Normal tension

glaucomaDr. Meenank

• 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

Classification Open angle glaucoma Angle closure glaucoma Child-hood glaucoma

Primary glaucoma Secondary 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

• 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

Normal tension glaucoma

• seen mostly with – Advancing ageMyopesMonozygoticsType 2 D.M , systemic hypertension Atherosclosis, ischemic vascular disGLClB and GLC1E genesAtypical – unilateral, dec central Vn, NRR

pallor, VF loss not consistent with optic disc appearance, anemia , heart dis, syphilis, temporal arteritis, young age

• Clinical feat : higher prevalence of vasospastic

disorders migraine, Raynaud phenomenon,

ischemic vascular dis., coagulopathies Bilateral and progressive Normal but, asymmetric IOPProgressive visual field lossPeripapillary atrophy – senile sclerotic, focal

ischemicDense Para central scotoma

• 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,

• 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

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

• 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

• 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

• 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)

Disc hemorrhage

Thank you