Neuralgia and the Diseases that Resemble it

Nor are we likely to reach a different conclusion, if we test the matter by the consideration of a rarer, but still sufficiently common kind of case, such as I have described in Chapter I., in which a very strong peripheral influence (traumatic) produces neuralgia, accompanied by vaso-motor and secretory phenomena, and by anæsthesia, but not in the district of the painful nerve, but in the territory of a quite different nerve. How can we doubt, in the case, e. g., of a trigeminal neuralgia thus complicated, the exciting cause of which was a wound of the ulnar nerve, that the morbid influence, traveling inward from the lesion, would have passed without any special consequences (as happens in thousands of such nerve-wounds), had it not, in its passage along the medulla, encountered a locus minoris resistentiæ in the roots of the trigeminus? It seems impossible to account for the phenomena on any other theory. [Eulenburg says, in reference to my reported cases of the kind: "Solche Falle begunstigen in hohem Grade die Annahme pradisponirender Momente, die in der ursprunglich schwacheren Organisation einzelner Abschnitte des centralen Nerven-apparates beruhen." Op. cit., p. 56.]

It is necessary, in the next place, to consider a very important question, how far irritation can pass over from one nerve to another, without reflection through a spinal centre, solely in virtue of a connection through the medium of a nervous plexus. The case which apparently presents such phenomena in the most unmistakable way is that of angina pectoris.

The site to which the essential heart-pain is referred in this disease is probably the cardiac, or this and the aortic plexus; in a comparatively small number of cases the pain does not extend farther. But much more frequently it spreads in various directions, and we have to account for its presence (a) in intercostal nerves, (b) cervical nerves, (c) nerves springing from the brachial plexus.

Before we inquire into the mechanism by which this extension of the pain takes place, we ought in strictness to ask ourselves whether the essential heart-pain is felt only in the spinal sensory branches, or whether the sympathetic fibres are themselves capable of feeling pain. The latter supposition, notwithstanding all that has been argued in its favor from the supposed analogies of the pain of colic, gall-stone, etc., seems to me very doubtful. It would appear more probable that both the latter pains, and also those of angina, are really connected with branches either of the vagus or of other spinal nerves. And there is no need to invoke the sympathetic as a sensory nerve, to account either for the essential heart-pain of angina, or for its extension into arm, chest-wall, and neck. For the plexus cardiacus receives spinal branches, both from the vagus and also (through the medium of the sympathetic ganglia of the neck) from the whole length of the cervical and the uppermost part of the dorsal cord-centres. And, in this way, it would seem quite possible intelligibly to account for the pain radiating into intercostal, cervical, and brachial nerves, merely by extension of a morbid process essentially seated in the cord. Usually, however, one sees it explained not in this way, but by the inter-communications that exist outside the spine, between the branches from the cervical ganglia and the lower cervical and upper dorsal nerves; and the pain in the arm is especially explained by the connection (outside the spinal canal) of the inferior cervical ganglion, on the one hand with the lower cervical nerves, which go to the brachial plexus, and, on the other hand, with the heart itself. There remains to be explained, however, the singular tendency of the arm-pain to be one-sided (this happens in at least four cases out of five); and this explanation seems to me insuperably difficult, on the theory that the transference of morbid action to the brachial nerves takes place through external anastomoses. It appears greatly more probable that angina is essentially a mainly unilateral morbid condition of the lower cervical and upper dorsal portion of the cord; liable of course to be seriously aggravated by such peripheral sources of irritation as would be furnished by diseases of the heart, and especially by diseases of the coronary arteries; the latter affection probably involving constant mechanical irritation of the cardiac and the aortic plexuses. It is noteworthy that the arm-pain is sometimes (I do not know how often) accompanied by vaso-motor paralysis in the limb; this phenomenon could also certainly be more easily accounted for on the supposition of radiation from a spinal vaso-motor centre (to which the morbid process had extended from a posterior nerve-root) than on that of communication between painful sensory nerves and vaso-motor nerves; through either of the plexuses independently of the spinal centres.

In truth, I suspect that, whatever part the plexuses, with their reenforcing ganglionic cells, may play during physiological life, they are not often the channels of mutual pathological reaction of one kind of nerve with another. It would be possible to argue this even more strongly in the case of trigeminal neuralgias; but I must not unnecessarily expand this already too lengthy discussion.

From the varied considerations which have now been adduced, the reader, unless I altogether miscalculate the value of the facts, will probably have arrived at the following conclusions: (1) That the assumption of a positive material centric change as the essential morbid event in neuralgia is almost forced upon us; (2) that, whereas the morbid process, if centric, is a priori infinitely more likely to be seated in the posterior root of the painful nerve, or the gray matter immediately connected with it, than anywhere else; so, again, the assumption of this locality will explain, as no other theory could explain, the singular variety of complications (all of them nearly always unilateral, and on the same side as the pain) which are apt to group themselves around a neuralgia; and some of which are very seldom absent in neuralgia of any considerable severity. To this we may certainly add that it is extremely probable that the vast majority of neuralgic patients inherit the tendency to this localized centric change; in support of this we may finally mention two considerations derived from the sex and the ages most favorable to neuralgia. Eulenburg saw a hundred and six cases of neuralgia of all kinds, of which seventy-six were in women and only thirty in men; my own experience is very similar; namely, sixty-eight women and thirty-two men out of a hundred hospital and private patients. The strong connection between the hysteric and the neuralgic temperament in women, and the great preponderance of women among neuralgics, strengthen in no small degree the probability of inherent tendencies to unstable equilibrium as a very common predisposing factor in neuralgia. And, on the subject of age, I need only recall what I have said so strongly about the coincidence of neuralgia with particular epochs in life, as affording evidence of the most powerful kind that neuralgics are, save in exceptional instances, persons with congenitally weak spots in the nervous centres, which break down into degeneration, temporary or permanent, under the strains imposed by one or other of the physiological crises of the organism, or the special physical or psychical circumstances which surround the patient's life.

Having thus decidedly expressed my belief in the essential material participation of the nerve-centre in neuralgia, it remains for me to discuss two points: first, as to the character of the material change in the nerve-root, and next, as to the extent to which mere peripheral influence, without special inherited tendencies, may suffice to set this process going.

The morbid change in the nerve-centre is probably, in the vast majority of cases, an interstitial atrophy, tending either to recovery, or to the gradual establishment of gray degeneration, or yellow atrophy, of considerable portions of the whole of the posterior root, and the commencement of the sensory trunk as far as the ganglion.

It is probable, however, that in a certain number of cases, the atrophic stage may be preceded by a process of genuine inflammation, and that this inflammation is centripetally produced in consequence of inflammations of peripheral portions of the nerve. The considerations which make this probable are chiefly derived from the analysis of cases in which a more or less chronic, but severe, visceral disorder has been followed by so-called reflex paralysis, but in which neuralgic phenomena, have been conspicuous. In reference to this subject I recommend to the reader's attention the very interesting paper on "Reflex Paralyses" by Prof. Leyden, of Konigsberg.28 He is immediately commenting upon a case in which dysenteric affection of the bowel were followed by the symptoms of myelitis, attended with febrile exacerbations, and also with severe pains in the region of the sacrum, in the course of the dorsal intercostal nerves of the right side, and in the knees, and semi-paralytic weakness of the lower extremities, and with pains between the shoulder-blades and the left arm. Leyden discusses the doctrine of reflex paralyses in general, starting from the cases of urinary paraplegia brought forward by Stanley, in 1835, and tracing the growth of opinion through the phases represented by Graves, Henoch, and Romberg, by Valentine and Hasse, then by Pfuger, and other professors of the inhibitory doctrine; by Brown-Sequard (in his well-known, and now very generally discredited, theory of spasm of the vessels in the nervous centres), by Jaccoud in the "Erschopfung" (exhaustion) theory, down to the more careful and reliable researches of Levisson on the temporary reflected paralyses induced by experimental squeezing of the kidney or uterus of animals; and then gives the history of the more recent doctrine of a positive material change in the cord centripetally introduced. Gull29 (1856) may be said to have inaugurated the new doctrine of a morbid process transmitted along the pelvic nerves to the cord, and causing material changes there. Remak,30 on the other hand, suggested a material change operating in the opposite direction; a neuritis descendens, starting in the very nerves (within the pelvis) which showed the paralysis in the extremities. The symptoms are supposed by him to be distinctive, inasmuch as there is both violent pain in the nerves of the soles of the feet, and also tenderness of the same. On the other hand, Remak said that myelitis, with neuritis, might be the origin of paraplegia and simultaneous palsy of bladder and rectum. The theory of neuritis descendens was supported by Kussmaul,31 in the record of a case where disease of the bladder was complicated with pelvic inflammation, atheromatous degeneration of the arteries, and consequent fatty degeneration of the sciatic nerves, causing direct paraplegia. We return to the centripetal theory of urinary paralysis with Leyden's own cases, published in 1865; of three patients with urinary paraplegia, two died, and the existence of a secondary (centripetal) myelitis seems to have been established, and by all analogy it must have existed in the third case, which recovered. The only puzzle and doubt that ensued was caused by the fact that there was an absence of neuritis in the different nerves themselves; though it seemed plain that the starting point of the myelitis was at the entrance of these nerves into the cord. This mystery seemed to be cleared up by the important experiments of Tiesler, ("Ueber Neuritis" Konigsberg, 1860) a pupil of Leyden's. This observer excited local traumatic inflammation in the sciatic nerve of rabbits and dogs; the rabbit became paraplegic and died three days afterward. At the site of the artificial irritation there was a localized formation of pus, and there was a second similar formation within the vertebral canal at the point where the posterior roots of the sciatic enter the cord; but there was no neuritis of the intervening portion of the nerve.

Upon this and similar evidence is based the modern doctrine of a neuritis migrans, with centripetal tendencies, upon which it is supposed that a very large proportion, at least, of the urinary, dysenteric, and uterine paraplegias, miscalled "reflex," depend; and it is clear that the application of the word "reflex" in such a case is a grave abuse, tending to produce such confusion of thought and error in practice. In relation to the subject of our own inquiry – neuralgia – it is obviously of the highest consequence to investigate the question whether peripheral irritations, analogous to those which produce urinary paraplegia, are at all frequently the cause of the changes in the posterior roots which produce true neuralgia; for of course an inflammation may be the beginning of an atrophy which may presently exhibit no distinction whatever from one of which the origin was altogether non-inflammatory. I think that there is strong reason for thinking that this is not at all frequently the case. In the first place, all the evidence that exists respecting these centripetal inflammations of the cord is opposed to the idea that, save in the rarest instances, the inflammatory process limits itself to one small segment of the cord. Secondly, the description of the pains that have usually accompanied such inflammations of the cord is considerably different from the strictly localized, frankly intermittent character of a true neuralgia; in fact, all we know of the history of myelitis (except when complicated with a large amount of meningitis) forbids us to suppose that severe pain would be an immediate symptom. But, thirdly, a far more important objection to the theory of an origin in localized centripetal myelitis, the result of a neuritis migrans, is the rarity of motor paralysis as an early symptom, instead of which we ought to find a very distinct history of decided paralysis (much more decided than those secondary paralyses which actually do occur in some neuralgias) of the muscles supplied by the anterior roots of the painful nerve, in every case in which such a peripheral origin could be assumed. Again, the totally feverless commencement of neuralgias, a character which is maintained throughout the progress of the milder cases, is entirely opposed to the idea of a direct connection between myelitis and neuralgia. The superficial appearance of pyrexia is sometimes given by a local vaso-motor paralysis, which makes the neuralgic part, after a long bout of pain, hot and red; but of general pyrexia there is nothing.

Taking every thing into consideration, one is inclined to say that there is a probability that in a very limited number of cases peripheral irritation does cause actual limited myelitis, which escapes recognition at the time, but which issues in an atrophy, the subjective expression of which is actual neuralgic pain. We may well ask ourselves, also, whether there is not some likelihood that a peripheral irritation, which stops short of producing an actual neuritis migrans capable of centripetally exciting a myelitis, may not, by a lower degree of centripetal irritation, give a bias toward certain forms of non-inflammatory atrophy in cells of posterior nerve-roots which are congenitally of weak organization. I am inclined to believe strongly that this does occur. For example, I should explain thus the majority of the peripheral cases of ciliary neuralgia, migraine, etc., that we meet with in poor young needle-women, especially the hypermetropic, who, at an age when they can ill afford the strain, work so constantly and strenuously at an occupation which fearfully taxes the eye.

I would also go farther, and express the opinion that peripheral influences of an extremely powerful and continuous kind, where they occur with one of those critical periods of life at which the central nervous system is relatively weak and unstable, can occasionally set going a non-inflammatory centric atrophy which may localize itself in those nerves upon whose centres the morbific peripheral influence is perpetually pouring in. Even such influences as the psychical and emotional, be it remembered, must be considered peripheral – that is, they are external to the seat and centre of the neuralgia. And there are probably few practitioners of large experience who have not seen a patient or two in whom the concurrence of some unfortunate psychical with some other noxious peripheral influence, the whole taking place at some critical period of life (especially in the years between puberty and marriage), seems to have totally deranged the general balance of nervous forces, and induced morbid susceptibilities and morbid tendencies to some particular neurosis. It is a comparatively frequent thing, for example, to see an unsocial solitary life (leading to the habit of masturbation), joined with the bad influence of an unhealthy ambition, prompting to premature and false work in literature and art. The bad peripheral influence of constant fatigue of the eyes in study may so completely modify a young man's constitution as to make a wreck of him in a very few years, changing him from the state of habitual and conscious health to that of chronic neurosis of one sort or another. And, though it is doubtless on persons with congenital tendencies to nervous diseases that such a combination of bad influences produces its most serious effects, yet there unquestionably are a few persons in whom they appear to entirely generate the neurotic constitution. I have already touched upon the part that misdirected psychical influences, especially religious and other forms of emotional excitement, may play in this unfortunate perversion of the natural and healthy nervous functions, more especially in youth; and need only add, here, that perhaps the most fatal combination of all the bad influences is the melancholy union of highly-strained religious sentiment with peripheral sexual irritation, which is, unfortunately, a too common phenomenon under certain systems of education. The most frequent neurotic consequences of the class of influences which have now been referred to are probably neuralgia – in the form either of migraine, of nervous angina, or of sciatica – or else asthma.

But, if the combination of several such centripetal influences may generate the neurosis unaided, even a single one of them operating powerfully for a long period may produce most serious consequences in those who are hereditarily predisposed. The influence of prolonged fatigue of the eyesight, independently of any special intellectual or emotional strain, was strongly illustrated in my own case about three years ago. I was then engaged upon a piece of scientific writing which demanded no great intellectual effort, but was being done against time, and by working, night after night, many hours by gas-light. My neuralgic (trigeminal) attacks came on with great severity, accompanied by vertiginous sensations of so alarming a kind as to make me fear the invasion of some serious brain-mischief. I broke off all work, and went to the sea-side, but was greatly disappointed to find, for the first few days, that the symptoms were not in the least mitigated. The mystery was soon explained. The weather had been such as to confine me a good deal to the house, and, thinking it would do no harm, I amused myself with reading newspapers and novels. At last I suspected that the use of my eyes in reading was altogether mischievous; I desisted from reading any thing, and in forty-eight hours every symptom had vanished.

Among peripheral influences of a more mechanical kind there is one cause of neuralgia, the force of which has been variously estimated, but which some authors rate as very important, viz.: the influence of the pressure, and especially of the varying pressure, of blood-vessels, or other hollow viscera, upon the trunks of the nerves. We must set aside one such action which is undoubtedly very powerful, as essentially differing from the others; I mean the pressure of dilated blood-vessels, especially aneurisms, when this happens to be exerted upon the ganglion of the sensory trunk. Here there can be no doubt of the mischief; for the pressure, if at all severe, gradually destroys the life of the ganglion, upon which, as was proved by Waller, the nutrition of the posterior nerve-root hangs with very intimate dependence, and the pulsations of the vessel seem greatly to aggravate both the irritation and the centripetal tendency to atrophy. In short, it is plain that such lesion of a ganglion may be the whole and sufficient cause of a neuralgia of the most desperate and incurable kind. It is another matter when we are asked to believe that the mere varying pressure of intestines, in different states of fullness, or plexuses of pelvic veins liable to temporary congestions, can so affect the sciatic nerves as to set up neuralgia. Considering the extreme frequency of cases in which such momenta must be partially coming into operation, especially in women – a frequency altogether out of proportion to that of sciatica – I cannot admit the probability that this influence is more than an occasional and very secondary factor, and that only in cases where the disposition to neuralgia is uncommonly strong.

A sufficiently complete explanation of my theory as to the pathology and etiology of neuralgia has now been given, although the subject might be elaborated at far greater length; and I hope it will be apparent to the reader that the view now advocated is at once important, and also vouched for by strong evidence. I claim for it that the whole argument shall be taken together, for it is a case of cumulative proof; every link must be weighed and tested, before the remarkable strength of the chain can be felt. And it may fairly be said that, if the proof of a definite kind of material change in a definite organ, as the essential factor in neuralgia, has been established upon reasonable grounds, an important step has been taken toward removing a serious opprobrium and difficulty in practical medicine. Although the true neuralgias are not among the most frequent of human diseases, they form a class of enormous practical importance, for they are sufficiently common to be sure to occur in considerable numbers in the practice of every medical man, and, both from the suffering which they inflict, and the rebelliousness which they often show to treatment, they are among the gravest sources of anxiety which the practitioner is likely to encounter. There are probably few disorders which so often occasion mortification and loss of professional credit to the physician. The helplessness which men, who do not enjoy special opportunities of seeing those diseases with frequency, so often show in dealing with them, is largely caused by the extreme timidity and vagueness with which the standard treatises on medicine deal with the question of their pathology; and a very unfair advantage has thus been given to the specialists, who, by the mere force of opportunity, and continual blind "pegging away" in an entirely empiric manner, have acquired a certain rude skill in the treatment of these maladies which enables them to outshine practitioners who often have far more in them of the veritable homme instruit as regards general scientific education and habits of mind. It will be evident, as a mere abstract proposition, that the enunciation of a reasonable pathology of the disease, and the sweeping away of a mass of unmeaning phrases about "mysterious functional affections" and the like, must be a distinct gain to practitioners of plain common-sense and good general knowledge, to whom neuralgia is merely one of a vast number of different diseases among which their attention and study are divided. And I hope that, in the further remarks on Diagnosis, Prognosis, and Treatment, yet to be made, the value of clear pathological ideas of disease will be brought more practically and clearly into view. [The reader will find, at the end of Part I. of this volume, a note which contains a brief discussion on the "Erschopfung" theory of Jaccoud, and the doctrines of Dr. Handfield Jones respecting inhibition, with which I thought it best not to encumber the text of the present chapter.]

CHAPTER IV.

DIAGNOSIS AND PROGNOSIS OF NEURALGIA

Diagnosis.– This subject is much simplified and shortened, in regard to our present purpose, by the plan of the present work, which, by separately describing (in Part II.) the other disorders which resemble neuralgia, and are liable to be confounded with it, avoids the necessity for stating here the negative diagnosis of neuralgia itself. We are only concerned here to give a clear picture of the positive signs which it is necessary to verify before we can suppose disease to be neuralgia. The special modes of searching for these are interesting, and in some respects peculiar;