Vitrectomy with residual internal limiting membrane covering and autologous blood for a secondary macular hole: A case report.

BACKGROUND: Myopic foveoschisis (MF) is a common complication of pathological myopia. A macular hole (MH) usually results from the natural progression of MF and is a common complication of vitrectomy. Vitrectomy combined with residual internal limiting membrane (ILM) covering and autologous blood was effective for closing a secondary MH. CASE SUMMARY: A 52-year-old woman presented to our clinic with a complaint of blurred vision in the right eye for 7 years. Her best corrected visual acuity (BCVA) was 20/100, axial length was 25.79 mm and standard equivalent refractive error was -10.5 dioptres. Preoperative optical coherence tomography revealed foveoschisis in the right eye. Vitrectomy with fovea-sparing ILM peeling was performed. An MH developed and gradually expanded 5 mo after the initial vitrectomy. Vitrectomy with residual ILM covering and autologous blood was performed. The MH closed 3 wk after the second vitrectomy. CONCLUSION: Fovea-sparing ILM peeling can provide residual ILM for the treatment of MH secondary to vitrectomy for MF. Vitrectomy combined with residual ILM covering and autologous blood is effective for closing secondary MH and improving BCVA.

Dopamine Receptor Subtypes Mediate Opposing Effects on Form Deprivation Myopia in Pigmented Guinea Pigs.

Purpose: We reported previously that changes in dopamine receptor (DR) subtype activation modulate spontaneous myopia progression in albino guinea pigs. To determine if DR control of refractive error development is different than in its normal counterpart, we evaluated the contribution of dopaminergic pathways to emmetropization and form deprivation myopia (FDM) progression in pigmented guinea pigs. Methods: Monocular myopia was induced by unilateral form-deprivation (FD). The effects of agonists of D1R (SKF38393) and D2R (quinpirole), the corresponding antagonists (SCH23390 and sulpiride), and vehicle were tested by peribulbar injection around FD or untreated control eyes. High-performance liquid chromatography with electrochemical detection quantified retinal and vitreous dopamine (DA) and 4-dihydroxyphenylacetic acid (DOPAC) levels. Ocular refraction and axial dimensions were measured using eccentric infrared photoretinoscopy (EIR) and A-scan ultrasonography, respectively, initially and after 2 or 4 weeks of treatment. Results: After treatment with any of these four agents for 2 weeks, retinal and vitreal DA and DOPAC levels were not significantly different in drug- and vehicle-treated eyes. Neither agonism nor antagonism of D1R or D2R activity affected emmetropization. In contrast, D1R activation by SKF38393 inhibited FDM progression, while D2R activation by quinpirole augmented this response. On the other hand, D2R antagonism with sulpiride slowed FDM progression while D1R antagonism with SCH23390 had no effect. Conclusions: In pigmented guinea pigs, D1R activation inhibited, whereas D2R activation enhanced, FDM. These results closely mirror previous findings in albino animals and offer further evidence that DA and its cognate receptors affect refractive error regulation in guinea pigs.

Daily Injection But Not Continuous Infusion of Apomorphine Inhibits Form-Deprivation Myopia in Mice.

PURPOSE: To compare the effects of daily injection versus continuous infusion of a nonspecific dopamine agonist, apomorphine (APO), on refraction and ocular growth in normal postnatal mice and mice with form-deprivation myopia (FDM). METHODS: The C57BL/6 mice were subjected (or not) to monocular FD by covering the left eye with a frosted goggle and leaving the right (fellow) eye uncovered. During postnatal days 28 to 56, both groups received APO (5 mg/kg/d) or vehicle either as daily intraperitoneal injection or by continuous subcutaneous infusion with mini-pumps. After these treatments, binocular refractions were measured by photoretinoscopy and binocular ocular dimensions were measured by optical coherence tomography. Monocular photopic flash electroretinograms were recorded from non-FD mice. RESULTS: In normal mice, daily injection or continuous infusion of APO did not affect normal postnatal development of refraction. However, in the FD group, daily APO-injection attenuated ocular growth and also myopia development, as reflected in the interocular differences for APO-injected mice compared with vehicle-injected mice: (1) refraction, -1.04 ± 0.37 diopter (D) (APO-injection) compared with -4.14 ± 0.77 D (vehicle-injection) (P < 0.05); (2) vitreous chamber depth: -0.002 ± 0.005 mm compared with 0.032 ± 0.009 mm (P < 0.05); and (3) axial length: 0.000 ± 0.005 mm compared with 0.057 ± 0.007 mm (P < 0.05). By contrast, continuous APO-infusion failed to affect these biometric parameters. Furthermore, daily APO-injection decreased the ERG a- and b-wave amplitudes, whereas continuous APO-infusion increased these responses. CONCLUSIONS: In monocularly FD mice, daily APO-injection, but not continuous infusion, attenuated myopia development. Therefore, evaluating different dopamine agonist administration paradigms is important for identifying effective dopamine-based treatment for myopia.

Effects of dopaminergic agents on progression of naturally occurring myopia in albino guinea pigs (Cavia porcellus).

PURPOSE: Disruption of dopaminergic signaling has been implicated in the abnormalities of ocular development in albinism, and many experiments have shown that retinal dopamine is a major regulator of postnatal eye growth and myopia in animal models. Therefore, in the present study we investigated whether progressive myopia, which can occur in albino guinea pigs without experimental manipulation of visual conditions, is affected by dopaminergic agents. METHODS: Two-week-old albino guinea pigs, selected for being myopic (range refractive error [RE], -2 to -10 diopters [D]), received unilateral peribulbar injections of apomorphine (nonselective dopamine receptor agonist; 0, 7.5, 25, 75, 250, 750, and 2500 ng; n = 112), SKF38393 (D1-like agonist; 0, 10, 100, 1000 ng; n = 63), SCH23390 (D1-like antagonist; 0, 2500 ng; n = 27), quinpirole (D2-like agonist; 0, 10, 100, 1000 ng; n = 58), or sulpiride (D2-like antagonist; 0, 2500 ng; n = 24) once a day for four weeks. One noninjected group (n = 19) served as untreated control. Refractive states and axial dimensions of the eyes were measured without cycloplegia or general anesthetic, using eccentric infrared photoretinoscopy and A-scan ultrasonography, respectively, before treatment, and after 2 and 4 weeks of treatment. The main drug effects were analyzed by paired t-test or 2-way repeated measures ANOVA, as required. RESULTS: The naturally occurring progression of myopic RE was inhibited by apomorphine at relatively high doses (250 and 750 ng), SKF38393 at 100 ng (D1-like agonist), and sulpiride at 2500 ng (D2-like antagonist), but promoted by apomorphine at a lower dose (25 ng), quinpirole at 100 ng (D2-like agonist), and SCH23390 at 2500 ng (D1-like antagonist). All drugs affected primarily vitreous chamber depth, rather than anterior segment dimensions. CONCLUSIONS: Our data suggest that the activation of D1-like receptors inhibits, whereas activation of D2-like receptors promotes, progressive myopia in this animal model. The robust effects of antagonists suggest that ocular dopamine receptors in these albinos may be in a chronic state of partial excitation. The precise location and identity of the receptors responsible for these effects remain to be determined.