It is customary to "explain" these cases of monocular amblyopia by previously existing squint, and one is quite satisfied if by the examination of patients it is only possible to prove that they have occasionally squinted, although the advocates of the amblyopia ex anopsia disallow the presence of the same under these conditions, that is, in periodic squint. Of course a theory which cannot exist without the assertion that occasional alternation suffices to hinder the development of defective vision caused by disuse, cannot possibly hold periodic squint to be the cause of it. Certainly permanent squint may also disappear, but this much I have been able to determine, that this seldom happens before the twelfth year of life, and one may surely reckon that children in whom permanent squint is developed at the usual early period of life, still squint at the age of ten years. Cases 24 and 26 to 30 can under no circumstances be explained by previous squint, notwithstanding that they represent the extremest degrees of amblyopia, but the question is undoubtedly that of congenital defective vision; moreover I have excluded from the statistics of congenital amblyopia all cases in which the previous presence of squint could even be supposed. A table of the cases above described with reference to the defective condition is interesting; when a determination of refraction existed for the weak eye I have given it, and when this was not the case I have stated that of the better eye, thus it is seen that among 85 cases in which the refraction was determined, hypermetropia (including hypermetropic astigmatism) was present in 39. Hypermetropia was found then in 47 per cent of all the cases. The percentage would probably be higher, if all weak-sighted eyes had been examined from the beginning as to their state of refraction, but as I only learnt to know the relation between hypermetropia and the higher degrees of congenital amblyopia from my statistics, I did not take notice of this relation when investigating individual cases. How does congenital amblyopia now stand in relation to that disturbance of vision which we observe in squint? I see no difference; whether squint is present or not, the form of defective vision is precisely the same, and nothing happens in the combination with squint which could not also be proved without it. The relation to hypermetropia, which is proved with congenital amblyopia, also appears in squint. A collective table of cases of convergent and divergent squint included in the statistics (pp. 19 and 47) shows: