Glaucoma suspects are controversial clinical dilemmas. These individuals harbor certain risk factors or demonstrate some clinical features suggestive of an increased probability to develop glaucomatous optic atrophy in the future. These characteristics range from high intraocular pressure; optic disc, visual field, or retinal nerve fiber layer abnormalities; or abnormal angles to a positive family history of glaucoma and other risk factors. Individuals having these characteristics should be assessed diligently before a diagnosis of glaucoma is made. Glaucoma is a chronic, lifelong condition, having a negative impact on the quality of life, with an increased risk of medication-related side-effects, adverse economic impacts, and the need for lifestyle changes in the patient. Overdiagnosis and unnecessary treatment of such individuals is bereft of any advantage. This review aims to provide a practical blueprint for the proper diagnosis and management of such glaucoma suspects.

An understanding of the pathogenesis of glaucoma is one of the foundations in glaucoma management. A number of theories have been presented to explain glaucomatous neural degeneration. The vascular theory attempts to explain the causation of glaucoma on the basis of vasogenic factors and altered he-modynamics in the body; however, this theory remains controversial. There are proponents for and against the role played by vascular factors in the development of glaucomatous optic nerve degeneration. This review aims to analyze the various studies performed to provide evidence for and against the vascular theory of glaucoma. It also affirms the need to undertake further studies regarding the path-ogenesis of glaucoma and integrate them into our management strategies. The literature search for this systemic analysis was performed using search engines, such as PubMed, The Virtual Library of the Ministry of Health Malaysia, Google Scholar, and ClinicalKey.

Glaucoma is a multi-factorial neurodegenerative disorder. The common denominator in all types of glaucomas is retinal ganglion cell death through apoptosis. However, this cellular demise in glaucoma is detected late by structural or functional analyses. There can be a 10-year delay prior to the appearance of visual field defects and pre-perimetric glaucoma is an issue still being addressed. However, a new cutting-edge technology called detection of apoptosing retinal cells (DARC) is being developed. This technique is capable of non-invasive, real-time visualization of apoptotic changes at the cellular level. It can detect glaucomatous cell damage at a very early stage, at the moment apoptosis starts, and thus management can be initiated even prior to development of visual field changes. In future, this technique will also be able to provide conclusive evidence of the effectiveness of treatment protocol and the need for any modifications which may be required. This article aims to provide a concise review of DARC technology.

Presently the management of glaucoma is limited to lowering of intra-ocular pressure (IOP). Since this modality does not appear to be successful in all cases there is increasing focus on non-IOP lowering medications. Coenzyme Q is a naturally occurring compound similar to vitamins. There are a few reports suggesting the neuroprotective efficacy of this agent in glaucoma models. The present systematic review was undertaken to study the pharmacology, physiology, metabolism and role of Coenzyme Q in glaucoma. An English-language search for relevant items was undertaken using PubMed, Google Scholar, Scopus and other databases. The present review found a positive outcome of Coenzyme Q as a neuroprotectant being reported in all studies. However, the review also found that the majority of studies on Coenzyme Q have been reported by a single group of researchers. In order to have a more wide-ranging impact regarding the efficacy of Coenzyme Q in glaucoma, it would be useful to undertake further multi- center trials.

SummarySpontaneous absorption of lenses or cataracts is rare. We report a case of bilateral spontaneous lens absorption in a 36-year-old woman for which no cause could be determined despite extensive laboratory testing. Case ReportA 36-year-old female presented at the eye clinic of Queen Elizabeth Hospital, Kota Kinabalu, Malaysia, with a complaint of poor vision in both eyes since childhood. She had not previously seen an ophthalmologist and had no history suggestive of trauma, surgery, red eyes, or pain. No systemic illnesses were reported. She was born at home; no additional birth history was available. Family and social histories were noncontributory.On examination, visual acuity was hand movements in both eyes. Intraocular pressures were 14 mm Hg in the right eye and 17 mm Hg in the left. The eyes were orthophoric, with full extraocular motility. Slit-lamp biomicroscopic examination was remarkable for whitish membranous structures in the anterior chambers of both eyes that appeared to be empty capsular bags located in the lower part of the anterior chambers (Figures 1, 2A, 3A). No residual zonules or signs of inflammation were evident. The pupils were 3-4 mm and reacted to light sluggishly. Both eyes were aphakic; an intact anterior vitreous face was present. The optic discs of both eyes were hypoplastic and pale ( Figures 2B, 3B, 4, 5).The patient was sent for refractive correction, but her vision failed to improve beyond hand movements in both eyes. Her refraction was +10.00 +3.50 × 55 in the right eye and +11.00 +2.50 × 108 in the left. Routine blood tests, including full blood count, fasting blood sugar, erythrocyte sedimentation rate, blood urea, and serum electrolytes and creatinine, were normal. Testing for congenital infections, including toxoplasmosis, rubella, cytomegalovirus, leptospirosis, and herpes simplex virus were also performed and found to be negative. Computed tomography of the brain and orbits with contrast agents revealed no abnormalities.