Primary Open Angle Glaucoma: The Pathophysiolgy, Mechanisms, Future Diagnostic and Therapeutic Directions

Abstract

Primary open angle glaucoma (POAG) is a multifactorial chronic optic neuropathy, characterized by progressive loss of retinal ganglion cells (RGC), leading to structural damage to the optic nerve head (ONH), retinal nerve fiber layer (RNFL), with visual field defects. It is occasioned by major risk factors of high intraocular pressure (IOP) and age. The pathogenesis of POAG is the imbalance between the production and drainage of the aqueous humour (AH). The resultant fluid back-up increases the IOP with consequent optic nerve damage, causing POAG. Modern diagnosis, using scanning laser polarimetry (SLP), confocal scanning laser ophthalmoscopy (CSLO), optical coherence tomography (OCT) etc, plays a vital role in the assessment of the ONH, RNFL and the macular, in POAG. OCT operates on the principles of interferometery, utilizing light beams and their pattern of back-scattering, to build high resolution cross-sectional images of ocular tissues. It gives an objective evaluation of structural alterations in the ONH or macular area of the retina in vivo. POAG is managed medically using classes of drugs like α-adrenergic agonists, beta-adrenergic receptor antagonist, prostaglandin agonists, carbonic anhydrase inhibitors, ccholinergic agonists etc. Surgical intervention is indicated with laser or incisional surgeries, when medical option fails. Future pharmacotherapeutic directions in POAG management consider transgenic model, genetic model, neuroregeneration (stem cell technique), neurodegeneration (Seeing glaucoma as a neurologic disorder much like in Parkinson's and Alzheimer's diseases and the mechanisms that cause the degeneration of RGCs), autoimmune response and T-cell autoimmune response attack.