Acute myositis is the second most common component of non-specific orbital inflammation. We will describe its clinical features and natural history. This is a retrospective study of 10 cases. The diagnosis of acute myositis was based on clinical and imaging criteria. Our study includes five men and five women. The average age was 35.8 years (17-59 years). Clinical symptoms were: pain increased on eye movement (10/10), diplopia (4/10), proptosis (6/10), visual loss (3/10), lid edema (6/10), conjunctival hyperemia (7/10), anterior scleritis (2/10), episcleritis (2/10), chemosis (4/10), upper lid retraction (1/10), limitation of eye movement (3/10), fundus abnormalities (2/10). Imaging showed thickening of one or more extraocular muscles (10/10). Recovery was complete with anti-inflammatory therapy in six patients. Three patients experienced recurrence, and one patient had a clinical rebound upon tapering the treatment. Acute myositis can be defined by pain on eye movement, signs of inflammation, and extraocular muscle thickening on imaging. If the clinical presentation is typical, histopathological analysis can be deferred but remains necessary in cases of poor response to treatment, chronic duration or suspicion of tumor infiltration. The diagnosis of acute myositis may be suspected in the presence of consistent, well-defined clinical signs. Contiguous inflammation is often associated. Treatment is based on steroids or non-steroidal treatment anti-inflammatory therapy, administered alone or consecutively. Recurrences are frequent but do not alter the final prognosis.

PURPOSE:

: To compare the interocular asymmetry of visual field loss in newly diagnosed normal-tension glaucoma (NTG), primary open-angle glaucoma (POAG), and chronic angle-closure glaucoma (CACG) patients.

METHODS::

Visual field results of 117 newly diagnosed, treatment-naive glaucoma patients (42 NTG, 38 POAG, and 37 CACG) were studied retrospectively. The following 3 visual field defect parameters were used to evaluate the interocular asymmetry: (1) global indices; (2) local mean deviations (MDs) of 6 predefined visual field areas; and (3) stage designated by glaucoma staging system 2. The differences of the above parameters between the trial eye (the eye with greater MDs) and the fellow eye in each subject were defined as interocular asymmetry scores.

RESULTS::

Interocular asymmetry of visual field loss was presented in all the 3 groups (all P<0.05). CACG group had greater total MD interocular asymmetry score compared with the NTG and POAG groups (among groups, P=0.008; NTG vs. CACG, P=0.005; POAG vs. CACG, P=0.009). CACG also presented with significantly higher local MD interocular asymmetry scores at central, inferior, and temporal areas compared with those of the POAG group and at inferior area compared with that of NTG group. No significant difference in either total or local MDs was detected between NTG and POAG (all P>0.05). Interocular asymmetry scores of glaucoma staging system 2 had no significant difference among the 3 groups (P=0.068).

CONCLUSIONS::

All CACG, POAG, and NTG groups presented with interocular asymmetric visual field loss at the time of diagnosis. CACG had greater interocular asymmetry compared with NTG and POAG. No significant interocular asymmetry difference was observed between NTG and POAG.

A 22-year-old lady presented with gradually progressive visual loss and chronic pain in both the eyes of 3 months duration. The clinical examination and fundus fluorescein angiography were suggestive of bilateral ocular ischaemic syndrome. Her upper limb pulses were feeble and blood pressure was not recordable in the same. Carotid Doppler revealed a bilateral carotid artery occlusion. Systemic markers for inflammation were elevated. Diagnosis of Takayasu arteritis was made on the basis of clinical and laboratory findings. Takayasu arteritis should be considered in the differential diagnosis of ocular ischaemic syndrome, particularly in young Asian women.

Abstract

Purpose:

To present a unique case of a 33-year-old woman using paroxetine who presented with acute unilateral visual loss due to chronic angle-closure glaucoma.

Methods:

Case report.

Results:

A 33-year-old women who had been under paroxetine treatment for the past four months presented at the emergency room due to a sudden loss of visual acuity (VA) in the left eye (LE). Narrow anterior chamber was detected. Intraocular pressure (IOP) was 29 mmHg right eye (RE) and 42 mm Hg LE. A fundus exam revealed a cup-to-disc ratio of 0.9-1 for the LE and of 0.1-0.2 for the RE. Paroxetine treatment was suspended, and after 48 h IOP was 10 mm Hg in both eyes (BE). ND-YAG laser iridotomy was performed in BE. In the subsequent visit, IOP was 25 mm Hg in the RE and 41 mm Hg in the LE; on her own initiative the patient had resumed paroxetine treatment. After requesting the patient again to stop taking the anti-depressant, IOP was 10 mm Hg in BE in the next exam 48 h later.

Conclusions:

As far as we are aware, there are no other reports of chronic angle-closure glaucoma related to the use of paroxetine. We thus consider that, before initiating treatment with this drug, patients should be informed of its potential ocular risks and they should be subjected to an ophthalmologic examination before its use is authorized.

To evaluate retina and optic nerve damage following experimental blast injury.Healthy adult mice were exposed to an overpressure blast wave using a custom-built blast chamber. The effects of blast exposure on retina and optic nerve function and structure were evaluated using the pattern electroretinogram (pERG), spectral domain optical coherence tomography (OCT), and the chromatic pupil light reflex.Assessment of the pupil response to light demonstrated decreased maximum pupil constriction diameter in blast-injured mice using red light or blue light stimuli 24 hours after injury compared with baseline in the eye exposed to direct blast injury. A decrease in the pupil light reflex was not observed chronically following blast exposure. We observed a biphasic pERG decrease with the acute injury recovering by 24 hours postblast and the chronic injury appearing at 4 months postblast injury. Furthermore, at 3 months following injury, a significant decrease in the retinal nerve fiber layer was observed using OCT compared with controls. Histologic analysis of the retina and optic nerve revealed punctate regions of reduced cellularity in the ganglion cell layer and damage to optic nerves. Additionally, a significant upregulation of proteins associated with oxidative stress was observed acutely following blast exposure compared with control mice.Our study demonstrates that decrements in retinal ganglion cell responses can be detected after blast injury using noninvasive functional and structural tests. These objective responses may serve as surrogate tests for higher CNS functions following traumatic brain injury that are difficult to quantify.

Abstract

Purpose:

To identify the causes of visual loss associated with uveitis and its risk factors.

Methods:

Review of 359 patients attending a uveitis service.

Results:

Anterior uveitis (n = 229, 63.8%) was most common, followed by panuveitis (n = 55, 15.3%). There were 82 infective cases with 29.3% associated with tuberculosis. Visual loss occurred in 100 (27.9%) patients, of which 27 (7.5%) had severe visual loss. The main causes of visual loss were cataract (26%) and glaucoma (12%). Cystoid macular edema (14.8%) accounted for severe visual loss. Panuveitis was predictive for visual loss (p = 0.022, odds ratio (OR) 2.22) and severe visual loss (p = 0.01, OR 3.47). Posterior uveitis (p = 0.005, OR 5.01) and chronic uveitis (p = 0.008, OR 3.83) also showed higher risk for severe visual loss.

Conclusion:

With panuveitis being the second most common presentation, early specialist referral is essential in preventing visual loss.

PURPOSE:

To determine the safety and efficacy of low-voltage, external-beam, stereotactic radiotherapy (SRT) for patients with neovascular age-related macular degeneration (nvAMD).

DESIGN:

Randomized, double-masked, sham-controlled, multicenter, clinical trial.

PARTICIPANTS:

Two hundred thirty patients with onset of nvAMD within 3 years who received 3 or more injections of ranibizumab or bevacizumab within the preceding year and who needed continuing ranibizumab or bevacizumab treatment.

INTERVENTIONS:

Participants were randomized 2:1:2:1 to 16 Gy plus pro re nata (PRN) ranibizumab, sham 16 Gy plus PRN ranibizumab, 24 Gy plus PRN ranibizumab, or sham 24 Gy plus PRN ranibizumab, respectively.

MAIN OUTCOME MEASURES:

The primary efficacy end point was the mean number of ranibizumab injections at 52 weeks. Secondary end points were change in mean best-corrected visual acuity (VA), loss of fewer than 15 Early Treatment Diabetic Retinopathy Study letters, gain of 0 or more and 15 or more letters, and change in angiographic total lesion size and choroidal neovascularization (CNV) lesion size.

RESULTS:

Both the 16-Gy and 24-Gy SRT arms received significantly fewer ranibizumab treatments compared with the sham arms: mean number of treatments, 2.64 (median, 2), 2.43 (median, 2), and 3.74 (median, 3.5), respectively (P = 0.013 and P = 0.004, respectively, vs. sham). Change in mean VA was -0.28, +0.40, and -1.57 letters for the 16-Gy, 24-Gy, and sham arms, respectively. The 16-Gy, 24-Gy, and sham arms lost fewer than 15 letters in 93%, 89%, and 91% of eyes, respectively, with 53%, 57%, and 56% gaining 0 or more letters, respectively, and 4% gaining 15 letters or more in all arms. Mean total angiographic lesion area changed by -1.15 mm(2), +0.49 mm(2), and +0.75 mm(2), respectively; mean CNV lesion area decreased by 0.16 mm(2), 0.18 mm(2), and 0.10 mm(2), respectively. Optical coherence tomography central subfield thickness decreased by 85.90 μm, 70.39 μm, and 33.51 μm, respectively. The number of adverse events (AEs) and number of serious AEs (SAEs) were similar across arms. No AEs were attributed to radiation. No SAEs occurred in the study eye.

CONCLUSIONS:

A single dose of SRT significantly reduces ranibizumab retreatment for patients with nvAMD, with a favorable safety profile at 1 year. Whereas chronic nvAMD typically results in loss of VA over time, SRT is associated with relatively well-preserved VA over 1 year. FINANCIAL DISCLOSURE(S): Proprietary or commercial disclosure may be found after the references.

IMPORTANCE This study provides further evidence from a national sample to generalize the relationship between depression and vision loss to adults across the age spectrum. Better recognition of depression among people reporting reduced ability to perform routine activities of daily living due to vision loss is warranted.

OBJECTIVES

To estimate, in a national survey of US adults 20 years of age or older, the prevalence of depression among adults reporting visual function loss and among those with visual acuity impairment. The relationship between depression and vision loss has not been reported in a nationally representative sample of US adults. Previous studies have been limited to specific cohorts and predominantly focused on the older population. DESIGN The National Health and Nutrition Examination Survey (NHANES) 2005-2008. SETTING A cross-sectional, nationally representative sample of adults, with prevalence estimates weighted to represent the civilian, noninstitutionalized US population. PARTICIPANTS A total of 10 480 US adults 20 years of age or older. MAIN OUTCOME MEASURES Depression, as measured by the 9-item Patient Health Questionnaire depression scale, and vision loss, as measured by visual function using a questionnaire and by visual acuity at examination.

RESULTS

In 2005-2008, the estimated crude prevalence of depression (9-item Patient Health Questionnaire score of ≥10) was 11.3% (95% CI, 9.7%-13.2%) among adults with self-reported visual function loss and 4.8% (95% CI, 4.0%-5.7%) among adults without. The estimated prevalence of depression was 10.7% (95% CI, 8.0%-14.3%) among adults with presenting visual acuity impairment (visual acuity worse than 20/40 in the better-seeing eye) compared with 6.8% (95% CI, 5.8%-7.8%) among adults with normal visual acuity. After controlling for age, sex, race/ethnicity, marital status, living alone or not, education, income, employment status, health insurance, body mass index, smoking, binge drinking, general health status, eyesight worry, and major chronic conditions, self-reported visual function loss remained significantly associated with depression (overall odds ratio, 1.9 [95% CI, 1.6-2.3]), whereas the association between presenting visual acuity impairment and depression was no longer statistically significant.

CONCLUSIONS

AND RELEVANCE Self-reported visual function loss, rather than loss of visual acuity, is significantly associated with depression. Health professionals should be aware of the risk of depression among persons reporting visual function loss.

Glaucoma is a heterogeneous group of conditions involving progressive damage to the optic nerve, deterioration of retinal ganglion cells and ultimately visual field loss. It is a leading cause of blindness worldwide. Open angle glaucoma (OAG), the commonest form of glaucoma, is a chronic condition that may or may not present with increased intraocular pressure (IOP). Neuroprotection for glaucoma refers to any intervention intended to prevent optic nerve damage or cell death.The objective of this review was to systematically examine the evidence regarding the effectiveness of neuroprotective agents for slowing the progression of OAG in adults.We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2012, Issue 9), Ovid MEDLINE, Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, Ovid OLDMEDLINE, (January 1950 to October 2012), EMBASE (January 1980 to October 2012), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to October 2012), the metaRegister of Controlled Trials (mRCT) (www.controlled-trials.com), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. The electronic databases were last searched on 16 October 2012.We included randomized controlled trials (RCTs) in which topical or oral treatments were used for neuroprotection in adults with OAG. Minimum follow up time was four years.Two review authors independently reviewed titles and abstracts from the literature searches. Full-text copies of potentially relevant studies were obtained and re-evaluated for inclusion. Two review authors independently extracted data related study characteristics, risk of bias, and outcome data. One trial was identified for this review, thus we performed no meta-analysis. Two studies comparing memantine to placebo are currently awaiting classification until additional study details are provided. We documented reasons for excluding studies from the review.We included one multi-center RCT of adults with low-pressure glaucoma (Low-pressure Glaucoma Treatment Study, LoGTS) conducted in the USA. The primary outcome was visual field progression after four years of treatment with either brimonidine or timolol. Of the 190 adults enrolled in the study, 12 (6.3%) were excluded after randomization and 77 (40.5%) did not complete four years of follow up. The rate of attrition was unbalanced between groups with more participants dropping out of the brimonidine group (55%) than the timolol group (29%). Of those remaining in the study at four years, participants assigned to brimonidine showed less visual field progression than participants assigned to timolol (5/45 participants in the brimonidine group compared with 18/56 participants in the timolol group). Since no information was available for the 12 participants excluded from the study, or the 77 participants who dropped out of the study, we cannot draw any conclusions from these results as the participants for whom data are missing may or may not have progressed. The mean IOP was similar in both groups at the four-year follow up among those for whom data were available: 14.2 mmHg (standard deviation (SD) = 1.9) among the 43 participants in the brimonidine group and 14.0 mmHg (SD = 2.6) among the 48 participants in the timolol group. Among the participants who developed progressive visual field loss, IOP reduction of 20% or greater was not significantly different between groups: 4/9 participants in the brimonidine group and 12/31 participants in the timolol group. The study authors did not report data for visual acuity or vertical cup-disc ratio. The most frequent adverse event was ocular allergy to study drug, which occurred more frequently in the brimonidine group (20/99 participants) than the timolol group (3/79 participants).Although neuroprotective agents are intended to act as pharmacological antagonists to prevent cell death, this trial did not provide evidence that they are effective in preventing retinal ganglion cell death, and thus preserving vision in people with OAG. Further clinical research is needed to determine whether neuroprotective agents may be beneficial for individuals with OAG. Such research should focus outcomes important to patients, such as preservation of vision, and how these outcomes relate to cell death and optic nerve damage. Since OAG is a chronic, progressive disease with variability in symptoms, RCTs designed to measure the effectiveness of neuroprotective agents would require long-term follow up (more than four years) in order to detect clinically meaningful effects.

Chronic cicatrizing conjunctivitis is a relatively uncommon condition resulting in significant ophthalmic morbidity, including keratoconjunctivitis sicca, cicatricial entropion, trichiasis, corneal scarring, significant discomfort, and visual loss. The potential causes of cicatrizing conjunctivitis are varied and include commonly encountered entities such as ocular cicatricial pemphigoid, Stevens-Johnson syndrome, and trachoma and many more rare causes which are particularly difficult to diagnose and treat and may not be familiar to the ophthalmologist. The authors herein present a case of chronic cicatrizing conjunctivitis, cicatricial entropion, and trichiasis caused by a rare entity called linear IgA bullous dermatosis. The case presentation conforms to the tenets of the Declaration of Helsinki and is Health Insurance Portability and Accountability Act compliant. This chronic dermatosis has a varied presentation, and the ophthalmic manifestations in particular have been infrequently described. This case demonstrates the benefits of immunohistochemistry in diagnosis and the difficulties in medical and surgical management of linear IgA bullous dermatosis while underscoring the lifelong difficulties in managing chronic inflammatory conditions causing ocular cicatrization.