Neuralgia and the diseases that resemble it

by Francis Edmund Anstie

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.