Medical hypothesis discovery and innovation in ophthalmology

Editorial/ No abstract

Central serous chorioretinopathy is a common acquired maculopathy. Multiple studies showed that photodynamic therapy is useful treatment for acute and chronic central serous chorioretinopathy. The exact mechanism of photodynamic therapy in treating central serous chorioretinopathy is not clear, but it is thought to be caused by short-term choriocapillaris hypoperfusion and long-term choroidal vascular remodeling, leading to a reduction in choroidal congestion, vascular hyperpermeability and extravascular leakage. Furthermore, photodynamic therapy seems to be an effective means of improving or stabilizing visual acuity in patients with central serous chorioretinopathy.

To evaluate the effects of intravitreal triamcinolone acetonide (TA) as a monotherapy of serous Pigment Epithelial Detachment (PED) associated with AMD (Age-Related Macular Degeneration), this study has been performed. Seventeen patients (19 eyes) with serous PED associated with AMD were observed. All patients received 0.1ml (4mg) of intravitreal TA. The mean follow-up period was 18 months. Re-attachment of serous PED was observed in 37% of cases to the end of follow-up. In other cases, the height and length of serous PED significantly decreased. Visual acuity remained stable in all cases. No evidence of RPE tear or CNV development were noted. Before TA administration, intraocular pressure (IOP) was 20.18 ± 2.58 mmHg however, after intravitreal TA, IOP increased gradually and reached its maximum of all period of observation (23.25±1.85mmHg) six months after injection (P=0.031). In 7 (37%) of the cases, progression to cataract was observed after treatment. After surgery, the visual acuity in all cases increased by 0.2 to 0.5. As a conclusion, intravitreal TA decreases of both the height and length of serous PED associated with AMD after 18 months follow-up in most cases. The presented data provides support for the hypothesis regarding the possibility of monotherapy of serous PED with intravitreal TA.

The retina is the most oxygen consuming tissue of the body. Rod and cone photoreceptors efficiently carry out visual cascades, which are energetically costly processes. Data has recently been published that suggests that the metabolic support to phototransduction in the rod outer segment (OS) may originate directly in the OS, which is able to conduct aerobic metabolism. This oxygen-handling activity of the rod OS, which was never suspected before, appears to be a primary cause of the generation of reactive oxygen species directly inside the OS. Oxidative stress has been hypothesised to contribute to most of the neurodegenerative retinal pathologies, such as diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa and photoreceptor cell death after retinal detachment. Many natural antioxidant compounds are routinely used in experimental or human therapies for preventing or delaying photoreceptor degeneration in those pathologies. Here it is proposed that the ultimate reason for the beneficial actions of antioxidants in preventing or retarding the effect on the retinal degenerative pathologies can be found in their action on reactive oxygen species generated by the ectopic mitochondrial electron transport chain (ETC) coupled to FoF1-ATP synthase in rod OS disks. In fact, if not adequately coupled, the ETC generates reactive oxygen species that, in turn, can act on the polyunsaturated fatty acids which the rod OS is rich in. If correct, the mechanism put forward here would provide a potential for the molecular basis of therapies with antioxidants for retinal degenerative diseases.

Electroconvulsive treatment (ECT) has developed over 70 years to a modern, effective way of lifting depressive moods. Memory loss and visual acuity after electroconvulsive treatment is the only remaining relevant criticism of the treatment modality when considering the overall rate of remission from this treatment compared to all other treatment modalities. A depressive state impedes memory, and memory improves on several qualities of cognition after treatment. However, the comparison of a person’s memory ability from the months before depression started to the level after a course of ECT is never performed, for obvious reasons. Some infectious diseases are known to influence memory negatively through effects on the dopamine receptors. More specifically, former toxoplasmosis infection may be a factor. Preliminary data on titres of toxoplasma IgG may indicate a connection to the development of long-standing memory problems after ECT.

Terson’s syndrome has had multiple definitions. The original definition is unlikely to have included Terson’s original case. An updated definition based on mechanism is proposed and related to the original case described by Terson.