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 Table of Contents  
Year : 2013  |  Volume : 1  |  Issue : 3  |  Page : 175-181

Nuggets in clinical approach to diagnosis of glaucoma

Department of Ophthalmology, Amina Hospital and ESIS Hospital, Solapur, Maharashtra, India

Date of Submission12-Feb-2013
Date of Acceptance06-Jun-2013
Date of Web Publication23-Aug-2013

Correspondence Address:
Sayyed Mazhar
158-A Railway Lines, Parijat Complex, Solapur, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2320-3897.116865

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Having a high index of suspicion and comprehensive examination are key to success in early diagnosis of glaucoma. The diagnosis of glaucoma is many a time straight forward in mid or late stages, but becomes elusive in early stages. Once a diagnosis of glaucoma is made then the patient is to be treated ether by medical line of treatment or with surgical intervention or with lasers and the follow-up remains to be life-long. So, one has to be very astute in making a diagnosis of glaucoma. Glaucoma not only affects the quality of vision, but also the quality-of-life. We all know the glaucoma is an irreversible blindness so early diagnosis is of prime importance. Opportunistic screening at our clinics with comprehensive eye examination is very important. This article deals with importance history taking and diagnostics in case of glaucoma. Perfecting our basics makes our life easier for further management.

Keywords: Gonioscopy, history, perimetry

How to cite this article:
Mazhar S. Nuggets in clinical approach to diagnosis of glaucoma. J Clin Ophthalmol Res 2013;1:175-81

How to cite this URL:
Mazhar S. Nuggets in clinical approach to diagnosis of glaucoma. J Clin Ophthalmol Res [serial online] 2013 [cited 2022 Jul 1];1:175-81. Available from: https://www.jcor.in/text.asp?2013/1/3/175/116865

Glaucoma is defined as chronic progressive optic neuropathy that has common characteristic morphological changes at the optic nerve head (ONH) and retinal nerve fiber layer (RNFL) in the absence of other ocular disease and congenital anomalies. Progressive retinal ganglion cell death and visual field (VF) losses are associated with these changes. Intraocular pressure (IOP) is a definite risk factor. Among the emerging causes of blindness glaucoma needs a special attention. Prevalence of glaucoma is 4% in the population aged above 30 years. In children, it is estimated to be 3%; hence, we should sharpen our clinical skills for diagnosing and managing glaucoma.

The diagnosis of glaucoma is based on structural and functional changes in the ONH. History, IOP, gonioscopy, central corneal thickness (CCT) and newer diagnostic modalities are complimentary to the diagnosis.

  History Top

In any illness history, taking is a prospective aspect in making a diagnosis, but in glaucoma it is a retrospective history, which plays a major role in management of the case. Here is small acronym for history taking.

A= Asthma, Arthritis, Allergy, Attacks in the past

In asthma non-selective beta blockers are to be avoided and selective beta blockers are to be given with care. [1],[2] Salbutamol can precipitate an attack of angle closure (AC). Arthritis and allergies are many times treated with the long-term use of steroids. Steroids through any root of administration can cause an increase in IOP in steroid responders. Allergy to sulphate has to be checked before using carbonic anhydrase inhibitors (CAI). History of attacks in the past suggesting the increase in IOP is very important when we are dealing with a case of narrow angles.

B= Blood pressure, Breathlessness, Blood loss, Blow to the eye

In patients using systemic beta blockers, topical administration of beta blockers may be less effective. [3] So also systemic beta blockers are to be avoided at night times to prevent further dip of IOP. Breathlessness may be a sign of cardio pulmonary problems so care is to be advocated while administering mannitol and topical beta blockers. [4] Blood loss either due to major surgery or accident causing severer hypovolemia may show changes in ONH, which mimic normal tension glaucoma (NTG). Blow to the eye (trauma) can direct us to see angle recession and other correlated subtle changes. No matter what the duration of trauma was or how trivial it was.

C = Cardio vascular system (CVS): Blocks, arrhythmias, cardiac failure, Central nervous system: Migraine, head injury, convulsions, depression, Calculus: Urinary.

blockers adverse effects with CVS have already been mentioned. Migraine history is important, especially in cases of NTG. Head injury may cause optic disc pallor and one has to carefully look for VFs for neurological defects. Convulsions and depressions are important because of the type of drug being taken, which is discussed later. Calculus-CAIs when used for a long-term can precipitate renal calculus because higher urine calcium levels.

D = Diabetes, Drugs-systemic/topical/local/inhalators.

Although Baltimore I study did not find any association of diabetes with open angle glaucoma (OAG), but recent population studies support an association with diabetes. [5] Drugs-use of any current medications needs to be considered along with certain specific past medications, including. Steroids-any route of administration is associated with ocular hypertension (OHT) and OAG, sometimes found in traditional medicines. Glaucoma eye drops (prolonged use may increase the likelihood of trabeculectomy failure) Anticholinergics/tricyclic antidepressants can cause AC Anticonvulsants: Topiramate can cause acute AC. Vigabatrin linked to nasal peripheral VF loss without disc changes. Systemic beta-blockers/calcium channel blockers-may interact with topical beta blockers. Alpha agonists are contraindicated for patients taking monoamine oxidase inhibitors (prescribed for depression, migraine prophylaxis, or Parkinson's disease) and in infants and children check for sulphur allergy prior to using CIAs.

E = Endocrine (thyroid), Error of refraction, Economic status.

A more recent study confirmed the association of graves diseases with primary open angle glaucoma (POAG) and NTG. [6] Patient can be hypothyroid, euthyroid or hyperthyroid when the eye problem begins. Other pituitary problems can be associated with anomalies of angle or the lens. Refractory errors around ± 6D are not much significant, but high myopes are thought as a risk factor for POAG and high hypermetropes are risk factors for primary angle closure glaucoma (PACG). Economic status of patients helps us to prescribe a drug according to the patient life-style and needs and hence increasing compliance in glaucoma management.

F = Family history of glaucoma, Family status.

Risk of developing POAG in the first degree relatives is 4-16%. Rotterdam found the risk to be as high as 10 times. [7] Family status regarding female patient a history of amenorrhea and lactation are of prime importance as drugs can act on the fetus or the new born.

  Slit Lamp Examination Top

Before we put our hands on to specific diagnostic tools of glaucoma, a basic slit lamp examination is a must. Attention must be paid to the following areas. Cornea and anterior chamber for central and peripheral anterior chamber depth (Von-Herick test) presence of keratic precipitates, haab's striae and corneal dimensions. Iris should be seen for reactions, which is slowly reacted after and acute, attack. Other abnormalities in the iris to be look for are rubeosis iridis, patchy atrophy, synechiae, ectropion of uveal pigment, pseudoexfoliative material, transillumination defects, iris nodules and displaced pupil with iris atrophy. Examination of lens also reveals certain diagnostic clues such as pseudoexfoliation, glaucoma fleckens, phacodonesis or abnormal lens shape.


Type-tonometers can be classified as:

  1. Direct or indirect
  2. Low displacement tonometer or high displacement tonometer
  3. Contact and non-contact tonometer
  4. Indentation tonometer or applanation tonometer
  5. Dynamic contour matching tonometer.
Goldmann applanation tonometry (1954) until today is considered as the gold standard.

Whom: Every OPD patient above the age of 40 years.

When: Every visit. If diurnal variation is required then at 8 am, 11 am, 2 pm, 6 pm.

Astigmatism: When above 3D turn the prism head to 90° and take the average of horizontal and vertical meridians OR rotate prism head at 45° corresponding to least curved meridian. [8]

Procedure: Performed under topical anesthesia, fluorescein staining, blue light, set knob at 1 g, turn the knob until inner borders of Fl rings touch each other at the midpoint of their pulsations. Take the average of three readings. Calibration of tonometer should be checked frequently [Figure 1].
Figure 1: Caliberation of applanation tonometer. Current glaucoma practice from glaucoma society of india year 2002

Click here to view

Sterilizations: I wipe it with sterlium and then with normal saline swab. Calibration-should be done monthly. The calibration rod should be tested at (0, 20, 60) mm of Hg potential errors-thin cornea, thick cornea, astigmatism more (>) three diopters, inadequate fluorescein, too much fluorescein, irregular cornea, tonometer out of calibration, elevating the eyes >15°, repeated tonometry, pressing on the eyelids or globe, squeezing of the eyelids, observer bias (expectations and even numbers).

Tips: After taking IOP turn over to normal light to examine if prism head had made any damage to the cornea.

Gonioscopy should not be followed by tonometry, but it should be vice versa.

CCT [9],[10]

Goldmann tonometer is calibrated for average corneal thickness of 520 microns. Excessive thick or thin corneas either over estimate or under estimate IOPs Normal CCT is 520 microns (Indians) Correction factor is 2.5 mm of Hg for every 50 microns. Increase or decrease target IOP by one standard deviation (SD) for every 1 SD of CCT. 1 SD of IOP = 3 mm of Hg 1 SD of CCT = 30 microns.

Whom: Ideally for all glaucoma patients on making a diagnosis more important for OHT/NTG and resetting of target IOP when - ideally ½ h after awakening.

Frequency: Once in 5 years.

Why: It is risk factor for progression. Thin corneas are a risk factor for progression especially in case of raised IOP.

How: Ultrasonic pachymetry is gold standard.

Expression: Thin - < 500 microns/average - 500-600 microns/thick - >600 microns. [11]


It is biomicroscopic examination of the anterior chamber angle of the eye.

Principal: The gonio lens eliminates the total internal reflection of the cornea by exceeding the critical angle of 46°.

When: Initially for all patients. Repeat more frequently for patient with AC.

Which lens: To start learning single mirror after learning curve shift to four mirrors [Table 1].
Table 1: Comparison of Goldmann single mirror and zeiss four mirror

Click here to view

Indications [12]


  1. To study topography of the anterior chamber angle [Figure 2]
    Figure 2: Peripheral Anterior Synechiae Gonioscopy a text and  Atlas More Details (Tanuja Dada)

    Click here to view
  2. To assess degree of opening of anterior chamber angle recess
  3. To assess risk of closure on dilatation of pupil
  4. Visualization of congenital anomalies
  5. Classification of glaucoma (primary/secondary)
  6. To note the presence and extent of angle neovascularization
  7. Assessment of abnormal angle pigmentation
  8. Visualization of pseudoexfoliative material in the angle
  9. To look for post-traumatic angle recession, cyclodialysis
  10. Rule out foreign body in the angle after open globe injury
  11. Neoplastic invasion into angle structures (ciliary body tumor)
  12. Diagnosis of epithelial down-growth
  13. To look for vitreous strands incarcerated in the surgical wound
  14. To view copper deposition on Descemet's membrane
  15. To study patency of trabeculectomy fistula
  16. To view a peripheral laser iridotomy
  17. To visualize the internal ostium of glaucoma drainage device
  18. To see orientation of haptics of an anterior chamber intraocular lenses.

  1. Laser trabeculoplasty
  2. Excimer laser trabeculotomy
  3. Goniotomy/gonioplasty
  4. Laser goniophotocoagulation
  5. Reopening of a blocked trabeculectomy opening
  6. Neodymium-doped yttrium aluminum garnet laser after deep sclerectomy
  7. Laser of suture tied around tube of a glaucoma drainage device
  8. Indentation gonioscopy to break an acute attack of PACG.
How: Gonioscopy should be performed to look for iridotrabecular contact. Gonioscopy needs to be performed in a dark room with a small slit-lamp beam.

  1. Minimal room illumination
  2. Good anesthesia
  3. Shortest slit practicable
  4. High magnification
  5. Dim slit illumination
  6. Set slit lamp or upper cornea, beam off-center 30°-45° nasally
  7. If necessary, elevate upper lid
  8. Place lens gently on eye while looking through slit lamp (as if you are doing tonometry) no gel needed with Zeiss-type lenses
  9. Look through the upper mirror (inferior angle) as you place lens on eye, stop pushing when you can see the iris
  10. Move slit-lamp beam inferiorly (avoid pupil) to examine superior angle
  11. Turn beam 90° and move on axis
  12. Move to Nasal side (temporal angle) then to temporal side (nasal angle)
  13. Record findings on goniogram
  14. In the presence of appositional closure, indentation should be performed to look for Peripheral Anterior ynechiae
  15. It may be necessary to alter the position of the mirror or the position of the gaze to look over a convex iris to visualize the angle
  16. In steep iris profile do manipulative gonioscopy (over the hill view)
  17. Indentation gonioscopy is used to open up the angle and differentiate between oppositional or synechial closure.
What can happen on indentation

  1. Concave iris opening (oppositional)
  2. Angle widens but synechial closure seen
  3. Iris moved backwards peripherally, but role of iris bulges out and doesn't assume concave configuration (plateau iris)
  4. Iris moves slightly backwards, but maintains its convex profile (large/displaced lens).
What to see

  1. Level of iris insertion
  2. Shape of peripheral iris profile
  3. Width of the angle recess
  4. Degree of trabecular pigmentation
  5. Areas of iridotrabecular apposition
  6. Areas of iridocorneal synechiae.
Normal adult angle

  1. Ciliary body band
  2. Scleral spur
  3. Schlemm's canal
  4. Pigmented trabecular meshwork
  5. Non-pigmented trabecular meshwork
  6. Schwalbe's line.

  1. Start form top mirror
  2. Identify corneal wedge to locate Schwalbe's line
  3. Avoid folds in descemet's membrane, which is a sign excessive pressure
  4. Avoid excess illumination
  5. Avoid direct light on pupil.

There are four angle grading systems: [13],[14]

  1. Shaffer
  2. Spaeth
  3. Scheie
  4. RPC classification (Dr. Rajendra Prasad Centre for ophthalmic sciences.

Practically document what you see [Figure 3]:
Figure 3: Diagraming gonioscopy with concentric circles. Dianosis and therapy of the glucomas (Becker-Shaffer's)

Click here to view

Pigmentation ± (Trabecular Meshwork 1-4)

Iris shape - S/R/Q

S - Straight; R - Regular; Q - Queer.


ONH evaluation is gateway to diagnosis of glaucoma [Figure 4]. Structural damage of ONH and RNFL are first to occur in glaucoma. 30-50% of ganglion cells are lost before a change is observed on w/w perimetry.
Figure 4: Neuroretinal rim Diagnosis and management of glaucoma (Jaypee Highlights) (Arvind Eye Care System) Auther – R. Ramakrishnan, SR Krishnadas, Mona Khurana, Alan L Robin

Click here to view

Why: It defines glaucoma.

When: At every visit.

What: Qualitative:
  • Neuroretinal rim (NRR)
  • Optic disk hemorrhage
  • Para papillary choroidal atrophy
  • Barred circum linear vessels (CLV)
  • Nerve fiber layer (NFL) defect.
  • Vertical disk diameter
  • Vertical cup to disk ratio (C:D)
  • Rim to disk ratio (R:D) at thinnest portion of rim
  • NFL height optical coherence tomography (OCT).
Size-average: 1.5-2 mm. Classify discs as small/average/large.

Stereoscopic views with the slit lamp using indirect condensing lens and considering magnification factor.

60 D × 0.88
78 D × 1.1
90 D × 1.3.

Welch Allyn ophthalmoscope smallest aperture casts an illumination of 1.75 Sq. mm.

Does refractive status play a role. Up to −5 D to +5D - no change seen. Hyperopes more than +5D - small discs. Myopes more than −5D - large discs note-small discs need more attention.

Cup disc ratio

  1. Vertical cup disc ratio is important
  2. Stereoscopic view is required
  3. Small discs have small C:D
  4. Larger discs have large C:D
  5. Change in C:D ratio indicates progression over period of time
  6. Difference of 0.2 in C:D of two eyes is very significant
  7. C:D changes super seed the perimetric changes
  8. C:D of 0.7 is taken as cut off from healthy eye and glaucomatous eye.
Rim discs ratio

It is designed by Spaeth. Takes into consideration the vertical long axis where the rim is thinned. It makes more sense than C:D.


  1. The rim is more important than the cup
  2. Cardinal feature of G ON is a loss of tissue from inner edge of rim
  3. Check inferior superior nasal temporal (ISNT) rule-in majority of eyes the rim is broadest in the inferior disc region followed by the superior disc region, the nasal disc region and finally a temporal disc region
  4. ISNT rule is followed in 50-60% of cases
  5. Early rim loss is manifested at superior temporal and inferior temporal region [15]
  6. Bared of circum linear vessel (CLV) is an early sign of NRR thinning
  7. Color - pallor more than cupping is suggestive of neurological disc
  8. Cataractous eye gives a hyperemic hue
  9. Localized pallor of NRR may be seen after an acute attack.
RNFL [16]

Where: To be seen in superior and inferior are arcuate zone within two disc diameter of the disc.

Appearance: RNFL are thickest in upper and lower poles hence double hump seen in imaging.

Loss is of two types wedge shaped and diffuses loss. Apex of wedge is on a disc margin and fans out in arcuate zone. Vessels appear darker.

How to see: On slit lamp with green filter or fundus photograph or on imaging technologies.

Difficult is to be seen in older persons and lens opacities.

Parapapillary atrophy (PPA) changes [17],[18],[19],[20]

Beta zone-marked atrophy of retinal pigment epithelium (RPE) leading to good visibility of large choroidal vessel and sclera. It is seen besides or next to disc margin. Alpha zone-hyper or hypo pigmentation of RPE. It is next to alpha zone. PPA has high prevalence in glaucomatous eyes. PPA is a risk factor for progression. [21] PPA is a useful in detection of glaucoma progression in myopia.

Vascular signs of glaucoma

Disc hemorrhage

  1. They are splinter shaped or flame shaped at the border of optic disc
  2. Important risk factor for glaucoma progression
  3. Suggestive of ongoing damage to the ONH
  4. Independent risk factor for development of glaucoma
  5. In OHT disc hemorrhage presence increases conversion risk by 6 times [22]
  6. Recurrent hemorrhages increases risk by 3-4 times [23]
  7. 70% hemorrhages are not glaucomatous.
Bayonetting of vessel

Bayonetting is rarely seen in normal discs even in presence of large physiological cups.

Retinal arteriolar narrowing

The diameter of arteriole is narrower at the immediate region around the optic disc compared with its diameter in more peripheral region of retina. It is not specific of glaucomatous change.

BCLV: A small branch of central retinal artery or vein recedes from the inner disc margin as the cup enlarges. Barring of CLV should prompt us to look for other signs of glaucoma.

Nasalization of vessel: Progressive nasalization may occur as a result of progressive NRR loss.

Acquired pit of optic nerve (APON) [24]

The difference between notch and pit is that an APON is localized loss of optic nerve tissue extending deep into lamina and disc margin. Notch doesn't extend deep into lamina.

Steps in clinical examination of ONH

  • Determine disc size
  • Check for unusual disc shape
  • Determine the vertical C:D
  • Determine cup and rim size in relation to disc size
  • Evaluate rim shape (which is the narrowest rim) and apply the ISNT rule
  • Check RNFL (red free illumination)
  • Look for disc hemorrhages
  • Look for vascular changes: Bending of vessels, BCLV, collaterals, anterior constriction
  • PPA (beta zone)
  • High myopia: Rule out glaucoma
  • Rule out non-glaucomatous causes of cupping
  • Correlate VFs with optic disc changes.

  • Disc drawings using colored pencils
  • Disc photographs monoscopy
  • Disc photographs stereoscopy
  • Newer imaging technologies like Heidelberg Retinal Tomogram /Optical Coherence Tomography/Glaucoma Diagnostics -Variable Corneal Compensator.
Features of non-glaucomatous optic atrophy

  • Pallor more than cupping
  • Marked asymmetry between fellow eyes
  • VF defects respect vertical meridian an are out of proportion to degree of cupping
  • Visual acuity out of proportion to degree of cupping
  • Relative Afferent Pupillary Defect in presence of C:D <0.3
  • Younger age
  • Unilateral progression.

  Perimetery Top

Why: Defines state of optic nerve function. Define visual impairment.
When: When Glaucoma in suspected on examination.
Machine: Humphrey/octopus/medmont.
Which test: Central fields 30.2 threshold, 24.2 threshold.
Defects approaching fixation use macular program.
How to read: GRADES.
Foveal threshold: V/A should correspond.
Patient's reliability decreases with age health and fatigue.
Take care of: Pupil size at least 3 mm.
Refractive correction ± 3 D.
G - General information
R - Reliability
A - Abnormal/normal
D - Defect
E - Evaluate clinically
S - Subsequent evaluation.
  • Interpretation-1. Global indices
  • Mean deviation (MD) = generalized depression.
  • Pattern standard deviation (PSD) = localized loss
  • Glaucoma hemi field test (GHT) = early affected and most sensitive in early disease process.
2. Anderson criteria to be satisfied.

Approach of interpretation of VF defects according to the stage of glaucoma is given in [Table 2].
Table 2: Approach of interpretation of visual fi elds based on the stage of glaucoma

Click here to view

Tips [25]

  1. When we use decibels (dB) to express light sensitivity a high dB value indicates dim light and low dB value indicates bright light.
  2. In the point pattern the bare area around the fixation spot is a circle of 3° radius because the distance between the points to the axis is 3°.
  3. Raw data is strategy specific. Different strategies will have different raw data hence for comparison same test strategy should be used in the same patient.
  4. Statistical Packagecalculates the P value for the points where there is loss of sensitivity.
  5. The pattern deviation plot is nothing but the total deviation minus a generalized field defect worth of the dB value that converts the 7 th best sensitivity points of Total Deviation Numerical Plot to 0 deviations.
  6. During follow-up tests, the most important index to assess field progression is MD index.
  7. The increase in MD >0.08 dB/year should be considered abnormal.
  8. Never come to a conclusion of foveal split unless you see 0 dB sensitivity in any four points on 1° circle around fixation point of 10-2 raw data.
  9. GHT is useful only in early cases.
Andersons criteria

At least two consecutive occasions GHTs outside normal limits.

Cluster of three or more non-edge points in location typical for glaucoma, all of which are depressed on PSD at a P < 5% and one of which is depressed P < 1% (P = Probability) PSD that occur in <5% of normal individuals.

How many times fields should be done

  1. At least twice/ideally thrice to establish base line field.
  2. Two consecutive reproducible fields to establish progress.
  3. Mild glaucoma-yearly.
  4. Moderate glaucoma-6 monthly.
  5. Severe Glaucoma with macular area threatened-quarterly.
Field progression

  • Event based-shows changes
  • Trend based-shows rate of change.

  1. Overview printout
  2. Glaucoma change analysis
  3. Glaucoma change probability
  4. VF index.

  Conclusion Top

Glaucoma being an important cause of irreversible blindness, its early detection and appropriate management goes a long way in reducing the socio economic burden of the individual's family and this country. Currently the optimal method for detection of glaucoma at our clinic is comprehensive eye examination of individuals attending our clinic for any reasons.

  References Top

1.Murthy GV, Gupta SK, Bachani D, Jose R, John N. Current estimates of blindness in India. Br J Ophthalmol 2005;89:257-60.  Back to cited text no. 1
2.Neufeld AH, Bartels SP, Liu JH. Laboratory and clinical studies on the mechanism of action of timolol. Surv Ophthalmol 1983;28 Suppl:286-92.  Back to cited text no. 2
3.Schuman JS. Effects of systemic beta-blocker therapy on the efficacy and safety of topical brimonidine and timolol. Brimonidine Study Groups 1 and 2. Ophthalmology 2000;107:1171-7.  Back to cited text no. 3
4.Jones FL Jr, Ekberg NL. Exacerbation of asthma by timolol. N Engl J Med 1979;301:270.  Back to cited text no. 4
5.Dielemans I, de Jong PT, Stolk R, Vingerling JR, Grobbee DE, Hofman A. Primary open-angle glaucoma, intraocular pressure, and diabetes mellitus in the general elderly population. The Rotterdam Study. Ophthalmology 1996;103:1271-5.  Back to cited text no. 5
6.Wiersinga WM, Smit T, van der Gaag R, Koornneef L. Temporal relationship between onset of Graves' ophthalmopathy and onset of thyroidal Graves' disease. J Endocrinol Invest 1988;11:615-9.  Back to cited text no. 6
7.François J, Heintz-De Bree C. Personal research on the heredity of chronic simple (open-angle) glaucoma. Am J Ophthalmol 1966;62:1067-71.  Back to cited text no. 7
8.Moses RA. The Goldmann applanation tonometer. Am J Ophthalmol 1958;46:865-9.  Back to cited text no. 8
9.Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh) 1975;53:34-43.  Back to cited text no. 9
10.Tonnu PA, Ho T, Newson T, El Sheikh A, Sharma K, White E, et al. The influence of central corneal thickness and age on intraocular pressure measured by pneumotonometry, non-contact tonometry, the Tono-Pen XL, and Goldmann applanation tonometry. Br J Ophthalmol 2005;89:851-4.  Back to cited text no. 10
11.Schaknow PN, Samples JR, editors. The Glaucoma Book: A Practical, Evidence-Based Approach to Patient Care. Springer (India); 2010. p. 79-90.  Back to cited text no. 11
12.Gonioscopy a Text and Atlas. (Tanuja Dada). [Table 1].1 indications for gonioscopy. New Delhi, India: Jaypee Brothers Medical Publishers; 2006. p. 4.  Back to cited text no. 12
13.Spaeth GL. The normal development of the human anterior chamber angle: A new system of descriptive grading. Trans Ophthalmol Soc U K 1971;91:709-39.  Back to cited text no. 13
14.Spaeth GL. Gonioscopy: Uses old and new. The inheritance of occludable angles. Ophthalmology 1978;85:222-32.  Back to cited text no. 14
15.Jonas JB, Fernández MC, Stürmer J. Pattern of glaucomatous neuroretinal rim loss. Ophthalmology 1993;100:63-8.  Back to cited text no. 15
16.Tuulonen A, Airaksinen PJ. Initial glaucomatous optic disk and retinal nerve fiber layer abnormalities and their progression. Am J Ophthalmol 1991;111:485-90.  Back to cited text no. 16
17.Jonas JB, Fernández MC, Naumann GO. Parapapillary atrophy and retinal vessel diameter in nonglaucomatous optic nerve damage. Invest Ophthalmol Vis Sci 1991;32:2942-7.  Back to cited text no. 17
18.Jonas JB, Naumann GO. Parapaillary chorioretinal atrophy in normal and glaucoma eyes. II. Correlations. Invest Ophthalmol Vis Sci 1989;30:919.  Back to cited text no. 18
19.Jonas JB, Nguyen XN, Naumann Go. Parapaillary chorioretinal atrophy in normal and glaucoma eyes I, Morphometric data. Invest Opthalmol Vis Sci 1989;30:908   Back to cited text no. 19
20.Jonas JB, Xu L. Parapapillary chorioretinal atrophy in normal-pressure glaucoma. Am J Ophthalmol 1993;115:501-5.  Back to cited text no. 20
21.Teng CC, De Moraes CG, Prata TS, Tello C, Ritch R, Liebmann JM. Beta-Zone parapapillary atrophy and the velocity of glaucoma progression. Ophthalmology 2010;117:909-15.  Back to cited text no. 21
22.Siegner SW, Netland PA. Optic disc hemorrhages and progression of glaucoma. Ophthalmology 1996;103:1014-24.  Back to cited text no. 22
23.Kim SH, Park KH. The relationship between recurrent optic disc hemorrhage and glaucoma progression. Ophthalmology 2006;113:598-602.  Back to cited text no. 23
24.Radius RL, Maumenee AE, Green WR. Pit-like changes of the optic nerve head in open-angle glaucoma. Br J Ophthalmol 1978;62:389-93.  Back to cited text no. 24
25.Ramakrishnan R, Krishnadas SR, Khurana M, Robin AL. Diagnosis and Management of Glaucoma. 1 st ed. Interpretation of Visual Fields. New Delhi (India): Jaypee Highlights Medical Publishers; 2013. p. 182-95.  Back to cited text no. 25


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]

This article has been cited by
1 Application of clinical techniques relevant for glaucoma assessment by optometrists: concordance with guidelines
Khalid F. Jamous,Michael Kalloniatis,Andrew Hayen,Paul Mitchell,Fiona J. Stapleton,Barbara Zangerl
Ophthalmic and Physiological Optics. 2014; 34(5): 580
[Pubmed] | [DOI]


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