The term ‘‘glaucoma’’was derived from the Greek word glaύkvma (Glaucosis) during the Hippocratic era of 400 BC 1 which essentially meant the greenish pupillary hue in eye which is much different from the normal pupillary color. Until 17th century, the clinical differentiation of poor visual acuity due to cataract or glaucoma was not so well defined. In ancient Indian Medicine, glaucoma has been described as black cataract (in Hindi:'Kala Motia'), a term which is popular among the Indian rural population even today. The classical description of greenish blue hue in pupillary area narrated in the ancient era corresponds to two main forms of glaucoma. In the first category, also known as acute primary angle closure glaucoma (PACG), pupillary blockage leads to sudden rise of intraocular pressure (IOP) which manifests as severe headache and intense ocular pain, redness, clouding, or haziness of cornea. These symptoms are further compounded with acute and marked diminution or even loss of vision within next few hours. Hence, acute PACG often presents itself as an emergency and warrants immediate therapeutic intervention to save vision. A typical acute PACG is easy to diagnose even by general physicians. Contrary to the PACG, the second form of glaucoma, known as the primary open angle glaucoma (POAG), remains silent for several years until slow and gradual rise in IOP leads to manifest optic nerve damage and peripheral visual fields changes. POAG is invariably diagnosed as an incidental finding in ocular examination or linked with the family history. However, the end stage of open angle glaucoma also leads to cloudy cornea and peculiar blind gate of the patient. Due to this gradual and very slow progression of visual loss, open angle glaucoma is also known as silent killer of vision or the ‘‘sneak thief of sight’’. Whereas PACG occurs mainly in elderly age group, POAG is a disease of late fourth or fifth decade. In addition to the adult onset primary glaucoma, there can be a congenital variant (known as congenital glaucoma) due to structural ocular anomalies. Glaucoma may also be the manifestation of a variety of aetiologies such as post-traumatic ocular changes, uveitis, or side effects of topical or systemic administration of steroids in which case it is known as secondary glaucoma. However, it is important to note that vast majority of the cases seen in day-to-day clinical practice are one of the variants of primary glaucoma. The term glaucoma does not denote disease per se but describes a group of symptoms which is characterized by raised IOP associated with optic nerve damage and subsequent damage or loss of retinal ganglion cells. However, raised IOP is not the only essential feature of all glaucoma or linked with optic nerve damage or visual field changes. In certain cases of ocular hypertension (IOP above 21 mmHg), optic nerve and visual fields remain normal for several years despite persistently raised IOP. Contrary to this situation, a good number of cases, commonly known as low-tension glaucoma, have been found to have definite evidence of optic nerve damage and visual fields changes despite normal IOP. Hence, in addition to raised IOP, several other factors like inadequate blood supply to retinal ganglion cells and optic nerve fibers due to atherosclerosis or advanced age-related connective tissue changes are also thought to play an important role in the progression of glaucoma. This possible vasculogenic theory has led to the genesis of another term ‘‘vascular optic neuropathy’’to glaucoma.

It is extremely important to understand here that glaucoma is the third largest cause of blindness all over the world following cataract and …