CHAPTER III.

PATHOLOGY AND ETIOLOGY OF NEURALGIA.

The pathology and the etiology of neuralgia cannot be considered apart; they must be discussed together at every step. I do not mean to say that neuralgia is singular among diseases in this respect; it seems to me merely a case in which the intrinsic defects of the conventional system of separating the "causes" of disease from its pathology happen to be more glaring and more easily demonstrable than usual.

Neuralgia possesses no "pathology," if by that word we intend to signify the knowledge of definite anatomical changes always associated with the disease, in a manner that we can exhibit or exactly describe. It also possesses no demonstrable causes, if we employ the word "causes" in the old metaphysical sense. And yet I am very far from admitting, what seems to be so generally taken for granted, that we know less about the seat, the nature, and the conditions of neuralgia than of other diseases. On the contrary, I believe, with all deference to the supporters of the ordinary opinion, that we know more about neuralgia, in all these respects, than we do about pneumonia, only our knowledge is not of the superficial and obvious kind, but requires the aid of reason and reflection to develop and turn it to account. It has long been a matter of surprise to me, that even able writers have been content to talk about this disease (as, indeed, they have been content to speak of many nervous diseases) with an inexplicable looseness of phraseology. They speak of its "protean" forms; whereas, in my humble judgment, its forms are by no means specially numerous. They insist on the mysterious and unintelligible manner of its outbreaks, remissions and departure; but I shall try to show that, although, in the investigation of neuralgia, we are continually stopped in particular lines of inquiry by what seems to be ultimate facts, susceptible of no further immediate solution, the channels of information open to us are so unusually numerous as to enable us to accumulate a mass of information which, upon further reflection, will be found to furnish the materials of a synthesis of the disease singularly clear and effective for every practical purpose of the physician. In one important particular I especially hope to convince the reader that a large proportion of the mystification as to the pathology of neuralgia is gratuitous, and the result of great carelessness in estimating the comparative value of different facts. I hope to show clearly that, as regards both the seat of what must be the essential part of the morbid process, and the general nature of the process itself, we possess very definite information indeed. I expect, in short, to convince most readers that the essential seat of every true neuralgia is the posterior root of the spinal nerve in which the pain is felt, and that the essential condition of the tissue of that nerve-root is atrophy, which is usually non-inflammatory in origin. This doctrine seems, at first sight, presumptuous,[16] in the confessed absence or extreme scarcity of dissections which even bear at all upon the question. But one source of the extraordinary interest which the pathology of neuralgia has long possessed for me resides in this very fact, that I am convinced we can demonstrate the above apparently difficult theorem by means of pathological observations on the living subject, taken in conjunction with physiological experiments, and with only the aid of a very few isolated facts of positive morbid anatomy. I need hardly say that I am none the less anxious for that further assurance which we shall one day, perhaps, obtain by means of greatly-improved processes for microscopic detection of minute changes in nerve-centres; but, looking to the necessary rarity of opportunities for post-mortem examinations of the nervous system in any but the most advanced stages of neuralgias, it will hardly be disputed that, if I am right in my main position, we are singularly fortunate to be so unusually independent of the need for this source of information.

1. The first fact which strikes me as of decided importance is the position of neuralgia as an hereditary neurosis; and this character of the disease is so pregnant with significance, that I shall take some considerable pains to put the fact beyond doubt in the reader's mind.

There are two series of facts which support the theory of the inheritance of the neuralgic tendency: (_a_) instances in which the parent of the sufferer had also been affected with the disease; and (_b_) instances in which the family history of the patient being traced out more at large it appeared that, among the members of two or more generations, while one, two, or more individuals had been actually neuralgic, other members had suffered from other serious neuroses (such as insanity, epilepsy, paralysis, chorea, and the tendency to uncontrollable alcoholic excesses), and, in many instances, that this neurotic disposition was complicated with a tendency to phthisis.

(_a_) The question of the direct transmission of neuralgia itself from the parent seems the easiest of decision, though even this cannot always be satisfactorily cleared up by the hospital patients, among whom one collects the largest part of one's clinical materials. However, I have been at the pains of investigating a hundred cases of all kinds of neuralgia, seen in hospital and private practice, with the following results: twenty-four gave distinct evidence that one or other parent had suffered from some variety of neuralgia; fifty-eight gave a distinctly negative answer; and eighteen would not undertake to give any answer at all. Among the twenty-four affirmatives are inserted none in which the history of the parent's affection did not clearly specify the liability to localized pain, of intermitting type, but recurring always in the same situation during the same illness. In three of these twenty-four instances, the patient stated that both parents had suffered from such attacks, and, in one of these, it appeared that the grandfather had likewise suffered.

(_b_) The question of the tendency of a family, during two or more generations, to severe neuroses of more or less varying kinds, including neuralgia, is difficult to work out perfectly, though in a large number of instances we may get enough information to be very useful. I have spent much time and trouble in endeavoring to collect such information; but there are two main difficulties in connection with all such attempts. From hospital patients you frequently can get no reliable information whatever respecting any members of the family farther back than the immediate parents; and, even respecting uncles and aunts and first cousins, it is often impossible to learn any thing. And when you get to a higher class of society, especially when you approach the highest, although the information may exist, it may be withheld, or you may be purposely mystified. One would doubt beforehand, under these circumstances of difficulty, whether it would be possible to obtain affirmative evidence of the neurotic temperament of the families of neuralgic patients in general; but, in truth, the evidence is so overwhelming in amount, that more than enough can be obtained for our purpose. I shall give, first, the results of one special inquiry which, by the kindness of a patient, I have been able to carry out with more than usual completeness; it relates to the medical genealogy of a sufferer from sciatica; the account is fairly complete for four generations. The great-grandfather was a man of splendid physique (an only son), who lived very freely, but died an old man. His children were three sons, one of whom (though strictly temperate) was a man of eccentric and somewhat violent temper, and suffered from a spasmodic facial affection. This one, the grandfather of my patient, married a lady who died of phthisis, and among the ten children she bore him, two sons died of phthisis, two sons became chronically insane, one son died, probably of mesenteric tubercular disease (aged fifty-six), two sons are still alive at very advanced ages, and have always been perfectly healthy and strong; one daughter died in middle age, it is not certain from what cause; one daughter lived healthily to the age of eighty, and then was attacked by facial erysipelas, followed by violent and intractable epileptiform tic, which clung to her for the remaining four years of her life; and the remaining daughter, an occasional sufferer from migraine, died at the age of sixty-seven, almost accidentally, from exhausting summer diarrhoea. The fourth generation, in this branch of the family, consisted of thirty-one individuals; of whom seven have died of phthisis, or scrofulous disease; one from accidental violence, one from rheumatic fever, one from scarlet fever; and among the surviving twenty-two one has been insane, but recovered; two are decided neuralgics; one is occasionally migraineuse, and once had a smart attack of facial erysipelas, corneitis, and iritis, as the climax to a severe neuralgic attack; one has been a sufferer from chorea; one has become phthisical; one developed strumous disease, but has fairly recovered from it. The remaining fifteen enjoy good health, but are distinguished, almost without exception, by a markedly neurotic temperament, indicated by an anxious tendency of mind, quickness of perception, æsthetic taste, disposition to alternations of impulse and procrastination. Of the young fifth generation growing up, there have been twenty-five children, of whom only one has died (from fever), the rest are apparently healthy (most of them specially so); but, as few have yet reached the age for the development either of phthisis or of neurotic diseases, the future of this generation can only be guessed at. [It is unnecessary to trace the other descendants of the second generation, but I may state that their medical history, also, strongly supports the theory of inheritance of the neurotic tendency, and of the influence of an imported element of phthisis in aggravating the latter.] I suspect that, as regards the young children now growing up, everything will depend on the care with which they are fed, and the kind of moral influences brought to bear on them, two subjects which will be fully dwelt on in the chapter on Treatment.

Of less perfect inquiries on the subject of neurotic disposition inherited by neuralgic patients, I have made a great number, though I regret to say that I have not attempted the task in the whole number of those from whom I inquired as to direct inheritance of neuralgia from their parents. However, in eighty-three cases this was done with all possible care, and any deficiency of completeness in the results is not my fault. I shall take first those that were private patients, twenty-two in number, respecting whom, I may say, that the evidence is of the best, as far as it goes, since I was better able to discriminate as to the worth of statements, than in dealing with hospital patients, and have rejected every case in which the informant did not seem intelligent enough, or otherwise to have the means, to give a thoroughly reliable account.

I. Neuralgia cervico-brachialis; in a lady, aged seventy-one. Mother suffered from epileptiform facial tic; uncle was paralyzed; patient herself eccentric to the verge of insanity.

II. Bilateral sciatica of great severity; in a gentleman, aged seventy-three. Gout, paralysis, and neuralgia, have been frequent in the family.

III. Cardiac neuralgia; in a man, aged twenty-four. Father epileptic and a drinker; grandfather died of softening of the brain, aged thirty-eight.

IV. "Cerebral" neuralgia; in a single lady, aged thirty-eight. Mother has been insane; first cousin epileptic.

V. Lumbo-abdominal neuralgia; in a gentleman, aged fifty-two. Father a drinker; mother insane; maternal grandfather phthisical.

VI. Severe neurotic angina pectoris; in a gentleman, aged fifty. Almost every one of the graver neuroses among patient's near relations.

VII. Migraine and cervico-occipital neuralgia; in a young lady, aged twenty-five. Immediate causes, brain-work, and influence of cold weather. Father and brother both epileptic; father's family much affected with neurotic diseases.

VIII. Sciatica; highly-nervous temperament. Father died insane from drink; and probably other members of the family also nearly or quite insane.

IX. Auriculo-temporal neuralgia; in a married lady, aged twenty-eight. Father's family markedly phthisical and neuralgic.

X. Intercostal neuralgia; in a girl (phthisical), aged twenty-four. Mother and two uncles phthisical; maternal grandfather epileptic and a drinker.

XI. Facial neuralgia (third branch trigeminal); in a gentleman, aged fifty-four, a great whiskey-drinker. Drinking hereditary for three generations; father died insane; grandfather epileptic; sister phthisical; two brothers very "eccentric."

XII. Migraine, severe; in a lady, aged thirty-three. Grief was the immediate cause. Mother hemiplegic at forty-second year; first cousin insane; two aunts (maternal) epileptic.

XIII. Extremely severe sciatica and cervico-brachial neuralgia of the left side, with singular inflammatory consequences; in a lady, aged fifty-two. A family history remarkably free from neurotic diseases and from phthisis. The neuralgia was probably caused partly by excessive ptyalism, partly by over brain-work.

XIV. Migraine; in a young lady, aged sixteen; very profuse menstruation, which had lasted for two years. Family history very free both from phthisis and neuroses.

XV. Frontal and nasal neuralgia; in a man. Repeated attacks of localized facial erysipelas; drinking-habits for some years; fatal acute insanity in middle age. Father insane, committed suicide; mother subject of violent epileptiform tic.

XVI. Angina pectoris (neurotic); spasmodic asthma, twenty years; facial neuralgia and erysipelas; in a gentleman, aged fifty. Family medical history scanty and imperfect; but, as far as it goes, entirely without evidence of either phthisis or neuroses.

XVII. Neuralgia of testis, immediately caused by local irritation. Father died of phthisis; paternal uncle epileptic and insane.

XVIII. Ovarian neuralgia; in a girl, aged twenty-six, liable to occasional migraine. Mother has suffered sciatica; brother died of phthisis.

XIX. Gastralgia; in a man, aged twenty-seven; highly intellectual and nervous. Family history very free from neuroses; but some evidence of phthisis, in two previous generations, on mother's side.

XX. Sciatica; in a lady, aged sixty; second attack. Ancestors, on both sides, for some generations, clever, and in several instances decidedly eccentric, if not insane; much neuralgia in the family.

XXI. Migraine; in a young lady, aged seventeen; menstrual difficulties. No neurotic nor phthisical family history.

XXII. Sciatica; in a married lady, aged twenty-seven; first pregnancy; had rheumatic fever and subsequent chorea in childhood. Paternal uncle epileptic; mother had rheumatic fever and cardiac disease; paternal grandfather suffered from sciatica late in life.

No one, I think, can look down the above list and fail to be struck with the great preponderance of cases in which the general neurotic temperament plainly existed in the patients' families; and let me add that, in not a few of these cases, the neuralgia in the individual under observation might have been easily set down as dependent merely upon peripheral irritation, which, indeed, plainly did act as a concurrent cause.

Fortunately, however, I am not dependent upon my own evidence alone, for the proofs of the proposition that neuralgia is eminently a development of hereditary neuroses. The great French alienists, Morel and Moreau of Tours, some years ago laid the foundations of the doctrine of hereditary neurosis. They enforced this chiefly with reference to the manner in which insanity is transmitted through a chain of variously-neurotic members of a family stock; and Moreau laid special stress on the deeply interesting connection of the phthisical with the neurotic tendency. Since then various observers have insisted on the same thing. Of late, Dr. Maudsley has worked out this subject with great ability, in his work "On the Physiology and Pathology of Mind," and in his recent "Gulstonian Lectures;" and Dr. Blandford dwells on it with emphasis in his interesting "Lectures on Insanity." [Dr. Blandford does not, however, admit that the phthisical diathesis has any such close and causal relation with neuroses as has been imagined by some recent pathologists; and, on the other hand, he points out that phthisis in neurotic subjects, _e. g._, the insane, must, in a large measure, be considered the product of the accidentally unhealthy circumstances in which they pass their lives. In the latter opinion I entirely agree.] Indeed, it may be taken as a recognized fact, among the more advanced students of nervous diseases, that hereditary neurosis is an important antecedent of neuralgia, in at least a very large number of instances. I shall conclude this part of the argument by stating the general results of my inquiries respecting sixty-one hospital patients. Of these cases, twenty-two were migraine, or some other affection of the ophthalmic division of the fifth nerve; seven were sciatica; two were epileptiform facial tic; ten were neuralgias affecting chiefly the second and third divisions of the fifth nerve; three were intercostal neuralgias pure; one was intercostal neuralgia plus anginoid pain; seven were intercostal neuralgias with zoster; three were brachial neuralgias; and five were abdominal neuralgias (hepatic, gastric, mesenteric, etc.) Of eighty-three hospital and private patients [It must be understood that the respective numbers do not indicate with any accuracy the relative frequency of the different neuralgias as seen in my practice. (Sciatica, _e. g._, was proportionally more frequent.) They represent but a small part of the neuralgic patients whom I have seen during fourteen years of dispensary, hospital, and private practice, and they were selected for inquiry merely because I happened to be able to give the time for the necessary questions. Every one who knows out-patient practice will understand how seldom this happened.] I obtained evidence of the presence, among blood-relations, of the following diseases: Epilepsy, fourteen cases (eight were examples of migraine); hemiplegia or paraplegia, nine cases; insanity, twelve cases; drunken habits, fourteen cases; "consumption," eighteen cases; "St. Vitus's dance," four cases. I am well aware that these figures must be taken with caution, and that considerable doubt must rest on the accuracy of some of these details, more especially with regard to "epilepsy," as it was impossible, with the greatest care, to be sure that this was not given, by mistake, for hysteria in some cases; and the same may apply to the statement that relations had suffered from "consumption." The facts are given for what they are worth, and with the express reservation that their total reliability is far less than that of the accounts obtained respecting private patients belonging to the more educated classes. But, in one respect, viz., as regards drunken habits, it is possible that a truer estimate is gained from the statements of hospital patients than from those of private patients, who would usually be more prone to reticence on such a topic.

The evidence as to the hereditary character of neuralgia assumes a yet higher importance when supplemented by the facts respecting the alternations of neuralgia with other neuroses as the same individuals. Every practitioner must be aware how frequent is the latter occurrence. Nothing is more common, for example, than to see insanity developed as the climax of minor nervous troubles, especially of neuralgia. And there is one form of neuralgia, the true epileptiform tic, which is intimately bound up with a mental condition of the nature of melancholia, and even with the markedly suicidal form of the latter affection. I have lately had under my care a lady in whom the prodromata of a severe facial neuralgia were mental; the disturbance commenced with frightful dreams, and there was great mental agitation even before the pain broke out; this disturbance of mind, however, continued during the whole period of the neuralgia, and was relieved simultaneously with the cessation of the attacks of pain. This is contrary to what happens in some cases; thus, Dr. Maudsley quotes the case of an able divine who was liable to alternations of neuralgia and insanity, the one affection disappearing when the other prevailed. Dr. Blandford has met with several instances in which neuralgia has been followed by insanity, the pain vanishing during the mental disturbance, and reappearing as the latter passed away. And he remarks that, in the transition of a neuralgia (to mental affection), we may well believe that the neurotic affection is merely changed from one centre to another, from the centres of sensation to those of mind. He says that the ultimate prognosis of such cases is bad; a point to which we shall have to refer again.

The prominent place which quasi-neuralgic pains hold in the earlier history of locomotor ataxy is a fact that cannot but engage attention. In this volume we have not treated these pains as belonging to the truly neuralgic class, for the very practical reason that they are but incidents in a most important organic disease, and that in a diagnostic and prognostic point of view it is necessary to dwell on their connection with that disease. But, in considering the pathological relations of neuralgia, it would be improper to omit the consideration of the pains of locomotor ataxy, which bear a striking semblance to neuralgic pains. The fact that they are an almost if not quite constant feature of a disease which is from first to last an atrophic affection (mainly of the posterior columns of the cord), in which the posterior roots of the nerves are almost always deeply involved, has a bearing on our present inquiry too obvious to need further remark.

Equally important to our investigation is the fact that pains, closely resembling neuralgia, are not very uncommonly a part of the phenomena of commencing, and more frequently of receding, spinal paralysis. I have the notes of three cases of partial recovery from paraplegia, in all of which the patients remained for years, in one case for nearly twenty years (ending with death), the victims to a singularly intractable neuralgia of both lower extremities. In the worst of the cases the patient was the victim of excessive and continuous labor at literary work of a kind which hardly exercised the mental powers, but was extremely exhausting to the general power of the nervous system; he broke down at about the age of fifty, but dragged on a painful existence for the long period above mentioned.

We are also certainly entitled to adduce the example of the so-called neuralgic form of chronic alcoholism as an instance of the close relationship of neuralgia to other central neuroses. I refer to those cases, more common perhaps than is generally admitted, in which pains in the extremities, often quite resembling neuralgia in their intermittence, are either superadded to or take the place of the muscular tremors and general restlessness that are more popularly considered as the essential nervous phenomena of chronic alcoholic poisoning. That the pains are usually bilateral, and more diffuse in their character than those of ordinary neuralgia, is a fact which it is not difficult to explain by the _modus operandi_ of the cause; but we shall have more to say on the general relations of alcoholic excess to neuralgia presently. The pains themselves will be fully described in the second part of this book, which treats of the affections that simulate neuralgia; here we need only remark that it is not uncommon for them to occur interchangeably with true neuralgia in the same person.

The occasional interchangeability of migraine with epilepsy is a well-known fact; every practitioner who has seen much of the latter disease will have seen some cases in which the patient had been liable, at some point of his medical history, to "sick-headaches" of a truly neuralgic kind; although it is quite true, as Dr. Reynolds points out, that the kind of sensorial disorder specially premonitory of the attacks consists rather in indefinable distressing sensations, than in actual pain. The genealogical connection between migraine and epilepsy is, as I have already stated, apparently very close. Such instances as one mentioned by Eulenburg are rightly explained by him; it is the case of a girl who suffered at an unusually early age (nine) from migraine; her mother had been a migraineuse, and her sister was epileptic; the strong neurotic family tendency is believed by Eulenburg to account for the appearance of migraine at such a period of life.

This seems the fitting place to introduce some special remarks on migraine in its relations to other neuralgias of the head, because Eulenburg has mentioned and combated my view, according to which migraine is a mere variety of neuralgia of the ophthalmic division of the fifth nerve. I call it my view, because, though several other authors had previously expressed it, I was first lead to entertain it by observations made before I had studied their works, and especially by the impressive teaching of my own case, as to which more will be presently said. Eulenburg, though he fully allows that migraine is a neuralgia, urges a series of objections to the identification of migraine with ophthalmic neuralgias; of which objections one, based on the doctrine of Du Bois Reymond as to the action of the sympathetic in migraine, must be reserved for consideration when we discuss the general pathology of the vaso-motor complications of neuralgia. The other grounds of distinction that he urges are the following: In the first place, he remarks that the site of the pain is by far less distinctly referred to definite foci on the outside of the skull than in trigeminal neuralgia; the patient's sensations very usually lead him to declare that the pain is in the brain itself. Secondly, he says that the points douloureux (in Valleix's sense) are almost constantly absent in true migraine. Thirdly, he specifies the character of the pain in migraine--dull, boring, straining, etc.--as differing from that of trigeminal neuralgia, which is ordinarily much more acute and darting. Fourthly, he notes the long duration of individual attacks of migraine, and the long intervals (very commonly three or four weeks) between them. Fifthly, he dwells on the frequent prodromata of migraine referable to the organs of sense (flashes before the eyes, noises in the ears), or to the stomach (nausea), or more generally to the reflex functions of the medulla oblongata (_e. g._, convulsive rigors, excessive yawning, etc.)

Now, I should have nothing to say against the accuracy of this description, did it apply merely to the distinctions between highly-typical cases of the "sick-headache" of the period of bodily development, and highly-typical cases of the ophthalmic neuralgias which are commonest in the middle and later periods of life; nor indeed should I greatly care if it were finally decided that migraine and clavus should be separated from the true trigeminal neuralgiæ, provided the following points were well impressed on the minds of practitioners. In the first place, I must insist that in my own experience the great majority of undoubtedly neuralgic headaches, which subordinate stomach disturbance, are far less sharply separated than the above description would allow from the unmistakable trigeminal neuralgias; it is only a minority of cases that wear this extreme type, and a far larger number shade imperceptibly away toward the type of ophthalmic neuralgia pure and simple. And so, again, of the so-called clavus there is every variety, from a form bordering closely on the migraine type to another, differing in nothing from an unusually severe ocular and frontal neuralgia of the fifth, except in the presence of a tremendously painful parietal focus. But the fact on which I would most particularly insist is one that was first taught me by my personal experience, viz., that migraine is, with extraordinary frequency, the primary or youthful type of a neuralgia which, in later years, entirely loses the special characters of sick-headache, and assumes those of ordinary frontal neuralgia, with or without complications. In my own case, the "sick-headache" character of the affection was strongly marked during the first two or three years, after which time it gradually but steadily lost all tendencies to stomach complications, and, what is more, the type of the recurrence became entirely changed. Yet it is quite impossible to believe that the malady is now a different one, in any essential pathological point, from what it was at first; if any disproof of this were needed, it might be remarked that the singular series of secondary trophic changes which have complicated my case have been impartially distributed between the respective periods when the affection was frankly migraineuse, when it was mixed, and when it was simply ophthalmic neuralgia (as it is at present;) indeed, some of the most decided of these trophic complications (orbital periostitis, corneal ulceration, fibrous obstruction of the nasal duct) occurred within the period in which every attack of pain, unless I succeeded in getting to sleep very shortly, ended in violent vomiting. The experience thus gained has made me very attentive to the past history of those who, in later life, complain of frontal neuralgia without stomach complication, and it is surprising to find in how many cases patients, who at first declare that they never had neuralgia before, on reflection will recall the fact that they were often "bilious" in their youth; which "biliousness" turns out to have been regularly preceded by one-sided headache, and to have been severe in proportion to the severity and duration of that previous headache.

I ask the reader to dwell with fixed attention on this fact of the exclusiveness, or almost exclusiveness, with which the neuralgias of the anterior part of the head are represented during the period of bodily development, and especially in the years just succeeding puberty, by migraine or by clavus. When this fact has thoroughly entered the mind, we can hardly help joining with it that other and most important fact already noticed, of the close connection between the predisposition to migraine and the predisposition to epilepsy, and reflecting further on the strong tendency which epilepsy likewise shows to infest the earlier years of sexual life. In view of these things, it is difficult to avoid the inference that both the epileptic and the neuralgic affections of this critical period of life are the expression of a morbid condition of the medulla oblongata, in which the sensory root of the trigeminus has its origin; and further, that this morbid condition (tending to explosive and atactic manifestations of nerve-force) must have its basis in defective nutrition. For, be it remembered, the epoch of sexual development is one in which an enormous addition is being made to the expenditure of vital energy; besides the continuous processes of the growth of the tissues and organs generally, the sexual apparatus, with its nervous supply, is making by its development heavy demands upon the nutritive powers of the organism; and, it is scarcely possible but that portions of the nervous centres, not directly connected with it, should proportionally suffer in their nutrition, probably through defective blood-supply. When we add to this the abnormal strain that is being put on the brain, in many cases, by a forcing plan of mental education, we shall perceive a source not merely of exhaustive expenditure of nervous power, but of secondary irritation of centres like the medulla oblongata, that are probably already somewhat lowered in power of vital resistance, and proportionably irritable. Let us suppose, then, that to all these unfavorable conditions there was added the circumstance that the structure of the medulla oblongata, or of parts of it, was congenitally weak and imperfect; then surely it would be scarcely possible for these loci minimæ resistentiæ to escape being thrown into that state of weak and disorderly commotion which eminently favors pain in the sensory, and convulsion in the motor apparatus.

2. We have so far been mainly considering the relations to the production of neuralgia of certain conditions of the central nervous system which indisputably are inherent from birth. Let us now pass quite to the other extreme, and consider a class of momenta which take a decided part in producing many neuralgiæ, but which are altogether accidental and factitious, and cannot be included among the necessary hostile conditions of life. To push the contrast to the utmost, let us inquire first, what amount of influence in the production of neuralgia can be given by such a purely "functional" influence as educational misdirection of intellect and emotion?

It is somewhat strange, though every one accepts as a mere truism the maxim that sudden emotional shock may produce almost any degree or variety of nervous disorder, the slower but far surer influence of long-continued mental habit is often practically ignored. It cannot, indeed, be left out of sight as a cause of disorders of the mind itself, nor are there many who would deny that such diseases as cerebral softening are, in a considerable number of cases, the premature ending to a life that has been broken down by harassing work and anxiety. But what is far less appreciated is the tendency of certain unfortunate mental surroundings and modes of mental life to produce a generally neurotic condition, which may express itself in a variety of functional disorders, among which not the least common is neuralgia.

I may fairly hope to be acquitted of any predisposition to lay exaggerated stress on this kind of influence in the production of neuralgia, considering all that I have said of the importance of that inevitable cause, the neurotic inheritance, and all that I shall have to say presently as to the effects of a variety of external influences of a totally different kind. But I confess that, with me, the result of close attention given to the pathology of neuralgia has been the ever-growing conviction that, next to the influence of neurotic inheritance, there is no such frequently powerful factor in the construction of the neuralgic habit as mental warp of a certain kind, the product of an unwise education. This work is not intended as a treatise either on religion or psychology, and yet it is impossible for me to avoid some few words that may seem to trench on the province of each: for I believe that there are certain emotional and spiritual and intellectual grooves into which it is only too easy to direct the minds of young children, and which conduct them too often to a condition of general nervous weakness, and not unfrequently to the special miseries of neuralgia. As regards the working of the intellect, it is easier to speak in a free and unembarrassed manner than respecting the other matters. There can be no doubt that, of intellectual work, that sort which exhausts and harasses the nervous system is the forced, the premature, and the unreal kind; and this it is which predisposes, among other nervous maladies, to neuralgia. It is more difficult to speak the truth about emotional influences generally, and especially about those which are concerned with the highest spiritual matters; but I should do wrong were I to suppress the statement of my convictions on this point. I believe that a most unfortunate, a positively poisonous influence upon the nervous system, especially in youth, is the direct result of efforts, dictated often by the highest motives, to train the emotions and aspirations to a high ideal, especially to a high religious ideal. It is not the object that is bad, but the machinery by which it is sought to be attained. In modern society there are two principal methods which are popularly employed for this purpose; I shall describe them, by two epithets which are selected with no offensive intention, as the Conventual and the Puritan methods of spiritual training. By the former is meant that kind of education which deliberately dwarfs the nervous energy, with the hope of preserving the mind from the contamination of unbelief and of sinful passion. It is a system which is not peculiar to the Roman Church, nor even to the Christian religion, and it need the less detain our attention, as its effects, so far as they are evil, are mainly seen in general nervous and mental enfeeblement, rather than in the outbreak of explosive nervous disorders, such as convulsion, insanity, or neuralgia. There are doubtless exceptions to the rule; but that is the rule. It is far otherwise with the spiritual education which is here called Puritan, but which is confined to no party in the Church. This is a system which seeks to purify and exalt the mind, not by enforcing obedience to a series of spiritual rules for which another mind is responsible, but by compelling it to a perpetual introspection directed to the object of discovering whether it comes up to a self-erected spiritual standard. The reader will understand that I have not the remotest intention to depreciate either a true and manly self-restraint in obedience to the direction of "pastors and masters," or an honest watchfulness over one's own conduct and thoughts. But the lessons which our psychologists are rapidly learning, as to the evil effects on the brain of an education that promotes self-consciousness, are sorely needed to be applied to the pathology of nervous diseases generally, and of neuralgia among the rest. Common sense and common humanity, when united with the physician's knowledge, cry out against the system under which religious parents and teachers subject the feeble and highly mobile nervous systems of the young to the tremendous strain of spiritual self-questioning upon the most momentous topics. More especially is such a practice to be condemned in the case of boys and girls who are passing through the terrible ordeal of sexual development--an epoch which, as we have already seen, is peculiarly favorable to the formation of the neurotic habit, and I must emphatically state my belief that among the seriously-minded English middle classes, more especially, whose life is necessarily colorless and monotonous, the mischief thus worked is both grave and widely spread.

Perhaps the maximum of damage that can be inflicted through the mind upon the sensory nervous centres is effected when to the kind of self-consciousness that is generated by an excessive spiritual introspection there is added the incessant toil of a life spent in sedentary brain-work, and checkered with many anxieties, and many griefs which strike through the affections. Doubtless, such a combination of morbid mental influences is sufficient of itself to generate the neuralgic disposition in its severest forms, without any hereditary neurotic influence, and without any other peripheral irritations; I have more than one such instance in my mind at this moment. But, if they can do this, much more can such influences arouse inherent tendencies to neuralgia; to persons who are predisposed in this manner they are most highly deleterious.

3. We come now to the peripheral influences which in a more obvious manner become factors in the production of neuralgia. Of such influences there are an immense variety, and the only common quality that can be predicated of all is the tendency directly to depress the life of the sentient centre upon which their action impinges.

If we search among the external influences which contribute to the production of neuralgia for one that is apparently trivial as to the amount of material disturbance which it can cause, and yet is very frequently effective, we may select the agency of cold. The effect of a continuous cold draught of air impinging on the naked skin for some time is comparatively frequently seen in the provocation of neuralgic attack: we say comparatively, because this influence is more frequently effective than blows, wounds, or temporary irritations of any kind, applied to the peripheral ends of sensory nerves. But if neuralgia be a more frequent consequence of cold than of these other influences, a moment's reflection will show that it is by no means an absolutely common result. One has only to think of the numerous omnibus-drivers, engine-drivers, cab-drivers, etc., etc., who pass their whole working lives in presenting the (more or less) naked expanse of their trigeminal and their cervico-occipital nerves to every variety of wind, to perceive that, were this sort of influence very potent in itself, male neuralgic patients should swarm as thick as bees in our hospital and dispensary out-patient rooms; which is notoriously quite contrary to the fact. The same remarks, in both directions, may be applied to the direct influence of atmospheric moisture, either with or without the effect of wind (of course I am not speaking of the more recondite effects of damp soil on the persons who live about it). [Among the hundred patients who formed the basis of the inquiries mentioned in this work, forty-one accused external cold of producing the attack, but many of these produced insufficient evidence that such was the case.] In short, the direct effects of atmospheric cold would seem to be these. Mere lowness of temperature goes for something, but not much; [The most marked instance of the effect of cold, _per se_, that I have seen, was exhibited by a young lady who was under my care during the past severe winter (1870-'71). During much of the time she was confined to a carefully-warmed apartment, on penalty of a violent paroxysm if she left it.] for about as much, perhaps, as it does in the way of aggravating all neurotic tendencies. Cold joined with wind is much more powerful. And the maximum of ill-effect seems reached by very cold wind mingled with sleet or driving rain, which keeps the skin sodden. But the conclusion at which I long ago arrived is, that none of these influences ever take more than a small (though it is sometimes an important) part in the production of neuralgia; and that in the majority of cases there is no pretence for supposing that they had the slightest share in its causation.

A word or two must be said as to the _modus operandi_ of cold and cold wind, as these are the most frequent of external, so-called "exciting" causes. The popular use of such phrases as the latter has an extraordinary influence in disguising the plain fact, which is, that these influences operate wholly in the direction of robbing the nerves of force. The continuous abstraction of heat from the surface, which of course is materially aided by rapid movement of the air, must necessitate a readjustment of the distribution of energy, the only result of which must be to drain the sensory nervous centre of its reserve of force. But, in fact, there is an experiment, ready performed to our hands, which may amply satisfy us as to the kind of influence exerted by cold on superficial nerves, viz., the sensations experienced in recovering from frost-bite, which has been severe enough to paralyze the nerves without causing actual gangrene of the tissues. The passage of the nerves back from temporary death to full functional life is marked by a half-way stage in which there is agonizing pain.

4. We must next consider the effects of a class of peripheral influences which act, where they exist, in a more constant manner than any others; viz., those in which the trunk or periphery of a sensory nerve either receives a severe injury, or becomes more or less engaged in inflammatory processes, or compressed or otherwise damaged by the growth of tumors or the spread of destructive ulcerations.

With regard to ordinary nerve-wounds as a cause of neuralgia, we have already said (_vide_ Chapter II.) nearly as much as it is necessary to say; we need only here point out that, like the influence of cold applied to superficial nerves, that of wounds must necessarily be a depressing one to the centre with which the wounded nerve is connected, and the resulting neuralgia must be regarded as an expression of impeded and imperfect nerve-energy, not of heightened nerve-function. The pain is set up during the process of nerve-healing; that is to say, at a stage intermediate between those of abolished function and completely restored function; and there can be little doubt that the obstinacy with which it is often protracted is due to the slowness with which a wounded nerve recovers its full functional activity; when once the latter is completely restored there is an end of neuralgic pain. It is exactly analogous to the course of events in recovery from freezing.

There remain for consideration, however, (a) a small class of cases of nerve-wounds in which the healing process is not simple; but the lesion is followed by the development of a tumor of the kind denominated true neuroma. The process consists of hyperplastic changes in the nerve-fibres; its commonest examples are seen in the extraordinarily painful swellings that occur on the ends of nerves left in stumps after amputations; but, in fact, a neuroma of this kind may occur after any kind of severe nerve-injury, as, _e. g._, a cut from broken glass, the impaction of foreign bodies, etc. The true neuromata are composed mainly of nerve-tissue, with a relatively small element of connective tissue: the nerve-fibres can be traced directly to the nerve-tumor. Besides the traumatic neuromata which form permanent tumors, incapable of being got rid of except by actual excision, a minor variety of the same kind of change has in several cases been known to take place in consequence of an abiding local irritation from the impaction of a foreign body, on the removal of which the neuromatoid enlargement completely disappeared. (b) There are likewise a certain number of cases in which a tumor is developed from the neurilemma, and does not consist of nervous tissue; these are distinguished as false neuromata, and may be of various kinds, the fibromatous and gliomatous being far the most common, but cysts and cystic tumors also sometimes occurring.

The case of the neuromata is well worth reflecting upon, in the course of our endeavors to clear up the Pathology and Etiology of Neuralgia. If ever we could find a merely peripheral influence which would of itself be invariably competent to excite neuralgic pains, it would surely be found in neuroma; but the case is not merely not so, it is strikingly contrary. Just as wounded and inflamed nerves frequently go through the whole processes of disease and recovery without once eliciting a neuralgic pang, so is it with neuromata; they are not unfrequently quite indolent, and neither excite neuralgia, nor are themselves at all particularly tender to the touch. And what is most remarkable is, that, as Eulenburg correctly remarks, among the pseudo-neuromata the kind of tumor which is most frequently associated with neuralgia is by no means the dense fibroma or glioma, which might be expected by its mechanical pressure to excite inevitable neuralgic pain, but the far softer and more yielding cystic tumors. I do not know how the facts may affect the reader, but to me they suggest the strongest possible arguments against the belief that peripheral irritation can of itself produce neuralgia without the intervention of some centric change. The tendency to such change (from inherent constitution) in the sensory root of the nerve must surely be the reason why neuroma causes neuralgia in a given number of subjects, instead of letting them go scot-free, as it does other persons.

The same remarks apply to the result of observations on the effect of tumors commencing in tissues altogether unconnected with the nerve, and merely coming to involve it, secondarily, in pressure. It has been often noted that, among these tumors, fluid-containing cysts and soft medullary cancers are far more frequently the cause of decided and distressing neuralgia than the denser and less yielding neoplasms. Of kinds of tumors that are specially apt to produce severe and even intolerable neuralgia by the pressure on nerves, it has been remarked that aneurisms are among the worst: here every pulsation often sends a dart of agony through the nerve. There is a reason here, however, which is often left out of sight; not merely is the perpetually varying pressure specially harassing and exhausting to the nerve, but in many of these cases there is general arterial degeneration, and the sensory root of the nerve is exceedingly likely to be very badly nourished. [This result will be more directly brought about when the aneurism happens to press on the ganglion of a posterior root.] We pass now to the consideration of the influence exerted by other great series of peripheral impressions in the production of neuralgia. These impressions are connected chiefly with the functions of the digestive and of the genito-urinary organs, the functions of the eye, and the nutrition of the teeth.

To take the least important of these first, I may surprise some readers by the statement, which I nevertheless make with much confidence, that irritation of any part of the alimentary canal is, on the whole, a rare concurrent cause, even in the production of neuralgia. There are, as has been already fully explained, cases of neuralgia seated in these viscera themselves (or the plexuses in their immediate neighborhood), although their number is immensely smaller than that of the neuralgias of superficial nerves. But it is not at all common--it is even exceedingly rare--for irritation conveyed from the alimentary canal to take any important part in setting up neuralgia of a distant nerve, even when that nerve has close connections, through the centres, with those coming from the irritated portion of the alimentary canal. Valleix had the great merit to perceive this, even in the case of neuralgias of the head, where appearances are so likely to lead the observer to a contrary opinion. And it is not a little remarkable that this should be the case, when we consider the close central connections which the vagus, the great sensory nerve of a large portion of the alimentary canal, has with the sensory root of the trigeminus. In fact, however, there are certain peculiar forms of gastric irritation which do react upon the trigeminus; for instance, a lump of unmelted ice, suddenly swallowed, almost invariably produces acute pain in the supra-orbital branch of the fifth, on one side or the other, and occasionally (as in a case cited by Sir Thomas Watson) in other nerves. But that common dyspeptic troubles at all frequently or importantly contribute to the production of neuralgia, I do not for a moment believe: it needs some very powerful irritation, such as that just mentioned, or as impaction of great masses of scybalæ in the intestines, or severe irritation from worms, to produce such an effect.

It is far otherwise with the genito-urinary apparatus; in a large number of cases, irritations proceeding from these organs do undoubtedly contribute to the production of neuralgia, though by no means in the important degree which many authors seem to have assumed. There can be no doubt, for example, that the irritation of a calculus, either within the kidney itself, in the ureter, or in the bladder, may set up violent neuralgia, which for the most part is localized in the branches of the lumbo-abdominal nerves. The instance of the eloquent Robert Hall is an example of renal calculus acting in this way: he suffered the most excruciating agony for years, and was obliged to take enormous quantities of opium in order to make life endurable. An instance of calculus impacted in the ureter, in a gentleman somewhat past middle age, occurred in my own practice; the lumbo-abdominal neuralgia occurred in frequent paroxysms of dreadful severity; and another case, already referred to was that of a woman, in whom ovarian neuralgia was undoubtedly in great part due to the irritation of an impacted calculus in the ureter. These cases, however, are very rare in comparison with others in which the peripheral source of the neuralgia is either the uterus or ovary, or the external genitals. I have no means of ascertaining, with anything like accuracy, the frequency with which the internal sexual organs are the starting-point of neuralgia, because the majority of such cases pass, naturally, to the care of physicians who practice chiefly in the diseases of women, and consequently not adequately represented either in my hospital or my private practice; still, I have seen a good many of these affections, and, though I speak with the reserve necessitated by the circumstances just named, I am much inclined to believe that even such powerful centripetal influences as those of the states of commencing puberty, of pregnancy, of the change of life, and uterine diseases generally, are very rarely the cause of true unilateral neuralgia, except in subjects with congenital tendencies to neuralgia. But in predisposed subjects there can be no doubt that these influences assist most powerfully in producing the malady.

Of the power of irritation of the external genitalia to act as a so-called "exciting cause" of neuralgia, there is abundant evidence. I would especially call attention to the remarkable monograph of M. Mauriac, ["_Etude sur les Nevralgies Reflexes symptomatiques de l'Orchi-epididymite blenorrhagique_" Par C. Mauriac, Medecin de l'Hospital du Midi. Paris, 1870.] on the neuralgias consecutive to blenorrhagic orchi-epididymitis, as illustrating this with a force that was to me, for one, surprising. I shall, perhaps, have further occasion to these researches; here it will be enough to mention that M. Mauriac's enormous experience of blenorrhoea and orchitis at the Midi has shown that, in an exceedingly large number of cases, certainly not less than four per cent., this combination is followed by reflex neuralgias, of which a large number are not seated in the genital apparatus, but affect the track of some distant sensory nerve, through the intermediation of the spinal centres; and that with these reflex pains there is often profound general disturbance, including very often an extremely profound general anæmia. The most frequent kind of these neuralgias is rachialgia, _i. e._, pain in the superficial posterior branches of spinal nerves; next comes lumbo-abdominal neuralgia; then sciatic and crural, visceralgic (abdominal), etc.; and besides all these there are numerous instances of neuralgia in the testis. As to the nervous "reflection," more hereafter.

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 anæsthesia 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 palpebræ 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 anæmia 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 anæmia and of mal-nutrition undoubtedly aggravate every existing neuralgia, and bring out lurking tendencies to the disease. But I do not believe that anæmia, 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 toxæmiæ, 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 "hyperæsthesia" may depend on three sorts of causes--(1) On local disease of the peripheral ends of nerves; (2) on alterations of the psychical centres; and (3) on morbidly exaggerated conduction in the nerve-trunks themselves; and it is to this third source that he attributes many of the phenomena of the neuralgic painful points, and especially their multiplicity, in many cases. The _locus in quo_ of the mischief which sets up this exaggerated conduction of sensory impression is, upon this theory, between the psychical centre and the main point of branching of the nerves; hence a large number of peripheral nerve-termini might be practically sensitive to touch, because the mischief, though localized in a comparatively small spot, might easily affect many bundles of fibres, which diverge widely from each other in their course. It will be seen presently with what limits and for what reasons we believe this to be a true theory. But to return to the question of painful points in Valleix's sense, we must state one or two facts which seem certain from our own experience, but have not been adequately recognized, we believe, by others. The first is, that localized tender spots, accurate pressure on which will set up or aggravate the neuralgic pain, are not early phenomena, save in neuralgias of exceptional severity of onset; but that a certain persistence and severity of neuralgia are always followed by the formation of one or more true points douloureux. The second fact relates to the clinical history of migraine. Roughly speaking, it is true, as Eulenburg states, that, in pure migraine, painful points in Valleix's sense are not to be found; in place of them we observe, after the paroxysms have passed away, a more generalized soreness of considerable tracts of the scalp, forehead, etc., or diffuse tenderness of the eyeball. But I must here again refer to the fact, first observed in my own case, and afterward verified in many others, that migraine may be only the youthful prelude to a regular trigeminal neuralgia attended with the formation of characteristic localized painful points at a later period. And the third fact that must be specially mentioned is that the true Valleix's point, when it has become established for some time, is not a mere spot of sensitive nerve, but is the scene of trophic changes, involving hyperæmia and thickening of parts surrounding the nerve. To give one example, it is quite a frequent thing to find a patch of tender and sensibly thickened periosteum of irregular shape, but equal sometimes to a square inch in size, over the frontal bone at and immediately above the inner end of the eyebrow, in cases where supra-orbital neuralgia has recurred frequently during some years, although no such thing was present when the neuralgia first commenced. In my own case, the bone has become sensibly thickened at that point.

The general result of such post-mortem and clinical information as can be had seems clearly to be that positive anatomical changes, either of nerve-terminals or superficial nerve-branches, are but casual and infrequent factors in the first production of neuralgia, and, in particular, it would seem that inflammation of a nerve itself by no means necessarily produces neuralgic pain, but (far more commonly) simple paralgesia or anæsthesia of the parts external (peripheral) to the lesion. The one marked exception to this general proposition is to be found in the case of the severe and peculiar injuries inflicted on the trunks of nerves by gunshot-wounds which, as we have seen (from the American experiences), can produce some of the most dreadful forms of neuralgia. But the nature of the injury here inflicted is, it must be remembered, quite different from any thing which either disease or accident in civil life would produce, save in the most exceptional instances. For the chief material element in the production of the neuralgias of ordinary life we are really driven, by exclusion, to the condition of the posterior roots of special nerves, in some cases, perhaps, to the (spinal) ganglia on which the nutrition of these roots probably is considerably dependent.

With the field thus narrowed for us, it is surely legitimate, in the necessary scarcity of anatomical records referring directly to the state of the nerve-roots in ordinary neuralgia, to place great weight on the facts of a disease like locomotor ataxy, in which the main anatomical change is a progressive atrophy of the posterior columns which usually falls with peculiar severity on the posterior nerve-roots, or on the parts of the gray matter immediately adjoining these, and in which neuralgia may be said, for practical purposes, to be a constant and most characteristic phenomenon. If any one desires to see how strikingly the connection of the neuralgic phenomena with the anatomical-change comes out, I recommend him to study Dr. Lockhart Clarke's papers on locomotor ataxy (_vide_ "St. George's Hospital Reports, i." 1866; _Lancet_, June, 10 1865; "Med.-Chir. Soc. Transactions," 1869), or the excellently reported case by Nothnagel (_Berlin Klin. Wochensch._, 1865). It is really not too much to say that the only important difference between the clinical aspect of the pains of locomotor ataxy and those of ordinary neuralgia is simply such as depends on the fact that the anatomical change in the former case is bilateral, and usually affects the roots of several, sometimes of a great many pairs of nerves. I infer, from a conversation with Dr. Clarke, that he fully recognizes the force of the analogy, and the great strength of the presumption which it sets up in favor of an atrophic change of the posterior roots in neuralgia.

It may, of course, be urged, against the view that neuralgia depends on any change analogous to those which occur in ataxy, that quantities of cases of the former recover speedily, and must be supposed to be either independent of material change altogether or, at any rate, to have involved only very trivial anatomical changes, not formidable diseases, like atrophy of nerve-centres. I find it impossible to admit that this argument has the slightest force. Are we to suppose that the posterior nerve-roots alone, of all tissues and organs of the body, are incapable of minute and partial changes in the direction of molecular death which may be perfectly recovered from in weeks, months, or even days? I, for one, cannot doubt, that such changes are of frequent occurrence, in all parts of the central nervous system, when I can consider the absolute dependence of these portions of the organism upon a perfect blood-supply, and the immense number of possible causes of temporary interference with that source of nutrition. And I can see no probable difference, except in degree and persistence between the effects on sensation which would be produced by such a change of the posterior roots as this, and that which would result from the more serious and fatally continuous change which is involved in locomotor ataxy.

9. We come now to a most important but most complex and difficult portion of the argument respecting the _locus in quo_ of the essential pathological process (if such there be) in neuralgia; viz., as to the paths and the character of the so-called "reflex" influences which intervene in the causation, both of neuralgia itself, and also of the numerous complications with which we have seen that neuralgia is liable to be attended. The clinical facts which confront us here, and demand explanation, are the following: (1) Irritation so called, of sensory fibres may apparently evoke pains attributed to the site of the irritation, or to the parts on the peripheral side which are supplied by the same sensory nerves. (2) Peripheral irritation of a particular sensory nerve may evoke neuralgic pains in nerves connected with that irritated only through the spinal centre. (3) Neuralgia in a sensory nerve may (and almost always does, to some extent) produce secondary vaso-motor paralyses: these paralyses may affect fibres which run in the same branch of the nerve as that which is painful, or fibres that run in another branch of the same nerve, or fibres that run with another sensory nerve, or the ganglionic chain of the sympathetic itself. (4) In like secondary manner, neuralgia may produce vaso-motor spasms in any of the directions just specified; this is usually a short-lived phenomenon, giving place quickly to paralysis; but Du Bois Reymond's often-quoted analysis[19] of his own sufferings from migraine seems to show that spasm-producing irritation of the trunk of the sympathetic may last during some hours. (5) Neuralgia in a sensory nerve may increase, alter, or (more rarely) suspend the secretions of glands supplied by fibres bound up either in the same branch, or in another branch of the same nerve, or in a different nerve with which it is connected only through the centre or (possibly) only through a plexus. (6) Neuralgia in a sensory nerve can produce paralysis of muscles supplied by motor fibres bound up with the painful branch, or with another branch of the same nerve, or in muscles supplied by a totally distinct nerve connected only through the centre. (7) It may produce convulsion and spasms of muscles, in all the above directions; this usually alternates with great weakness, or actual paralysis of the same muscles. (8) It may produce partial or complete loss of common or special sensation in nerve-fibres that run either with the same branch, or with another branch of the same nerve. (9) It may produce trophic changes, either in the direction of simple atrophy or of subacute inflammation with proliferation of lowly-vitalized tissue (_e. g._, connective) in the parts with which are supplied with sensation by the painful branches or by other branches of the same nerve.

It is necessary to go over again the proof of these facts; they are given pretty copiously in the chapter on Complications; and could have been made much more numerous. But the point to which I desire to compel the reader's attention is the impossibility as it seems of me, of accounting for the variety and complexity of these phenomena, except by the supposition that there is in every case of neuralgia a central change, which is the one most important factor in the producing both of the pain and of the secondary phenomena. For the result of my experience is that neuralgia, unless very slight and brief, is never unattended by these complications and in the great majority of cases involves several different secondary alterations of function which must (so to speak) radiate from the central end of the sensory nerve, and from no other place whatever. And it must be remembered that the most elaborate "_symptome-complexe_" is found equally in cases where no suggestion of any peripheral origin of the pain can be made, and in cases where, at first sight, one might fancy there was a very obvious peripheral cause for pain. I am quite willing to admit, with Eulenburg and others, that the evidence, powerful and varied though it be of the relations of neuralgia to hereditary neuroses, to alcoholic and senile degeneration, etc., only raises a strong probability that some part of the central nervous system is the _locus in quo_ of the essential morbid processes in the majority of neuralgias. But the case stands far otherwise now that we are able to show, not merely that the majority of neuralgic patients suffer from such influences as those above mentioned, but that every variety of neuralgia is liable to be complicated with secondary affections of the most divergent nerves, the only common meeting-place of which is in the spinal centre of the painful nerve; and when we find moreover, that many of these secondary affections can equally be produced by undoubted atrophic changes (as in ataxy of those same posterior roots).

At this point we must introduce a remark relative to the true nature of so-called "reflex" effects. The word is constantly used, and is also much abused, as Eulenburg remarks. We all understand, of course, what is intended by the commonest use of the word: the case of sneezing produced by the irritation of snuff applied to the peripheral branches of the fifth nerve in the nose is a stock example. But another application of the phrase, of much more questionable propriety, is that where it is employed to designate functional nervous actions, which merely arise simultaneously with or subsequently to sensory phenomena as to which there is no proof whatever that they were produced by peripheral irritation. This particular inaccuracy of customary speech has probably contributed largely to the inveteracy with which writers on nervous disease have insisted on assuming a peripheral origin in every case for neuralgia itself. In the case of sciatica, for example, complicated, secondarily, with paralysis of the flexors of the limb, it seemed easy and scientific to speak both of the neuralgia and the paralysis as "reflex" effects of a local peripheral mischief--gouty, rheumatic, or the like; and it appears to have been perfectly forgotten by many that the whole phenomena might be explained by an original morbid action in the sensory root of the nerve, extending subsequently to the motor root, without any intervention of peripheral irritation whatever, or under the influence only of the ordinary peripheral impressions, which, in health, evoke no painful nor paralytic symptoms. It is by this kind of extension of a central morbific process, leading to radiation of the perturbing influence centrifugally along divers nervous paths, that I believe we must explain the facts observed in complicated cases.

Take, for example, the following case, which, in its history of twenty-three years, presents a fair example of a type of trigeminal neuralgia which I believe to be the rule rather than the exception, though the trophic changes were somewhat unusually varied and interesting. The following would be the pathological order of events, according to the radiation theory: First or true migrainous stage; failure of nutrition of a portion of the sensory root of the right fifth nerve within medulla oblongata, lesser degree of the same condition in the adjoining and closely-connected vagus root (hence supra-orbital pain, local anæsthesia and vomiting); extension of the morbid process to the motor root (hence vaso-motor paralysis and secretory and trophic changes in the cornea, superciliary periosteum, etc). Second period: recovery, to a large extent, of the nutrition of the posterior root of the trigeminus, complete recovery of the root of the vagus (hence alteration of the type of recurrence of the pains, which now occur at increasingly long intervals, and needed special provocation, _e. g._, excessive fatigue, to bring them on; hence, also, disappearance of the stomach symptoms); continuance of the affection of the motor portion of the nerve (hence, continuance of the tendency to trophic, secretory, and vaso-motor changes); development of the true points douloureux during and after the paroxysms, instead of the diffused tenderness following the old attacks of migraine. Third stage: neuralgic attacks become rare and comparatively unimportant; tendency to trophic changes greatly lessened; local anæsthesia persists. Presumption, that the nutrition of the nerve-centre has nearly recovered itself, but that that centre is still the _locus minimæ resistentiæ_ of the central nervous system, liable to suffer from any cause of general nervous depression.

Now, in interpreting the above phenomena, as I do, upon the theory of one essentially uniform nutritive change affecting the fifth nerve within the medulla oblongata, I shall be met with the following objections: First, there is the common and superficial difficulty that pain and paralysis of sensation must be opposite states, and that it is impossible to refer them both to one and the same pathological process. I have already in many places given instances how constantly pain and sensory paralysis interchange in a manner which is totally incomprehensible except upon the supposition that their physiological basis is essentially the same; but the most satisfactory evidence, perhaps, that could possibly be produced on this point is to be found in the perusal of a group of cases observed by Hippel,[20] and entitled by him "Anæsthesia of the Trigeminus," the loss of sensation being the most remarkable feature. The cases are so deeply interesting that I would gladly transfer them bodily to these pages, but must abstain from want of space. Suffice it to say here, that, in the first place, the anæsthesia was accompanied, in every one of these cases, by a most distinct and typical neuralgia; and, secondly, that trophic changes occurred which most interestingly (though not with absolute completeness) reproduced the phenomena observed after complete section of the trigeminus at the Gasserian ganglion.

The second objection sure to be raised to the theory of a simple spreading of a nutritive central change, as the cause of all the phenomena in such a case as the above, is this: It will be asked how the process extended itself to the motor root, which, in the case of the fifth nerve, is removed by a somewhat formidable anatomical distance from the sensory root. I am, of course, well aware of the latter fact, and it is an additional reason for selecting neuralgia of the fifth, as an extra difficult test of the value of my theory. A few words must be premised, reminding the reader of the physiological anatomy of the nerve.

The trigeminus is in all its characters a spinal nerve; but it has sundry peculiarities both of structure and of connections with other nerves. Its posterior or sensory root is enormous, and, as Schroder van der Kolk showed, takes a direction from behind downward and forward, which is intended to facilitate its numerous and important connections with the nuclei of other nerves: of these the most notable are its connections with the vagus, facial, glosso-pharyngeal, and hypo-glossal nuclei. The motor root, much smaller than the sensory, was shown by Lockhart Clarke to be traceable as low as the inferior border of the olivary body, as a column of cells which occupies a situation corresponding to that of the anterior course of the spinal gray matter.

As this column passes onward in the medulla oblongata, on a level with the glosso-pharyngeal nerve, it forms a group of cells of large size. Besides numerous other connections which it forms, Clarke describes the motor root as sending processes forward, like tapering brushes or tails of fibres, in connection with more scattered cells lying in their course, which may be frequently seen to communicate with the transverse bundles which traverse the "gray tubercle" and the sensory roots of the fifth contained therein. In this way the sensory root, though seemingly much separated from, is really in very direct connection with, the motor root.

Now, proofs, which must be considered almost positive, have recently been adduced to show that the nerve-fibres concerned in those peculiar alterations in the tissues supplied by the ophthalmic division of the fifth, which occur in section of the trigeminus, come entirely from the motor root of the fifth, and form a very small band in the inner or medial margin of the ophthalmic trunk. The observation of Meissner[21] goes to show that it is possible (by good luck) to divide the trunk in such a partial manner as to cut only the inner fibres, and thereby produce the trophic eye-changes without any anæsthesia, or only the sensory fibres, and thereby induce anæsthesia without any trophic changes; and it must be owned that this really affords the only reasonable explanation of the discrepancy between the experimental results obtained by Magendie and Bernard; and also the facts of such cases as those related by Mr. Hutchinson,[22] who in two instances found that a completely anæsthetic eye recovered perfectly well from the wound made in a surgical operation. The nature of the nervous influence (whether ordinary vaso-motor only, or a special trophic function) has been greatly disputed. Dr. Wegner,[23] from observing the remarkable group of glaucomatous cases under Horner (of which one has been related), made experiments, from which he concluded that the augmentation of intra-ocular pressure in glaucoma was a phenomenon dependent upon the sympathetic, which was irritated by reflection from the trigeminus. But the researches of Hippel and Grunhagen, especially their latest,[24] give a different explanation, excluding the sympathetic; they found that irritation of the medulla oblongata, in the neighborhood of the trigeminus root, produced a lasting and very pronounced augmentation of intra-ocular blood-pressure, an effect which, they remark, could not depend on irritation of the vaso-motor centre, since that must produce contraction of the vessels and lowering of the blood-pressure. They conclude that "the trigeminus contains specific fibres which possess the property of actively dilating the blood-vessels of the eye;" and in reference to the secretion of the fluid humors of the eye, they conclude also that "the trigeminus also plays the part of an (active) nerve of secretion."

Of these conflicting opinions I can have no difficulty in at any rate rejecting that of Wegner; for the clinical phenomena of the complications attending trigeminal neuralgia, such as they are described in my last chapter (and could have been described at much greater length), seem to me utterly to exclude vaso-motor spasm except as a temporary phenomenon at the commencement of the attacks of acute pain. Vaso-motor palsy undoubtedly is very often present, in fact every attack of neuralgia of a certain severity is thus complicated; and there is no reason to doubt that this paralysis could be caused by lesions within the medulla. Are we, then, to admit functions of active dilatation of vessels, and active impulse to secretion in certain fibres of the fifth? It is necessary at any rate to clear the ground in one respect: it must not be supposed that I for a moment entertain the idea that there can be direct active dilatation, _i. e._, that there can be any system of muscular fibres (and nerve-fibres stimulating them) whose office is to open the calibre of the vessels; the idea is wildly improbable--in fact almost inconceivable by any one who reflects on the necessary machinery--and there is not a single observed anatomical fact to give it support. If, then, I speak of the possibility of "active" dilatation, it must be understood that I refer to a theory of "inhibition," which supposes certain fibres to be gifted with the power of paralyzing or inhibiting the vaso-motor nerves. It is my duty to speak with all reasonable reserve on that most difficult _quæstio vexata_, the existence of special inhibiting systems of nerves, and the extent to which a double series of opposed nervous actions is generalized in the body; but it is impossible to avoid the subject altogether, and I offer the following remarks, with deference, to our professional physiologists. The strongest instances of the apparent inhibiting action are probably afforded by the _nervi erigentes_, as shown by Loven, the cardiac depressor, by Ludwig and Cyon, and the splanchnics (upon the intestine), by Pfluger. But there is not a single one of these examples that has not been challenged by experimenters of repute. Thus the theory of the distinctive restraint-action of the splanchnics upon the intestine, and of the vagus upon the heart, has been especially controverted by Piotrowski, who, indeed, rejects the whole theory of special inhibitory nerves.[25] And, from another point of view, Mr. Lister long ago attacked the views of Pfluger, maintaining that it was possible to produce exactly opposite effects through the medium of the very same nerves, according as the experimental irritation applied to them was weak or strong. To Dr. Handfield Jones[26] this seems a still unanswerable objection to the inhibitory theory. And in the remarkably able and judicial summary of the "Physiology and Pathology of the Sympathetic or Ganglionic System,"[27] by Dr. Robert T. Edes, a less decided but still tolerably strong acquiescence is given to Mr. Lister's criticisms of this theory. Personally, I must express very strongly the distrust (which is probably felt by many others) of doctrines which assert an exact opposition between the functions of any two nerves, on the basis of an observation that the same apparent effects may be produced by section of the one and galvanization of the other; both processes seem far too pathological, and too remote from the conditions of ordinary vitality, to admit of any such absolute deductions from their results.

In the present state of our information I am inclined to explain all the congestive complications of trigeminal neuralgia on the basis of vaso-motor paralysis. And I further believe that the cause of that paralysis is a direct extension of the original morbid process from the sensory root to the motor, affecting the origin of fibres in the latter, which are destined to govern the calibre as ocular and facial vessels. These fibres I suppose it is that Meissner succeeded in dividing when he partially cut the trigeminus, and got nutritive and vascular changes without anæsthesia.

There must be more than this, however, to account for the whole of the trophic phenomena; for there is a great body of evidence to show that mere vaso-motor paralysis does not produce any phenomena of such an actively morbid kind as those we are endeavoring to explain. The phenomena on the side of secretion might indeed be possibly explained by vaso-motor paralysis. [It must be remembered that I am speaking of such augmented secretion as is seen in neuralgia. I agree with Prof. Rutherford (Lectures on Experimental Physiology, Lancet, April 29, 1871) that it is difficult thus to explain the effects of galvanization of the chorda tympani on the submaxillary gland.] Consisting as they do (a), in the great majority of cases, of a mere outpour of what seems little more than the aqueous part of the secretion, and (b) in a few cases of arrested secretion, a phenomenon otherwise by no means unfamiliar as the result of sudden, passive engorgement of glands. But the mere cessation of vaso-motion will not account for such facts as the rapid and simultaneous development of erysipelatous inflammation, of corneal clouding and ulceration, of iritis and glaucoma, of nutrition-changes in hair and mucous membrane. I must, for the present, be content to believe it probable that there is a special set of efferent fibres in the trigeminus, emanating from the motor-root, whose office it is in some unknown way to preside over the equilibrium of molecular forces in the tissues to which the nerve is distributed; trophic nerves, in fact, though not active dilators of blood-vessels.

It seems to me that, without enlarging further on this almost endless topic, I should be justified in assuming that I had shown the very high probability that the common starting-point both of the neuralgia and of its vaso-motor secretory, and trophic complications, was in the sensory root of the trigeminus. But the argument is greatly strengthened when we consider the fact that loss of peripheral common, and also tactile sensation, to a greater or less degree, is constantly observed to occur simultaneously with the pain and with the other complications. When we observe a patient suffering from racking supra-orbital and ocular neuralgia, and discover that at the very same period the skin round the eye is markedly insensitive to impressions, except in the _points douloureux_, what can we rationally suppose, except that both pain and insensibility are the result of one and the same influence, which radiates from the sensory centre?

Nor are we likely to reach a different conclusion, if we test the matter by the consideration of a rarer, but still sufficiently common kind of case, such as I have described in Chapter I., in which a very strong peripheral influence (traumatic) produces neuralgia, accompanied by vaso-motor and secretory phenomena, and by anæsthesia, but not in the district of the painful nerve, but in the territory of a quite different nerve. How can we doubt, in the case, _e. g._, of a trigeminal neuralgia thus complicated, the exciting cause of which was a wound of the ulnar nerve, that the morbid influence, traveling inward from the lesion, would have passed without any special consequences (as happens in thousands of such nerve-wounds), had it not, in its passage along the medulla, encountered a _locus minoris resistentiæ_ in the roots of the trigeminus? It seems impossible to account for the phenomena on any other theory. [Eulenburg says, in reference to my reported cases of the kind: "_Solche Falle begunstigen in hohem Grade die Annahme pradisponirender Momente, die in der ursprunglich schwacheren Organisation einzelner Abschnitte des centralen Nerven-apparates beruhen._" _Op. cit._, p. 56.]

It is necessary, in the next place, to consider a very important question, how far irritation can pass over from one nerve to another, without reflection through a spinal centre, solely in virtue of a connection through the medium of a nervous plexus. The case which apparently presents such phenomena in the most unmistakable way is that of _angina pectoris_.

The site to which the essential heart-pain is referred in this disease is probably the cardiac, or this and the aortic plexus; in a comparatively small number of cases the pain does not extend farther. But much more frequently it spreads in various directions, and we have to account for its presence (_a_) in intercostal nerves, (_b_) cervical nerves, (_c_) nerves springing from the brachial plexus.

Before we inquire into the mechanism by which this extension of the pain takes place, we ought in strictness to ask ourselves whether the essential heart-pain is felt only in the spinal sensory branches, or whether the sympathetic fibres are themselves capable of feeling pain. The latter supposition, notwithstanding all that has been argued in its favor from the supposed analogies of the pain of colic, gall-stone, etc., seems to me very doubtful. It would appear more probable that both the latter pains, and also those of angina, are really connected with branches either of the vagus or of other spinal nerves. And there is no need to invoke the sympathetic as a sensory nerve, to account either for the essential heart-pain of angina, or for its extension into arm, chest-wall, and neck. For the plexus cardiacus receives spinal branches, both from the vagus and also (through the medium of the sympathetic ganglia of the neck) from the whole length of the cervical and the uppermost part of the dorsal cord-centres. And, in this way, it would seem quite possible intelligibly to account for the pain radiating into intercostal, cervical, and brachial nerves, merely by extension of a morbid process essentially seated in the cord. Usually, however, one sees it explained not in this way, but by the inter-communications that exist outside the spine, between the branches from the cervical ganglia and the lower cervical and upper dorsal nerves; and the pain in the arm is especially explained by the connection (outside the spinal canal) of the inferior cervical ganglion, on the one hand with the lower cervical nerves, which go to the brachial plexus, and, on the other hand, with the heart itself. There remains to be explained, however, the singular tendency of the arm-pain to be one-sided (this happens in at least four cases out of five); and this explanation seems to me insuperably difficult, on the theory that the transference of morbid action to the brachial nerves takes place through external anastomoses. It appears greatly more probable that angina is essentially a mainly unilateral morbid condition of the lower cervical and upper dorsal portion of the cord; liable of course to be seriously aggravated by such peripheral sources of irritation as would be furnished by diseases of the heart, and especially by diseases of the coronary arteries; the latter affection probably involving constant mechanical irritation of the cardiac and the aortic plexuses. It is noteworthy that the arm-pain is sometimes (I do not know how often) accompanied by vaso-motor paralysis in the limb; this phenomenon could also certainly be more easily accounted for on the supposition of radiation from a spinal vaso-motor centre (to which the morbid process had extended from a posterior nerve-root) than on that of communication between painful sensory nerves and vaso-motor nerves; through either of the plexuses independently of the spinal centres.

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

From the varied considerations which have now been adduced, the reader, unless I altogether miscalculate the value of the facts, will probably have arrived at the following conclusions: (1) That the assumption of a positive material centric change as the essential morbid event in neuralgia is almost forced upon us; (2) that, whereas the morbid process, if centric, 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 assumption of this locality will explain, as no other theory could explain, the singular variety of complications (all of them nearly always unilateral, and on the same side as the pain) which are apt to group themselves around a neuralgia; and some of which are very seldom absent in neuralgia of any considerable severity. To this we may certainly add that it is extremely probable that the vast majority of neuralgic patients inherit the tendency to this localized centric change; in support of this we may finally mention two considerations derived from the sex and the ages most favorable to neuralgia. Eulenburg saw a hundred and six cases of neuralgia of all kinds, of which seventy-six were in women and only thirty in men; my own experience is very similar; namely, sixty-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 circumstances which surround the patient's life.

Having thus decidedly expressed my belief in the essential material participation of the nerve-centre in neuralgia, it remains for me to discuss two points: first, as to the character of the material change in the nerve-root, and next, as to the extent to which mere peripheral influence, without special inherited tendencies, may suffice to set this process going.

The morbid change in the nerve-centre is probably, in the vast majority of cases, an interstitial atrophy, tending either to recovery, or to the gradual establishment of gray degeneration, or yellow atrophy, of considerable portions of the whole of the posterior root, and the commencement of the sensory trunk as far as the ganglion.

It is probable, however, that in a certain number of cases, the atrophic stage may be preceded by a process of genuine inflammation, and that this inflammation is centripetally produced in consequence of inflammations of peripheral portions of the nerve. The considerations which make this probable are chiefly derived from the analysis of cases in which a more or less chronic, but severe, visceral disorder has been followed by so-called reflex paralysis, but in which neuralgic phenomena, have been conspicuous. In reference to this subject I recommend to the reader's attention the very interesting paper on "Reflex Paralyses" by Prof. Leyden, of Konigsberg.[28] He is immediately commenting upon a case in which dysenteric affection of the bowel were followed by the symptoms of myelitis, attended with febrile exacerbations, and also with severe pains in the region of the sacrum, in the course of the dorsal intercostal nerves of the right side, and in the knees, and semi-paralytic weakness of the lower extremities, and with pains between the shoulder-blades and the left arm. Leyden discusses the doctrine of reflex paralyses in general, starting 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 Hasse, then by Pfuger, and other professors of the inhibitory doctrine; by Brown-Sequard (in his well-known, and now very generally discredited, theory of spasm of the vessels in the nervous centres), by Jaccoud in the "Erschopfung" (exhaustion) theory, down to the more careful and reliable researches of Levisson on the temporary reflected paralyses induced by experimental squeezing of the kidney or uterus of animals; and then gives the history of the more recent doctrine of a positive material change in the cord centripetally introduced. Gull[29] (1856) may be said to have inaugurated the new doctrine of a morbid process transmitted along the pelvic nerves to the cord, and causing material changes there. Remak,[30] on the other hand, suggested a material change operating in the opposite direction; _a neuritis descendens_, starting in the very nerves (within the pelvis) which showed the paralysis in the extremities. The symptoms are supposed by him to be distinctive, inasmuch as there is both violent pain in the nerves of the soles of the feet, and also tenderness of the same. On the other hand, Remak said that myelitis, with neuritis, might be the origin of paraplegia and simultaneous palsy of bladder and rectum. The theory of neuritis descendens was supported by Kussmaul,[31] in the record of a case where disease of the bladder was complicated with pelvic inflammation, atheromatous degeneration of the arteries, and consequent fatty degeneration of the sciatic nerves, causing direct paraplegia. We return to the centripetal theory of urinary paralysis with Leyden's own cases, published in 1865; of three patients with urinary paraplegia, two died, and the existence of a secondary (centripetal) myelitis seems to have been established, and by all analogy it must have existed in the third case, which recovered. The only puzzle and doubt that ensued was caused by the fact that there was an absence of neuritis in the different nerves themselves; though it seemed plain that the starting point of the myelitis was at the entrance of these nerves into the cord. This mystery seemed to be cleared up by the important experiments of Tiesler, ("Ueber Neuritis" Konigsberg, 1860) a pupil of Leyden's. This observer excited local traumatic inflammation in the sciatic nerve of rabbits and dogs; the rabbit became paraplegic and died three days afterward. At the site of the artificial irritation there was a localized formation of pus, and there was a second similar formation within the vertebral canal at the point where the 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, analogous to those which produce urinary paraplegia, are at all frequently the cause of the changes in the posterior roots which produce true neuralgia; for of course an inflammation may be the beginning of an atrophy which may presently exhibit no distinction whatever from one of which the origin was altogether non-inflammatory. I think that there is strong reason for thinking that this is not at all frequently the case. In the first place, all the evidence that exists respecting these centripetal inflammations of the cord is opposed to the idea that, save in the rarest instances, the inflammatory process limits itself to one small segment of the cord. Secondly, the description of the pains that have usually accompanied such inflammations of the cord is considerably different from the strictly localized, frankly intermittent character of a true neuralgia; in fact, all we know of the history of myelitis (except when complicated with a large amount of meningitis) forbids us to suppose that severe pain would be an immediate symptom. But, thirdly, a far more important objection to the theory of an origin in localized centripetal myelitis, the result of a neuritis migrans, is the rarity of motor paralysis as an early symptom, instead of which we ought to find a very distinct history of decided paralysis (much more decided than those secondary paralyses which actually do occur in some neuralgias) of the muscles supplied by the anterior roots of the painful nerve, in every case in which such a peripheral origin could be assumed. Again, the totally feverless commencement of neuralgias, a character which is maintained throughout the progress of the milder cases, is entirely opposed to the idea of a direct connection between myelitis and neuralgia. The superficial appearance of pyrexia is sometimes given by a local vaso-motor paralysis, which makes the neuralgic part, after a long bout of pain, hot and red; but of general pyrexia there is nothing.

Taking every thing into consideration, one is inclined to say that there is a probability that in a very limited number of cases peripheral irritation does cause actual limited myelitis, which escapes recognition at the time, but which issues in an atrophy, the subjective expression of which is 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 practitioners of large experience who have not seen a patient or two in whom the concurrence of some unfortunate psychical with some other noxious peripheral influence, the whole taking place at some critical period of life (especially in the years between puberty and marriage), seems to have totally deranged the general balance of nervous forces, and induced morbid susceptibilities and morbid tendencies to some particular neurosis. It is a comparatively frequent thing, for example, to see an unsocial solitary life (leading to the habit of masturbation), joined with the bad influence of an unhealthy ambition, prompting to premature and false work in literature and art. The bad peripheral influence of constant fatigue of the eyes in study may so completely modify a young man's constitution as to make a wreck of him in a very few years, changing him from the state of habitual and conscious health to that of chronic neurosis of one sort or another. And, though it is doubtless on persons with congenital tendencies to nervous diseases that such a combination of bad influences produces its most serious effects, yet there unquestionably are a few persons in whom they appear to entirely generate the neurotic constitution. I have already touched upon the part that misdirected psychical influences, especially religious and other forms of emotional excitement, may play in this unfortunate perversion of the natural and healthy nervous functions, more especially in youth; and need only add, here, that perhaps the most fatal combination of all the bad influences is the melancholy union of highly-strained religious sentiment with peripheral sexual irritation, which is, unfortunately, a too common phenomenon under certain systems of education. The most frequent neurotic consequences of the class of influences which have now been referred to are probably neuralgia--in the form either of migraine, of nervous angina, or of sciatica--or else asthma.

But, if the combination of several such centripetal influences may generate the neurosis unaided, even a single one of them operating powerfully for a long period may produce most serious consequences in those who are hereditarily predisposed. The influence of prolonged fatigue of the eyesight, independently of any special intellectual or emotional strain, was strongly illustrated in my own case about three years ago. I was then engaged upon a piece of scientific writing which demanded no great intellectual effort, but was being done against time, and by working, night after night, many hours by gas-light. My neuralgic (trigeminal) attacks came on with great severity, accompanied by vertiginous sensations of so alarming a kind as to make me fear the invasion of some serious brain-mischief. I broke off all work, and went to the sea-side, but was greatly disappointed to find, for the first few days, that the symptoms were not in the least mitigated. The mystery was soon explained. The weather had been such as to confine me a good deal to the house, and, thinking it would do no harm, I amused myself with reading newspapers and novels. At last I suspected that the use of my eyes in reading was altogether mischievous; I desisted from reading any thing, and in forty-eight hours every symptom had vanished.

Among peripheral influences of a more mechanical kind there is one cause of neuralgia, the force of which has been variously estimated, but which some authors rate as very important, viz.: the influence of the pressure, and especially of the varying pressure, of blood-vessels, or other hollow viscera, upon the trunks of the nerves. We must set aside one such action which is undoubtedly very powerful, as essentially differing from the others; I mean the pressure of dilated blood-vessels, especially aneurisms, when this happens to be exerted upon the ganglion of the sensory trunk. Here there can be no doubt of the mischief; for the pressure, if at all severe, gradually destroys the life of the ganglion, upon which, as was proved by Waller, the nutrition of the posterior nerve-root hangs with very intimate dependence, and the pulsations of the vessel seem greatly to aggravate both the irritation and the centripetal tendency to atrophy. In short, it is plain that such lesion of a ganglion may be the whole 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 cumulative proof; every link must be weighed and tested, before the remarkable strength of the chain can be felt. And it may fairly be said that, if the proof of a definite kind of material change in a definite organ, as the essential factor in neuralgia, has been established upon reasonable grounds, an important step has been taken toward removing a serious opprobrium and difficulty in practical medicine. Although the true neuralgias are not among the most frequent of human diseases, they form a class of enormous practical importance, for they are sufficiently common to be sure to occur in considerable numbers in the practice of every medical man, and, both from the suffering which they inflict, and the rebelliousness which they often show to treatment, they are among the gravest sources of anxiety which the practitioner is likely to encounter. There are probably few disorders which so often occasion mortification and loss of professional credit to the physician. The helplessness which men, who do not enjoy special opportunities of seeing those diseases with frequency, so often show in dealing with them, is largely caused by the extreme timidity and vagueness with which the standard treatises on medicine deal with the question of their pathology; and a very unfair advantage has thus been given to the specialists, who, by the mere force of opportunity, and continual blind "pegging away" in an entirely empiric manner, have acquired a certain rude skill in the treatment of these maladies which enables them to outshine practitioners who often have far more in them of the 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 mass of unmeaning phrases about "mysterious functional affections" and the like, must be a distinct gain to practitioners of plain common-sense and good general knowledge, to whom neuralgia is merely one of a vast number of different diseases among which their attention and study are divided. And I hope that, in the further remarks on Diagnosis, Prognosis, and Treatment, yet to be made, the value of clear pathological ideas of disease will be brought more practically and clearly into view. [The reader will find, at the end of Part I. of this volume, a note which contains a brief discussion on the "Erschopfung" theory of Jaccoud, and the doctrines of Dr. Handfield Jones respecting inhibition, with which I thought it best not to encumber the text of the present chapter.]

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.

[19] _Journal de la Physiologie, v._

[20] "Ernährungsstörungen der Augen bei Anæsthesie des Trigeminus." Mitgetheilt von Dr. v. Hippel in Konigsberg in Preussen. Archiv f. Ophthalm. Band. xiii.

[21] Zeitsch. f. rat. Med., 1867. There is corroborative evidence, from independent sources, of the truth of Meissner's views. His own observation only proved half the case; but he quotes an observation of Buttman's in which the exact converse of his own experience happened, the external fibres being affected without the inner band, and anæsthesia without trophic changes being the result. Moreover, Schiff (Gaz. hebdom., 1867) obtained experimental results (in operating on cats and rabbits) which coincide with Meissner's.

[22] London Hospital Reports, vol. iii., p. 305.

[23] Wegner, loc. cit.

[24] Archiv f. Ophthalm., xv., 1.

[25] "Deutsches Archiv f. klin. Med.," ii., 2, 1866. I am not aware whether Piotrowski has at all altered his opinions since the (subsequent) observations of Ludwig and Cyon upon the "depressor" nerve.

[26] "Functional Nervous Disorders." Churchill, 2d edit., 1870.

[27] "Prize Essay of the New York Academy of Medicine." New York: Wood & Co., 1869.

[28] Volkmann's Sammlung klinischer Vortrage, No. 2. "Ueber Reflex Lahmungen," von E. Leyden. Leipzig, 1870.

[29] "Cases of Urinary Paraplegia," Med.-Chir. Trans., 1856.

[30] Wurzburg. Med. Zeitsch., iv., 56-64.

[31] Med. Cent. Ztg. 21, 1860.