Tics and Their Treatment

by Henry Meige; E. Feindel

An interesting case (says Brissaud), and one that is everywhere quoted, is reported by Schultz, in which an aneurism of the vertebral artery, at the point where the basilar arises, compressed the trunk of the left facial nerve, and occasioned a "tic" of ten years' duration. As a matter of fact, one could not have a better example of spasm pure and simple.

Féré[43] cites the following incident in support of the contention that encephalic trauma may engender a tic:

A man in falling on his head sustained an injury to the cranial vault over the posterior section of the left parietal bone, at a spot exactly corresponding to the posterior part of the angular gyrus, and immediately became afflicted with a convulsive tic of the zygomatics and orbicularis palpebrarum on the right. Conformably to Ferrier's experimental localisation of the motor centre for the eye muscles and lids in the angular gyrus, irritation of this centre by the cranial injury was the diagnosis made.

The proffered interpretation of the motor phenomena by cortical excitation is entirely justifiable, but no convulsion consecutive to traumatism can ever pass muster as a tic.

A no less frequently quoted experiment of Gilbert, Cadiot, and Roger,[44] supposed to confirm certain results obtained by Nothnagel, is now a standard case in the history of tic hypotheses. The animal in question was a dog affected with spasmodic twitches of the ear, which the successive removal of cortical facial centre, internal capsule, corpora striata, and cerebellum, signally failed to alleviate, and which disappeared only with the destruction of the corresponding nucleus in the pons. Their inability to find any anatomical change determined the experimenters in favour of the view that the trouble was functional, and they described it as a tic.

It would be foolhardy to deny the existence of a lesion on the ground that it was not discovered. Negative findings of this sort are valueless. The sole conclusion to draw from the incident is the all-important rôle played by the bulbar centres in the production of convulsive movements, which are in such circumstances, of course, nought else than spasms.

Compression of cranial nerves by tumours or aneurisms of the base has been the cause of symptoms imagined to be identical with those of tic. The case of intracranial neoplasm mentioned by Oppenheim, in which irritation of the upper branch of the trigeminal was accompanied by homolateral facial contraction, is wholly comparable to the so-called "tic douloureux."

No less positive is our refusal to accept as tics spasmodic contractions in association with or subsequent to facial palsy or contracture of peripheral or central origin. They are spasms, not tics. Cruchet, for instance, describes indifferently as labial tic or intermittent labial hemispasm clonic elevation or depression of the oral aperture developing in central facial paralysis, especially in children. As example he refers to the case of a child in whom an ictus at the age of three years was followed by a typical spastic hemiplegia on the left side, with athetoido-choreic movements chiefly in the arm.

At first the left side of the face was flaccid and deviated in the other direction, but at the time of examination it presented no unusual feature beyond a continual twitching, a real convulsive tic, of the upper lip.

Now, whatever a facial convulsion of apoplectic origin, secondary to facial palsy and accompanied with spastic hemiplegia and athetosis, may be, it is at all events no tic.