Neuralgia And The Diseases That Resemble It Part 8

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 a.n.a.logous 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 ill.u.s.trate 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 Ga.s.serian 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 ill.u.s.tration 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. a.s.suredly, 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 pa.s.sing through ca.n.a.ls, 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 periost.i.tis, or from concentric hypertrophy in narrowed bony ca.n.a.ls, 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 ca.n.a.ls; 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 p.r.o.nounced 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 ent.i.tled 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 "hyperaesthesia" 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 pa.s.sed 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 hyperaemia 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 anaesthesia 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 a.n.a.logy, 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 a.n.a.logous to those which occur in ataxy, that quant.i.ties 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 a.n.a.lysis[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).

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 a.s.suming 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 anaesthesia 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 anaesthesia persists. Presumption, that the nutrition of the nerve-centre has nearly recovered itself, but that that centre is still the _locus minimae resistentiae_ 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 ent.i.tled by him "Anaesthesia 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 s.p.a.ce. Suffice it to say here, that, in the first place, the anaesthesia 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 Ga.s.serian 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 pa.s.ses 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 anaesthesia, or only the sensory fibres, and thereby induce anaesthesia 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 anaesthetic 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 p.r.o.nounced 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 _quaestio 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 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 a.s.sert 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 anaesthesia.

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, pa.s.sive 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 a.s.suming 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 anaesthesia, 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 pa.s.sed without any special consequences (as happens in thousands of such nerve-wounds), had it not, in its pa.s.sage along the medulla, encountered a _locus minoris resistentiae_ 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 pa.s.s 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 a.n.a.logies 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 ca.n.a.l) of the inferior cervical ganglion, on the one hand with the lower cervical nerves, which go to the brachial plexus, and, on the other hand, with the heart itself. There remains to be explained, however, the singular tendency of the arm-pain to be one-sided (this happens in at least four cases out of five); and this explanation seems to me insuperably difficult, on the theory that the transference of morbid action to the brachial nerves takes place through external anastomoses. It appears greatly more probable that angina is essentially a mainly unilateral morbid condition of the lower cervical and upper dorsal portion of the cord; liable of course to be seriously aggravated by such peripheral sources of irritation as would be furnished by diseases of the heart, and especially by diseases of the coronary arteries; the latter affection probably involving constant mechanical irritation of the cardiac and the aortic plexuses. It is noteworthy that the arm-pain is sometimes (I do not know how often) accompanied by vaso-motor paralysis in the limb; this phenomenon could also certainly be more easily accounted for on the supposition of radiation from a spinal vaso-motor centre (to which the morbid process had extended from a posterior nerve-root) than on that of communication between painful sensory nerves and vaso-motor nerves; through either of the plexuses independently of the spinal centres.

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

From the varied considerations which have now been adduced, the reader, unless I altogether miscalculate the value of the facts, will probably have arrived at the following conclusions: (1) That the a.s.sumption of a positive material centric change as the essential morbid event in neuralgia is almost forced upon us; (2) that, whereas the morbid process, if centric, is _a priori_ infinitely more likely to be seated in the posterior root of the painful nerve, or the gray matter immediately connected with it, than anywhere else; so, again, the a.s.sumption 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 s.e.x and the ages most favorable to neuralgia. Eulenburg saw a hundred and six cases of neuralgia of all kinds, of which seventy-six were in women and only thirty in men; my own experience is very similar; namely, sixty-eight women and thirty-two men out of a hundred hospital and private patients. The strong connection between the hysteric and the neuralgic temperament in women, and the great preponderance of women among neuralgics, strengthen in no small degree the probability of inherent tendencies to unstable equilibrium as a very common predisposing factor in neuralgia. And, on the subject of age, I need only recall what I have said so strongly about the coincidence of neuralgia with particular epochs in life, as affording evidence of the most powerful kind that neuralgics are, save in exceptional instances, persons with congenitally weak spots in the nervous centres, which break down into degeneration, temporary or permanent, under the strains imposed by one or other of the physiological crises of the organism, or the special physical or psychical circ.u.mstances which surround the patient's life.

Having thus decidedly expressed my belief in the essential material partic.i.p.ation 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 interst.i.tial 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 a.n.a.lysis of cases in which a more or less chronic, but severe, visceral disorder has been followed by so-called reflex paralysis, but in which neuralgic phenomena, have been conspicuous. In reference to this subject I recommend to the reader's attention the very interesting paper on "Reflex Paralyses" by Prof. Leyden, of Konigsberg.[28] He is immediately commenting upon a case in which dysenteric affection of the bowel were followed by the symptoms of myelitis, attended with febrile exacerbations, and also with severe pains in the region of the sacrum, in the course of the dorsal intercostal nerves of the right side, and in the knees, and semi-paralytic weakness of the lower extremities, and with pains between the shoulder-blades and the left arm. Leyden discusses the doctrine of reflex paralyses in general, starting from the cases of urinary paraplegia brought forward by Stanley, in 1835, and tracing the growth of opinion through the phases represented by Graves, Henoch, and Romberg, by Valentine and Ha.s.se, 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 r.e.c.t.u.m. 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 a.n.a.logy 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 ca.n.a.l at the point where the posterior roots of the sciatic enter the cord; but there was no neuritis of the intervening portion of the nerve.

Upon this and similar evidence is based the modern doctrine of a neuritis migrans, with centripetal tendencies, upon which it is supposed that a very large proportion, at least, of the urinary, dysenteric, and uterine paraplegias, miscalled "reflex," depend; and it is clear that the application of the word "reflex" in such a case is a grave abuse, tending to produce such confusion of thought and error in practice. In relation to the subject of our own inquiry--neuralgia--it is obviously of the highest consequence to investigate the question whether peripheral irritations, a.n.a.logous 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 a.s.sumed. Again, the totally feverless commencement of neuralgias, a character which is maintained throughout the progress of the milder cases, is entirely opposed to the idea of a direct connection between myelitis and neuralgia. The superficial appearance of pyrexia is sometimes given by a local vaso-motor paralysis, which makes the neuralgic part, after a long bout of pain, hot and red; but of general pyrexia there is nothing.

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

I would also go farther, and express the opinion that peripheral influences of an extremely powerful and continuous kind, where they occur with one of those critical periods of life at which the central nervous system is relatively weak and unstable, can occasionally set going a non-inflammatory centric atrophy which may localize itself in those nerves upon whose centres the morbific peripheral influence is perpetually pouring in. Even such influences as the psychical and emotional, be it remembered, must be considered peripheral--that is, they are external to the seat and centre of the neuralgia. And there are probably few pract.i.tioners 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 p.u.b.erty 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 const.i.tution 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 const.i.tution. 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 s.e.xual irritation, which is, unfortunately, a too common phenomenon under certain systems of education. The most frequent neurotic consequences of the cla.s.s 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 ill.u.s.trated in my own case about three years ago. I was then engaged upon a piece of scientific writing which demanded no great intellectual effort, but was being done against time, and by working, night after night, many hours by gas-light. My neuralgic (trigeminal) attacks came on with great severity, accompanied by vertiginous sensations of so alarming a kind as to make me fear the invasion of some serious brain-mischief. I broke off all work, and went to the sea-side, but was greatly disappointed to find, for the first few days, that the symptoms were not in the least mitigated. The mystery was soon explained. The weather had been such as to confine me a good deal to the house, and, thinking it would do no harm, I amused myself with reading newspapers and novels. At last I suspected that the use of my eyes in reading was altogether mischievous; I desisted from reading any thing, and in forty-eight hours every symptom had vanished.

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

A sufficiently complete explanation of my theory as to the pathology and etiology of neuralgia has now been given, although the subject might be elaborated at far greater length; and I hope it will be apparent to the reader that the view now advocated is at once important, and also vouched for by strong evidence. I claim for it that the whole argument shall be taken together, for it is a case of c.u.mulative 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 cla.s.s 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 pract.i.tioner 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 outs.h.i.+ne pract.i.tioners who often have far more in them of the veritable _homme instruit_ as regards general scientific education and habits of mind. It will be evident, as a mere abstract proposition, that the enunciation of a reasonable pathology of the disease, and the sweeping away of a ma.s.s of unmeaning phrases about "mysterious functional affections" and the like, must be a distinct gain to pract.i.tioners 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 enc.u.mber the text of the present chapter.]

FOOTNOTES:

[16] Eulenburg, to whose excellent work ("Lehrbuch der functionellen Nervenkrankheiten," Berlin, 1871) I shall have frequent occasion to refer, has partly misunderstood the drift and scope of my argument, a misfortune which I owe to the impossibility of giving, in the "System of Medicine," more than the briefest and most superficial sketch, both of my ideas and of the facts on which they rest.

[17] _Op. cit._, p. 60.

[18] This opinion is somewhat stronger than that expressed in my article in the "System of Medicine." I can only say it is the result of much increased experience.