Role of optical coherence tomography angiography in myopic choroidal neovascularization after intravitreal injections of Ranibizumab / 国际眼科杂志(Guoji Yanke Zazhi)

AIM: To investigate the change of myopic choroidal neovascularization treated by ranibizumab and evaluate their value in monitoring the effect of anti-vascular endothelial growth factor ( VEGF) therapy. ·METHODS: The study enrolled 30 patients ( 30 eyes ) diagnosed with myopic choroidal neovascularization. All affected eyes were treated with intravitreal ranibizumab 0. 05mL ( 10mg/mL ). Best corrected visual acuity ( BCVA ) , non-contact tonometer, ophthalmoscope, fundus fluorescein angiograph ( FFA ) and OCTA were evaluated monthly until 6mo. The changes of BCVA and central macular thickness ( CMT) were compared at 1, 3 and 6mo after treatment. ·RESULTS:All patients received an average of 1. 70±0. 65 injections. BCVA was 0. 96 ± 0. 17 ( LogMAR ) before therapy, and BCVA 1, 3 and 6mo after treatment respectively improved by 0. 23 ± 0. 09, 0. 34 ± 0. 07, 0. 38 ± 0. 11. The differences were significant ( t=5. 461, 8. 191, 8. 894; P<0. 05 ). Mean CMT decreased form 281. 07 ± 13. 72μm to 261. 33 ± 13. 13μm, 243. 47 ± 16. 65μm, 234. 73 ± 17. 52μm respectively 1, 3 and 6mo after treatment, showing significant differences (t=12. 007, 13. 360, 9. 531;P<0. 05). OCTA revealed a progressively smaller vascular lesion and reduction in capillary density. · CONCLUSION: Intravitreal ranibizumab for CNV secondary to pathologic myopia is effective and safe;OCTA is a noninvasive and time-saving new technology, and it also is a promising tool for clinicians to make preliminary diagnosis and assess treatment efficacy in the follow-up visits.

Neuroprotective Effect of Compound Anisodine in a Mouse Model with Chronic Ocular Hypertension / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Compound anisodine (CA) is a compound preparation made from hydrobromide anisodine and procaine hydrochloride. The former is an M-choline receptor blocker with the function of regulating the vegetative nervous system, improving microcirculation, and so on. The latter is an antioxidant with the activities of neuroprotection. This study aimed to investigate the potential neuroprotection of CA, which affects the degeneration of the retinal ganglion cells (RGCs) in an animal model with chronic ocular hypertension.</p><p><b>METHODS</b>Female C57BL/6J mice (n = 24) were divided randomly into four groups: normal control group without any treatment (Group A, n = 6); CA control group with feeding the CA solution (Group B, n = 6); microbeads (MBs) control group with injecting MB into the anterior chamber (Group C, n = 6); CA study group with MB injection and with feeding the CA solution (Group D, n = 6). Intraocular pressure (IOP) was measured every 3 days after MB injection. At the 21st day, neurons were retrograde-labeled by Fluoro-Gold (FG). Animals were sacrificed on the 27th day. Retinal flat mounts were stained immunohistologically by α2-III-tubulin. FG-retrograde-labeled RGCs, α2-III-tubulin-positive RGCs, and α2-III-tubulin-positive nerve fibers were quantified.</p><p><b>RESULTS</b>Mice of Groups C and D expressed the incidence of consistent IOP elevation, which is above the IOP level of Group A with the normal one. There is no significant difference in IOP between Groups A and B (P > 0.05). On the 27th day, there were distinct loss in stained RGCs and nerve fibers from Groups C and D compared with Group A (allP < 0.001). The quantity was significantly higher in Group D as compared to Group C (allP < 0.001) but lower than Group A (allP > 0.001). There was no significant difference in the quantity of RGCs and nerve fibers between Groups A and B (allP > 0.05).</p><p><b>CONCLUSIONS</b>These findings suggest that CA plays an importantly neuroprotective role on RGCs in a mouse model with chronic ocular hypertension.</p>

Clinical features of retinal diseases masquerading as retrobulbar optic neuritis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Managements of optic neuritis (ON) included high-dose corticosteroids or combined with systemic immunomodulatory agents. It was important to make a correct diagnosis of ON before initiation of treatment. The purpose of the study was to report and analyze the clinical features of retinal diseases in patients who were misdiagnosed as having retrobulbar ON.</p><p><b>METHODS</b>Retrospective review of 26 patients (38 eyes) initially diagnosed with retrobulbar ON but were ultimately diagnosed with retinal or macular diseases. Data obtained from fundus examination, fluorescence fundus angiography (FFA), automated static perimetry, full-field electroretinogram (ffERG), multifocal electroretinogram (mfERG), and optical coherence tomography (OCT) were evaluated.</p><p><b>RESULTS</b>Thirty-eight eyes of 26 patients were found to have misdiagnosis of retrobulbar ON, based on normal or slight abnormal fundus findings and abnormal visual evoked potentials (VEP). The mean age of the patients was 34 years and the correct diagnosis of the patients included acute zonal occult outer retinopathy (AZOOR, 15 eyes, 14 patients), occult macular dystrophy (OMD, 8 eyes, 4 patients), cone or cone-rod dystrophy (10 eyes, 5 patients), acute macular neuroretinopathy (AMNR, 3 eyes, 2 patients), and cancer-associated retinopathy (CAR, 2 eyes, 1 patient).</p><p><b>CONCLUSION</b>When attempting to diagnose retrobulbar ON in clinical practice, it is crucial to carry out necessary examinations of the retinal function and morphology to decrease misdiagnosis.</p>