Normal tension glaucoma
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Normal Tension Glaucoma
Presenter: Dr. Niket GandhiModerator: Dr.Vijay Shetty
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IntroductionNormal-tension glaucoma (NTG) is a form of
open-angle glaucoma characterized by glaucomatous optic neuropathy and corresponding visual field defects in patients with IOP measurements consistently lower than 21 mmHg
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Case Presentation47 Year old, femaleTeacherMumbaiVisited our institute with primarily for a
squint opinion
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HistoryH/o of using glassesShe reported as being a hypotensive patientFamily h/o: Mother – High myopia, ?
Glaucoma
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ExaminationBCVA:
1. (RE): -6.00/-0.75x30 add +1.50ds 6/6,N62. (LE): -5.00/-1.00x130 add +1.50ds 6/6,N6
(LE) Exotropia On PBCT: 70 pd base in deviation for
distance and near with good fusion
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RE LE
Lid N N
Conjunctiva Quiet Quiet
Cornea Clear Clear
AC Deep and quiet
Deep and quiet
Iris CPN CPN
Pupil 7mm 7mm
Lens Clear Clear
Fundus CDR=0.85 :1 Inferior NotchDull FR
CDR=0.85 :1 Inferior NotchDull FR
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Investigation Perimetry GonioscopyOCTDVTPachymetry - (RE) 509 u (LE) 505 u
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GonioscopyBE- PTM seen in all quadrants Hence, wide open angles were observed.
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DVTBP- 94/60 mmhg to 110/70 mmhgIOP – (RE) 12-18 mmhg (LE) 10-16 mmhg For both eyes - Min : 2 am & Max : 2 pm
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ManagementDiagnosed as NTGStarted on e/d Travaprost hsShe underwent B/L Lateral Rectus recession
and MR resection on 24/06/2014
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EpidemiologyNTG is a disease of the elderly. Beaver Dam Eye Study:
The prevalence of likely NTG increased from 0.2% in the 43–54 years age group to 1.6% in those over 75 years of age
Below 50 years - 11% to 30% of all glaucoma casesMore prevalent in the female populationPositive family history - 5% to 40% * Higher prevalence in Japanese population
*1.Miglior M. Low critical tension glaucoma: present problems. Glaucoma 1987;9:77.*2.Geijssen HC. Studies on normal pressure glaucoma. Amsterdam: Kugler, 1991;1:1.
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Pathogenesis
Pressure dependent Pressure independent groups
Factors involved in the etiology of glaucomatous optic neuropathy
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Pressure dependent factorsIOP in NTG : A “risk factor” for the development
and progression of the diseaseImpaired optic nerve blood flow or a structurally
abnormal lamina cribrosa, which cannot withstand a normal range of IOP.
The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma was studied by:
Collaborative Normal-Tension Glaucoma Study Group
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Collaborative Normal-Tension Glaucoma Study Group
PURPOSE: To determine if intraocular pressure plays a part in the pathogenic process of normal-tension glaucoma.
METHODS: 1. One eye of each eligible subject was randomized either
to be untreated as a control or to have intraocular pressure lowered by 30% from baseline.
2. Eyes were randomized if they met criteria for diagnosis of normal-tension glaucoma and showed documented progression or high-risk field defects that threatened fixation or the appearance of a new disk hemorrhage.
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RESULTS:
Sample size: 140 eyes of 140 patients Groups : Treatment group : 61 Untreated control: 79 Patients reaching end points (specifically defined
criteria of glaucomatous optic disk progression or visual field loss)1. 28 (35%) of the control eyes2. 7 (12%) of the treated eyes
Of 34 cataracts developed during the study, 11 (14%) occurred in the control group and 23 (38%) in the treated group (P = .0075), with the highest incidence in those whose treatment included filtration surgery.
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CONCLUSIONS
Intraocular pressure is part of the pathogenic process in normal-tension glaucoma.
Therapy that is effective in lowering intraocular pressure and free of adverse effects would be expected to be beneficial in patients who are at a risk of progression
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Pressure independent factorsAbnormal blood flowSystemic hypotensionAbnormal blood coagulability,Misc.
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Systemic Hypotension
Various study show the role of systemic hypotension in the pathogenesis of the optic
neuropathy in NTG :1. Greater nocturnal decrease and a lower level of
diastolic BP2. In both NTG and HTG groups, lower BP at night
resulted in pts having progressive disease 3. Overall glaucoma pts, those on
antihypertensives who had a larger nocturnal decrease in systolic pressure tended to have deteriorating visual fields
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Abnormal Blood flowOptic nerve blood vessel diameter may be
affected by vasospasm and the association between vasospastic disorders
Drance et al found decreased finger capillary flow in NTG patients suggesting vasospasm as an underlying aetiological factor
Close associations: Migrainous headache and Raynaud’s phenomenon
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Mean Ocular Perfusion Pressure
Ocular perfusion pressure (OPP), the relationship between systemic blood pressure and IOP
Mean ocular perfusion pressure(MOPP)MOPP = 2/3 [DBP + 1/3(SBP – DBP)] – IOP
Risk factor for open-angle glaucoma. Because low blood pressure lets OPP drop, and
low OPP is similar to elevated IOP,hence it has consistently and strongly been associated with OAG.
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Misc factors
Other factors include:Abnormal blood coaguability Endothelin (ET1), a potent and continuous
vasoacting peptide is associated with NTG.Obstructive sleep apnea/hypopnea syndrome
(OSAHS)- Prevalence overall : 5.7% & In severe: 7.1%
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Systemic AssociationsPatients with normal-tension glaucoma have been noted to
haveA higher prevalence of hemodynamic crisesHypercoagulability;Hypertension/Hypotension Increased blood viscosityElevated blood cholesterol and lipidsCarotid artery disease Slowed parapapillary, choroidal, and retinal circulationsPeripheral vasospasmMigraine.
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Main CriteriaA mean IOP off treatment <=21 mm Hg on
diurnal testing, with no single measurement greater than 24 mm Hg
Open drainage angles on gonioscopyAbsence of any secondary cause for a
glaucomatous optic neuropathyTypical optic disc damage with glaucomatous
cupping and loss of neuroretinal rimVisual field defect compatible with the
glaucomatous cupping (disc/field correlation)Progression of glaucomatous damage.
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Work Up for NTGHistoryPhysical ExaminationDiagnostic ProceduresDDxManangement
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History
Neurologic symptoms :Headache, weakness, dizziness,
diplopia, or loss of consciousness
Ocular trauma or inflammation:
Possible prior intraocular pressure elevation or other causes of optic
neuropathy.
Medications:Systemic, topical, inhaled, or nasal
steroids, that can elevate intraocular pressure
Compromised ocular perfusion:
Sleep apnea, syncope, Raynaud’s phenomenon, anemia,
hypotension, blood transfusions.
Systemic hypertension or
hypotension and any current
treatments for these.
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ExaminationVisual acuity Color vision testing (to help differentiate from non-
glaucomatous optic neuropathies) IOP measurement also Diurnal and if possible supine Pachymetry Afferent pupillary response testing Gonioscopy Complete slit lamp examination of the anterior segment Dilated fundus examination with optic nerve head and
retinal nerve fiber layer (RNFL) assessment
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SignsThe following features may be more frequently
seen in NTG compared to POAG:- Flame shaped hemorrhages of the optic nerve rim (Drance hemorrhage)
- Deep, focal notching of the rim - Peripapillary atrophy
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Optic nerve in NTGOptic nerves with a larger surface area and with
thinner inferior/inferotemporal rimsPPA in a crescent or halo configuration PPA: adjacent to areas of greatest disc thinning
and corresponding visual field loss While thinning of the optic nerve rim is observed
in all POAG, focal thinning or ‘notching’ is more commonly observed in NTG.
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Acquired pits of optic nerveAcquired pits of optic nerve [APON] which
are thought to be due to focal loss of neuroretinal rim tissue and shown as localised excavations of the lamina cribrosa, are more frequent in NTG.
More prevalent in lower pressure glaucoma than in higher pressure glaucoma.
Inferior part of disc> Superior
Acquired pits of the optic nerve in glaucoma: prevalence and associated visual field loss.Nduaguba C1, Ugurlu S, Caprioli J.
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Disc Hemorrhages
Flame or splinter shaped, often with feathered ends, and is radially oriented and perpendicular to the disc margin
Extends from within the optic nerve head to the adjacent retina, crossing any peripapillary zone of absent or disrupted retinal pigment epithelium
13.8 to 28.0% in NTG
Soares AS, Artes PH, Andreou P, Leblanc RP, Chauhan BC, Nicolela MT. Factors associated with optic disc hemorrhages in glaucoma. Ophthalmology. 2004;111:1653-7.. Diehl DL, Quigley HA, Miller NR, Sommer A, Burney EN. Prevalence and significance of optic disc hemorrhage in a longitudinal study of glaucoma. Arch Ophthalmol. 1990;108:545-50
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Disc HemorrhagesNerve fiber layer hemorrhage and arteriolar
narrowing were found more frequentlyOptic disk hemorrhages showed significantly
higher percentages of progressed points within the 10-degree area compared with the group without optic disk hemorrhage
Comparative optic disc analysis in normal pressure glaucoma, primary open-angle glaucoma, and ocular hypertension.Tezel G1, Kass MA, Kolker AE, Wax MB.Disk hemorrhage is a significantly negative prognostic factor in normal-tension glaucoma.Ishida K1, Yamamoto T, Sugiyama K, Kitazawa Y
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SymptomsAsymptomatic until very advanced. Subjective scotoma near fixation as these
defects can occur early on in the disease process of NTG
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Diagnostic TestsVisual Field testingPachymetryOptic Disc imagingOCT 24 Hr IOP evaluation
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Visual field testingVisual field defects may include those
common to POAG including nasal step and arcuate scotoma.
However, defects noted in NTG tend to be more focal and occur closer to fixation early in the disease
Dense paracentral scotomas may characteristically be noted at initial diagnosis
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Role of Corneal Thickness in NTGPatients with NTG have a thinner CCT than do
patients with POAG or controls. Underestimation of the IOP in patients with
POAG who have thin corneas may lead to a misdiagnosis of NTG, while overestimation of the IOP in normal subjects who have thick corneas may lead to a misdiagnosis of OHT.
Corneal Thickness in Ocular Hypertension, Primary Open-angle Glaucoma, and Normal Tension Glaucoma
René-Pierre Copt, MD; Ravi Thomas, MD; André Mermoud, MD
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Optic Disc ImagingOptic nerve head photography is important to
document the status of the optic nerve at baseline and for future comparisons
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OCT RNFLNormally a double-hump pattern with a dual prominence
at the superior and inferior borders. Pattern lost with superior and inferior RNFL flattening in
glaucomatous eyes Inferior quadrant> Superior quadrantThe mean RNFL thickness/disc area ratio showed a
significantly lesser value for NTG despite the fact that absolute values for mean RNFL thickness and disc area was larger for NTG
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24 Hr IOP evaluation24 Hour IOP evaluation helps to determine
the pressure spikes Normal eyes : between 3 and 6 mmHg and
the variation may increase in glaucomatous eyes
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Progression
Signs:Increased disc cuppingOptic nerve disc hemorrahgesIncreased peripapillary atrophy Visual field lossMonitoring:Optic nerve head photosVisual field testingOCT
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Neurological Work upMarked asymmetry or unilateral optic nerve
involvement Unexplained visual acuity loss Color vision deficits in the absence of visual field
deficits Visual field defects not corresponding or out of
proportion to optic nerve damage Vertically aligned visual field defects Atypical neurologic symptoms for glaucoma Optic nerve pallor in excess of cupping Age less than 50 years
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Differential DiagnosisGlaucomatous etiology
Primary open angle glaucoma with diurnal fluctuation between normal and elevated IOP
Diurnal Variation Test helps in detecting pressure spikes throughout the day
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Intermittent acute angle closure glaucoma – r/o via Gonioscopy
Tonometric underestimation of actual IOP (e.g. thin central corneas) - Pachymetry
Resolved corticosteroid-induced, uveitic, or traumatic glaucoma
Uveitic glaucoma/glaucomatocyclitic crisis (Posner-Schlossman)
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Burned out pigmentary glaucomaSigns: Iris transillumination defects, Pigmented
angle structures, krukrnberg spindles
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Myopia with peripapillary atrophy Optic nerve coloboma or pits Congenital disc anomalies/cupping
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Compressive, metabolic, toxic, inflammatory or infectious optic
neuropathy - Pituitary Adenoma
- Meningioma- Empty sella syndrome- Leber’s optic atrophy- Methanol optic neuropathy- Optic neuritis- Syphilis
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Vascular injuries - Giant cell arteritis
- Non-arteritic anterior ischemic optic neuropathy- Posterior ischemic optic neuropathy- Central retinal artery occlusion- Carotid/ophthalmic artery occlusion
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ManagmentThe main focus for treating NTG is on
lowering the INTRAOCULAR PRESSUREIt can be achieved by:
1. Medical Therapy2. Surgery
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Medical RxStudies suggest a 25%-30% reduction in IOP Topical Prostaglandin analogues are the
preferred drug Adjuntive use of Carbonic anhydrase
inhibitors and B-blockersThough use of B-blockers should be avoided
at nightStudies show brimonidine showed less visual
field progression than twice daily use of timolol Low-Pressure Glaucoma Treatment Study.A randomized trial of brimonidine versus timolol in preserving visual function: results from the Low-Pressure Glaucoma Treatment Study.Krupin T1, Liebmann JM, Greenfield DS, Ritch R, Gardiner S; Low-Pressure Glaucoma Study Group.
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SurgeryFilteration surgeries with peri/intra operative
use of anti- metabloites like MMC and 5-FU show enhanced success of surgery
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Non IOP related RxThe role of different neuroprotective agents
still remains controversialAgents under study include
1. Memantine (NMDA blocker)2. Unoprostone( Prostanoid and synthetic
docasanoid)3. -Statins (HMG-CoA reductase inhibitor)4. Ginkgo Biloba5. Resveratrol
Calcium channel blockers use remains doubtful in cases where vasospasm is a factor
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Thank You