Chapter III: Pathology and Etiology of Neuralgia (2)

It has surprised me, somewhat, that while M. Mauriac has seen so many reflex neuralgias set up by orchi-epididymitis, he does not appear to have noticed cases of trigeminal neuralgia from this source; because, in the very analogous instance of the peripheral irritation produced by excessive masturbation, we undoubtedly do frequently get a development of the tendency to migraine, and also to other forms of neuralgia of the fifth: moreover the effect of such local irritation can be occasionally traced with much distinctness in the trigemini, by a tendency to certain forms of eye-disease without positive neuralgia. This was remarkably exemplified in a case which was under my care some years ago, and in which both eyes were greatly damaged by vaso-motor and trophic changes; partial insanity also supervened with hallucinations of sight and hearing.

We come now to one of the most powerful sources of peripheral irritation tending to set up neuralgia; viz., functional abuse of the eye. This is one of the very few peripheral influences which occasionally we see producing neuralgia unaided by hereditary predisposition, or any other observable cause whatever, and in a far larger number producing it with the sole aid of more or less defective general nutrition. The latter occurrence is well exemplified by a case which Mr. Carter sent me the other day, and which also illustrates (second attack) the effect of the superaddition of syphilitic taint:

Matilda W----, aged thirty-three, married, and has three very healthy children. Comes of a remarkably healthy family, of which she told me the entire history for three generations, with unusual intelligence and clearness. No neuroses, properly so-called, in any of her relatives during all this time. She herself was a very strong and hearty girl until the age of seventeen; between this date and her marriage, three years later, she was obliged to work tremendously hard at fine sewing, by which means she gained a very scanty livelihood. After a comparatively short period of this work she began to suffer from typical attacks of migraine, very severe, and recurring every three or four weeks, but in no particular connection with the menstrual function, which was normal. On her marrying and ceasing to do needle-work, the migraine entirely disappeared, and she retained perfect health till the commencement of 1871. At this time she had suckled a very hearty baby for ten months, and was not able to furnish such good living as usual. She was attacked early in January, with violent neuralgia affecting all three branches of the right fifth, and she the more readily applied for advice because she soon found that the neuralgia was becoming complicated with dimness of vision in the eye of the affected side, "as if she was going to have a cast." Was quite unconscious of ever having had syphilis. The medical man encouraged to believe that the whole malady was nervous, and would soon disappear under appropriate remedies, and gave her quinine, under which treatment she declares that she was rapidly improving, both as to pain and vision, but that her resources came to an end, and she could no longer pay for the medicine. She then neglected herself, and rapidly got worse in all regards, till at last she was compelled to apply to the South London Ophthalmic Hospital, whence Mr. Carter sent her to me, on the 6th of April. At this time the paroxysms were excessively violent and frequent, though brief. On examination, tender points were found at the supra-orbital notch, at the infra-orbital foramen; in front of the ear; in the temporal region; in the parietal region, and the inferior dental region. There was strongly marked anaesthesia of the skin of the right half of the face, of the gums, and of the side of the tongue. The teeth were absolutely perfect: not one spot of caries could be seen. Taste was completely destroyed in left half of anterior part of the tongue. Smell was totally lost on both sides, and had been so, the woman declared, from a very early period in the illness. The right eye showed complete paralysis of the levator palpebrae and of the external rectus; nearly complete paralysis of the superior and inferior rectus, rather less marked paralysis of the internal rectus. Pupil normal, conjunctiva moderately congested, lachrymation profuse, photophobia partial. The functions of the retina were perfect. Accommodation was affected in the following degree and manner. The vision of the affected eye was perfect at long distances, very imperfect at short distances. With both eyes open she saw every thing double, but could still count all the bricks in a whitewashed wall at sixteen feet distant. There was no secondary disturbance of the stomach whatever. On the first visit she assuredly had no visible signs, in skin or throat, of syphilis; the perfect health of her children, and absence of abortions, made syphilis the less probable. But on her second visit she complained of sore throat, and a week later a palpably specific sore appeared on the soft palate. She declared, with apparent sincerity, that it was the first symptom of the kind she had ever had. The neuralgia rapidly disappeared under thirty grains of iodide of potassium daily. The lesions of taste and smell disappeared exactly pari passua with the trigeminal pains. The ocular paralysis threaten to be much slower in departing. I think we must believe that this woman contracted syphilis after the birth of her last child. It is at any rate certain that the migraine of her youth was perfectly unconnected with syphilis, being as unlike the pains evoked by the latter as it is possible for two kinds of pain to be. In all probability she was infected during her last lactation.

Last among the peripheral influences of sufficient importance to be specially mentioned as effective factors in the production of neuralgia, must be mentioned caries of the teeth, and the comparatively rare accident of the mal-position or abnormal growth of a "wisdom-tooth." It is an undoubted fact that these things may cause neuralgia even of a very serious type, and attended with extensive complications; as in Mr. Salter's cases, already mentioned, of reflex cervico-brachial neuralgia from carious teeth. Looking to the extreme frequency of caries, however, as compared with the rarity of true neuralgia (not mere toothache) as a consequence of it, it is impossible not to suppose that the share of the carious teeth in the production of such neuralgia must be very small, compared with that of other influences.

5. The next influence which we shall mention as undoubtedly very effective in assisting the production of neuralgia in certain cases is that of anaemia and mal-nutrition generally; but it is not necessary to dwell on this at any length. The fact is notorious that severe loss of blood is always followed by headache; and if there be the least predisposition to neuralgia, this headache will very commonly take the form of the severest clavus. And, in like manner, chronic states of anaemia and of mal-nutrition undoubtedly aggravate every existing neuralgia, and bring out lurking tendencies to the disease. But I do not believe that anaemia, or starvation pure and simple, ever generates true neuralgia by its sole influence.

6. The question how far, and in what way, the neuralgic tendency is helped by certain constitutional diatheses, such as rheumatism and gout, and by certain toxaemiae, such as malaria, alcoholism, lead-poisoning, etc., is a very much more difficult one than might be supposed from the off-hand manner in which many writers speak of the "rheumatic," the "gouty," or the "alcoholic" forms of "neuralgia." We may, however, simplify it a good deal. In the first place, it seems obvious to me that the only manner in which alcohol helps the production of true neuralgia is by its tendency, after long abuse, to produce degeneration of the nervous centres: it will therefore be considered, shortly, under another division of the present subject. Lead-poisoning, again, only produces so highly special a form of neuralgia (if colic be neuralgia at all) that it need not detain us here. The influence of malaria is, for the most part, an utter mystery to us, but by so much as we can see it appears plain that one of the most important features in the disease is a powerful disturbance of the spinal vaso-motor centres. But the most interesting consideration that we have to deal with is the question of the supposed relations of the rheumatic and the gouty diatheses, and the syphilitic dyscrasia, to the neuralgic tendency. On this point I am obliged to disagree _in toto_ with the popular view that assigns these diatheses among the most frequent predisposing causes of neuralgia.

To take the case of rheumatism first, I am willing to allow that there are a number of facts which superficially appear to countenance the idea of a close connection of this disease with neuralgia. But of these facts a considerable proportion consist only of examples of inflammation of the nerve-sheath, with a certain amount of effusion within and around it, occurring in persons who have never shown any symptoms which warrant the assumption of a general rheumatic diathesis; and these local phenomena really differ in nothing from many trophic and vaso-motor changes which have been already described as plainly secondary to ordinary neuralgia in which there could be no pretence of a rheumatic pathology except on the slender foundation of a suspicion that the affection was immediately excited by the influence of cold, which is really no argument at all. Such patients will be found to have exhibited, not special rheumatic, but special neuralgic tendencies in their past history. On the other hand, there undoubtedly are a certain number of patients who, having previously given signs of a tendency to generalized rheumatic inflammation of fibrous membranes, are, on some particular occasion, attacked with similar inflammation extending over a more or less considerable tract (not a small limited spot) of a nerve sheath. But so far from agreeing with those who think that this is a frequent case, my experience teaches me that it is quite exceptional; nor do I believe that the common opinion could ever have arisen had it not been for the rage that exists for connecting every disease with a special diathesis which the profession flatters itself that it understands. Few persons have taken more pains than myself to ascertain the frequency with which neuralgic patients show a history of previous rheumatism, whether in the so-called "fibrous," or in the synovial form; but it is remarkable how seldom I have found this to be the case--a result which surprised me, because it happened that I, a neuralgic subject, had suffered in youth from regular acute rheumatism, and had fancied that I should discover a close connection between rheumatism and neuralgia. Eulenburg states that neuralgia caused by cold more frequently attacks the sciatic nerve than any other, and thinks that the tendency to sciatica is characteristic of the relations of rheumatism to sensory nerves. For my own part, I see no reason to call in the rheumatic diathesis as a _deus ex machina_ to explain the frequency with which sciatica follows comparatively trifling peripheral impressions like that of cold. The true reason I believe to be, that what would have been a slight and trivial neuralgia elsewhere, becomes a serious affection in the instance of the sciatic nerve, by reason of the strong muscular pressure end dragging which are always going on in the thigh in locomotion. I shall return to this subject when speaking of Treatment.

As regards the relations, of gout to neuralgia, I can hardly express my own view better than by quoting the words of Eulenburg:[17] "Much more doubtful is the influence of gout, which in rare cases, perhaps, produces neuralgia directly, by means of neuritis, or by the deposit of tophus-like calcareous concretions in the nerve-trunks. Gout has been reckoned as a great influence among the causes of superficial neuralgias (sciatica), and also of visceral neuralgia (angina pectoris, etc.,) but this influence is more probably only an indirect one, operating through circulation changes which are often produced by chronic liver-diseases or by diseases of the heart and vessels, (_e. g._ Valvular diseases and narrowing of the coronary arteries in angina)." To which I will add this argument against any close connection of gout with neuralgia, that it is exceedingly seldom that colchicum effects any decided good, a fact which is as unlike the relations of colchicum to true gout as any thing could be. For, whatever may be thought of the advantages or disadvantages, on the whole, of employing colchicum against gout, at least no one with any experience will deny that in the immense majority of cases of true gouty pain, it gives rapid relief to the acute suffering. I doubt if it ever[18] acts in that way in real neuralgia, though I have occasionally seen it apparently useful in a more limited way, as will be said hereafter.

As regards the relation of the syphilitic dyscrasia to neuralgia, I agree in general with Eulenburg. "Syphilis," he says, "may be the direct cause of neuralgia, either by the development of specific gummata in the nerve-trunks or in the centres, or by arousing chronic irritative processes in the nerve sheaths, the membranes of the brain and spinal cord, or, especially, in the bones and periosteum (syphilitic osteitis and periostitis)." The case of periostitis, however, is a doubtful one: it may be questioned whether this affection (which will be among the diseases discussed in Part II. of this work) ever give rise to true neuralgia. Persons who are, by inheritance, highly predisposed to neuralgia, may from the mere general lowering of their health produced by constitutional syphilis, become truly neuralgic simultaneously with, or subsequently to, the appearance of painful nodes on their bones. And as regards the whole relations of syphilis to neuralgia, I must, from my experience, conclude that the former is, after all, but rarely concerned in the production of the latter. Syphilis has a strong specialty for producing limited motor paralyses, but a much weaker one for producing limited affections of the sensory system.

7. We now come to the discussion of a group of momenta whose influence in the production of neuralgia is at once very powerful, and of the highest significance as regards the general pathology of the disease. These are the degenerative changes of the arterial and capillary systems which are a part of the normal phenomena of old age, but may occur at earlier periods of life, in consequence either of certain constitutional diseases, especially gout, or of special toxic influences on nutrition, of which persistent alcoholic excess is very far the most important.

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 "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 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 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 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).

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 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 entitled 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 space. 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 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 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 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 _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 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 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, 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 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 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 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 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.