The general result of such post-mortem and clinical information as can be had seems clearly to be that positive anatomical changes, either of nerve-terminals or superficial nerve-branches, are but casual and infrequent factors in the first production of neuralgia, and, in particular, it would seem that inflammation of a nerve itself by no means necessarily produces neuralgic pain, but (far more commonly) simple paralgesia or anæsthesia of the parts external (peripheral) to the lesion. The one marked exception to this general proposition is to be found in the case of the severe and peculiar injuries inflicted on the trunks of nerves by gunshot-wounds which, as we have seen (from the American experiences), can produce some of the most dreadful forms of neuralgia. But the nature of the injury here inflicted is, it must be remembered, quite different from any thing which either disease or accident in civil life would produce, save in the most exceptional instances. For the chief material element in the production of the neuralgias of ordinary life we are really driven, by exclusion, to the condition of the posterior roots of special nerves, in some cases, perhaps, to the (spinal) ganglia on which the nutrition of these roots probably is considerably dependent.
With the field thus narrowed for us, it is surely legitimate, in the necessary scarcity of anatomical records referring directly to the state of the nerve-roots in ordinary neuralgia, to place great weight on the facts of a disease like locomotor ataxy, in which the main anatomical change is a progressive atrophy of the posterior columns which usually falls with peculiar severity on the posterior nerve-roots, or on the parts of the gray matter immediately adjoining these, and in which neuralgia may be said, for practical purposes, to be a constant and most characteristic phenomenon. If any one desires to see how strikingly the connection of the neuralgic phenomena with the anatomical-change comes out, I recommend him to study Dr. Lockhart Clarke's papers on locomotor ataxy (vide "St. George's Hospital Reports, i." 1866; Lancet, June, 10 1865; "Med. – Chir. Soc. Transactions," 1869), or the excellently reported case by Nothnagel (Berlin Klin. Wochensch., 1865). It is really not too much to say that the only important difference between the clinical aspect of the pains of locomotor ataxy and those of ordinary neuralgia is simply such as depends on the fact that the anatomical change in the former case is bilateral, and usually affects the roots of several, sometimes of a great many pairs of nerves. I infer, from a conversation with Dr. Clarke, that he fully recognizes the force of the analogy, and the great strength of the presumption which it sets up in favor of an atrophic change of the posterior roots in neuralgia.
It may, of course, be urged, against the view that neuralgia depends on any change analogous to those which occur in ataxy, that quantities of cases of the former recover speedily, and must be supposed to be either independent of material change altogether or, at any rate, to have involved only very trivial anatomical changes, not formidable diseases, like atrophy of nerve-centres. I find it impossible to admit that this argument has the slightest force. Are we to suppose that the posterior nerve-roots alone, of all tissues and organs of the body, are incapable of minute and partial changes in the direction of molecular death which may be perfectly recovered from in weeks, months, or even days? I, for one, cannot doubt, that such changes are of frequent occurrence, in all parts of the central nervous system, when I can consider the absolute dependence of these portions of the organism upon a perfect blood-supply, and the immense number of possible causes of temporary interference with that source of nutrition. And I can see no probable difference, except in degree and persistence between the effects on sensation which would be produced by such a change of the posterior roots as this, and that which would result from the more serious and fatally continuous change which is involved in locomotor ataxy.
9. We come now to a most important but most complex and difficult portion of the argument respecting the locus in quo of the essential pathological process (if such there be) in neuralgia; viz., as to the paths and the character of the so-called "reflex" influences which intervene in the causation, both of neuralgia itself, and also of the numerous complications with which we have seen that neuralgia is liable to be attended. The clinical facts which confront us here, and demand explanation, are the following: (1) Irritation so called, of sensory fibres may apparently evoke pains attributed to the site of the irritation, or to the parts on the peripheral side which are supplied by the same sensory nerves. (2) Peripheral irritation of a particular sensory nerve may evoke neuralgic pains in nerves connected with that irritated only through the spinal centre. (3) Neuralgia in a sensory nerve may (and almost always does, to some extent) produce secondary vaso-motor paralyses: these paralyses may affect fibres which run in the same branch of the nerve as that which is painful, or fibres that run in another branch of the same nerve, or fibres that run with another sensory nerve, or the ganglionic chain of the sympathetic itself. (4) In like secondary manner, neuralgia may produce vaso-motor spasms in any of the directions just specified; this is usually a short-lived phenomenon, giving place quickly to paralysis; but Du Bois Reymond's often-quoted analysis19 of his own sufferings from migraine seems to show that spasm-producing irritation of the trunk of the sympathetic may last during some hours. (5) Neuralgia in a sensory nerve may increase, alter, or (more rarely) suspend the secretions of glands supplied by fibres bound up either in the same branch, or in another branch of the same nerve, or in a different nerve with which it is connected only through the centre or (possibly) only through a plexus. (6) Neuralgia in a sensory nerve can produce paralysis of muscles supplied by motor fibres bound up with the painful branch, or with another branch of the same nerve, or in muscles supplied by a totally distinct nerve connected only through the centre. (7) It may produce convulsion and spasms of muscles, in all the above directions; this usually alternates with great weakness, or actual paralysis of the same muscles. (8) It may produce partial or complete loss of common or special sensation in nerve-fibres that run either with the same branch, or with another branch of the same nerve. (9) It may produce trophic changes, either in the direction of simple atrophy or of subacute inflammation with proliferation of lowly-vitalized tissue (e. g., connective) in the parts with which are supplied with sensation by the painful branches or by other branches of the same nerve.
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 the locus in quo of 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 inaccuracy of 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 the locus minimæ resistentiæ of 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 inferior border 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 Meissner21 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 reflection from 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 difficult quæstio 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 the nervi erigentes, as shown by Loven, the cardiac depressor, by Ludwig and 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 Jones26 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 such augmented 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 the points 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 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.