It is necessary to go over again the proof of these facts; they are given pretty copiously in the chapter on Complications; and could have been made much more numerous. But the point to which I desire to compel the reader's attention is the impossibility as it seems of me, of accounting for the variety and complexity of these phenomena, except by the supposition that there is in every case of neuralgia a central change, which is the one most important factor in the producing both of the pain and of the secondary phenomena. For the result of my experience is that neuralgia, unless very slight and brief, is never unattended by these complications and in the great majority of cases involves several different secondary alterations of function which must (so to speak) radiate from the central end of the sensory nerve, and from no other place whatever. And it must be remembered that the most elaborate "symptome-complexe" is found equally in cases where no suggestion of any peripheral origin of the pain can be made, and in cases where, at first sight, one might fancy there was a very obvious peripheral cause for pain. I am quite willing to admit, with Eulenburg and others, that the evidence, powerful and varied though it be of the relations of neuralgia to hereditary neuroses, to alcoholic and senile degeneration, etc., only raises a strong probability that some part of the central nervous system is thelocus in quoof the essential morbid processes in the majority of neuralgias. But the case stands far otherwise now that we are able to show, not merely that the majority of neuralgic patients suffer from such influences as those above mentioned, but that every variety of neuralgia is liable to be complicated with secondary affections of the most divergent nerves, the only common meeting-place of which is in the spinal centre of the painful nerve; and when we find moreover, that many of these secondary affections can equally be produced by undoubted atrophic changes (as in ataxy of those same posterior roots).
At this point we must introduce a remark relative to the true nature of so-called "reflex" effects. The word is constantly used, and is also much abused, as Eulenburg remarks. We all understand, of course, what is intended by the commonest use of the word: the case of sneezing produced by the irritation of snuff applied to the peripheral branches of the fifth nerve in the nose is a stock example. But another application of the phrase, of much more questionable propriety, is that where it is employed to designate functional nervous actions, which merely arise simultaneously with or subsequently to sensory phenomena as to which there is no proof whatever that they were produced by peripheral irritation. This particular inaccuracyof customary speech has probably contributed largely to the inveteracy with which writers on nervous disease have insisted on assuming a peripheral origin in every case for neuralgia itself. In the case of sciatica, for example, complicated, secondarily, with paralysis of the flexors of the limb, it seemed easy and scientific to speak both of the neuralgia and the paralysis as "reflex" effects of a local peripheral mischief—gouty, rheumatic, or the like; and it appears to have been perfectly forgotten by many that the whole phenomena might be explained by an original morbid action in the sensory root of the nerve, extending subsequently to the motor root, without any intervention of peripheral irritation whatever, or under the influence only of the ordinary peripheral impressions, which, in health, evoke no painful nor paralytic symptoms. It is by this kind of extension of a central morbific process, leading to radiation of the perturbing influence centrifugally along divers nervous paths, that I believe we must explain the facts observed in complicated cases.
Take, for example, the following case, which, in its history of twenty-three years, presents a fair example of a type of trigeminal neuralgia which I believe to be the rule rather than the exception, though the trophic changes were somewhat unusually varied and interesting. The following would be the pathological order of events, according to the radiation theory: First or true migrainous stage; failure of nutrition of a portion of the sensory root of the right fifth nerve within medulla oblongata, lesser degree of the same condition in the adjoining and closely-connected vagus root (hence supra-orbital pain, local anæsthesia and vomiting); extension of the morbid process to the motor root (hence vaso-motor paralysis and secretory and trophic changes in the cornea, superciliary periosteum, etc). Second period: recovery, to a large extent, of the nutrition of the posterior root of the trigeminus, complete recovery of the root of the vagus (hence alteration of the type of recurrence of the pains, which now occur at increasingly long intervals, and needed special provocation,e. g., excessive fatigue, to bring them on; hence, also, disappearance of the stomach symptoms); continuance of the affection of the motor portion of the nerve (hence, continuance of the tendency to trophic, secretory, and vaso-motor changes); development of the true points douloureux during and after the paroxysms, instead of the diffused tenderness following the old attacks of migraine. Third stage: neuralgic attacks become rare and comparatively unimportant; tendency to trophic changes greatly lessened; local anæsthesia persists. Presumption, that the nutrition of the nerve-centre has nearly recovered itself, but that that centre is still thelocus minimæ resistentiæof the central nervous system, liable to suffer from any cause of general nervous depression.
Now, in interpreting the above phenomena, as I do, upon the theory of one essentially uniform nutritive change affecting the fifth nerve within the medulla oblongata, I shall be met with the following objections: First, there is the common and superficial difficulty that pain and paralysis of sensation must be opposite states, and that it is impossible to refer them both to one and the same pathological process. I have already in many places given instances how constantly pain and sensory paralysis interchange in a manner which is totally incomprehensible except upon the supposition that their physiological basis is essentially the same; but the most satisfactory evidence, perhaps, that could possibly be produced on this point is to be found in the perusal of a group of cases observed by Hippel,[20]and entitled by him "Anæsthesia of the Trigeminus," the loss of sensation being the most remarkable feature. The cases are so deeply interesting that I would gladly transfer them bodily to these pages, but must abstain from want of space. Suffice it to say here, that, in the first place, the anæsthesia was accompanied, in every one of these cases, by a most distinct and typical neuralgia; and, secondly, that trophic changes occurred which most interestingly (though not with absolute completeness) reproduced the phenomena observed after complete section of the trigeminus at the Gasserian ganglion.
The second objection sure to be raised to the theory of a simple spreading of a nutritive central change, as the cause of all the phenomena in such a case as the above, is this: It will be asked how the process extended itself to the motor root, which, in the case of the fifth nerve, is removed by a somewhat formidable anatomical distance from the sensory root. I am, of course, well aware of the latter fact, and it is an additional reason for selecting neuralgia of the fifth, as an extra difficult test of the value of my theory. A few words must be premised, reminding the reader of the physiological anatomy of the nerve.
The trigeminus is in all its characters a spinal nerve; but it has sundry peculiarities both of structure and of connections with other nerves. Its posterior or sensory root is enormous, and, as Schroder van der Kolk showed, takes a direction from behind downward and forward, which is intended to facilitate its numerous and important connections with the nuclei of other nerves: of these the most notable are its connections with the vagus, facial, glosso-pharyngeal, and hypo-glossal nuclei. The motor root, much smaller than the sensory, was shown by Lockhart Clarke to be traceable as low as the inferiorborder of the olivary body, as a column of cells which occupies a situation corresponding to that of the anterior course of the spinal gray matter.
As this column passes onward in the medulla oblongata, on a level with the glosso-pharyngeal nerve, it forms a group of cells of large size. Besides numerous other connections which it forms, Clarke describes the motor root as sending processes forward, like tapering brushes or tails of fibres, in connection with more scattered cells lying in their course, which may be frequently seen to communicate with the transverse bundles which traverse the "gray tubercle" and the sensory roots of the fifth contained therein. In this way the sensory root, though seemingly much separated from, is really in very direct connection with, the motor root.
Now, proofs, which must be considered almost positive, have recently been adduced to show that the nerve-fibres concerned in those peculiar alterations in the tissues supplied by the ophthalmic division of the fifth, which occur in section of the trigeminus, come entirely from the motor root of the fifth, and form a very small band in the inner or medial margin of the ophthalmic trunk. The observation of Meissner[21]goes to show that it is possible (by good luck) to divide the trunk in such a partial manner as to cut only the inner fibres, and thereby produce the trophic eye-changes without any anæsthesia, or only the sensory fibres, and thereby induce anæsthesia without any trophic changes; and it must be owned that this really affords the only reasonable explanation of the discrepancy between the experimental results obtained by Magendie and Bernard; and also the facts of such cases as those related by Mr. Hutchinson,[22]who in two instances found that a completely anæsthetic eye recovered perfectly well from the wound made in a surgical operation. The nature of the nervous influence (whether ordinary vaso-motor only, or a special trophic function) has been greatly disputed. Dr. Wegner,[23]from observing the remarkable group of glaucomatous cases under Horner (of which one has been related), made experiments, from which he concluded that the augmentation of intra-ocular pressure in glaucoma was a phenomenon dependent upon the sympathetic, which was irritated by reflectionfrom the trigeminus. But the researches of Hippel and Grunhagen, especially their latest,[24]give a different explanation, excluding the sympathetic; they found that irritation of the medulla oblongata, in the neighborhood of the trigeminus root, produced a lasting and very pronounced augmentation of intra-ocular blood-pressure, an effect which, they remark, could not depend on irritation of the vaso-motor centre, since that must produce contraction of the vessels and lowering of the blood-pressure. They conclude that "the trigeminus contains specific fibres which possess the property of actively dilating the blood-vessels of the eye;" and in reference to the secretion of the fluid humors of the eye, they conclude also that "the trigeminus also plays the part of an (active) nerve of secretion."
Of these conflicting opinions I can have no difficulty in at any rate rejecting that of Wegner; for the clinical phenomena of the complications attending trigeminal neuralgia, such as they are described in my last chapter (and could have been described at much greater length), seem to me utterly to exclude vaso-motor spasm except as a temporary phenomenon at the commencement of the attacks of acute pain. Vaso-motor palsy undoubtedly is very often present, in fact every attack of neuralgia of a certain severity is thus complicated; and there is no reason to doubt that this paralysis could be caused by lesions within the medulla. Are we, then, to admit functions of active dilatation of vessels, and active impulse to secretion in certain fibres of the fifth? It is necessary at any rate to clear the ground in one respect: it must not be supposed that I for a moment entertain the idea that there can be direct active dilatation,i. e., that there can be any system of muscular fibres (and nerve-fibres stimulating them) whose office is to open the calibre of the vessels; the idea is wildly improbable—in fact almost inconceivable by any one who reflects on the necessary machinery—and there is not a single observed anatomical fact to give it support. If, then, I speak of the possibility of "active" dilatation, it must be understood that I refer to a theory of "inhibition," which supposes certain fibres to be gifted with the power of paralyzing or inhibiting the vaso-motor nerves. It is my duty to speak with all reasonable reserve on that most difficultquæstio vexata, the existence of special inhibiting systems of nerves, and the extent to which a double series of opposed nervous actions is generalized in the body; but it is impossible to avoid the subject altogether, and I offer the following remarks, with deference, to our professional physiologists. The strongest instances of the apparent inhibiting action are probably afforded by thenervi erigentes, as shown by Loven, the cardiac depressor, by Ludwigand Cyon, and the splanchnics (upon the intestine), by Pfluger. But there is not a single one of these examples that has not been challenged by experimenters of repute. Thus the theory of the distinctive restraint-action of the splanchnics upon the intestine, and of the vagus upon the heart, has been especially controverted by Piotrowski, who, indeed, rejects the whole theory of special inhibitory nerves.[25]And, from another point of view, Mr. Lister long ago attacked the views of Pfluger, maintaining that it was possible to produce exactly opposite effects through the medium of the very same nerves, according as the experimental irritation applied to them was weak or strong. To Dr. Handfield Jones[26]this seems a still unanswerable objection to the inhibitory theory. And in the remarkably able and judicial summary of the "Physiology and Pathology of the Sympathetic or Ganglionic System,"[27]by Dr. Robert T. Edes, a less decided but still tolerably strong acquiescence is given to Mr. Lister's criticisms of this theory. Personally, I must express very strongly the distrust (which is probably felt by many others) of doctrines which assert an exact opposition between the functions of any two nerves, on the basis of an observation that the same apparent effects may be produced by section of the one and galvanization of the other; both processes seem far too pathological, and too remote from the conditions of ordinary vitality, to admit of any such absolute deductions from their results.
In the present state of our information I am inclined to explain all the congestive complications of trigeminal neuralgia on the basis of vaso-motor paralysis. And I further believe that the cause of that paralysis is a direct extension of the original morbid process from the sensory root to the motor, affecting the origin of fibres in the latter, which are destined to govern the calibre as ocular and facial vessels. These fibres I suppose it is that Meissner succeeded in dividing when he partially cut the trigeminus, and got nutritive and vascular changes without anæsthesia.
There must be more than this, however, to account for the whole of the trophic phenomena; for there is a great body of evidence to show that mere vaso-motor paralysis does not produce any phenomena of such an actively morbid kind as those we are endeavoring to explain. The phenomena on the side of secretion might indeed be possibly explained by vaso-motor paralysis. [It must be remembered that I am speaking of suchaugmented secretion as is seen in neuralgia. I agree with Prof. Rutherford (Lectures on Experimental Physiology, Lancet, April 29, 1871) that it is difficult thus to explain the effects of galvanization of the chorda tympani on the submaxillary gland.] Consisting as they do (a), in the great majority of cases, of a mere outpour of what seems little more than the aqueous part of the secretion, and (b) in a few cases of arrested secretion, a phenomenon otherwise by no means unfamiliar as the result of sudden, passive engorgement of glands. But the mere cessation of vaso-motion will not account for such facts as the rapid and simultaneous development of erysipelatous inflammation, of corneal clouding and ulceration, of iritis and glaucoma, of nutrition-changes in hair and mucous membrane. I must, for the present, be content to believe it probable that there is a special set of efferent fibres in the trigeminus, emanating from the motor-root, whose office it is in some unknown way to preside over the equilibrium of molecular forces in the tissues to which the nerve is distributed; trophic nerves, in fact, though not active dilators of blood-vessels.
It seems to me that, without enlarging further on this almost endless topic, I should be justified in assuming that I had shown the very high probability that the common starting-point both of the neuralgia and of its vaso-motor secretory, and trophic complications, was in the sensory root of the trigeminus. But the argument is greatly strengthened when we consider the fact that loss of peripheral common, and also tactile sensation, to a greater or less degree, is constantly observed to occur simultaneously with the pain and with the other complications. When we observe a patient suffering from racking supra-orbital and ocular neuralgia, and discover that at the very same period the skin round the eye is markedly insensitive to impressions, except in thepoints douloureux, what can we rationally suppose, except that both pain and insensibility are the result of one and the same influence, which radiates from the sensory centre?
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 alocus minoris resistentiæin 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 ofangina 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 tendencyof 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, isa prioriinfinitely 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-eightwomen 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 fromthe 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. Gull[29](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 posteriorroots 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 actualneuralgic 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 andsufficient 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 veritablehomme instruitas 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 unmeaningphrases 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.]
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;
(1) The first and most essential characteristic of a true neuralgia is, that the pain is invariably either frankly intermittent, or at least fluctuates greatly in severity, without any sufficient and recognizable cause for these changes.
(2) The severity of the pain is altogether out of proportion to the general constitutional disturbance.
(3) True neuralgic pain is limited with more or less distinctness to a branch or branches of particular nerves; in the immense majority of cases it is unilateral, but when bilateral it is nearly always symmetrical as to the main nerve affected, though a larger number of peripheral branches may be more painful on one side than on the other.
(4) The pains are invariably aggravated by fatigue or other depressing physical or psychical agencies.
The above are characteristics which every genuine neuralgia possesses, even in its earliest stages; if they be not present, wemust at once refer the diagnosis to one or other of the affections described in Part II. of this work.
Supposing the above symptoms to be present, we expect to find—
(5) In by far the largest number of instances that the patient has either previously been neuralgic, or liable to other neuroses, or that he comes of a family in which the neurotic disposition is well marked. Failing this, we are strongly to doubt the neuralgic character of the malady, unless we detect that there has been—
(6) A poisoning of the blood by malaria (but this very rarely causes neuralgia, save in the congenitally predisposed); or—
(7) A powerfully operating or very long-continued peripheral irritation centripetally directed upon the sensory nucleus of the painful nerve; which irritation may be (a) "functional," as where the eye has been persistently and severely over-strained and trigeminal pain results, or a sudden severe shock has been received; or, (b) coarsely material, as where inflammation, ulceration, etc., of surrounding tissues involve the periphery of the painful nerves in a perpetually morbid action, or chronic but profoundly depressing psychical influences; or—
(8) A constitutional syphilis. In this case there will either be marked syphilitic local affection of the trunk of a nerve, or if, as is more common, the syphilitic change is in the nerve-centre, there will most likely be other syphilitic centric mischiefs, leading to scattered motor or vaso-motor paralyses, characteristic modifications of special sense-functions, etc.
If the neuralgia be of some standing and a certain degree of severity, there will inevitably be found—
(9) Some of the fixed tender points of Valleix, in such situations as have been described in Chapter I.; and—
(10) Secondary affections (a) of secreting glands, or (b) vaso-motor nerves; or (c) of nutrition of tissues; or secondary localized paralyses of muscles, or localized anæsthesia of a somewhat decided though not complete kind, as described in Chapter II.; any one or any number of these various complications may be present.
I must insist that the above picture includes only the essentials for a diagnosis of neuralgia; if the painful affection will not answer to the conditions therein included, we have no right to call it a neuralgia—it belongs, for every practical purpose, to some other category of disease. Let me add one more essential characteristic, which is, that the pain begins and assumes its characteristic type before any other of the phenomena appear, with the single and partial exception of anæsthesia.
There are some special modes of diagnosis of the varietiesof neuralgia, developed of late years, that require notice here; they are chiefly the result of the researches of Moriz Benedikt.
As regards the quality of the pain, Benedikt says that the curve of intensity has an intimate relation to thelocus in quoof the neuralgia (i. e., whether in the periphery, trunk, or roots). An inflammatory irritation set up at the periphery of a nerve (by a joint-inflammation, for instance) produces a continuous pain; the same kind of irritation, attacking a nerve-trunk (e. g., in the bony canals), produces a paroxysmal pain; an inflammation spreading from the vertebræ to the nerve-roots or the cord-centres produces momentary lancinating pains. The latter characteristic he supposes to be especially characteristic of the centrally-produced neuralgias; and I may observe, as so far confirmatory of this idea, that this is especially the character of the pains in locomotor ataxy. There are sundry special cases to be considered, however: thus, Benedikt himself remarks that the pain set up by the pressure of a pulsating aneurism is, from the nature of things, lancinating from moment to moment. Eulenburg,[32]moreover, says that Benedikt's tests of the locality of the primary mischief only hold good under the following circumstances: (1) When the irritability and the exhaustibility of the nerves are in a normal condition during the neuralgia; (2) when the irritation that calls forth the paroxysm is either identical with the original cause of the disease, or at least operates upon the same spot. The two conditions, however, do not concur. The irritability and exhaustibility may be sometimes excessive in neuralgias, sometimes normal, and perhaps, in certain cases, beneath the normal standard; by which means the form of the curve of intensity must be considerably modified. Moreover, the irritation that provokes an attack may from the periphery attack the primary seat of the disease, even when this is central, on account (says Eulenburg) of exaggerated conductivity of the nerves (his second cause[33]of "hyperæsthesia"), as is, in fact, very frequently the case. He also thinks the distinction between paroxysmal and lancinating pains too indefinite to serve as a sufficiently reliable basis of diagnosis, especially considering the endlessnuancesof the form which the pain is apt to take. I agree with Eulenburg upon this point; and am convinced, from my own observations, that such a distinction as that between lancinating and paroxysmal pains is illusory, [I have taken some pains to investigate the character of the pains, not only in neuralgia, but in locomotor ataxy. It is true that the lancinating character predominates, on the whole, in the latter disease; but there are great differences in different individuals, and even in the same patient at varioustimes, which plainly depend on subjective influences. Compare for instance, Dr. Headlam Greenhow's report on an ataxic patient, with a report on the same man by Dr. Buzzard and myself. ("Trans. Clin. Soc.," vol. i., 1868, pp. 152-162.)] the two kinds being frequently found alternate in the same case. The only useful distinction, in my opinion, is Benedikt's first one: he is probably right in saying that, where such an affection as an inflamed joint forms the source of peripheral irritation that immediately provokes a neuralgia, the pain is apt to be unusually continuous.
The extent to which the pain of neuralgia spreads into different termini of the same nerve has been made the basis of distinctions as to the seat of the original mischief. For example, it has been said that pain in the mental branch of the third division of the trigeminus, which does not invade the auriculo-temporal branch, can hardly depend on an irritation operating on the trunk of the inferior dental; it must be distinctly peripheral, or else it must act upon limited portions of the central origin of the fifth nerve. But the fact seems rather to be that, whether the neuralgia was excited by lesions at the periphery, in the nerve-trunk, or in the centre, it is equally possible that either a small or a large part of the peripheral expanse of the nerve may become the seat of the pain: this almost necessarily follows from the entire independence of individual fibres in nerves.
As regards the evidence afforded by the motor, vaso-motor, and trophic complications, there is this very positive diagnostic value in them—that they enable us to say, with greater assurance than we could otherwise do, that the disease is a real neuralgia. But, the only evidence that they afford as to the situation of the mischief is, that they uniformly point to the central end of a particular nerve; and accordingly I have already shown, in the chapter on Pathology, that the attentive study of these very complications furnishes us with some of the most powerful arguments upon which rests my theory that in neuralgia there is always centric mischief. What share in the production of the malady, in any given case, has been taken by the centric disease, and what if any by a peripheral irritation, the existence of these complications in no way helps us to determine; far less does it enable us to localize a peripheral lesion which may have acted as a concomitant cause; on the contrary, I believe that there is no more fertile source of erroneous judgment on this very point, than some of these complications, especially the vaso-motor and trophic. I suspect that it has happened, in hundreds of instances, that a localized congestion or inflammation, which is a mere secondary phenomenon, produced in the centrifugal manner already so fully explained, has been taken for the veritablefons et origoof the malady: hence the neuralgia has been confidently reckonedas one peripherally produced, and, what is even worse, the whole energy of treatment has been directed to a mere outlying symptom, under the idea that the primary source of mischief was being attacked.
The application of electricity as a test of the nature of a neuralgia has been employed by Benedikt,[34]who lays down certain laws as the result of his researches. He says that (a) in idiopathic peripheral neuralgias the nerves are not sensitive to the current; (b) in neuralgias dependent on neuritis or hyperæmia of the nerve-sheath there is general electric tenderness of the nerve; (c) in cases where the pain has been set up by morbid processes in tissues surrounding the nerve, there is electric tenderness only at the site of these changes. I may, in general terms, express concurrence in these statements; but I must add that, as diagnostic rules they apply only to the early stages of neuralgia; for the occurrence of secondary complications may and does altogether change the condition of electric sensitiveness. It need hardly be said that the above remarks on diagnosis apply for the most part only to the superficial neuralgias, which, however, include an immense majority of the cases of neuralgias. The diagnosis of visceral neuralgias is, it need hardly be said, in most cases, a far more difficult and complicated matter. In these diseases we have often little more to guide us, in the actual symptoms, than (a) the intermittence of the pain, and (b) the absence of commensurate constitutional disturbance, especially the complete freedom from sense of illness in the intervals between the pains. We shall be obliged to rely greatly on such historical facts as the presence or absence of neurotic tendencies in the patient and his family; the possibility of his having been exposed to blood-poisoning (e. g., from malaria or chronic alcoholic excess, or extreme over-smoking); the circumstance that he has been habitually overworked, or greatly exposed to agitating psychical influences; perhaps that he has been subject to a combination of several of these morbific momenta. To say truth, the diagnosis of visceral neuralgias must, at the best of times, be a difficult and anxious matter, and we can hardly ever thoroughly satisfy ourselves until we have procured some decided results from treatment; fortunately, however, it happens tolerably often that we can do this, and sometimes in a very striking way.
Prognosis.—The prognosis of neuralgia varies exceedingly, according to the form and situation of the disease, and many other considerations. There are, of course, in the first place, certain neuralgias in which the prospect is perfectly hopeless as to cure; such are the cases in which the nerve is involved in a continuously growing tumor (especially within a rigidcavity, like the skull), or a slow but persistent ulcerative process.
Supposing, however, that the case is none of these, the very first prognostic consideration is that of age.
Of the neuralgias of youth, the majority either disappear altogether after a first attack, or recur a certain number of times during some years, the neuralgic tendency either disappearing or becoming greatly mitigated when the process of bodily consolidation is over. In another group the neuralgic tendency is never lost, but the form of the attacks changes, and there is far less spontaneity in the manner of their production. It is exceedingly common to see delicate boys and girls between puberty and the age of eighteen or twenty, attacked with typical migraine, which recurs regularly every three or four weeks for perhaps two or three years, then ceases to occur at regular periods, then loses the tendency to stomach complication; and, by the age of twenty-five or somewhat later, has left, as its only relic, a tendency to attacks of ophthalmic neuralgia, which come on when the patient is excessively fatigued, or encounters the close air of a theatre, or undergoes an unusual strain of mental excitement or anxiety, etc.; but which never come on without some such special provocation. So, again, there is a variety of sciatica which belongs mainly to the period between puberty and the twenty-fifth to thirtieth year, and which seems really to belong, pathologically, to the age of unsettled and irregular sexual function, the tendency to it usually disappearing after the patient has settled down happily in married life. Ovarian and mammary neuralgia have very commonly a similar history.
On the other extreme we find the neuralgias of the period of bodily decay: these are of very bad prognosis. A neuralgia which first develops itself after the arteries and capillaries have begun to change decidedly in the direction of atheroma is extremely likely, even if apparently cured for a time, to recur again and again, with ever-increasing severity, and to haunt the patient for the remainder of his days. It therefore becomes exceedingly important, in a prognostic point of view, to assure ourselves as soon as possible whether this arterial degeneration has decidedly commenced; and for this purpose I am in the habit of insisting to pupils on the great importance of sphygmographic examination for all neuralgic patients who have passed the middle age. Where we get the evidence which is furnished by the formation of a distinctly square-headed radial pulse-curve, even though there be no palpable cord-like rigidity of superficial arteries, we are bound to be exceedingly cautious of giving a favorable prognosis.
In women the period of involution of the sexual apparatus forms a crisis which, in regard to neuralgias, is of great prognostic importance. On the one hand, if the general vital statusbe good, and the arterial system fairly unimpaired, we may look to the completion of the process of involution as a probable time of deliverance from neuralgic troubles that have hitherto beset a woman; we know that she will probably suffer a temporary aggravation of her pains, but we hope to see her lose them altogether. On the other hand, if it should happen that she enters on the period of sexual involution with her general nutrition considerably impaired and her arterial system decidedly invaded by atheroma, it is only too likely that neuralgias recurring now, or attacking her for the first time, will assume the worst and least manageable type.
Of almost or quite equal importance with the question of the physiological age of the patient is that of his personal and family history with regard to the tendency to neuralgia and to other severe neuroses. Upon this subject I have dwelt so very fully in other parts of this work, that it is merely necessary here to repeat, that the balance of chances is most heavily swayed to the bad side by all evidence tending to prove congenital neurotic tendencies in the patient and vice versa.
Of prognostic hints that are to be gathered from our knowledge of the immediate causes of the attack, there are none so valuable as those which we gather from the detection of a malarial or a syphilitic factor in the production of the malady. In the former case, we hope to cure the patient either with quinine or arsenic, with almost magical certainty and rapidity; in the latter, we expect an almost equally brilliant result from iodide of potassium.
The particular nerve in which the neuralgia is seated does not so decidedly influence the prognosis, according to my experience, as is stated by some authors; nevertheless, there are differences of this kind. For instance, sciatica, though by no means so frequently a mild and trifling complaint as Eulenburg would make it to be, is certainly, on the whole, more curable than the trigeminal neuralgias taken as a group. I, however, cannot share Eulenburg's opinion as to the rarity of a central cause for sciatica, nor his consequent explanation of its more frequent curability; the latter I explain by the fact that it is possible far more completely to remove the concomitant causes in sciatica than in trigeminal neuralgia. By simply keeping a sciatic patient in the prone posture, shielded from cold and from pressure on the nerve, we have it in our power to remove nearly all peripheral sources of irritation; but in trigeminal neuralgia there are many influences, particularly psychical ones, which cannot be shut out, and which will continue to act with disastrous effect in many cases. With all this, however, we see a sufficiently large number of incurable sciaticas, on the one hand, and of severe trigeminal neuralgia cured on the other. It is only the genuine epileptiform tic, occurring in subjects whose arterial system is an advancedstage of degeneration, that stands out clearly and unmistakably pre-eminent among neuralgias for rebelliousness to treatment of every kind.
I now approach what is really the most difficult portion of my task; for, although it would be easy enough to write copiously on the treatment of neuralgia, it is extremely difficult to keep a just medium between the opposite extremes of undue meagreness and of useless profusion of detail in the handling of this subject. There are also difficulties connected with the present uncertain and transitional state of opinion, even among high authorities, as to the value of particular remedies, and even of large groups of remedial agents, altogether there has been more hesitation in my mind as to this part of the present work than about any other, and the present chapter has been rewritten more than once. I mention this only to account for what there may very likely be found in it—an imperfect literary style such as too commonly marks work which has been repeatedly patched and corrected. At the same time, it should be said that my hesitation does not apply to the main principles of treatment which will be recommended below; it proceeds rather from the fear of seeming to ignore from carelessness modes of treatment which are still much used, but which I have really rejected, because, after full trial, they appeared to me valueless. Space is, after all, limited, and a complete account of all the remedies for neuralgia in vogue, in English and Continental clinics, would of itself fill a large volume.
The treatment of neuralgia may be divided into four branches: (1) Constitutional remedies; (2) narcotic-stimulant remedies; (3) local applications; (4) prophylaxis.
1. Constitutional treatment must be subdivided, as (a) dietetic, (b) anti-toxic, and (c) medicinal tonic.
(a) The importance of a greatly-improved diet for neuralgic patients is a matter which is more fully appreciated by the English school of medicine than by either the French or the German; it has, for instance, very much surprised me to notice the almost entire silence of Eulenburg on this topic. For my part, the opinions expressed three years ago[35]on this matter have only been modified in the direction of increasingcertainty; I have learned by further experience that the principle is even more extensively applicable than I had supposed.
That neuralgic patients require and are greatly benefited by a nutrition considerably richer than that which is needed by healthy persons, is a fact which corresponds with what may be observed respecting the chronic neuroses in general; and it gives me much satisfaction to point out this position of neuralgia as belonging to this large class of disorders, not merely by its pathological affinities, but by its nutritive demands. In a very excellent and suggestive paper by Dr. Blandford[36]it is stated, as the result of a large experience in mental and other nervous disorders, that the greater number of chronic insane and hypochondriacal cases, as well as neuralgic patients, are remarkably benefited by what might seem at first sight almost a dangerously copious diet. Occasionally it happens that the patients discover this by the teaching of their own sensations, and the apparent excesses in eating which some epileptic and hypochondriacal persons habitually commit are looked on by many practitioners as the mere indications of a morbidbulimiawhich represents no real want, but only the craving of a perverted sensation which ought to be interfered with and allayed rather than encouraged. It is now many years since I began to doubt the justice of this opinion; the particular instance which called my attention to it being that of epilepsy, of which disease I saw a considerable number of cases, within a short period of time, that were distinguished by the presence of enormous appetite for food; and I finally came to the conclusion that, so far from this symptom being of evil augury, and likely to lead to mischief, it is, with certain limitations, a most fortunate occurrence. It is hardly necessary to say that over-eating, such as produces dyspepsia and distention of a torpid intestine with masses of fæces, may distinctly aggravate the convulsive tendency; but the truth is that, with a little careful direction and management of the unusual appetite, these bulimic patients can in most cases be allowed to satisfy their desires without harm of this kind following; a larger portion of food really gets applied to the nutritive needs of the body, and the nervous system unmistakably benefits thereby, the tendency to atactic disorder being visibly held in check.
That which I have thus observed in the case of epilepsy, and which Dr. Blandford more particularly affirms concerning chronic mental diseases and the large number of neuroses that hover on the verge of insanity, has been most distinctly verified in my experience of the treatment of neuralgia. It is, unfortunately, by no means a frequent occurrence that the sufferer from this malady is inclined to eat largely, but the few patients of this type that I have seen were, in my judgment,distinctly the better for it. Far more common in neuralgia is a disposition of the patient to care little for food, to become nice and dainty, and in particular to develop an aversion—partly sensational and partly the result of morbid fear about indigestion—for special articles of diet. Dr. Radcliffe pointed out the special tendency of neuralgics to neglect all kinds of fat; partly from dislike, and partly because they believe it makes them "bilious;" and I have had many occasions to observe the correctness of this observation. In fact, by the time patients have become sufficiently ill with neuralgia to apply to a consulting physician, they have already, in the great majority of cases, got to reject all fatty foods, and have cut down their total nutriment to a very sufficient standard. Young ladies suffering from migraine are especially apt to mismanage themselves, to a lamentable extent, in this direction: this is natural enough, because the stomach disorder seems to them the origin of the pain, instead of being, as it is, a mere secondary consequence of the neurosis. But it is not only the sufferers from sick-headache in whom we find this tendency to insufficient eating, especially of fat; not to mention that all severe pain usually tends to disorder appetite and make it fastidious, there is nearly always some wiseacre of a friend at hand, ready to suggest that neuralgia is something very like gout, that gout is always aggravated by good living, and,ergo, that the patient should be "extremely cautious as to diet;" the end of which is that the poor wretch becomes a half-starved valetudinarian, but, so far from his pain getting better, it steadily becomes worse. I cannot too strongly express the benefits that I have seen accrue, in the most various kinds of neuralgic cases, from persistent efforts to remedy this state of things, and to convert the patient from a valetudinarian to a hearty eater; and I wish particularly to say that this success has always been most marked when I have from the first insisted on fat forming a considerable element of the food. Cod-liver oil is the form in which I much prefer to give it, if this be possible; there can be no mistake about the relatively greater power of this than of any other fatty matter, I believe simply from its great assimilability. But the very cases in which we most urgently desire to give fat are often those in which the patient's fantastic stomach openly revolts at the idea of the oil; we must then try other fats; and we should go on trying one thing after another—butter, plain cream, Devonshire cream, even olive or cocoanut oil (though these are the poorest things of the sort we can use)—till we get the patient well into the way of taking a considerable, if possible a decidedly large, daily allowance of fat, without provoking dyspepsia. It is surprising what can be done in this way by perseverance and tact, and it is no less striking to observe the good effects of the treatment. Nothing is more singular than to seea girl, who was a peevish, fanciful, and really very suffering migraineuse, brought to a state in which she will eat spoonful after spoonful of Devonshire cream, and at the same time lose her headaches, lose her sickness, and develop the appetite of a day-laborer; and, though such very marked instances as this are uncommon, they do sometimes occur, and a minor but still important degree of improvement is very frequent.
As for themodus operandiof the fatty food, there is no certainty. Dr. Radcliffe believe it acts as a direct nutrient of the nervous centres; and I also cannot help feeling that there is some evidence in favor of this idea. But, whether this be so or not, there is another kind of action of fat that is more simple and obvious; namely, it seems to be certain that the enrichment of the diet by fat greatly assists the assimilation of food in general, and thus the patient's nutrition is altogether improved.
It is not merely, however, by increasing any one element of food that we should seek to enrich the diet of neuralgics, but rather by such a steady and persistent effort as Dr. Blandford describes, to increase the total quantity of nutriment to perhaps as much as one-third more than the patient would probably have taken in health. To those who from prejudice are incredulous of the propriety of this method, I would say, "Try it, and I venture to say your incredulity will disappear." More especially I would urge the great importance of this system in modifying the nervous status of very young, and also of aged, sufferers from neuralgia; it is the indispensable basis of a sound treatment for such patients.
This seems the proper place for such remarks as must be made upon the function of alcohol in neuralgia; for, though this agent is a true narcotic when given in large doses, it is not under that aspect that I can recommend its use in neuralgia at all. I have written so much on this subject lately, that I shall here content myself with an emphatic repetition of my protest against the use of alcoholic liquors as direct remedies for pain. They ought only to be given, in neuralgia, in such moderate doses, with the meals, as may assist primary digestion without inducing any torpor, or flushing of the face, or artificial exhilaration. I cannot too expressly reprobate the practice of encouraging neuralgics, especially women, to relieve pain and depression by the direct agency of wine or spirit; it is a system fraught with dangers of the gravest kind.
(b) The anti-toxic remedies include agents addressed to the modification of a special condition of the blood and tissues induced by the presence of morbid poisons, of which syphilis, malaria, and (more doubtfully) gout and rheumatism, are the representative examples.
Of syphilitic neuralgia the treatment may be summed up in a few words: Give iodide of potassium in doses rapidlyincreased up to a daily quantum of twenty to thirty grains. If this fails, give one-twelfth of a grain of bichloride of mercury thrice daily.
Of malarial neuralgia I can only speak from such a limited experience that I am by no means in a position to give an exhaustive account of the treatment. Quinine is, of course, the remedy that should first be tried; and, as the paroxysms are usually regular in their recurrence, I prefer to give the drug after the plan which is, I think, incontestably the best in ordinary ague—i. e., to administer one large dose (five to twenty grains) about an hour before the time when the attack is expected. With a few exceptions the malady, unless it had taken very deep root before we were consulted, will yield to a few doses given in this way; after the morbid sequence has been thus interrupted, it will be proper to continue the action of quinine in smaller and more frequent doses, given for three or four weeks continuously. For the comparatively rare cases in which quinine fails, the prolonged use of arsenic (Fowler's solution, five to eight minims three times a day), especially with the simultaneous employment of cod-liver oil, is to be recommended.