Part 13 (1/2)

In the present transitional state of opinion concerning the mode in which the phenomena are produced that are popularly known under the name of ”reflex paralysis,” I cannot pa.s.s without notice the doctrines of these two observers. The reader will have perceived that, as regards the secondary paralytic symptoms observed in neuralgias, I explain the phenomena mainly on the theory of a process which is central, and not peripheral, in origin. And, even where, as in some few instances, it seems possible that the starting-point was an organic affection of some viscus, we must always consider the possibility that the link between this and the neuralgia and paralyses was a neuritis migrans travelling inward to the sensory centre, and from that pa.s.sing over to motor centres and thus producing paralysis; or that, without the intervention of any truly inflammatory process, the continual impressions streaming in upon the cord from the original seat of organic disease may damage the nutrition of the sensory nerve-root, producing a partial atrophy, and that this process may extend to the motor root.

It remains, however, to inquire whether the influence of powerful peripheral agencies may not, in a purely ”functional” manner, disable the nerve-centres for a time, causing paralysis with or without neuralgia. The main supporters of such a doctrine are Dr. Handfield Jones[46] and M. Jaccoud.[47]

Dr. Handfield Jones expressly rejects the theory of Brown-Sequard, as to spasm of the vessels in the nerve-centres, and we need not repeat his arguments on that head, because it seems to be generally felt that the vascular spasm theory will not account for the facts. Jones believes that the state produced in the nerve-centre by the peripheral influence is one of paresis from shock-depression, and that from the sensory centre this state can communicate itself to motor and vaso-motor centres, though commissural fibres. He does not believe in the existence of a special inhibitory portion of the nervous system: he believes that an impression may prove stimulating when it is mild, or paralyzing when it is strong; and that any afferent nerve may convey either the one influence or the other to the centres and thus produce secondary stimulus or secondary paralyses in various efferent nerves. Jones has the distinguished merit of being one of the first authors distinctly to perceive that pain must rank on the same level with paralysis: hence he sees nothing unintelligible in the communication of paralysis to a motor centre from a sensory centre that was in the state which the mind interprets as pain.

The _theorie d'epuis.e.m.e.nt_ of Jaccoud (Erschopfungs-theoric) also denies the possibility of Brown-Sequard's idea of prolonged spasm of the vessels of the centres. It imagines that powerful peripheral excitements exhaust the irritability of the nerve, and through that of the centres, and induce a state of unimpressibility--a.n.a.logous to that which exists in a nerve or nerve-centre, which is included in the circuit of a constant current. The nervous force is wasted, and, until an opportunity of repose is afforded to the centre, the faculty of impressibility cannot again revive.

I must say that of these two theories I decidedly incline to that of Handfield Jones (though I imagine that in reality the cases are extremely rare, if there be any, in which the change in the centres is really only functional and non-organic), I prefer the idea of paralyzing shock to that of exhaustion from over-excitement, from a consideration of the nature of that form of peripheral influence which has been specially mentioned by authors as competent to produce this sort of ”reflex” affections, namely, intense and persistent cold. It seems to me a mere abuse of words to speak of this as an agent that could exhaust the nerve by over-stimulation; it must surely exhaust it in a much more direct manner than this, namely by the direct physical agency of withdrawing heat from the nerve, and spoiling its physical texture, _pro tanto_. If such an effect as that which must thus be produced on the nerve, and through it on the centre, is to be looked on as a case of over-stimulated function, then, it seems to me, there is no meaning in language, and no possibility of attaining to clear ideas on the subject of nervous influence.

NOTE III.

a.r.s.eNICAL TREATMENT OF VISCERALGIae.

Since writing the above chapter on the Treatment of Neuralgia, I have had two fresh and very striking examples, in private practice, of the power of a.r.s.enic to break the morbid chain of nervous actions in angina pectoris.

The first example was that of a medical man, aged seventy-five, in whom a neuralgia, originally malarial in origin, and of some years' duration, had fixed itself for some time in the fifth and sixth left intercostal s.p.a.ces, and of late had become complicated with anginoid attacks of an unmistakable character, though not of the highest degree of severity.

The case certainly seemed very unpromising, looking at the patient's age and the consequent high probability that there was much arterial degeneration. However, the use of Fowler's solution (five minims three times a day) was commenced and steadily pushed. The anginoid attacks rapidly diminished in frequency and at the end of ten days' time were entirely gone, and after one month of treatment he still had no return of them, although they had previously been of daily occurrence. It is a curious fact, whether a mere coincidence or not I cannot say, that, some few days after the anginoid attacks ceased, he began to experience somewhat severe pains, rheumatic in feeling, but unattended with heat or swelling, in the elbows, wrists, and fingers, symmetrically. This has nearly disappeared, but he is still free from angina. There is no discoverable heart-lesion in this patient.

The other case was that of a fine old man of sixty-four, who, but for some few slight attacks of gout, a few small calculi, and a troublesome prostatic affection, had always enjoyed remarkably good health, until about five months ago, when he began to notice tightness across the chest, etc., when he walked uphill. About a fortnight before he came to me, he was seized with very violent and alarming paroxysms of pain across the chest and running down both arms, extreme intermittence of pulse, and a sense of impending dissolution. The attack had recurred daily, at the same hour (6 P. M.), ever since; besides which there was an abiding sense of uneasiness in the cardiac region, and a consciousness that the least excitement or exertion would bring on the paroxysm. I put the patient on five minims of Fowler, three times a day, with directions to take ether when the paroxysms came. At the end of the first week there was already much improvement, the paroxysms having been both less frequent and less severe. At the end of a fortnight's treatment he reported that there had been nothing like a paroxysm for the last eight days, although there was still a good deal of uneasiness from time to time. The hour at which the attack was expected pa.s.sed by absolutely without a trace of angina. It remains to be seen how long this improvement will last, but the altered state of things, and particularly the suddenness of the change, cannot be overlooked, and has very much struck the patient himself. It is now six weeks since he had any paroxysm.

It becomes more and more apparent that a.r.s.enic is generally applicable to neuroses of the vagus. In asthma, I have long held it to be the most powerful prophylactic tonic that we possess. It is also an excellent remedy in gastralgia; although I have rather dwelt (in the text of this work) on the action of strychnia in this disease, I would not omit my testimony to a.r.s.enic. Dr. Leared has related some exceedingly interesting cases bearing on this point. (See _British Medical Journal_, November 23 and 30, 1867.)

NOTE IV.

INFLUENCE OF GALVANISM ON CUTANEOUS PIGMENT.

Dr. Reynolds pointed out to me the exceedingly curious fact, which I have several times verified, that the constant current, in relieving facial neuralgia, not unfrequently disperses, almost instantaneously, the brown skin-pigment that has collected in the painful region; _e. g._, near the orbit.

NOTE V.

THE ACTUAL CAUTERY.

A remedy for inveterate neuralgia which of late years I had almost discarded--the actual cautery--has quite recently yielded me very good palliative results in two cases. Its omission from the text of the chapter on Treatment was an accident due to the effect of habit in making one, half unconsciously, reckon this remedy as a ”counter-irritant.” The longer I practise, however, the more decidedly I am convinced that the actual cautery, if properly applied, does not act as an irritant at all; and this fact was sufficiently in my mind, when writing of irritant remedies, to make me omit the cautery from that section. I should have inserted it under the heading of remedies that interrupt the conductivity of nerves, and thus give the centres temporary rest. The only useful way to apply it is, to make an iron white hot, and very lightly brush the skin over so as to make an eschar not followed by suppuration. The galvano-cautery (Stohrer's Bunsen) is the best for the purpose, but I have made the flat-iron cautery serve very well.

FOOTNOTES:

[35] Art. ”Neuralgia” (”Reynolds's System of Medicine,” vol. ii. 1868.)

[36] Pract.i.tioner, vol. iv., 1870.

[37] Berlin. klin. Wochensch., 1865.

[38] In a paper on the ”Hypodermic Use of Remedies,” in the _Pract.i.tioner_ of July, 1868, I gave the reasons for this opinion in full; and I see no reason to alter any thing I then said.

[39] Pract.i.tioner, vol. iv.