de Chirurgie_, vol. xxxviii. (1885), for a summary of vaso-motor physiology, and to Gerhardt's “Ueber Angio-neurosen,” _Volkmann's Sammlung klin. Vorträge_, No. 209. Gaskell's researches, published in the _Journal of Physiology_, are the most recent and satisfactory.]

PATHOGENESIS.—From this review of the physiology of the vaso-motor system it becomes evident that disturbances of vascular tone may be produced by many different causes acting upon many various parts. They may be due to local affections of the part in which the symptoms are present, as in the case of erythema[22] after burns or frost-bite, or congestion of any organ after injury. They may be due to affections of the vaso-motor nerves passing to the part affected, as in the case of vascular changes due to peripheral nerve lesions.[23] They may be due to affections of the sympathetic ganglia connected with the part affected, as in the case of migraine,[24] sudden flushing of one ear, certain cases of polyuria,[25] and Basedow's disease.[26] They may be due to lesions in the spinal cord affecting the vaso-motor centres[27] or compressing the nerve-roots on their way to and from the sympathetic ganglia,[28] as is the case in the various forms of myelitis and in Raynaud's disease or symmetrical gangrene, and in meningitis, tumors of the cord, or Pott's disease. They may also be caused by such conditions in the cord as cut off the vaso-motor centres from the medullary centres, such as transverse myelitis from compression or traumatism.[29] They may be due to lesions of the medulla oblongata,[30] as is seen in some cases of polyuria and glycosuria,[31] and in cases of universal erythema[32] following acute fevers. They may be due to diseases of the cerebral hemispheres, as is evident from the vaso-motor symptoms occurring in hemiplegia and hysteria. Finally, they may be of a reflex {1252} origin, dependent upon some obscure source of irritation in a part quite distant from the region in which the symptoms appear.[33]

[Footnote 22: Vol. IV. p. 511.]

[Footnote 23: Vol. V., “Neuritis.”]

[Footnote 24: Vol. V., “Migraine.”]

[Footnote 25: Vol. IV., “Polyuria.”]

[Footnote 26: Vol. III. p. 761.]

[Footnote 27: Vol. V., “Syringo-myelitis.”]

[Footnote 28: Vol. V., “Meningitis Spinalis.”]

[Footnote 29: Vol. V., “Transverse Myelitis.”]

[Footnote 30: Vol. V., “Medulla.”]

[Footnote 31: Vol. I., “Diabetes Mellitus.”]

[Footnote 32: Vol. IV. p. 512.]

[Footnote 33: Vol. V. p. 205.]

The DIAGNOSIS of the seat of the lesion in many cases of vaso-motor neurosis may be made if the organ or the exact limitation of the area affected be ascertained, and the history of the case, together with the concurrent symptoms of other kinds, be considered. In some cases no organic cause can be found, and in these a reflex cause should be diligently searched for.

SYMPTOMS.—A vaso-motor affection may manifest itself either by a spasm or a paralysis of the vessels. In angiospasm the part affected becomes pale, and irritation no longer causes a vaso-motor reflex. It looks shrunken, and if the skin over it is loose it may be thrown into folds or shrivelled, presenting the appearance seen in the hands after long immersion in hot water. The lack of blood in the part arrests the processes of metabolism which are normally constant, and if the condition continues this may result in such a disturbance of nutrition that ulceration, or even gangrene, may ensue. The local anæmia, combined with the cessation of metabolism, produces a fall of temperature in the affected part, which is then more easily affected by the temperature of the air than in a normal state, so that exposure to cold is very liable to cause freezing. These conditions necessarily produce an impairment of function, so that if the affection is located in the extremities, as the fingers, they are soon rendered useless. The term digiti mortui has been applied to this state. In the surface of the body angiospasm causes cutis anserina, pallor, numbness, tingling, slight anæsthesia, and analgesia. If it occurs in a limb, the finer motions are imperfectly performed, and in time the nutrition of the muscles may be so impaired as to produce atrophy and paresis. It may even lead to gangrene. Nothnagel has recorded[34] five cases of sciatica in which the pain produced a reflex spasm of the vessels of the leg, which, persisting, resulted in partial paralysis, atrophy, lowering of temperature, pallor, and sensory disturbances. Ross mentions[35] the sudden appearance of circumscribed patches on the hands and forearms of washerwomen, in which there is a pallor, coldness, and partial anæsthesia. These may be limited to the distribution of a single nerve, and may be accompanied by trophic affections.

[Footnote 34: _Arch. f. Psych._, v.]

[Footnote 35: Vol. I. p. 221.]

Spasm of the veins may occur as well as of the arteries,[36] or independently of them. In the latter case the blood will not pass out of the capillaries. The part will then be blue, swollen, œdematous, and painful; the temperature will be lowered by increased radiation of heat, and all the sensations and functions be impaired in greater or less degree. If this continues, nutrition may suffer, and in the end gangrene develop, which will take its course and lead to the throwing off of the part. Grainger Stewart has described such a condition occurring in both hands and feet.[37] It may be likened to a severe form of Raynaud's disease.

[Footnote 36: Weiss, “Symmetrische Gangrän,” _Wiener Klinik_, 1882.]

[Footnote 37: Grainger Stewart, _An Introduction to the Study of Nervous Diseases_, p. 138.]

Angio-paralysis is more frequent than angiospasm, and may be due either to paralysis of the vaso-constrictors or to excitement of the vaso-dilators. It shows itself by a bright-red or mottled appearance of the skin, and increase of local temperature, and more rapid processes of {1253} nutrition, together with an increase of secretion if the part is a gland or a mucous membrane, and an increase of sweat if it is the skin. In the latter case an increased sensitiveness to changes of temperature, a subjective sensation of heat, and hyperæsthesia and hyperalgesia may occur. The hyperæsthesia on the paralyzed side which is present in hemiparaplegia spinalis is ascribed to the vaso-motor paralysis. But these symptoms soon give place to others. The dilatation of the vessels, which at first caused an increased flow of blood to the part, produces a slowing of the blood-current in the part, just as a river runs less rapidly where it becomes wider. The slowing of the current in the skin allows of a more complete cooling of the part as the radiation of heat and the evaporation of moisture are increased, and the slowness of the renewal of blood impairs the processes of nutrition, so that to the first stage of redness, heat, and increased metabolism there ensues a stage of blueness, cold, and defective nutrition, and the function of the part may be impaired. In this stage it usually presents a mottled appearance, and may be slightly swollen and œdematous, and the continued increase of perspiration gives it a clammy coldness to the touch. In all of these conditions severe pain, sometimes of a burning character, is a very distressing symptom (causalgia). These conditions are seen in peripheral nerve-lesions, and give rise to the appearances which have been so admirably described by Weir Mitchell.[38]

[Footnote 38: _Injuries of Nerves_.]

A peculiar combination of symptoms may be mentioned here, to which Weir Mitchell has given the name of erythromelalgia.[39] This disease begins with tenderness and pain in the soles of the feet, which are soon followed by a marked distension of the capillary vessels. The congestion is attended by a sensation of burning pain similar to that produced by a blister. The surface is at first of a dull dusky-red color; later it appears purple. The redness is not uniformly distributed over the sole, but occurs in patches of irregular shape, being especially frequent over prominent parts exposed to pressure and friction, and the attacks seem to be brought on by long standing or walking. At first there is a rise of temperature in the affected surface, the arteries pulsate visibly, the veins are swollen, and there may be some œdema. Later, the foot is cold and pale. Sensations of touch and temperature are normal, but the part is so extremely tender that walking is impossible. There is no paralysis. One or both feet may be affected, but the patches of redness are rarely symmetrical. The hands are occasionally affected. The condition may occur in paroxysms or may remain for some time. It resists all known methods of treatment, although applications of cold relieve the burning pain to some extent and the tenderness enforces rest.

[Footnote 39: _Amer. Journ. of the Med. Sci._, July, 1878.]

With angio-paralysis may be classed the taches cérébrales of Trousseau no longer considered diagnostic of meningitis, but denoting a weakened condition of vaso-constrictor action in the local ganglia of the vessel-wall which may occur upon local irritation of the skin in any severe disease affecting the nutrition of the general nervous system.

Actual rupture of the capillaries in the course of vaso-motor diseases is rarely observed, although the stigmata appearing in hysterical and cataleptic patients may be ascribed to this cause. In this connection tabetic ecchymoses may be mentioned, which appear suddenly without local injury, {1254} and resemble an ordinary bruise, running a similar course. They occur only in the course of locomotor ataxia.[40]

[Footnote 40: Straus, _Arch. de Neurologie_, tome i. p. 536.]

In addition to these forms of vaso-motor affections there is a condition of instability of vascular tone which manifests itself by sudden transient changes in the circulation of various organs. This is a functional affection, usually due to malnutrition. It is seen in many cases of neurasthenia and hysteria, and manifests itself by sudden flushes or pallor, alternations of heat and cold, local sweating, attacks of mental confusion, and inability to use any organ continuously from disturbance of the power of the vaso-dilators to maintain a condition of functional hyperæmia.[41] Little is actually known about the causes of this state of the vascular system, although much has been written about it. (For a fuller description the article on Neurasthenia may be consulted.)

[Footnote 41: Anjel, _Arch. für Psychiatrie_, xv. 618.]

Many functional derangements of the internal viscera have been ascribed to such vaso-motor instability with more or less probability,[42] but hypothesis of this kind, however plausible, is evidently beyond confirmation. It is especially in affections of this kind that causes of reflex irritation are to be carefully sought. Cutaneous angio-neuroses, such as have just been described, may affect any part of the body. They usually appear suddenly, producing much discomfort and an impairment of function in the part if it is an extremity. They disappear as rapidly as they come. The duration of such attacks varies from a few minutes to several days. They are very liable to recur. If it is the vessels under the control of the cervical sympathetic which are affected, the symptoms will be those of migraine or of lesion of the ganglia.[43] If it is the vessels in the extremities which are involved, the condition of digiti mortui or erythromelalgia or symmetrical gangrene[44] may be produced.

[Footnote 42: Fox, _The Influence of the Sympathetic System in Disease_, London, 1885.]

[Footnote 43: See p. 1263.]

[Footnote 44: See p. 1257.]

A singular epidemic occurred in France in 1828 and 1830 which was termed acrodynia. Many persons were suddenly seized with vomiting and purging, and soon after the onset the extremities became red or mottled in blotches, swollen and œdematous, and hot, painful, and tender. The attacks lasted from a few days to two months, and during this time the skin became thick and hard, the muscles weak and subject to spasms, and the general health was impaired. Relapses occurred in many cases, but all finally recovered, and hence the exact nature of the disease was not ascertained.

COURSE.—In any case of vaso-motor neurosis the course of the disease and its termination will depend chiefly upon its cause. If the cause is some permanent lesion of the nervous system, the condition will remain, and in this case the termination will depend upon the severity of the symptoms. Angiospasm may be so severe as to lead to gangrene ana the separation of the part affected, or may be so slight as to cause only subjective discomfort and a little pallor. Angio-paralysis may lead to an extreme degree of congestion, which is attended by heat and pain at first, later by paræsthesia and coolness, with increased liability of the part to be affected by changes in the surrounding air. This stage is succeeded by one of less marked dilatation of the vessels and a spontaneous partial {1255} recovery, although the more moderate symptoms may continue indefinitely and seriously impair the function of the part. If the cause is a temporary derangement of function in the vascular mechanism, is reflex irritation which can be removed, or is a curable organic disease, the symptoms will subside rapidly or gradually and perfect recovery may follow. If the condition is one of irritability in the vaso-motor centres, producing alternations of flashing or pallor, such as is observed in nervous exhaustion, it may recur irregularly for a considerable length of time until the causative condition can be removed.

PROGNOSIS.—The prognosis must be determined in each case by a consideration of the cause of the affection, of the nature of the symptoms, of the severity of the disease, and of the possibility of success in both symptomatic and causative treatment. In the angio-paralytic cases an eventual spontaneous relief from much of the discomfort may be promised, although the duration of the symptoms cannot be predicted.

TREATMENT.—Treatment must be directed primarily to removing or diminishing the severity of the cause. A review of the section on Pathogenesis will indicate how wide a field this may include, and the reader must be referred to the special articles which are alluded to in that place for therapeutic measures. Special diligence is to be shown in searching for a source of reflex irritation. When the cause cannot be reached, and when the symptoms are of such severity as to demand immediate attention, treatment may be directed to them.

In all conditions of vaso-motor disease it is important to shield the part from external injury; for if the vessels are dilated they are liable to rupture, and any abrasion of the surface may produce serious inflammation and ulceration; and if the vessels are contracted any injury will be repaired slowly and imperfectly on account of the anæmia, and may even hasten the approach of gangrene.

Perfect rest, bandaging with cotton, and even the application of a light splint to the extremities will be advisable in cases of angiospasm. It is desirable to retain the animal heat, inasmuch as its supply is deficient. In angio-paralysis rest in a somewhat elevated position and applications of mild evaporating lotions are indicated in the early stage; later, the limb may be bandaged. It is not advisable to attempt by tight bandaging to counteract the effect of the vascular paralysis, for the nutrition of the limb is liable to suffer and gangrene may be induced.

Massage of a part affected with vaso-motor symptoms is of great service, since the circulation can be increased in the veins, and thus indirectly in the capillaries, and the nutrition of the part can thus be favored. It is more efficacious in angio-paralysis than in angiospasm. Too rough rubbing is of course to be avoided, lest the skin be injured. All counter-irritation is to be strictly forbidden.

Electricity has been used with varying results. According to Erb,[45] moderate faradic applications contract the vessels; strong faradic applications, especially with the brush, dilate the vessels. The galvanic current at first contracts the vessels, but this is followed by a secondary dilatation, which will be greater and occur more rapidly the stronger the current used.[46] Cathodal closures contract the vessels; the anodal {1256} continuous current dilates them widely. Stabile continuous currents through a nerve dilate the vessels which the nerve supplies. Inasmuch as vaso-constrictors and vaso-dilators pass together in many nerves, and are found together in all parts, it is impossible to apply electricity to either alone. In those cases, therefore, in which it has been ascertained which set of vaso-motors is affected, it is not always possible to produce a direct effect upon that set by electrical treatment. Erb recommends, in conditions of vaso-motor spasm a trial of the galvanic current, the cathode on an indifferent point, the anode being applied over the vaso-motor centres governing the part, and also over the area of the body which is affected, and held there while a moderate continuous current is passing, interruptions being avoided; or, the cathode being placed on the neck, the anode may be applied to the nerves passing to the affected part; or a strong continuous current may be sent through the nerve, its direction being changed several times during a moderately long application. Finally, the faradic brush applied to the part or a strong faradic current sent through its nerve may relax the spasm. In any case, all these methods should be tried before electrical treatment is abandoned.

[Footnote 45: _Electrothérapie_, 562.]

[Footnote 46: To this statement Lauder Brunton assents—_Pharmacology_, p. 250.]

In vaso-motor paralysis other methods are used. The cathode is placed on the part congested, and a weak galvanic current is employed with frequent interruptions or even with changes of the pole; or the cathode may be moved about upon the reddened skin while a mild continuous current is passing. A very weak faradic current with wet electrodes, or even a weak faradic current applied with a brush, may be of service. Here, again, various methods may be tried.

If the extremities are affected, it may be well to immerse them in a basin of water which is connected with one pole of the battery, and the current directed in the manner just described, according to the case. It must be confessed that no definite results can be predicted from the use of electricity in these cases, and much more experience is needed before definite rules can be laid down. The records show that in apparently similar cases opposite methods of application have produced favorable effects, while in other cases all methods have failed. Too much reliance should not be placed in electrical treatment. Erythromelalgia is an obstinate affection, and symptomatic treatment, directed chiefly to quieting the pain by opium and allaying the sensation of burning by cool baths, must be resorted to.

Internal remedies may be tried appropriate to the condition present. In angiospasm nitrite of amyl inhaled, or nitro-glycerin 1/100 gr. t. i. d., may give considerable relief, although both of these drugs are to be used with caution. Chloral hydrate is also of some service, and where the patient is in pain and suffers from insomnia this may fulfil several indications. In angio-paralysis ergot has been used with advantage. Oxygen inhalations are of service. Chloride of potassium may also be tried. It is evident, however, that such remedies, acting as they do upon the general arterial system, are not to be depended upon in the treatment of local conditions, since they have no selective action upon the affected part. The majority of the drugs known as sedatives and antispasmodics have been used in these conditions, but the records of individual cases show that they are not of much avail. Theoretical therapeutic measures based upon {1257} experimentation on animals have been fully discussed by Lauder Brunton,[47] but practical experience has not yet been sufficiently extensive to warrant any further statements.

[Footnote 47: _Pharmacology, Therapeutics, and Materia Medica_, pp. 229-360. Lea Bros., 1886.]

Symmetrical Gangrene.

SYNONYMS.—Local asphyxia, Asphyxie locale, Raynaud's disease; Symmetrische Gangrän.

DEFINITION.—Symmetrical gangrene is an affection of the nervous system characterized by arterial or venous spasm appearing in symmetrical parts of the body, especially in the phalanges of all the extremities, which may result in trophic changes or in gangrene. There are various stages in the disease, which have given rise to the various names by which it is known. The stage of local syncope, in which there occurs a moderate contraction of the arterioles and consequent pallor of the part, may be followed by a stage of local asphyxia, in which the complete contraction of the arterioles cuts off entirely the supply of arterial blood, and the regurgitation of venous blood produces cyanosis of the part; and this, if continued, may result in the gangrene of the part, which is then thrown off. Instead of a condition of local asphyxia, there may be a spasm of the smaller veins, resulting in a local erythema, which may go on to capillary stasis and then to gangrene. The spasm of the vessels may cease at any stage as suddenly as it began; and if this occurs in the first or second stage, no gangrene results.

HISTORY.—While isolated cases of this affection had been recorded as curiosities during the past two centuries,[48] the disease was first studied with care by Raynaud in his _Thèse de Paris_ in 1862. He collected twenty-eight cases which had been described with accuracy or had been personally observed in the hospitals of Paris, and after a thorough analysis of the symptoms defined the disease as “a neurosis characterized by an exaggeration of the excito-motor power of the cord presiding over the vaso-motor nerves.” He called particular attention to the condition of spasm in the vessels, and proposed the name asphyxie locale to designate the peculiar appearance of the parts affected. He also noticed the resulting gangrene as a new variety of gangrene, not dependent upon embolism or upon changes of an atheromatous nature in the coats of the vessels.

[Footnote 48: Schrader, 1629; Hertius, 1685; Bouquet, 1808; Moulin, 1830; Racle, 1859—cited in full by Weiss, “Symmetrische Gangrän,” _Wiener Klinik_, 1882.]

The condition was at once recognized by others, and several cases had been reported prior to 1873, when Raynaud published a more complete article on the subject in the _Dictionnaire de Médecine et de Chirurgie_ under the title gangrene symmétrique; in 1874 he recorded five new cases in the _Archives générales de Médecine_, vol. i. pp. 5 and 189.

The disease, having been thus established as a definite nervous affection, began to be noticed in other countries than France; and Billroth in Vienna,[49] Weir Mitchell,[50] Mills,[51] A. McL. Hamilton,[52] and J. C. Warren[53] {1258} in this country, and many other careful observers, published cases, together with more or less complete articles upon the disease. In 1882, Weiss produced a monograph[54] upon the subject containing references to all the cases which had appeared; and this is still the most complete article to be found, although the essay of R. Lauer[55] and the discussion of the disease by the Berlin Medical Society,[56] as well as the short articles of Schulz[57] and Lutz,[58] deserve mention, for they contain additional observations of cases and numerous facts not to be found elsewhere.

[Footnote 49: _Wiener Med. Wochensch._, 1878, No. 23.]

[Footnote 50: _Amer. Journ. of the Med. Sci._, 1878, July.]

[Footnote 51: _Ibid._, 1878, Oct.]

[Footnote 52: _N. Y. Med. Journ._, 1874, Oct.]

[Footnote 53: _Boston Surg. and Med. Journ._, 1879, No. 3.]

[Footnote 54: Weiss, _Wiener Klinik_, 1882, “Symmetrische Gangrän;” also _Zeitschrift für Prac. Heilkunde_, 1882.]

[Footnote 55: _Inaug. Dissert._, Strasburg, 1884.]

[Footnote 56: _Zeitschrift für klin. Med._, vi. p. 277, 1883.]

[Footnote 57: _Deut. Arch. f. klin. Med._, xxxv. 183, 1884.]

[Footnote 58: _Bäyr. ärzt Intell. Blatt_, 1884, xxxi. 24.]

SYMPTOMS.—The disease begins suddenly in all cases, and the constitutional symptoms are less prominent than the local ones. In some cases there are noticed a certain degree of mental disturbance, a condition of depression with a tendency to sigh and cry without cause, disturbed sleep with unpleasant dreams, irritability, and headache. A loss of appetite and disorders of digestion may follow, and then the local symptoms appear. In other cases, which seem to be the majority, the local condition develops without any such premonitory disturbances of the nervous and digestive systems, although these may ensue. The local symptoms first noticed may be paræsthesiæ or pain in all the extremities, usually limited to the tips of the fingers and the toes. These are continuous and severe, and are immediately followed (and occasionally preceded) by an appearance of ischæmia or of cyanosis or of erythema, in the order of frequency named.

(1) The fingers may look pale and dead, presenting the appearance of the so-called digiti mortui, and may be cold, painful, and anæsthetic. If this condition is moderate in degree, a certain amount of blood will continue to flow through the contracted arterioles, and then it corresponds to the description given by Raynaud of syncope locale. If it is extreme, the part may be wholly deprived of arterial blood, and then a true local asphyxia is present. In this stage the patients usually suffer considerably, although some do not complain of pain until the next stage. The ischæmia is attended with an impairment of sensation to touch, temperature, and pain, and finer motions become clumsy on account of the subjective numbness and actual anæsthesia. At the same time, the fingers look shrunken, the skin being thrown into folds, as if the hand had been soaked in hot water, or they may appear as if frozen, the skin being hard and immovable.[59] The secretion of perspiration may be increased, and the fingers feel damp as well as cold, or it may be suspended. The local temperature is lowered. If the part is cut, little or no blood will flow. At this stage the arterial spasm may suddenly relax and the part return gradually to its normal condition, the cessation of the constriction of the arteries and the return of blood being usually accompanied by burning pain, which may last for some hours. The duration of such an attack may vary from a few moments to several days. If it continues longer, this stage is usually succeeded by the second stage, of cyanosis.

[Footnote 59: Finlayson, _Medical Chronicle_, 1885, No. 4.]

(2) The stage of cyanosis results from one of two conditions: either the arterial spasm is so complete that no blood passes into the part, in {1259} which case venous blood from lack of vis a tergo or in response to gravitation regurgitates into the capillaries, distending them and producing a state of blueness; or a venous spasm occurs, preventing the exit of blood from the part, which then becomes actively congested, and the blood in the capillaries, from want of renewal, soon becomes venous and produces the cyanotic appearance. The stage of ischæmia may be so short that it is hardly noticed, so that the patient's attention is first attracted by the swollen, blue, and extremely painful condition. The skin may be stretched, the tissue infiltrated with products of exudation, which can be pressed out, as can also the venous blood, and the surface may itch as well as be painful. Anæsthesia is rarely present in this stage, and there may even be hyperæsthesia. The part is cool from the increased radiation of heat and cessation of the processes of metabolism, the local temperature being lowered. The small vessels on the surface will be visibly injected, and capillary ecchymoses may rarely be seen. There is less liability to difficulty in movement in this stage than in the former one, as the sensations of the part are not benumbed, but if present it is due to the swelling. This condition, like that in the former stage, may cease suddenly, the recovery of the normal appearance being, as a rule, slower than after a simple ischæmia. The duration of this stage has varied from a few seconds to several days. It is usually followed by gangrene.

(3) The condition of local erythema is described here because it may lead to gangrene, and has therefore been considered by Weiss as one of the early stages of the disease. As a rule, however, it is not followed by the death of the part, and the affection in these cases is probably one of erythromelalgia rather than of symmetrical gangrene. Like the stage of ischæmia, the stage of erythema may appear suddenly. The part presents a bright-red or a mottled appearance—is hot and swollen, and painful. The vessels are visibly injected, the local temperature is raised, the secretion of sweat may or may not be increased, and the patient feels a burning sensation rather than pain. Hyperæsthesia to touch and temperature and pain is usually present, or the sensations are normal. The blood can be pressed out, but returns immediately. In this condition of hyperæmia slight injuries lead frequently to an inflammatory process, ulcers may form in the pulps of the fingers or around the nails, and the eschars may appear dark and even gangrenous; or an actual condition of gangrene may appear in the tips of the fingers, the exact method of its occurrence being a matter of dispute. The erythematous condition is much more likely to be permanent than are the other stages of the disease—another fact which has led to some hesitation in considering it a true stage. This condition of erythema may be due to a paralysis of the vaso-constrictors, the converse of the spasm occurring in ischæmia. It has also been ascribed to an irritation of the vaso-dilators; and this appears to be the more probable hypothesis.

(4) The stage of gangrene is always preceded by that of cyanosis, and the death of the tissue is due to the arrest of nutrition consequent upon a stasis of the blood. It is not necessary to invoke the injury of trophic nerves to explain its appearance. In the tips of the cyanotic fingers, on their palmar surface, beneath the epidermis, a small blister appears, filled with a dark serous fluid or with pus or blood. This soon ruptures, and a dark dry scab forms, beneath which an ulceration may go on destroying {1260} the corium, but not penetrating deeper. In the majority of cases the gangrene is limited to a small area of the pulps of the fingers, and only involves the superficial layers of the corium. The gangrenous spot is surrounded by a purple margin. When the sphacelus has separated a scar remains which is frequently insensitive. In other cases when the sphacelus is thrown off it leaves a deep ulcer, which may look as if the lost tissue had been cut out with a punch, and this gradually granulates and heals. In still other cases the entire skin of the terminal phalanx may become black and dry, presenting a true gangrenous appearance. Then a line of demarcation is formed, usually at the junction of the terminal with the middle phalanx; separation of the gangrenous part occurs, and a stump is left covered with thin, glossy skin. This extensive gangrene, involving an entire phalanx, is the exception rather than the rule.

While the gangrenous process is in progress in the tip of the finger the nails cease to grow, and may become bulbous and rigid; the epidermis elsewhere may become dry and desquamate, and ulceration around the root of the nail may take place. With the completion of the stage of gangrene, which may last from one to five weeks according to its extent, the local symptoms terminate.

It is the symmetrical distribution of the local symptoms just enumerated which is the peculiar characteristic of the disease. The fingers of both hands, the toes of both feet, symmetrically situated spots upon the back, trunk, thighs, legs, forearms, and arms (in the order of frequency named), are affected either singly or in combination. In the majority of cases fingers and toes are affected together, and a few spots are seen on the trunk. In many cases the toes escape. In a large number of cases the face has been affected, spots of cyanosis appearing on the nose or ears or lips. As a rule, the stage of gangrene only ensues in the tips of the extremities, but a few cases are recorded in which little areas of skin elsewhere have passed through all the stages of the disease. Pigmentation occurs in spots upon the body when the process does not go on to gangrene.

Among the rare symptoms which have occurred in some cases are great impairment of temperature, pain, and electric sensations in the affected extremities; swelling, pain, redness about, and effusion into, the joints; considerable loss of motion in the muscles of the hands and feet, with diminution of electric excitability, but no qualitative change; and oculo-pupillary changes ascribed to an irritation of the cervical sympathetic fibres at their origin in the spinal cord.

In addition to the constitutional symptoms mentioned, which may usher in the disease and may continue during its course, there have been observed temporary albuminuria, glycosuria, and hæmaturia. Fever never occurs as a symptom of the disease, and if present must be ascribed to some other condition. The special senses have been affected in a few cases. In one case a spastic contraction of the retinal arteries alternated with attacks of ischæmia in the extremities.[60] The intellect is usually unaffected, but Weiss observed a case in which transient aphasia occurred, which he attributes to local spasm in the arteries of the cortex. The patient could find words only after long thought, and spoke slowly and with difficulty.

[Footnote 60: Raynaud, _Arch. gén. de méd._, 1874, p. 11; Galezowski examined the discs.]

{1261} COURSE AND DURATION.—The onset of the disease is sudden. The symptoms in the first two stages may last only for a few minutes and pass off, or the disease may pass through all the stages and terminate in gangrene. It is usual for the first stage of ischæmia to last several days, varying in severity; for the second stage to last several days; and for the stage of gangrene to occupy about three weeks. The shortest duration of a single attack has been ten days, the longest five months. If the gangrene begins simultaneously in all the fingers, the duration will be shorter than if it proceeds to one after another. In one-third of the cases a recurrence of the disease within a year of the first attack has been observed, and it is probable that the proportion would have been larger had all the patients been kept under observation. In some cases three and four attacks have succeeded each other with some rapidity, some of the attacks being much less severe and shorter than others. In some cases the condition of gangrene has developed only in one out of three attacks. When the condition is one of local erythema the duration may be indefinite, the state becoming chronic and lasting for several years.

NATURE.—The nature of the disease is a matter of deduction from the study of the symptoms, no autopsies having as yet been made. As already stated, the symptoms are explained on the theory of a vaso-constrictor irritation in the stages of ischæmia and cyanosis—of a vaso-dilator irritation in the stage of erythema. Whether this irritation is the direct result of abnormal processes going on in the vaso-motor centres in the spinal cord, or is the reflex result of irritation arising elsewhere, is undetermined. Raynaud held that it must be of central origin, since in his cases galvanization of the spinal cord modified the arterial spasm. The latter observation has not been confirmed by other observers. Weiss believes that the condition may occur in response to irritation arising in the skin, in the viscera, or in the brain, and thus prefers the theory of reflex origin. This theory is adopted by several observers, who find a source for such irritation in the female genital organs in their cases.

ETIOLOGY.—The disease occurs in adult life, only two cases having been observed in persons fifty years old. It is most frequent between the ages of fifteen and thirty, although children and adults beyond the age of thirty are about equally liable. Females are more liable to it than males, four-fifths of the recorded cases having been in women. It occurs more frequently in the winter months, exposure to cold being a common exciting cause. Other exciting causes are nervous exhaustion, especially occurring in those who are predisposed to nervous diseases by heredity; general weakness from anæmia, malnutrition, or the occurrence of acute fever or exhausting disease; and mental agitation, a fright having preceded the attack in several cases. In women menstrual disorders and uterine disease have been considered as etiological factors. Occupation has something to do with its occurrence, since washerwomen, waitresses, and chambermaids are the class most often affected. In many cases, however, no cause of local irritation can be found.

DIAGNOSIS.—The diagnosis rests upon the development of vaso-motor symptoms in the extremities, situated symmetrically, going on to gangrene, in a person not afflicted with cardiac disease or with endarteritis of any kind, and not having been exposed to frost-bite or ergot-poisoning. The age of the patient, the symmetrical position of the symptoms, the {1262} persistence of the pulse in the main arteries, and the limitation of the gangrene to the tips of the extremities distinguish it readily from senile gangrene. The history of the case, the absence of itching, and the presence of pain during the arterial spasm which passes off when the spasm ceases, serve to separate it clearly from chilblains. Congenital cyanosis is produced by cardiac anomalies, and the entire body is affected. Ergot-poisoning can be ascertained by the history.

PROGNOSIS.—Life is not endangered by this disease, no fatal cases having been recorded. Recovery from an attack is certain, but the duration cannot be stated, as it will depend in any case on the character, the extent, and the severity of the symptoms. The possibility of a recurrence of the attack should be stated to the patient.

TREATMENT.—The methods of treatment have varied, and none are wholly satisfactory. If the causes can be met—_e.g._ anæmia, nervous exhaustion—they should be treated. If not, the disease itself may be attacked by means of electricity. Or the symptoms may be treated as they demand it. Electricity has been used by almost all observers. The faradic current produces an aggravation of all the symptoms except in the stage of erythema, and has been discarded. The galvanic current may be employed in several ways. Two methods are in use. In the first the positive pole is applied over the cervical region, and the negative pole over the lumbar region, a descending current being thus sent through the spinal cord. The current should be of moderate strength, not above twenty-five milliamperes, few patients being able to endure the strength implied in Raynaud's statement that he used sixty-four cells of a Daniel battery. The duration of the application should be ten minutes, and the electricity may be applied once daily. In the second method the anode is applied over the brachial or lumbar plexus, as the case may be, and the cathode passed over the affected extremity, the current being constant and care being taken not to break it suddenly. The strength, duration, and frequency should be the same as in the first method. From these two methods, separately or combined, Raynaud claimed to have seen favorable results. His assertions have not been confirmed by other observers who have followed his directions closely, and hence considerable doubt at present prevails as to the efficacy of the electric current. The so-called electrical application to the cervical sympathetic is certainly useless. In the stage of erythema a very weak faradic current applied to the hands in a bath may be of service.

Many observers have found that the progress of the case to recovery was quite rapid if the limb were put at rest in an elevated position, were kept warm by cotton batting or similar bandaging, and were kept clean with antiseptic lotions when the stage of gangrene set in. Massage is to be used in all cases, the limbs or affected parts being gently rubbed with the dry hand or with aromatic liniments or oils. All local injury, however, and especially counter-irritation, are to be carefully avoided. General tonic treatment, especially iron and cod-liver oil, is to be used in all cases.

The pain occurring in the early stages is often so severe as to require the use of opium or other narcotics. And when the nervous symptoms are especially aggravated, and irritability and insomnia give the patient discomfort, bromide and chloral may be employed.

{1263} Diseases of the Cervical Sympathetic.

ETIOLOGY.—Diseases of the cervical sympathetic ganglia or cord may be of two kinds—either irritative or destructive.[61] They are produced by pressure upon the cervical ganglia or upon the sympathetic cord between these ganglia, by tumors, especially aneurisms, and enlarged glands; by abscesses; and by cicatrices of old wounds in the neck. They are also due to extension of inflammation from a thickened pleura in phthisis and chronic pleuritis of the apex. They may be caused by injuries, such as stab-wounds, gunshot wounds, etc. Any disease which produces marked irritation of peripheral branches of the sympathetic in the neck, or of the cerebro-spinal cervical nerves, may cause reflex phenomena resembling the symptoms of actual disease. From such phenomena it is not justifiable to conclude that the sympathetic cord and ganglia are the seat of lesions, and the only cases which will be considered here are those in which actual disease was proven to be present by an autopsy.