The reader does not need to be told the familiar story of the degenerative changes in the vessels which, commencing usually some time during the fifth decenniad, by degrees convert the elastic arterial coats, and the almost membranous walls of the capillaries, into more or less rigid tubes; nor does he need to be informed that the tendency of these changes, as they operate in the great motor and intellectual centres, is notoriously to produce innutrition of the tissues that depend for their blood supply on the affected vessels, whence cerebral softening so commonly results. That analogous changes take place in the vessels supplying the spinal centres is certain; but it is a remarkable fact that these do not very commonly produce motor paralysis. What they do produce is rather a slow enfeeblement both of (spinal) sensation and motion, but where the process of decay has been prematurely forced, or the inheritance of neurotic weakness is very marked, the process of sensorial decay (the decline, that is, of true sensorial function) is apt to be mingled with pain. That this pain should be localized, often in a single nerve, is no more surprising than the fact that the degenerative process itself should vary so greatly in the degree of its development at one point from that which it shows at others. I have already insisted (vide Chapter I.) on the marked correspondence between the period of life in which degenerative changes commence and progress (the last third, roughly speaking, of a fairly long life), and that in which the most severe, intractable, and progressively increasing neuralgias are developed. I must here notice a singular statement of Eulenburg's, that neuralgia never attacks people who are over seventy. That statement shows that persons of a greater age than seventy are rare in this world, and that no such patient happened to come under Eulenburg's notice; for I have (by mere chance, doubtless) seen several instances of first attacks occurring after seventy; and almost the worst case of epileptiform tic I ever saw began when the patient was eighty; she was a member of a highly neurotic family whose medical genealogy is given at a previous page. In general terms, it may be said that every additional year of life after fifty increases the probability that a neuralgia, should such arise, will be severe and rebellious to treatment; and in the very aged the cure of such affections is probably impossible.
8. This seems the proper place to introduce such facts as have been observed, and they are very few, that directly illustrate the material changes occurring in neuralgia.
Very much the most important of these facts is the history of a remarkable case recorded by Romberg. ["Diseases of Nervous System," Syd. Soc. Trans., vol. i.] The patient, a man sixty-five years old at the time of his death, had suffered for several years from the most violent and intractable epileptiform trigeminal neuralgia, complicated with interesting trophic changes of the tissues. Post-mortem examination showed that the pressure of an internal carotid aneurism had almost destroyed the Gasserian ganglion of the painful nerve, that the trunk and posterior root of the nerve were in a state of advanced atrophic softening, and the atrophic process had extended in less degree to the nerve of the opposite side. Now, the value of this case is by no means restricted to the fact that it records the existence of a particular anatomical change in one example of neuralgia. Its most striking teaching is the fact that the acutest agonies of neuralgia can be felt in a nerve, the central end of which is reduced to such a pitch of degeneration that conduction between centre and periphery must very shortly have entirely ceased had the patient lived. And hardly less important is its illustration of the fact that permanent injury to the ganglion of the posterior root of a spinal nerve impairs the vitality of the posterior root itself—a fact which has been independently made out by the physiological researches of Bernard and of Augustus Waller.
On the other hand, if we examine the tolerably numerous histories of cases in which the painful nerves have been examined at the apparent site of pain, we discover nothing to lead us to connect neuralgia definitely with any one sort of change. Assuredly, for example, local neuritis is by no means universally, it is probably even not commonly, present in the early stages of neuralgia; it has also been repeatedly detected in nerves that had been wholly free from neuralgia; and, on the other hand, it has been entirely absent in nerves that have been the seat of the severest pains. Moreover, many facts which have been put down without reflection, as showing a local peripheral cause for neuralgia, are at least open to another and, as I believe, truer explanation; as (e. g.) in the following remarks of Eulenburg on mechanical irritations of nerves as causes of neuralgia: "Diseases of bones are extraordinarily frequently the cause of neuralgias in consequence of compression or secondary disease, which affects the branches of nerves passing through canals, foramina, fissures, or over processes of bone. The appearances which the opportunities of resections of the trigeminus for facial neuralgia have permitted to be discovered, have given us valuable information in that direction. Flattening and atrophy of nerves from periostitis, or from concentric hypertrophy in narrowed bony canals, have frequently been discovered. The neurilemma at the narrowed parts was often seen reddened, ecchymosed, infiltrated with serum, or surrounded with fibrous exudation; occasionally inflammation had been followed by partial thickening of the neurilemma (fibrous knots) and turbidity (Trubungen) of the nervous cord at the corresponding spot. Similar appearances have been noted in other neuralgias (neuralgia-brachialis, sciatica)." For my own part, I believe that the above description represents the facts from an erroneous point of view. True neuralgia, if by that we understand a pain of intermittent character limited to one or more nerves, is in my experience an extremely uncommon result of periosteal disease, or of inflammation of the linings of bony canals; but in a great number of instances such diseases appear to be set up as the secondary consequence of the neuralgic process (whatever the essential nature of that may be) going on in sensory nerves which supply the parts when these inflammations appear. And it must be remembered that the specimens obtained by resection of nerves are comparatively few in number, and are taken universally from old-standing and desperate cases of disease; in short, from cases which are just in those advanced stages of neuralgia in which, as has already been amply shown, these secondary inflammations are almost always present. On the other hand, I have myself had one opportunity of examining the local condition of an intercostal nerve, which during life, and quite up to death, had been the site of the most pronounced neuralgia, which, however, had only existed for a few days. The patient, a young man, aged twenty-seven, was probably insane, and had attempted suicide. Not a trace of inflammation, either in the nerve itself or in any of the tissues to which it was distributed, could be detected. (This was a case in which I greatly regretted the impossibility of getting a family history that was at all reliable.) The spinal cord, unfortunately, could not be examined. And I strongly believe, from the marked absence of tenderness on pressure which is almost universally observed in ordinary cases of neuralgia at an early stage, that primary inflammation of neurilemma, periostem, etc., as a cause of neuralgia, is altogether exceptional; so much so, that we are entitled to believe it can never be more than a concurrent, and then not the most important, cause.
It is necessary here to inquire, more particularly than we have yet done, into the nature of the "painful points" first signalized by Valleix as a distinctive symptom of neuralgia. Very great differences of opinion have prevailed among subsequent writers, both as to the frequency and the significance of these points. It may be said, however, to be now quite settled that the presence of definite points, painful on pressure, and also corresponding to the foci of severest spontaneous pain, is far from universal in neuralgia. Upon this point there is probably no reason to doubt the correctness of Eulenburg's observations made in the surgical clinic of Greifswald and the polyclinic of the University of Berlin; he says that he discovered the existence of tender points in "Valleix's sense," in rather more than half the cases of superficial neuralgia, but in the rest he could not by any means discover them. In many other cases, however, he found more indefinite points of tenderness, not accurately corresponding to nerve-branches, but affecting individual portions of skin, bone, or joints; the relation of these to the neuralgic symptoms was difficult of explanation. Eulenburg lays down the principle that "hyperæsthesia" may depend on three sorts of causes—(1) On local disease of the peripheral ends of nerves; (2) on alterations of the psychical centres; and (3) on morbidly exaggerated conduction in the nerve-trunks themselves; and it is to this third source that he attributes many of the phenomena of the neuralgic painful points, and especially their multiplicity, in many cases. The locus in quo of the mischief which sets up this exaggerated conduction of sensory impression is, upon this theory, between the psychical centre and the main point of branching of the nerves; hence a large number of peripheral nerve-termini might be practically sensitive to touch, because the mischief, though localized in a comparatively small spot, might easily affect many bundles of fibres, which diverge widely from each other in their course. It will be seen presently with what limits and for what reasons we believe this to be a true theory. But to return to the question of painful points in Valleix's sense, we must state one or two facts which seem certain from our own experience, but have not been adequately recognized, we believe, by others. The first is, that localized tender spots, accurate pressure on which will set up or aggravate the neuralgic pain, are not early phenomena, save in neuralgias of exceptional severity of onset; but that a certain persistence and severity of neuralgia are always followed by the formation of one or more true points douloureux. The second fact relates to the clinical history of migraine. Roughly speaking, it is true, as Eulenburg states, that, in pure migraine, painful points in Valleix's sense are not to be found; in place of them we observe, after the paroxysms have passed away, a more generalized soreness of considerable tracts of the scalp, forehead, etc., or diffuse tenderness of the eyeball. But I must here again refer to the fact, first observed in my own case, and afterward verified in many others, that migraine may be only the youthful prelude to a regular trigeminal neuralgia attended with the formation of characteristic localized painful points at a later period. And the third fact that must be specially mentioned is that the true Valleix's point, when it has become established for some time, is not a mere spot of sensitive nerve, but is the scene of trophic changes, involving hyperæmia and thickening of parts surrounding the nerve. To give one example, it is quite a frequent thing to find a patch of tender and sensibly thickened periosteum of irregular shape, but equal sometimes to a square inch in size, over the frontal bone at and immediately above the inner end of the eyebrow, in cases where supra-orbital neuralgia has recurred frequently during some years, although no such thing was present when the neuralgia first commenced. In my own case, the bone has become sensibly thickened at that point.
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 analysis[19] 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).