For our part, we cannot apply the word tic to the convulsive phenomena of tuberculous meningitis. If localised spasms occurring in the course of a grave illness, associated with fever, headache, and delirium, with contractures and generalised convulsions, and if the spasmodic manifestations of rapidly fatal pyrexias, are all to be denominated tics, then the term has no longer any significance, and it would be wiser to give it at once its quietus.
We are well enough aware that Cruchet believes there is a "convulsive tic symptom"; in other words, certain symptoms in such and such a disease appear in the guise of convulsive tic, "a movement or combination of movements representing in a clonic fashion a physiological act." Nevertheless, we are not convinced that the convulsive movements of Cruchet's patients exhibit the sequence of "regulated physiological acts."
He further draws an analogy between the foregoing case and the partial convulsions of toxæmias, cerebral tumours, etc., "transient convulsions supervening in the course of acute or chronic affections, and readily recognisable." In exceptional circumstances they may "assume the form of convulsive tic." In strict truth the form may be the same, but examination of the patient will soon demonstrate that the two are alike merely in appearance, and compel the reconsideration of an immature diagnosis.
Our position is that tic is more than a symptom—it is a symptom-complex. Cruchet's definition of convulsive tic just quoted is by itself insufficient; the additional and indispensable factor is the characteristic mental defect, of which so illuminating an exposition was given by Charcot.
Finally, the knowledge derived from the pathological investigation of myoclonus and polyclonus does not of necessity throw light on the morbid anatomy of tic.
In the case of an epileptic who suffered from myoclonus in his last years, ischæmic degenerations were found by Rossi and Gonzales disseminated throughout the brain, especially in the rolandic area, but any inference to hold good for the tics would be premature.
The term polyclonus has been employed by Murri to designate a succession of clonic contractions of the limbs, due to the existence of punctiform hæmorrhages or areas of softening scattered throughout the rolandic cortex. The character of the motor reaction in these cases, however, bears no resemblance either to tic or to chorea, although the fact of the relation between diffuse cortical lesions and convulsive movements is calculated to enhance the difficulties of diagnosis.
Vincenzo Patella[48] has recently called attention to a case of polyclonus in which the disappearance of the symptoms during sleep suggested their purely functional origin, but histological examination of the rolandic grey matter at a subsequent period revealed the presence of numerous foci of degeneration. We are as yet, however, far from grasping the real meaning of such symptoms, which, moreover, from the clinical standpoint, cannot always be assimilated to those of the tics. Conclusive anatomical information is therefore still being awaited.
The functional nature of the movements we have had under discussion is unfortunately an obstacle in the way of our early knowledge of their pathology. As long as we remain ignorant of the actual cause of the neuroses and psychoses, so long will the pathological anatomy of tic continue a sealed book. All that has been written on this topic hitherto really concerns spasm and other convulsive affections secondary to irritation of nerve centres or conductors. If we may venture to express an opinion, it is that we should not be surprised if post-mortem examination rest constantly negative. As a matter of fact, we do not favour the view that the phenomena depend on an acquired lesion; rather are we inclined to believe that they represent some congenital anomaly, some arrest or defect in the development of cortical association paths or subcortical anastomoses, minute teratological malformations that our medical knowledge is still unhappily powerless to appreciate.