It is now generally recognized that the disease known as locomotor ataxia may include among its clinical manifestations symptoms other than those which depend on pathological changes in the spinal cord. A number of these are associated with the functions of the eyeballs. The Argyll-Robertson pupil is universally admitted as valuable confirmatory evidence of a diagnosis of locomotor ataxia; ocular paralyses, if less frequent, are certainly not less significant; and optic nerve atrophy is at least so well known in connection with the disease that its occurrence in any individual case would hardly call for comment. A further step forward in our knowledge of the clinical possibilities of locomotor ataxia has been the recognition of the fact that ocular disturbances may precede the evidences of any spinal lesion. This advance necessarily means that the occurrence of any one of the ocular events above mentioned must, unless otherwise explained, generate the suspicion that the case may in its later events display the phenomena known to depend upon sclerosis of the posterior columns of the spinal cord. It is very difficult to collect the evidence necessary to show in what proportion of cases this suspicion is justified by the event. For it is certain that ocular disturbances may long precede the manifestation of spinal symptoms. In the case of optic atrophy the interval may, according to Gowers, extend even to twenty years. Thus it can only be in very exceptional instances that one and the same physician will have the opportunity of observing at least a number of these cases through all the stages of their progress. Yet, if true, it is of manifest importance, for the sake both of exact knowledge and of accurate prognosis, that it should be clearly recognized that an optic-nerve atrophy, an ocular paralysis, or a loss of the pupil light reflex, unless capable of other explanation, belongs in all probability to the order of events incident to locomotor ataxia, and that any one of these may well be the introduction to a more widely-spread manifestation of the disease. For reasons stated above, the collection of complete histories necessary to afford actual demonstration of the truth of these propositions is difficult; and all the more so as there is reason to believe that in those cases in which the early stress of the disease falls upon the nervous apparatus of the eyeball the spinal symptoms are apt to be slight in degree as well as delayed in development. This is certainly the case when the ocular disturbance takes the form of optic-nerve atrophy. “In a large number of such cases,” says Gowers, “ataxy never comes on, the spinal malady becoming stationary when the nerve suffers.”