Neuralgia and the diseases that resemble it

by Francis Edmund Anstie

The course of cardiac neuralgia varies extremely. Supposing the malady to be purely neurotic, and not complicated with organic disease, which forms a constant source of cardiac embarrassment, then the patient may only experience one or two attacks, under some special circumstances of exhaustion, which may never recur; or, on the other hand, he may develop a strong tendency to cardiac neuralgia which may beset him during almost any number of years. In the latter case, it is an even chance whether the patient will at last sink from the anginal affection; for, even supposing him to escape any fatal intercurrent disease of an independent nature, the fatal event may be at last produced by cerebral softening, or by apoplexy, or other central nervous disease. In fact, the frequency with which the latter kind of termination occurs is very significant of the essential nature of the disease.

The manner in which cardiac neuralgia commences varies very greatly. In the celebrated case of Dr. Arnold, the first attack did not occur till he was forty-seven years of age; it at once assumed full intensity, and proved fatal in two hours and a half. There is also reason to believe that Dr. Arnold's father died in a first attack of angina. I have myself known a first attack prove fatal in the course of an hour; there was very considerable ossification of the coronary arteries and fatty degeneration of the heart-walls. Again, there are many cases which commence gradually, and with great mildness, and with little appearance of danger to life in the first attacks; but the subsequent attacks are progressively more severe and dangerous up to a fatal result, after weeks, months, or years. On the other hand, I have known three instances in which the first attacks of spasmodic heart-pain very nearly proved fatal, but the subsequent fits were milder (in one there was no second attack): all those patients are living, six, eight, and three years respectively, after their first attacks.

It can hardly be doubted that neuralgic spasm is the true cause of sudden death in some cases of stenosis of the aortic orifice, which, but for some accidental circumstances, would not have died suddenly at all, but would have gone through a long and gradual course of deterioration. I particularly remember an instance in which extreme and calcareous constriction of the aortic orifice, in a boy not yet come to puberty, was entirely unsuspected, until one day, in running fast, he screamed out and fell down, and was almost instantaneously dead. I remember another case very similar, in which extreme mitral constriction produced almost as sudden death, apparently from painful spasm, under the same kind of exertion. On the other hand, sudden death, when produced by the form of heart-disease which (as Dr. Walshe points out) is most likely to cause such a catastrophe, viz., aortic regurgitation pure, without hypertrophy, does not seem to be due to painful spasm, but to simple and complete failure of the muscular power, and is perhaps partly of the nature of paralysis from a syncopal condition of the brain, the unhypertrophied heart having become for the moment unable to supply blood enough to the brain to carry on nervous function at all.

A good instance of the form which angina takes, when the element of organic cardiac change is well pronounced, was afforded by the case of a young gentleman recently under my care. He was twenty-one years of age, and from early boyhood had been accustomed to a great deal of muscular exercise; in fact, it is probable that he had undermined his health by the frequent and extraordinarily long walks which he took, for his frame was particularly small and slight, and the muscles small and soft. He came of a family in whom the tendency to neurotic disorders is obviously very strong; both his father and his brother are subject to bad attacks of migraine, and he had himself repeatedly suffered from the same thing. The family disposition, altogether, is highly nervous and excitable. The remarkable circumstance in this young gentleman's case is, that although he had taken for years an extraordinary amount of pedestrian exercise (including mountain-climbing), and latterly had exchanged this for the even more trying exertion of rowing, he had never suffered from any noticeable symptom of cardiac distress up to the very day of his anginal attack. For some months, however, he had been growing thin and pale, and I had given him certain cautions, and had made him take cod-liver oil and steel, as I entertained some fears of his becoming phthisical. On the day of the attack there was nothing particular in his appearance, but he complained of a slight cold, and had no appetite for his six o'clock dinner. He retired to rest at eleven o'clock, having taken a small dose of laudanum and chloric ether for his cold. In less than half an hour he awoke out of his sleep in fearful agony; so severe and prostrating was the anginoid pain that he had the greatest difficulty in crawling out of bed to unlock his door. I found him bathed in cold sweat, pale as a sheet, and with livid lips. He groaned with pain, which he described as "cutting him across" from the sternal notch to the nipple, and going down the left arm; and there was so marked a catching of the breath as to make it almost certain that there was diaphragmatic spasm; in fact, it was this which alarmed him, and made him say that he was certainly dying. The heart, however, appeared to be pushed up somewhat, and it was thought that this might be partly due to stomachic distention, but a mustard emetic produced little effect. The heart-sounds were so weak that the presence or absence of bruit could not be safely predicated; meantime, the pulsations intermitted in a most alarming manner. Large doses of brandy and sulphuric ether at length (after several relapses) seemed to subdue the pain and spasm, and in an hour and a half from the commencement of the attack the patient, though utterly worn out, sank into a tolerably quiet sleep. The spasms did not recur, but for the next three or four days he was in a state of great exhaustion. When his tranquillity of mind had been somewhat restored, a careful physical examination was made, and it was discovered that there was a moderately loud and somewhat thrilling systolic bruit at the site of the aortic valves, and extending some distance into the vessels. The pulse still remained strikingly intermittent, and, though of fair volume, was very compressible. Percussion indicated considerable enlargement of the heart, and the physical signs pointed, on the whole, to dilatation without hypertrophy. Some doubtful signs of consolidation were observed at both apices of the lungs.

It is remarkable that, notwithstanding the serious degree of cardiac mischief indicated by the above signs, the patient, a very few days later, took a walk of some ten miles, and, though much exhausted, suffered no recurrence of his formidable spasmodic symptoms in consequence of this imprudence. He was sent to the mild climate of Mentone, and subsequently to Nice; the angina never recurred, but the patient remained weak, and liable to more or less dyspnœa for fifteen or sixteen months; now he lives an ordinary life, doing his duty as a Swiss citizen and officer. The cure of some hæmorrhoids, about twelve months after the anginal attack, seemed greatly to benefit him. What the future of this case may be it is impossible to say, but of course there is no security against the angina recurring on extraordinary excitement or over-exertion.

Of the purely neurotic variety of angina it is impossible to determine the frequency; but it seems certain that the affection is common, and I suspect that it occurs more often than is supposed, as a sequel to asthma. The probable relationship between the two affections was long ago indicated by Kneeland.[8] I have certainly seen several cases of asthma in which spasmodic pain of the heart has occurred on various occasions after or during a very severe asthmatic paroxysm. One case was that of a gentleman, of a highly delicate and neurotic temperament, who had suffered for fifteen or sixteen years from well-marked spasmodic asthma: this case is remarkable as an illustration of several points which will be dwelt upon in other parts of this volume. For some time before the outbreak of cardiac neuralgia, he had suffered repeatedly from severe facial neuralgia, and these attacks on more than one occasion culminated in facial erysipelas, or what was entirely indistinguishable from that affection. He then began to suffer from cardiac pain and spasm after his asthmatic paroxysms, and these new symptoms speedily assumed the form of a very severe intermittent angina: in several of the attacks he appeared about to die. The pain in these attacks is very severe; it occupies a large area in the centre of the chest, and runs down both arms; and, what is strange, the arms become remarkably swollen and hot after an unusually long bout of pain, I presume from vaso-motor paralysis. At present (nearly five years from the commencement of the cardiac neuralgia) the cardiac attacks, though of frequent occurrence, are decidedly more tolerable than they were at first, and the sense of squeezing or pressure, though never quite absent, does not amount to the dreadful sort of feeling which used to convince the patient that he was at the point of death. In this case, the heart has been repeatedly explored without any positive result, and the pulse has been frequently tested by the sphygmograph. The latter instrument is the only mode of examining by which I have been able to elicit even suspicious evidence that there is any organic change of the heart; by means of it I have lately obtained some grounds for suspecting that there is slight dilatation of the heart, but it is uncertain whether anything of the kind existed at the commencement of the anginal symptoms. In this case I am inclined, on the whole, to doubt whether the angina will ever prove fatal, unless the bronchitis, with which the patient's asthma has for some time past been liable to be complicated, should occur in a severe form; in that case it is likely that the additional embarrassment of the heart's action may bring on fatal spasms.

One of the best examples I ever saw of cardiac neuralgia (ultimately proving fatal) was one of which the origin was entirely nervous. It occurred in a gentleman in the prime of life, and naturally of a powerful physique, whose very active and capacious mind had been greatly overwrought. The whole weight of responsibility for an undertaking of national importance, and which involved great difficulties and much anxiety, for a long time rested on his shoulders. Under these influences he broke down, and never effectually recovered himself. At first, the symptoms were those of mere ordinary nervous exhaustion, but after a time he became subject to frequently recurring attacks of agonizing spasmodic heart-pain, with a sense of impending dissolution; from these he was invariably relieved by the inhalation of a small amount of chloroform. Not the slightest organic heart mischief could be detected, either during life or after death.

Pathology.—Angina stands in so peculiar a position that I deem it well to discuss it as a whole, and not merely its clinical history, in this place. As I have already said, there is nothing in the morbid appearances found after death which is characteristic of fatal angina, and in the milder kinds of cardiac neuralgia we are driven back upon the general probabilities which we deal with in reasoning as to the origin of neuralgias in general. As to morbid changes, it is impossible to say any thing more exhaustive of the facts known than the following words of Dr. Walshe:[9] "First, there are few, if any, structural diseases either of the heart, its orifices, and its nutrient arteries, or of the aorta, found recorded in the narratives of the post-mortem examination of different victims of angina pectoris. Secondly, there is no conceivable disease of these structures and parts which has not in various individuals reached the highest point of development, without anginal paroxysms, even of a slight kind, having occurred during life; to this proposition extensive calcification of the coronary arteries perhaps furnishes a solitary exception. Thirdly, the organic changes most frequently met with have been fatty atrophy and flabby dilatation of the heart; obstructive disease of the coronary arteries by atheroma and calcification of the orifice and arch of the aorta. Fourthly, the rarest have been hypertrophy and hypertrophy with dilatation. In truth, it may be doubted whether these conditions in their genuine form, without any combination of fatty atrophy, have ever been the sole morbid states present." From all this Dr. Walshe concludes that the fundamental mischief of angina is neurotic; and, while he believes that some textural change in the heart is necessary as an irritant to generate this neurotic susceptibility to dynamic disturbance from slight causes, he recognizes only one common quality in these various cardiac lesions, viz., that they indicate mal-nutrition and weakened power. Dr. Walshe does not appear to believe the neurotic disturbance can arise without the kind of irritation which is kept up by such cardiac changes. In spite, however of the great authority of this author, it certainly seems very probable that organic cardiac change is by no means necessary to the occurrence of angina, and this for two reasons: In the first place, though full reliance may be placed on the details of the post-mortem examinations made by Dr. Walshe himself, they are very few (twelve or fourteen) in number; and other observers who have recorded cases are as little trustworthy, considering their evident tendency to find some disease where none exists, as the older narratives which Dr. Walshe naturally distrusts were unreliable when they declared that no morbid change was present. And, secondly, his view hardly takes it into account that there are still two other alternatives, even supposing that one or other of the above changes is always present: (a) it is possible that the neurotic disturbance and the cardiac lesions might both be the result of a common cause; and (b) it is even possible that the alterations of tissue in the heart and vessels are due to a morbid influence proceeding from a diseased nervous centre, either spinal or sympathetic.

As for the state of the muscular fibre which immediately causes death, Dr. Walshe is of opinion that it is paralytic rather than spasmodic; and he urges in favor of this view the fact that in his large experience he has never known the pulse to intermit during the attack—it was always regular, however feeble. In this respect he is in opposition to some distinguished authors, however, and, as he allows that he has not seen original attacks in their height, but only when they were subsiding, it would be possible that the spasm stage had subsided. However Dr. Walshe admits that there may be exceptional cases in which spasm, or cramp (i. e., spasm with rupture or dislocation of fibre), really occurs, and suggests that this is very probable in the rare cases where death is attended by general tetanic spasm of the muscles. As far as my own opinion is worth anything, I could insist that at least Dr. Walshe must be right as against Dr. Latham and Dr. Inman, in affirming that cardiac cramp, if it occurs, is the consequence and not the cause of the neuralgic pain.

Causes.—In some respects it is impossible to deal with the etiology of angina apart from the pathology, just as we remarked with regard to neuralgias in general. But there are certain special features in the causation of angina pectoris which require separate notice, just as there are special features in its pathology.