CHAP, in.] SIGHT. 1181 



j t 



balance of evidence seems to be against the existence of a distinct 

 radial dilator muscle. 



Whatever be the view adopted as to the exact mode of action 

 of the sympathetic there remains the broad fact that the pupil is 

 under the dominion of two antagonistic mechanisms : one a con- 

 stricting mechanism, reflex in nature, the third nerve serving as 

 the efferent, and the optic as the afferent tract; the other a 

 dilating mechanism, apparently tonic in nature, but subject to 

 augmentation from various causes, and of this the cervical sym- 

 pathetic is the efferent channel. Hence, when the third or optic 

 nerve is divided, not only do constricting impulses cease to be 

 manifest, but the effect of their absence is increased, on account 

 of the tonic dilating influence of the sympathetic being left 

 free to work. When, on the other hand, the sympathetic is 

 divided, this tonic dilating influence falls away, and constriction 

 results. When the optic or third nerve is stimulated, the dilating 

 effect of the sympathetic is overcome, and constriction results ; 

 and when the sympathetic is stimulated, any constricting influence 

 of the third nerve which may be present is overcome, and dilation 

 ensues. 



The former, optic oculo-motor mechanism is the instrument 

 by means of which the pupil is adapted to. the amount of light, 

 the latter, sympathetic mechanism appears to be employed when 

 other influences are brought to bear on the pupil. Thus the 

 characteristic pupil-dilating effects of emotions such as fear, of 

 the painful stimulation of sensory nerves, of dyspnoea, and in 

 part of some drugs, appear to be carried out through the sym- 

 pathetic mechanism. 



729. In the case of many drugs, however, the effect produced 

 is either in part or wholly independent of both these nervous 

 mechanisms. A small quantity of atropin introduced into the 

 system, or even directly into the eye, causes a dilation of the pupil 

 which may be so great that the iris is reduced to a mere rim, 

 while physostigmin (eserin) similarly introduced into the system 

 or eye produces a constriction of the pupil which may be so great 

 that the pupil is narrowed to a mere pin's point. Since both these 

 drugs may produce their full effects after division of the optic- 

 oculo-motor and the sympathetic nerves, and indeed may produce 

 their effects in an extirpated eyeball, it is obvious that those 

 effects are not due to the drugs acting on the central parts of the 

 above mechanisms. Their action is a local one. They do not 

 act by means of the ciliary ganglion, for both drugs continue to 

 produce their effects to a most marked degree after the ganglion 

 has been excised. Nor have we any evidence that their action 

 is dependent on any other local nervous mechanism, such as 

 might be afforded by the nerve cells lying in the choroid or even 

 in the iris. They appear to act directly on the sphincter, 

 atropin paralyzing it or producing relaxation, and physostigmin 



