Glaucoma is a group of conditions affecting the main nerve of vision called the optic nerve. Damage to the optic nerve may cause loss of vision. Most of the time abnormally high intraocular pressure (pressure inside the eye) causes this damage. Glaucoma damages the vision slowly and gradually. Early diagnosis and treatment minimizes or prevents optic nerve damage and limits glaucoma-related vision loss.


Glaucomas can be categorized as open-angle or closed-angle. Primary open-angle and acute closed-angle glaucoma are the most common types. Another common type of glaucoma is low-tension glaucoma characterized with optic nerve damage despite normal intraocular pressure.

Glaucomas can also be categorized as primary or secondary conditions. If their cause is unknown, they are called primary conditions. In secondary condition, known factors like an eye injury, tumor, inflammation, diabetes, or advanced cataract result in glaucoma.


Symptoms depend on the type of glaucoma present.

  • Primary open-angle glaucoma: This type is characterized by gradual loss of peripheral vision, typically in both eyes. In the advanced stages, tunnel vision is reported.
  • Acute angle-closure glaucoma:
    – Severe pain in the eyes
    – Blurred vision
    – Nausea and vomiting
    – Visual disturbances in low light
    – Halos around lights
    – Redness in the eye

If not treated in time, glaucoma progresses to vision loss in three stages:

  1. Appearance of blind spots in the peripheral vision
  2. Tunnel vision
  3. Blindness


In the eyes, a fluid called aqueous humor, is constantly produced and drained through a tiny channel. A problem with the drainage leads to accumulation of aqueous humor. This generates intraocular pressure. Abnormally high intraocular pressure damages the optic nerve, resulting into glaucoma.

  • In primary open-angle glaucoma, a partial blockage of the drainage channels result in a slow drainage of aqueous humor. This builds up intraocular pressure within your eye.
  • In closed-angle glaucoma, iris bulges and blocks the drainage channel, increasing the eye pressure abruptly.
  • A sudden dilation of the pupils (like in darkness, low light, stress, excitement, and due to some medicines like anti-histamines and tricyclic antidepressants) may trigger acute angle-closure glaucoma.
  • In low-tension glaucoma, a reduced blood circulation to the optic nerve causes damage to it, despite a normal intraocular pressure.
  • Pigmentary glaucoma is associated with the accumulation of pigment granules on and in the drainage channel.

High intraocular pressure, increasing age, family history, medical conditions (like diabetes and hypothyroidism), other eye conditions (eye injuries, surgery, tumors, and inflammations), nearsightedness, and prolonged corticosteroid use increase the risks of developing glaucoma.


Treatment directs at reducing intraocular pressure, decreasing the production of aqueous humor, and preventing vision loss.


  • Prostaglandin-like compounds (latanoprost, bimatoprost), epinephrine compounds (dipivefrin), and mitotic or cholinergic agents (pilocarpine, and carbachol) increase the outflow of aqueous humor.
  • Beta blockers (timolol, metipranolol, and betaxolol), carbonic anhydrase inhibitors (dorzolamide, brinzolamide) and alpha-agonists (apraclonidine and brimonidine) reduce the production of aqueous humor.

Oral medication

Oral administration of carbonic anhydrase inhibitors may be recommended to some patients.


In treatment-resistant cases, surgery is performed. The surgical options include laser surgery ( trabeculoplasty), filtering surgery (trabeculectomy), drainage implant surgery, or iridotomy in case of acute angle-closure glaucoma.

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