AbstractAnterior segment Spectral domain–optical coherence tomography (SD‐OCT) is being increasingly used in glaucoma patients, primarily to investigate the anterior chamber angle and visualize the trabecular meshwork (TM) and Schlemm's canal (SC) in vivo. With the advent of angle surgery for glaucoma much interest has been generated in the aqueous outflow pathways. Our studies have shown that in vivo imaging of anterior chamber angle with ASOCT can been used to detect gross features of angle dysgenesis in primary congenital glaucoma (PCG), juvenile onset open angle glaucoma (JOAG) and adult onset primary open angle glaucoma (POAG), which has been described either as an absence of SC and/or the presence of abnormal tissue or a hyper‐reflective membrane within angle recess. This membrane is similar to what Barkan had described in PCG and was later described to be an angle cicatrization that portends a poorer success with goniotomy. Absence of development of SC was also shown by Hollander et al to be associated with a severe form of goniodysgenesis while its presence was seen in less severe goniodysgenesis on histopathological studies involving PCG. In fact, angle dysgenesis on ASOCT (ADoA), can be observed even in eyes with gonioscopically normal appearing angles. It is known that gonioscopy provides only a superficial representation of the histopathological anomalies affecting the angle. The presence of a thick compact tissue in the TM samples of Juvenile glaucoma patients has been observed, irrespective of whether they had an apparent goniodysgenesis or not. Hence, what appears to be morphologically normal angle on gonioscopy may harbour dysgenesis of the TM or even the SC. Primary congenital glaucoma, JOAG and adult onset POAG form a spectrum in terms of severity of angle dysgenesis. While most of the PCG eyes have features of ADoA, the same are present in 40% of JOAG eyes and in up to 35% of adult onset POAG. The size of the SC has also shown to be decreased in patients with adult‐onset open angle glaucoma based on in vivo OCT studies. We also present interesting observations of angle dysgenesis in fellow eyes of children with unilateral PCG.