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?