Double peeling during vitrectomy for macular pucker: the Charles L. Schepens Lecture.

Epiretinal membranes are commonly encountered in retinal practice, and they result in decreased vision. The present work addresses whether peeling of the internal limiting membrane is necessary during vitrectomy for macular pucker. We performed a retrospective analysis to investigate the effects of "single peeling," in which only the epiretinal membrane was peeled, and "double peeling," in which the internal limiting membrane was also stained and peeled. Although significantly more patients in the single-peeling group had an epiretinal membrane remaining in the central fovea postoperatively, visual acuity was not found to differ between the 2 groups in the short term. Patients who had an epiretinal membrane for more than 18 months had significantly worse visual acuity outcomes. Unexpectedly, there was a greater proportional decrease in central macular thickness in the single-peeling group than in the double peeling group, a finding that deserves further study.

Optic disk pit morphology and retinal detachment: optical coherence tomography with intraoperative correlation.

BACKGROUND: The pathogenesis of optic nerve head pits and associated retinal detachment, and the most effective surgical intervention when visual loss develops, remains unclear. METHODS: The morphology of the optic disk in patients with pits was investigated with optical coherence tomography. For those who underwent surgical treatment for pit-associated retinal detachment, the efficacy of treatment by vitrectomy and separation of the posterior hyaloid, with and without additional peeling of peripapillary tissue, was assessed. RESULTS: On optical coherence tomography imaging, 14 of 18 pits (78%) demonstrated a localized pit-like invagination, whereas 3 (17%) had disks with a generally excavated structure. For 16 of 18 pits (89%), there was evidence of condensed vitreous or glial tissue seen extending from the pit or inside the optic disk. Nine eyes with retinal detachment underwent vitrectomy, posterior hyaloid separation, and endolaser. The retinal detachment completely resolved in 6 of 6 cases where the surgeon additionally peeled the fibrous tissue from the pit and 2 of 3 cases where this was not performed. CONCLUSION: Spectral domain optical coherence tomography demonstrates the varying morphology of optic pit anatomy. Condensed vitreous strands or glial tissue in the optic nerve pit may also contribute to retinal detachment development.

Electroconvulsive therapy-induced persistent retrograde amnesia: could it be minimised by ketamine or other pharmacological approaches?

BACKGROUND: Certain pharmacological agents administered during electroconvulsive therapy may have the potential to prevent persistent retrograde amnesia induced during electroconvulsive therapy. This review examines mechanisms for electroconvulsive therapy-induced retrograde amnesia, and evaluates the suitability of the anaesthetic ketamine for preventing this amnestic outcome. METHODS: A review of human studies, animal models and theoretical models in light of memory dysfunction following electroconvulsive therapy was conducted. MEDLINE was searched from 1950 to April 2009 using the MeSH terms "electroconvulsive therapy", "memory", "memory short term", "memory disorders", "excitatory amino acid antagonists", and "ketamine". PREMEDLINE was searched using the terms "electroconvulsive therapy", "amnesia" and "ketamine". Additional keyword and reference list searches were performed. No language, date constraints or article type constraints were used. RESULTS: Disruption of long term potentiation as a mechanism for electroconvulsive therapy-induced retrograde amnesia is well supported. Based on this putative mechanism, an N-methyl-D-aspartate receptor antagonist would appear suitable for preventing the retrograde amnesia. Available evidence in animals and humans supports the prediction that ketamine, an anaesthetic agent and N-methyl-D-aspartate receptor antagonist, could effectively prevent electroconvulsive therapy-induced persistent retrograde amnesia. Whilst there are concerns about the use of ketamine with electroconvulsive therapy, such as possible psychotomimetic effects, on balance this anaesthetic agent may improve or hasten clinical response to electroconvulsive therapy. CONCLUSIONS: A clinical trial is warranted to determine if ketamine anaesthesia during electroconvulsive therapy can lessen persistent retrograde amnesia and improve therapeutic response. Electroconvulsive therapy with ketamine anaesthesia may provide effective antidepressant action with minimal side effects.