Purpose: To describe an observational case of closed‐angle glaucoma secondary to uveal effusion syndrome after a first episode of posterior scleritis. Methods: Morales Meseguer University Hospital. Ophthalmology service. Uveitis section. Results: A 76‐year‐old woman presented to the emergency department with a red, painful right eye (RO) and decreased visual acuity (VA). Initial VA was light perception and intraocular pressure was 40 mmHg, presenting a narrowed chamber and corticonuclear cataract. The fundus was not assessable due to media opacity. Optical coherence tomography showed choroidal folds in the left eye, and the OD was unapproachable. B‐mode ocular ultrasound showed scleral thickening of 2 mm in both eyes and a superior temporal hematic choroidal detachment in the left eye. She was diagnosed with acute glaucoma secondary to uveal effusion after the first outbreak of posterior scleritis. In the emergency department she was treated with intravenous mannitol, acetazolamide orally and hypotensive eye drops. Acute angle‐closure glaucoma and choroidal detachment remitted under systemic steroid treatment, cycloplegic eye drops and topical hypotensive agents. After screening for pathologies associated with posterior scleritis, idiopathic origin of the condition was concluded. Conclusions: Patients with posterior scleritis may develop uveal effusion syndrome, which can lead to secondary angle‐closure glaucoma. A screening for pathologies associated with posterior scleritis (Wegener's, rheumatoid arthritis, herpes zoster, tumours, porphyria, post‐surgical or pharmacological causes) should be performed, although most cases are idiopathic. Treatment differs from glaucoma due to pupillary block, being necessary the use of systemic corticosteroids.

Purpose: The purpose of this research was to compare the thickness of different retinal layers between dyslexic subjects and controls at the macula by means of optical coherence tomography (OCT). Methods: Each patient underwent a complete ophthalmic examination including macular OCT in both eyes. The thickness of the fovea, four sectors of the parafovea and four sectors of the perifovea were obtained according to the Early Treatment Diabetic Retinopathy Study protocol in the following 13 segmentations: complete retina, outer retina, inner retina, retinal nerve fibre layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), outer plexiform layer (OPL), outer nuclear layer (ONL), INL + OPL + ONL, IPL + INL, OPL + ONL and ganglion cell complex (RNFL + GCL + IPL). The results of the right and left eyes were independently compared between groups. Results: The thickness in all the four sectors of the parafovea was found significantly higher in the right and in the left eyes in the dyslexic group in the following segmentations: complete retina, inner retina, middle retinal layers and OPL + ONL. Several macular sectors were also thicker in IPL + INL, INL, IPL and ONL in dyslexia. In contrast, no thickness differences between both groups were found in any of the sectors of RNFL, GCL, GCC, or outer retina in any eye. Conclusions: Anatomy of the macula is different in dyslexic and normoreader subjects in middle retinal layers, especially in the parafovea. This fact suggests that the macula may play an important role in the development of dyslexia.

Purpose: To report by multimodality imaging the follow‐up of a patient with posterior uveitis presenting serpiginous choroiditis (SC). To highlight the importance of autofluorescence in the follow‐up of patients with atrophic scarring due to CS. Methods: We present an observational case of SC documented photographically. Clinical data were gathered retrospectively from several visits. The data included corrected visual acuity (BCVA), fundus examination, optical coherence tomography (OCT) and autofluorescence (AF). Results: Periodic revision of a 49‐year‐old female being followed up for SC secondary to tuberculosis. Mantoux test was positive in 2010 and she was treated correctly. Twelve years later, BCVA was hand movements in the right eye and in the left eye 20/40. Fundus examination revealed no presence of vitritis and atrophic scars post choroiditis serpiginosa. OCT displayed disruption of outer retinal layers. AF revealed atrophy plaque with a new diffuse hypoautofluorescence halo surrounding hyperautofluorescent rim. Aqueous humour and vitreous sample results were negatives. Finally, the lesion was diagnosed as a serpiginous choroiditis. She was treated with corticosteroid and biological therapy to improve her visual acuity. It should suggest a reactivation of SC the appearance of a new atrophy plaque with ill‐defined creamy rim, early block and diffuse oozing at late times, choroidal hypoperfusion, diffuse hypoautofluorescence halo surrounding hyperautofluorescent rim and disruption of outer retinal layers with ellipsoid loss. Conclusions: A differential diagnosis should be made between SC and posterior uveitis secondary to tuberculosis. Multimodal imaging by autofluorescence is important for the diagnosis and follow‐up of patients with atrophic scarring due to SC. Differential diagnosis of cause posterior uveitis is essential for the monitoring and treatment. In inflammatory diseases always rule out infection prior to corticosteroid treatment or biological therapy.

Purpose: Drugs mostly sulfa‐related compounds, have produced uveal effusions, forward rotation of the iris‐lens diaphragm, transient myopia, and secondary angle closure. It has been recently encountered one case in which uveal effusions have occurred after administration of topiramate, a new anticonvulsant medication. Methods: A 54‐year‐old woman was seen in our emergency department with severe headaches, progressively blurry vision and photophobia in both eyes starting that morning. On examination, her visual acuity was hand movement in both eyes. Central corneal edema was observed, narrow chamber and anterior lens‐iris complex displacement with an unreactive middle pupil in both eyes. The funduscopic examination was difficult to assess due to the media opacity. Intraocular pressure measured with an applanation tonometer was 45 mm of mercury (mmHg) in the right eye and 50 mmHg in the left eye. Her medications included topiramate which she had started 2 weeks prior to initial examination due to headaches followed by neurology. Results: Topiramate‐induced angle closure has even been described as an idiosyncratic reaction in patients with normal depth of anterior chamber. The drug causes a prostaglandins increasement that trigger ciliary body edema at the local level but without acting at the systemic level. Ultrasound biomicroscopy shows the presence of a ciliochoroidal effusion syndrome, edema and the ciliary body anterolateral rotation, with zonular relaxation, changes that lead to iris‐lens diaphragm anterior displacement and, as a consequence, narrowing of the responsible anterior chamber with an acute glaucoma crisis. Conclusions: Topiramate is a sulfamate monosaccharide and belongs to a new generation of antiepileptic drugs, widely prescribed throughout the world as treatment of generalized tonic–clonic seizures and partial seizures. Prophylaxis of migraine, bipolar disorder, depression and neuropathic pain are other recent indications of its use. Bilateral acute glaucoma due to uveal effusion syndrome should be considered as an infrequent complication of topiramate use. References. 1. Prithvi S. Sankar, MD; Louis R. Pasquale et al. Uveal Effusion and Secondary Angle‐Closure Glaucoma Associated With Topiramate Use. Arch Ophthalmol. 2001;119(8):1210–1211.