Uncertainty regarding the ultimate cause of Congenital Glaucoma persists and will persist as long as so much concerning the influence of heredity and the forces in prenatal life that make for maldevelopment continues to be wrapped in mystery.

We have concentrated on an investigation of the earliest specimens with this disease and we have sought for traces of pre-existing inflammation, and we have found little. Either such a state is far from being universal or its manifestations in foetal life are not recognised because they can rapidly disappear or because they differ from those so well known in adult tissues. If an attack of inflammation had been initiated early, its influence would be great enough to lead to grave and obvious malformation. One may ask, can such an attack commence prior to the development of an efficient blood-vascular system? If not, its onset must be restricted to the second half of pregnancy. If this attack be of any but the mildest degree, surely histological evidence of inflammation would be revealed in an examination of specimens obtained during the first few weeks of life.

Though the abnormal findings in the earliest specimens are varied and diverse yet they as a whole resemble defects in development. They suggest that growth has been retarded or has become aberrant. A study of human embryology and of comparative anatomy throws light on these anomalous states. Collateral evidence is supplied by the presence of other developmental defects in patients with congenital glaucoma. Not only do we find ocular defects but facial naevi or neurofibromatous changes on the same side of the face and head as the affected eye.

We cannot, however, assume that congenital glaucoma is due, as a rule, to defective development and nothing else, for one does not know what factors underlie errors in development in general. It is conceivable that a deficiency in some vitamin or some endocrine substance may exist, or that some upset in the maternal nervous system may so lower resistance that inflammation or some other dystrophic influence may be permitted to disturb the smoothness that characterises normal growth.