Primary open angle glaucoma , normotensive glaucoma

1. Primary Open Angle
Glaucoma, Normotensive
Glaucoma & Low-tension
Glaucoma
BIPIN BISTA
RESIDENT
OPHTHALMOLOGY
NATIONAL MEDICAL COLLEGE
& TEACHING HOSPITAL

2. Chronic Open Angle Glaucoma
Continued research , has shown the concept of primary and secondary glaucoma to be arbitrary.
Thus, this term would be used as COAG.
COAG is characterised by :
a) An open normal-appearing AC angle & increased IOP without any apparent ocular or
systemic abnormality.
b) Typical ON damage or glaucomatous VF.

3. Definition of COAG
It is a multifactorial Optic Neuropathy in which there is characteristic atrophy of the Optic Nerve.
Although abnormally elevated IOP had long been considered a risk factor for COAG.

4. Normal Tension Glaucoma
These are patients with open, normal-appearing anterior chamber angles who have
glaucomatous Optic Nerve Head and visual field damage despite pressure that has never been
documented above 21 mmHg.

5. Proposed Mechanism of COAG
•Histopathological observation
•Influence of Aqueous Humor
•Alterations of the Trabecular Meshwork
•Stress Response Markers
•Collapse of the Schlemm Canal : with or without bulge of TM into the canal.
•Alterations of the Intrascleral Channels

6. Influence of Aqueous Humor
Abnormal constituent of AH may adversely affect the outflow structures.
Transforming Growth Factors(TGFs) – multifunctional polypeptides with several cell regulatory
properties : Inhibition of epithelial cell proliferation, Induction of ECM protein synthesis, and
stimulation of mesenchymal cell growth.
Abnormal levels of TGF-β2 may decrease the cellularity of TM and promote a buildup of
excessive amounts of ECM materials with subsequent increased resistance of outflow.

7. Alterations of the Trabecular Meshwork
Juxtacanalicular tissue and inner wall of the Schlemm canal: Site of maximum resistance .
Increase in ECM and accumulation of ‘’plaque material’’ .

8. Stress Response Markers
Myocilin, first gene to be mutated in COAG appears to be in greater amount in time of Stress.
Heat-shock proteins , αB-crystalline and myocilin to be more in regions of the meshwork.
Endothelial cell lining are more active in COAG.
Cellularity of TM in COAG is lower than in non-glaucomatous eyes.
Cross-linked actin are found in higher levels and increase more in response to dexamethasone in
glaucomatous eyes.
Intertrabecular space showed general thickening of trabeculae, are thus narrowed.
Matrix vesicles, representing EC lysosomes, a sheath material like fibers, fibronectin , elastin is found
in abnormal amounts in the Juxtacanalicular connective tissue.
In COAG, hyaluronic acid was depleted in all layers and chondroitin sulphate was higher in JCCT.
Giant vacuoles have been reduced and pore density reduced and uneven.

9. Relationship of IOP to Corticosteroid
Sensitivity.
1) Hypothalamic-Pituitary-Adrenal Axis Theory
2) Cyclic-Adenosine-Monophosphate theory : permissive β ADRENERGIC stimulation of adenyl
cyclase , responsible for synthesis of cyclic-adenosine Monophosphate.
3) Glycosaminoglycans Theory : when polymerised,gets hydrated, swell and obstruct AO,
catabolic enzyme released from lysosomes depolymerise GAG. Corticosteroids stabilises
lysosome membrane.
4) Phagocytosis Theory : endothelial cell lining are normally phagocytic. They suppreses
phagocytosis.

10. Mechanism of Optic Neuropathy
Immunological Studies : elevated Antiphospholipid Cardiolipid antibodies, Immunoglob
Blood Flow :altered autoregulation of blood flow in the Optic Nerve and retinal circulations,
differences in Red cell aggregability, increased plasma viscosity and activation of Clotting
Factors.
Apoptotic Susceptibility of Ganglion Cells : Death of Ganglionic cell layer , accumulation of
Glutamate and imbalance of proteases
Possible Infectious Susceptibilty : H.pylori

11. Nature of Progressive Visual Loss
Pre-perimetric : Sub-clinical, subtle visual sensitivity changes, non-specific perimetric change.
But despite Normal VF, significant retinal ganglionic cell loss, progressive disc cupping and retinal
nerve fiber layer thinning may be present.
Threshold and Conversion : persistent visual field defects developing in previously normal visual
fields.
Conversion : previously pre-perimetric disease has worsened to become detectable.
Critical Phase :scotomas involve by deepening, but enlarging arcuate defects and the
appearance of new defects
Blindness : Higher incidence despite treatment : 27% & 9% respectively in U/L and B/l

12. Visual field Defects
1. Earliest changes : Increased variability of
responses.
2. Paracentral : 70 % of all defects. Since defects
respect the distribution of RNFL they
terminate at the horizontal line, defect
above/below are not aligned.
3. Nasal Step of Ronne
4. Arcuate shaped Defects
5. Enlargement of scotomas
6. Deepening of scotomas
7. Ring-scotoma
8. End-stage.

13. Scanning laser tomography

14. COAG VS NTG
COAG
1. Elevated IOP
2. ONH : Cupping, RNFL defects,
Saucerisation,Disc Hmrg,peripapillary
atropthy
3. VF : Previously mentioned
NTG
1. IOP : Normalcy
2. ONH : Similar defects to COAG
3. VF : deeper, more localised scotoma,
greater rate of progression

15. MANAGEMENT
GOALS : target pressure, proportional reduction of IOP, Monitoring of the ON and VF.

16. MEDICAL THERAPY
Commensing medical therapy
Review
Preimetry
Gonioscopy
OD examination

17. If doesn’t responds
Laser trabeculoplasty
Surgery

18. Prognosis
Diagnosed COAG will not be blind in their lifetime
Mean time for progression to blindness is 20 years.

19. Reference:
1.Glaucoma – Shield Textbook of Glaucoma 6th edition
2.Curbside Consultation in Glaucoma : Steven J. Gedde
3.Myron yanoff and jay s duker4th edition
Thank you