Normal tension glaucoma, also known as low tension glaucoma, is characterized by open angle glaucoma with typical optic nerve damage but intraocular pressure that is consistently normal or only slightly elevated. It has several risk factors such as older age, female sex, East Asian ethnicity, family history of glaucoma, and thin central corneal thickness. The pathogenesis involves vascular dysfunction, autoimmune mechanisms, vascular inflammation, and genetic mutations. Diagnosis involves a detailed medical history, eye examination, visual field testing, and sometimes additional imaging or blood work. Treatment aims to lower intraocular pressure by 30% using topical eye drops, laser trabeculoplasty, or filtering surgeries along with controlling any underlying vascular problems

1. Dr. Samarth Mishra
NORMAL TENSION
GLAUCOMA

2. INTRODUCTION
Also k/a low tension glaucoma
Characterized by:-
Open angle of AC
Typical glaucomatous cupping
 IOP (</= 21 mm of Hg)
VF loss
No obvious / apparent cause for these changes

3. Risk factors for NTG/LTG
 Age - > 50yrs
 Gender – F>M
 Race – Japan > Europe/ North America
 Family/H – POAG is more in families of NPG
- mutation of OPTN gene at chr 10

4. Risk factors for NTG/LTG
CCT
Vascular diseases--Hemodynamic crisis
Hypercoagulability
High blood viscosity
High cholesterol & lipids
CAD
Abnormal vasoregulation –Migraine & Raynauds
phenomenon
Syst. Hypotension –Nocturnal hypotension & pt. on
oral anti-HTN
Obs. Sleep apnoea syn.

5. PATHOGENESIS
I. LOCAL & SYSTEMIC VASCULAR
DYSFUNCTION

6. CONTD…
II. AUTOIMMUNE MECHANISM
 anti-Ro/SS-A positivity and heat shock protein
antibodies
III. VASCULAR INFLAMMATION
Elevated plasma C-reactive protein levels
IV. MUTATION & POLYMORPHISM
 located on chromosome 10
 E50K mutation optineurin gene severe disease and
progressive
 Polymorphisms OPA1 gene mutations dominant
optic atrophy

7. CLINICAL FEATURES
Usually asym.
Symp. of decreased vision, fluctuating vision / VF
loss
Diag. by routine exam. / screening programme
Borderline high IOP
Wide DVT & postural fluctuation

8. Contd…
FUNDUS FINDING :-
OD is more cupped (pallor > cupping)
Focal ischaemic
Diffuse sclerotic
Parapapillary atrophy is more
Diffuse & focal hypoflourescence of OD & abnormal
transit time on FFA
Splinter haemorrhages are more
VF CHANGES:-
defects are denser, steeper, and closer to fixation
Dense arcuate / dense hemifield scotoma

11. DIAGNOSIS
PROPER HISTORY TAKING
1) Past ocular history
 Migraine headaches
 Previous eye disease, eye surgery /head trauma
 Short-sightedness (myopia)
2)Current medication history

12. Contd…
3) ANY ILLNESS
 Vasospasms such as Raynaud’s phenomenon
 Coagulopathies
 Previous blood loss or shock-like episodes
 Nocturnal hypotension
 Autoimmune disorders
 Vascular diseases including atherosclerosis
 Thyroid disease
 Sleep apnoea
 Alzheimer’s disease

13. OCULAR EXAMINATION & TESTS
Slit lamp examination
Tonometry
Gonioscopy
Optic nerve
• Different imaging studies
• Doppler USG- to monitor blood flow to the eye
• Fundus photographs
Retinal exam.
VF analysis

14. CONTD…
SYSTEMIC EXAM. & TESTS
Auscultation & palpation of carotid A.
Neurologic exam.
Blood for Hematocrit, ESR, Hb, ANA
Serologic for Syphilis,
Serum –ACE level, plasma electrophoresis, auto
Ab
Doppler of Carotid A. / Angiography
CT
MRI

15. Extensive systemic work up to be done in pt’s –
< 60 yrs
OD pallor> cupping
IOP < 17 mm of Hg
Rapid progression inspite of adequate t/t

16. D/D
I. Glaucoma
A. Elevated intraocular pressure (IOP) not detected
1. Undetected wide diurnal variation
2. Low scleral rigidity
3. Systemic medication
4. Past systemic medication that may have
elevated IOP
5. Elevation of IOP in supine position only
B. Glaucoma in remission
1. Past corticosteroid administration
2. Pigmentary glaucoma
3. Associated with past uveitis or trauma
4. Glaucomatocyclitic crisis
5. Burned-out primary open-angle glaucoma

17. Contd…
II. Optic nerve damage
A. Congenital optic nerve conditions – Pits, Colobomas,
Tilted discs
B. Ischemic optic neuropathy
1. Arteritic
2. Non-arteritic
C. Compressed lesions
1. Tumors
2. Aneurysms
3. Cysts
4. Chiasmatic arachnoiditis
D. Optic nerve drusen
E. Demyelinating conditions
F. Inflammatory diseases
G. Hereditary optic atrophy
H. Toxic drugs or chemicals

18. Contd…
III Ocular disorders
A. Myopia
B. Retinal degeneration
C. Myelinated nerve fibers
D. Branch vascular occlusions
E. Choroidal nevus or melanoma
F. Choroidal rupture
G. Retinoschisis
H. Chorioretinal disease

19. Contd…
IV. Systemic vascular conditions
A. Anemia
B. Carotid artery obstruction
C. Acute blood loss
D. Arrhythmia
E. Hypotensive episodes
V. Miscellanenous
A. Hysteria
B. Artifact of visual field testing

20. T/T
MEDICAL
Aim is to reduce the IOP upto 30%
Control of systemic vascular disease
Topical agents including b-blockers
latanoprost
brimonidine
carbonic anhydrase inhibitor
miotics

21. SURGICAL
Laser trabeculoplasty (ALT / SLT)
Trabeculectomy with anti-metabolite (mitomycin
C / 5-FU)
Full-thickness filtering surgery

22. RECENT DRUGS-
 serotonin antagonist -- Naftidrofuryl
 a calcium channel blocker-- Nilvadipine
 a nimodipine-like agent -- brovincamines

23. CONCLUSION
With early diagnosis and medical treatment,
further optic nerve damage and/or vision loss
may be prevented
Follow up to be done every 3-6 mons
Target IOP to be maintained for each pt. to
prevent further progression of the disease

24. THANK YOU