Neuralgia and the diseases that resemble it

by Francis Edmund Anstie

NOTE II.

THE INHIBITION THEORIES OF HANDFIELD JONES AND JACCOUD.

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 pass 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 passing 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'epuisement 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—analogous 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.

ARSENICAL TREATMENT OF VISCERALGIÆ.

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 arsenic to break the morbid chain of nervous actions in angina pectoris.