Optic nerve in advanced<unk>  disease Screening for<unk>  is usually performed as part of a standard eye examination performed by optometrists and ophthalmologists. Testing for<unk>  includes measurements of the intraocular pressure using tonometry, anterior chamber angle examination or gonioscopy as well as examination of the optic nerve to discern visible damage, changes in the cup-to-disc ratio, rim appearance and vascular change. A formal visual field test is performed. The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography, scanning laser polarimetry or scanning laser ophthalmoscopy (Heidelberg retinal tomogram). Visual field loss is the most specific sign of the condition, though it occurs later in the course of the disease. As all methods of tonometry are sensitive to corneal thickness, methods such as Goldmann tonometry may be augmented with pachymetry to measure the central corneal thickness (CCT). A thicker cornea can result in a pressure reading higher than the true pressure but a thinner cornea can produce a pressure reading lower than the true pressure. Because pressure-measurement error can be caused by more than just CCT (such as by corneal hydration or elastic properties), it is impossible to adjust pressure measurements based only on CCT measurements. The frequency-doubling illusion can also be used to detect<unk>  with the use of a frequency-doubling technology perimeter. Examination for<unk>  is assessed with attention given to gender, race, history of drug use, refraction, inheritance and family history. +<unk>  tests What the test examines Eye drops used Physical contact with the eye Procedure Tonometry Inner eye pressure Eye drops may be used to numb the eye. The examiner then uses a tonometer to measure the inner pressure of the eye through pressure applied by a puff of warm air or a tiny tool. Ophthalmoscopy (dilated eye examination) Shape and color of the optic nerve Eye drops are used to dilate the pupil. Using a small magnification device with a light on the end, the examiner can examine the magnified optic nerve. Perimetry (visual field test) Complete field of vision The patient looks straight ahead and is asked to indicate when light passes the patient's peripheral field of vision. This allows the examiner to map the patient's field of vision. Gonioscopy Angle in the eye where the iris meets the cornea Eye drops are used to numb the eye. A hand-held contact lens with a mirror is placed gently on the eye to allow the examiner to see the angle between the cornea and the iris. Pachymetry Thickness of the cornea The examiner places a pachymeter gently on the front of the eye to measure its thickness. Nerve fiber analysis Thickness of the nerve fiber layer Using one of several techniques, the nerve fibers are examined.<unk>  has been classified into specific types: Primary<unk>  and its variants Primary<unk>  (H40.1-H40.2) *Primary open-angle<unk> , also known as chronic open-angle<unk> , chronic simple<unk> ,<unk>  simplex :*High-tension<unk>  :*Low-tension<unk>  *Primary angle closure<unk> , also known as primary closed-angle<unk> , narrow-angle<unk> , pupil-block<unk> , acute congestive<unk>  :*Acute angle closure<unk>  (aka AACG) :*Chronic angle closure<unk>  :*Intermittent angle closure<unk>  :*Superimposed on chronic open-angle closure<unk>  ("combined mechanism" – uncommon) Variants of primary<unk>  *Pigmentary<unk>  *Exfoliation<unk> , also known as pseudoexfoliative<unk>  or<unk>  capsulare *Primary juvenile<unk>  Primary angle closure<unk>  is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye, causing pain and redness (symptomatic, or so-called "acute" angle closure). In this situation, the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include a headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. However, the majority of cases are asymptomatic. Prior to the very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse and prevent contact between the iris and trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser iridoplasty, medication (pilocarpine) or incisional surgery may be required. Primary open-angle<unk>  is when optic nerve damage results in a progressive loss of the visual field. This is associated with increased pressure in the eye. Not all people with primary open-angle<unk>  have eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown to stop progression even in these cases. The increased pressure is caused by trabecular meshwork blockage. Because the microscopic passageways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is affected first, but eventually the entire vision will be lost if not treated. Diagnosis is made by looking for cupping of the optic nerve. Prostaglandin agonists work by opening uveoscleral passageways. Beta-blockers, such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing the formation of aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via inhibition of AC) and increase drainage. Developmental<unk>  Developmental<unk>  (Q15.0) *Primary congenital<unk>  *Infantile<unk> <unk>  associated with hereditary or familial diseases Secondary<unk>  Secondary<unk>  (H40.3-H40.6) *Inflammatory<unk>  :*Uveitis of all types :*Fuchs heterochromic iridocyclitis *Phacogenic<unk>  :*Angle-closure<unk>  with mature cataract :*Phacoanaphylactic<unk>  secondary to rupture of lens capsule :*Phacolytic<unk>  due to phacotoxic meshwork blockage :*Subluxation of lens<unk>  secondary to intraocular hemorrhage :*Hyphema :*Hemolytic<unk> , also known as erythroclastic<unk>  *Traumatic<unk>  :*Angle recession<unk> : Traumatic recession on anterior chamber angle :*Postsurgical<unk>  ::*Aphakic pupillary block ::*Ciliary block<unk>  *Neovascular<unk>  (see below for more details) *Drug-induced<unk>  :*Corticosteroid induced<unk>  :*Alpha-chymotrypsin<unk> . Postoperative ocular hypertension from use of alpha chymotrypsin.<unk>  of miscellaneous origin :*Associated with intraocular tumors :*Associated with retinal detachments :*Secondary to severe chemical burns of the eye :*Associated with essential iris atrophy :*Toxic<unk>  Neovascular<unk> , an uncommon type of<unk> , is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition. Neovascular<unk>  results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. People with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. A new treatment for this disease, as first reported by Kahook and colleagues, involves the use of a novel group of medications known as anti-VEGF agents. These injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure. Currently, there are no high-quality controlled trials demonstrating a beneficial effect of anti-VEGF treatments in lowering IOP in people with neovascular<unk> . Toxic<unk>  is open-angle<unk>  with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach . It characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to Schlemm's canal. This condition is differentiated from malignant<unk>  by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown. Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reported on four patients who had toxic<unk> . One of them underwent phacoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief, but further research is required. Absolute<unk>  Absolute<unk>  (H44.5) is the end stage of all types of<unk> . The eye has no vision, absence of pupillary light reflex and pupillary response, and has a stony appearance. Severe pain is present in the eye. The treatment of absolute<unk>  is a destructive procedure like cyclocryoapplication,
Glaucoma
Keratitis
Normal tension glaucoma
Conjunctivitis
Cat eye syndrome
Uveitis
Phacolytic glaucoma
Ocular hypertension