Glaucoma

Chronic progressive optic neuropathy caused by a group of ocular conditions leading to damage of optic nerve and loss of visual function.Most common risk factor being a raised intraocular pressure.

A sustained increase in IOP may be due to

-increased formation of aqueous humour (rare)

-difficulty in its exit (most common)

-raised pressure in episcleral veins (rare)

Raised IOP is essentially due to an increased resistance to the circulation of aqueous humour at the pupil &/or to its drainage through the angle of the anterior chamber.

If trabecular meshwork is blocked, some drainage does occur through the uveoscleral outflow, but these alternative channels are not efficient & they are icapable of dealing with sudden changes of IOP.

Mechanical Changes:

The coats of the eye can withstand fairly high IOPs except at the lamina cribrosa, the fenestrated region through which optic nerve fibres enter the eye. Here, nerve fibres are supported by glial tissue & have to bend over the edge of the disc. A raised IOP causes mechanical pressure on the lamina cribrosa altering capillary blood flow & decreasing axoplasmic flows in the initial stages.Later, significant backward displacement & compaction of the laminar plates narrows the openings through which the axons pass, directly damaging the nerve fibre bundles.

Vascular Perfusion:

The perfusion of the optic nerve head may be affected because of a lack of an adequate autoregulatory mechanism. A substantial rise in IOP can also decrease the capillary blood flow due to mechanical compression of vessels at lamina cribrosa or a decreased flow at the annulus of Zinn, which supplies nutrition to the laminar & post laminar optic nerve head. A fall in perfusion pressure at optic disc can also be caused by systemic factors such as hypotension, vasospasm & acute blood loss.

Other Factors:

Patients with Primary Open Angle Glaucoma have a susceptibility to damage, in some part, because of the presence of larger openings in the lamina cribrosa that allows for greater mechanical displacement of the nerve fibres coursing through.

Dysfunctional axoplasmic transport, because of these mechanical or vascular changes, lead to fewer trophic factors reaching the ganglion cells-damage & eventual death of ganglion cells-triggers apoptosis of adjacent cells. As the loss of nerve fibres extends beyond the normal physiological overlap of functional zones, visual field defects become apparent.initially & predominantly @ superior & inferior poles.The normal distribution of nerve fibres in retina is such that polar loss of nerve fibres translates into an arch above & below the macular area, ending in a horizontal line nasally, with neither crossing it.


Diagnosis:
-charactaristic changes in optic nerve head
-abnormalities in the visual field
-rise in IOP

-type of glaucoma is determined by clinical features & status of anterior chamber determined by gonioscopy
-primary open angle glaucoma is diagnosed if at least two of the three abnormalities are detected
-in acute & subacute primary angle closure glaucoma & the secondary glaucomas- the presence of raised IOP is enough to make a diagnosis

Optic nerve head changes in glaucoma
Ratio of normal cup-disc diameter= .3:1
to diagnose glaucoma:
1.asymmetry of cup:disc between two eyes
cup:disc::>.2
2.localized notch/thinning of neuroretinal rim
3.enlarged cup-disc ratio >.5, especially in vertical axis
4.pallor of neuroretinal rim
5.superficial disc hemorrhages
6.vascular signs suggestive of an acquired cupping, such as baring of the circumlinear vessels & overpass of central vessels
7.parapapillary atrophy

Visual field abnormalities:
initially observed in Bjerrum area,10-25 degrees from fixation-correlate with abnormalities on optic nerve head
common glaucomatous visual field defects as seen in kinetic perimetry as follows:

1.Relative paracentral scotomas- areas where smaller or dimmer targets are not visualized by the patient-but larger/brighter targets are appreciated
2.Nasal step-The appearance of a horizontal shelf in the nasal visual field is caused by an asymmetry in the nerve fibre loss at the two poles
3.Siedel scotoma- one that appears to start@the poles poles of the blind spot & arches over the macular area, without reaching the horizontal meridian nasally
4.Arcuate scotomar-appear to start @the superior/inferior poles of the blind spot & arch over the macular area, widening as they curve down or up to end as a horizontal line nasally, never crossing the horizontal divide of the field
5.Double arcuate/ring scotoma- advanced glaucomatous field defects- only central & temporal islands of vision are left when two arcuate scotomas expand to involve the peripheral visual field
6.End stage/near total field defect-only a residual temporal island of vision left