According to the classical description,* the Argyll Robertson syndrome is characterized by the following essential features: (1) the absence or diminution of the pupillary reflex to light; (2) an active or hyperactive pupillary contraction to near vision, and (3) the presence of miosis.
The cause of the miosis in the Argyll Robertson syndrome and in related pupillary disturbances has never been satisfactorily explained. In the abundant literature, extending over almost a century, two main theories have evolved:
The miosis is due to an interruption of the sympathetic dilator fibers.
The miosis is due to irritation within the parasympathetic reflex arc.
It is the purpose of this paper to discuss, on the basis of pupillographic and pharmacodynamic tests, the mechanism by which miosis is produced in the Argyll Robertson and related pupillary syndromes. An attempt will be made to clarify some of the basic problems which have perpetuated the controversies involved.