To evaluate the effects of repeated intravitreal dexamethasone implant. We reviewed the charts of 12 patients with diabetic macular edema, who received at least 2 intravitreal Ozurdex (0.7 mg) on an "as needed" basis. Main outcome measures included changes in best-corrected visual acuity, central macular thickness, retreatment interval, and incidence of side effects. A total of 15 eyes of 12 patients (6 men, 6 women; mean age 62 ± 12 years) were included. Retreatment was judged necessary after mean of 7.8 ± 4.1 months from the first Ozurdex (median, 6 months) (15 of 15 eyes), mean of 4.8 ± 0.9 months from the second Ozurdex (median, 5 months) (7 of 15 eyes), mean of 5.3 ± 1.5 months from the third Ozurdex (median, 5 months) (3 of 15 eyes), and mean of 5.6 ± 2 months from the fourth Ozurdex (median, 5 months) (3 of 15 eyes). Mean baseline best-corrected visual acuity was 0.67 ± 0.33 logMAR in the overall diabetic macular edema population; it significantly improved to 0.53 ± 0.31 logMAR after mean of 40.9 ± 18.2 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 0.53 ± 0.29 logMAR after mean of 34.4 ± 9.0 days from the second Ozurdex (peaking efficacy) (P < 0.003), and stabilized to 0.62 ± 0.26 logMAR after mean of 29.8 ± 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.05), to 0.5 ± 0.26 logMAR after mean of 36.3 ± 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.2), and to 0.50 ± 0.26 logMAR after mean of 37.0 ± 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.2). Mean baseline central macular thickness significantly decreased from 546 ± 139 μm to 292 ± 43 μm at 39.4 ± 17.9 days from the first Ozurdex (peaking efficacy) (P < 0.001), to 297 ± 47 μm at 33 ± 9.4 days from the second Ozurdex (peaking efficacy) (P < 0.001), to 293 ± 22 μm at 29.8 ± 12.1 days from the third Ozurdex (peaking efficacy) (P = 0.01), and stabilized to 309 ± 35 μm at 36.3 ± 3.2 days from the fourth Ozurdex (peaking efficacy) (P = 0.1), and to 295 ± 7 μm at 37.0 ± 2.6 days from the fifth Ozurdex (peaking efficacy) (P = 0.1). No serious adverse events were observed; three eyes developed a transient intraocular pressure increase, and cataract was extracted in one eye. Repeated intravitreal Ozurdex on an "as needed" basis with a variable retreatment interval may produce long-term clinically meaningful benefits in the treatment of diabetic macular edema, without other significant side effects than expected after intraocular corticosteroid treatment.

Background To evaluate the effects of dexamethasone implant in eyes affected by recalcitrant diabetic macular oedema (DME) associated with proliferative diabetic retinopathy (PDR). Methods Thirteen consecutive patients with centre-involving DME associated with PDR, central macular thickness (CMT) ≥300 µm, previous therapy with panretinal photocoagulation, focal/grid laser treatment and anti-vascular endothelial growth factor injection were prospectively enrolled. A complete ophthalmological examination included: best-corrected visual acuity (BCVA) assessment, spectral-domain optical coherence tomography and fluorescein angiography. After the first dexamethasone implant, each patient was evaluated on a bi-monthly basis and re-treated according to persistence/recurrence of DME from the fourth month on. Primary outcome measures were the changes in mean BCVA and CMT at the 12-month examination. Secondary outcome measures included changes to the outer retinal layers. Results BCVA improved from 0.99±0.31 LogMAR (logarithm of the minimum angle of resolution; Snellen Equivalent: 20/196) to 0.77±0.25 LogMAR (Snellen Equivalent: 20/117) (p<0.001) at the 12-month examination. CMT passed from baseline value 510±169 µm to 423±171 µm (p=0.018) at 12 months. The data showed a significant improvement in the integrity of the external limiting membrane (ELM, p=0.02), the ellipsoid zone (EZ, p=0.025) and retinal pigment epithelium (RPE, p=0.008), significantly correlated with the upturn in BCVA. Conclusions Dexamethasone implant results in a recovery of morphology of the outer retinal layers even in patients displaying a compromised clinical situation. The qualitative status of the ELM and EZ might provide prognostic value for the final visual acuity and disease regression.

We investigated how the abnormalities of fixation eye movements (FEMs) of the amblyopic eye were linked with treatment outcomes following part-time patching therapy in children with amblyopia. We recruited 53 patients, with at least 12 months of patching, and measured FEMs at the end of treatment. Subjects were classified based on FEM waveforms (those without nystagmus = 21, those with nystagmus without fusion maldevelopment nystagmus (FMN) = 21, and those with FMN = 11) and based on clinical type of amblyopia (anisometropic = 18, strabismic = 6, and mixed = 29). The treatment outcomes such as duration of treatment of receiving part-time patching therapy, visual acuity and stereo-acuity deficits at the end of treatment were determined. Bivariate contour ellipse area (BCEA), fast (fixational saccade/quick phases), and slow (inter-saccadic drifts/slow phases) FEMs of the fellow and amblyopic eye were analyzed. Anisometropic group had less residual amblyopia (0.23±0.19logMAR acuity) compared to strabismic/mixed (0.36±0.26) groups (p = 0.007). Treatment duration in patients without nystagmus was lower (12.6±9.5months) compared to nystagmus without FMN (25.6±23.2) and FMN (29.5±20.4) groups (p = 0.006). Patients without nystagmus had better stereopsis at the end of treatment (2.3±0.84logarcsecs) compared to nystagmus without FMN (2.6±0.84) group (p = 0.003). The majority of patients with FMN (8/11) had absent stereopsis. BCEA of the amblyopic eye was higher in patients with greater residual visual acuity deficits in patients without nystagmus. No such association was seen in Nystagmus no FMN and FMN groups. Increased amplitude of fast FEMs, increased eye position variance and eye velocity of slow FEMs were seen in patients who had received longer duration of part time patching therapy and in those with greater residual amblyopia, and poor stereopsis at the end of treatment. Assessment of FEM waveforms and fast and slow FEM characteristics are important measures while describing fixation instability in amblyopia. Several FEM abnormalities were associated with stereo-acuity and visual acuity deficits and treatment duration in patients with amblyopia treated with part time patching therapy.

Several extraorbital findings have been described in morning glory disc anomaly (MGDA), including optic pathway abnormalities. We want to emphasize the importance of looking for ipsilateral optic nerve and chiasm thickening in MGDA-affected patients because we think that it may be a relevant common associated finding to date not stressed by anyone. We report three cases of clinically diagnosed unilateral MGDA in which magnetic resonance imaging revealed enlargement of the ipsilateral optic nerve and chiasm. A literature analysis was made and previously reported MGDA cases, and case series were checked, looking for described, or misunderstood similar magnetic resonance imaging findings. Three other cases with very similar prechiasmatic optic nerve and chiasm findings were identified from the literature. Two further cases are discussed as possibly characterized by similar misinterpreted magnetic resonance features. Our study broadens the constellation of intra- and extraorbital findings of MGDA. Though magnetic resonance imaging is not sufficient to determine the neuropathological substrate of this finding, clinicians and radiologists should be aware of the possible association of MGDA with ipsilateral thickening of the optic nerve and chiasm, to properly plan the clinical and imaging follow-up.

Purpose: To analyze the outer retinal layer changes on spectral-domain optical coherence tomography after dexamethasone implant for the treatment of macular edema secondary to central retinal vein occlusions (CRVO). Methods: Thirty patients affected by macular edema related to CRVO (8 patients less than 50 years of age with nonischemic CRVO [50-niCRVO], and 10 patients with ischemic CRVO [iCRVO]) were included in a prospective study. After a comprehensive ophthalmologic examination, including best-corrected visual acuity, fluorescein angiography, and spectral-domain optical coherence tomography, each patient received a first implant. Further retreatments were performed on the basis of macular edema detection from the fourth month. Main outcome measure was the change in outer retinal layers at the 12-month examination. Results: The retinal layers of interest (external limiting membrane; ellipsoid zone; and retinal pigment epithelium) were classified as absent, disrupted, or present. The best baseline optical coherence tomography profile was found in <50-niCRVO group (absent external limiting membrane, ellipsoid zone, and retinal pigment epithelium layers in no patients; present and disrupted external limiting membrane in 25% and 75% of cases, respectively; disrupted ellipsoid zone and retinal pigment epithelium in 100% of cases), whereas the worst was detected in the iCRVO group (absent external limiting membrane, ellipsoid zone, and retinal pigment epithelium in 40%, 40%, and 10% of cases, respectively). A significant recovery of the retinal layers was observed in all CRVO subgroups; the greatest improvement was found in <50-niCRVO group. Median best-corrected visual acuity in the whole group improved from 0.85 to 0.45 (P = 0.0001). It is noteworthy that a significant best-corrected visual acuity gain was achieved only in eyes showing present or disrupted layers at baseline regardless of the CRVO subgroup examined, whereas eyes with absent layers at baseline were unable to attain any improvement. Conclusion: Dexamethasone implant can promote the resolution of macular edema in patients affected by any CRVO subform, but a beneficial functional outcome could be achieved by eyes showing no absence of outer retinal layers on spectral-domain optical coherence tomography at baseline.