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Material can be deposited in the cornea as a result of a wide range of systemic and ophthalmic diseases, as well as local and systemic therapies. Causes include local infection or trauma, systemic malignancy, a wide range of medications and a host of genetic and metabolic diseases. Some of these can be acutely life threatening, so generalists caring for both children and adults should have a basic awareness of the pattern and distribution of corneal deposits to facilitate timely diagnosis, investigation, management or onward referral to avoid significant morbidity or mortality. This article outlines causes of corneal deposits found in patients presenting to primary care, ophthalmic clinics or encountered on the wards to help generalists avoid missing serious pathology. It also provides insight into the natural history of underlying causative conditions and their possible treatments.

Nystagmus is the repetitive to and fro movement of the eyes, which may be physiological or pathological. The movements can be horizontal, vertical, torsional or a combination of these movements. It starts by a slow movement of the eye away from the visual target. The second movement brings the eye back to the visual target. If this second movement is quick, the nystagmus is called jerk nystagmus. If the second movement is slow, the nystagmus is said to be pendular. Maintaining steady gaze is dependent upon visual fixation, the vestibulo-ocular reflex and the gaze-holding neural integrator system. Pathological nystagmus typically presents with the symptom of oscillopsia, which is the illusory movement of the surrounding environment. Nystagmus that develops outside of early infancy is termed acquired nystagmus. There may be serious underlying pathology that will require further investigation and management. This article reviews the terminology, pathophysiology, causes and treatment of acquired nystagmus.

Background/aims To evaluate the vitreous signals obtained on spectral domain optical coherence tomography (SD-OCT) in patients with uveitic cystoid macular oedema (CMO) and compare these signals before and after sub-Tenon9s triamcinolone acetonide injection. Methods Retrospective study with standardised longitudinal imaging preintervention and postintervention. The study cohort comprises 22 patients (22 eyes) with uveitic CMO receiving a sub-Tenon9s triamcinolone acetonide (STTA) injection. Post hoc analysis of SD-OCT images using custom software provided an ‘absolute’ measurement of vitreous signal intensity, which was expressed as a ratio to the retinal pigment epithelium intensity (‘VIT/RPE-relative intensity’) in arbitrary units. Main outcome measure Difference in VIT/RPE-relative intensity before and after treatment. Results Treatment with STTA resulted in a significant reduction in VIT/RPE-relative intensity, which was associated with both a reduction in central retinal thickness (CRT) and improvement in visual acuity. Mean (SD) VIT/RPE-relative intensity pretreatment was 0.139 (0.074) versus 0.053 (0.028) post-treatment (p=3×10 −5 ). Mean (SD) CRT was 581 μm (119 μm) pretreatment versus 333 μm (95 μm) post-treatment (p=2×10 −8 ); the mean reduction in CRT was 248 (95% CI 189 to 306). The correlation coefficient between VIT/RPE-relative intensity and CRT was 0.534 (p=0.011) and between VIT/RPE-relative intensity and visual acuity was 0.702 (p=0.0001). Conclusions This study provides evidence that the OCT-derived VIT/RPE-relative intensity may be useful as a quantitative and objective marker of disease activity and treatment response in uveitis complicated by CMO. This first longitudinal study of this novel OCT parameter is an encouraging step in the development of sensitive objective OCT-based endpoints for trials of efficacy in uveitis.

“As the UK House of Lords considers the effects of the Mental Capacity Act 2005, we report on how the act came into being and how the assessment of mental capacity varies around the globe”