1. Normal tension
glaucoma
Dr. Meenank

2. • Glaucoma : Multifactorial optic neuropathy in
where there is characteristic atrophy of optic nerve.
• Although elevated IOP is clearly the most frequent
causative risk factor
• Normal IOP 10 – 21 mmHg

3. Classification
 Primary glaucoma
 Secondary glaucoma
 Open angle glaucoma
 Angle closure glaucoma
 Child-hood glaucoma
Primary glaucoma : not ass. With known ocular (or)
systemic diseases that cause an inc. resistance to aq.
Flow (or) angle closure. Usually bilateral
Secondary glaucoma : associated with ocular or
systemic disorders responsible for dec. aq. Flow
usually asymmetric and unilateral

4. Normal tension glaucoma
• Type of open angle glaucoma without raise in IOP
• Also called low tension glaucoma
• Cause - Chronic low vascular perfusion, which
makes optic nerve head susceptible to normal IOP
• Stress markers –myocilin and aβ- crystalline in TMW
• Inc. age, female, mutation of OPTN gene, sleep
apnea, auto-antibodies, migraine and Raynaud's

5. • seen mostly with –
 Advancing age
 Myopes
 Monozygotics
 Type 2 D.M , systemic hypertension
 Atherosclosis, ischemic vascular dis
 GLClB and GLC1E genes
 Atypical – unilateral, dec central Vn, NRR pallor,
VF loss not consistent with optic disc
appearance, anemia , heart dis, syphilis,
temporal arteritis, young age

6. • Clinical feat :
 higher prevalence of vasospastic disorders
migraine, Raynaud phenomenon, ischemic
vascular dis., coagulopathies
 Bilateral and progressive
 Normal but, asymmetric IOP
 Progressive visual field loss
 Peripapillary atrophy – senile sclerotic, focal
ischemic
 Dense Para central scotoma

7. • Clinical features :
• Optic nerve head – thin neuro-retinal rim, disc Hx,
retinal nerve fiber defects
• Visual fields – more deeper and localized scotoma
with constant progression
• IOP –normal asymmetric IOP, wide diurnal variation
• Ocular vascular abr - vascular perfusion of optic
head
 Non-progressive – transient vascular shock
 Progressive – Ch. Insufficiency
• Sys vascular abr - alt BP (nocturnal dip) + elevated
diastolic,
 Asymptomatic MI , frequent headache ± migraine,

8. • Differential diagnosis :
 Several contd. Mimic NTG causing arcuate-type of
visual field defects , some are progressive
 IOP – raised IOP is noted with systemic β-blockers
 Tonometer – low readings due to
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Reduced scleral rigidity
Corneal thickness
Assessment of CCT – NTG (530 -545 μm)
Refractive surgery
Myopic disc with VF changes
Previously elevated IOP
Intermittent angle closure
POAG with diurnal variation

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Diagnostic evaluation :
Repeated testing
Applanation tonometry at various times
Gonioscopy
Stereoscopic disc evaluation
Complete medical history
Provocation test
 Water drinking test
 Steroid provocation test
 Jugular vein compression test
 imaging – CT, MRI, OCT

10. • Prognosis and therapy :
• According to Collaborative Normal-Tension
Glaucoma Study (CNTGS)
• Goal - to achieve an lOP that is as low as possible,
without the development of complications.
• Aggressive reduction in IOP by 30% to reduce
progressive VF loss from base line
• Criteria for initiation of thx
 Visual field loss threatening fixation
 Disc hemorrhage
 Documented VF or optic nerve progression
• If independent of IOP check cvs, anemia, htn, CHF,
TIH
• Ensure maximum optic nerve head perfusion

11. • Systemic and tropical  Calcium channel blockers – inc. capillary perfusion of optic
nerve, dec. in progression
 Prostaglandin analogs – achieve target IOP , below
episcleral venous pressure
• Others –
 Tropical β-blockers, CAI, alpha agonist
• Surgery –
 laser trabeculoplasty, glaucoma filtering Sx ±(anti-fibrotic
agent)

12. Disc hemorrhage

13. Thank you