Glaucoma Week Series 2011- episode 6 ( Understanding Glaucoma)

Optom
The eyeball is a pear-like globe surrounded  by the uveal body and reinforced by the sclera and the cornea externally which actually provides its (the eyeball's) toughness. It is filled with two types of liquid that defer basically,only, in their viscous status. They are the vitreous humor, occupying the posterior eyeball and bound by the retina posteriorly and the posterior crystalline lens, the pars plana and the ciliary process. the vitreous humor, a gel, faces the optic nerve head and the lamina cribosa. it is always almost static & rather behaves like a connective tissue!
The aqueous humor occupies the anterior portion of the eyeball, separated from the vitreous humor by the crystalline lens, pars plicata, anterior cilliary process and bound anteriorly by the endothelium of the cornea. The fluid is in a constant flux by a process known as inflow and outflow mechanisms. This two mechanisms, though poorly understood, provides the basis of intra-ocular pressure (I.O.P)of the eyeball. I.O.P is an important factor in glaucoma though its effect on individual eyeballs suggests an arbitrary relationship, yet it remains the only controllable factor in Glaucoma management.
Inflow mechanism originates from the ciliary body, anterior crystalline lens on  the posterior channels, the pupillary aperture and ends @ the trabecular meshwork. @ the trabecular meshwork, the outflow mechanism commences. the trigger factor of these two mechanisms of flow is poorly understood but undoubtedly contributes hugely in the pathophysiology of glaucoma. Another outflow channel that dont really influence I.O.P is the uveo-sleral flow located around the junction of the pars plicata and the sclera. It contributes about 10% of total outflow while the trabecular meshwork contributes almost 90% of outflow & influences I.O.P & is influenced by I.O.P too.
The outflow mechanism commences from the trabecular meshwork, the Sinus Venosus Sclerae or Canal of Schlemm, into the larger episcleral venous spaces then into the vena cava...etc etc & the process repeats itself again. The indirect outflow @ the uveo-scleral spaces follows through the capillaries of that part of the ciliary body and escapes into the episcleral spaces & straight into the larger veins- the vena cava!
Any process that disrupts these dual mechanisms results in a disrupted equillibruim of flow with subsequent rise in I.O.P with a resultant pressure on the optic nerve head, the most vulnerable part of the sclera the lamina cribosa becomes a culprit, choking the optic nerve fibres and subsequent death of those fibres.
Cell mediated apoptosis especially on the lamina cribosa and/or the optic nerve fibres can also can contribute to glaucoma formation in some case of 'normal' tension glaucoma.
Ishcaemia of blood vessel supplying the optic nerve head can result to Optic nerve fibre deaths. Also neovascularisation on the optic nerve head, as in Diabetic patients for instance has been implicated in optic nerve death. These all contributes to the formation of Glaucoma but the process is poorly understood, though well articulated.
We will treat the different types of Glaucoma subsequently...
To be continued!
Dr Ezebuiroh Victor Okwudiri.