Pathologies of the optic nerve could result as primary insults in the visual tract or as secondary deficits due to inflammation, demyelination, or compressing effects of the surrounding tissue. The extent of damage may vary from mild to severe, differently affecting patient vision, with the most severe forms leading to complete uni‐ or bilateral visual loss. The aim of researchers and clinicians in the field is to alleviate the symptoms of these, yet uncurable pathologies, taking advantage of known and novel potential therapeutic approaches, alone or in combinations, and applying them in a limited time window after the insult. In this review, we discuss the epidemiological and clinical profile as well as the pathophysiological mechanisms of two main categories of optic nerve pathologies, namely traumatic optic neuropathy and optic neuritis, focusing on the demyelinating form of the latter. Moreover, we report on the main rodent models mimicking these pathologies or some of their clinical aspects. The current treatment options will also be reviewed and novel approaches will be discussed.

Purpose To evaluate the efficacy and duration of action of an intravitreal (dexamethasone (Ozurdex)) implant in vitrectomised and non-vitrectomised eyes with persistent diabetic macular oedema (DMO). Methods We retrospectively analysed the records for 18 eyes that had or had not been vitrectomised but required an intravitreal dexamethasone implant for DMO after a poor response to anti-vascular endothelial growth factor. Optical coherence tomography and visual acuity (VA) examinations were performed before and 1, 3 and 6 months after implantation. The six months following implantation constituted one treatment round; up to three rounds were studied. Results Ten of 18 eyes had undergone vitrectomy. Best-corrected visual acuity (BCVA) and central macular thickness (CMT) were significantly improved by months 1-3 after implantation of the Ozurdex device in all rounds of treatment. The BCVA and CMT deteriorated gradually after month 3 through to month 6 post implantation. There were no statistically significant differences between the vitrectomised and non-vitrectomised groups at any time point. When the implantation interval was <6 weeks from the end of each treatment round, the improvement in BCVA and CMT was obvious even after 18 months of treatment. Conclusions Vitrectomy did not have a negative effect on the duration of action or efficacy of the Ozurdex implant in patients with persistent DMO. The implant started working from the first month after implantation regardless of whether vitrectomy had or had not been performed. The maximum functional and anatomic improvement was achieved in the first 3 months post implantation in all treatment rounds.

The olfactory system provides mammals with the abilities to investigate, communicate and interact with their environment. These functions are achieved through a finely organized circuit starting from the nasal cavity, passing through the olfactory bulb and ending in various cortical areas. We show that the absence of transient axonal glycoprotein-1 (Tag1)/contactin-2 (Cntn2) in mice results in a significant and selective defect in the number of the main projection neurons in the olfactory bulb, namely the mitral cells. A subpopulation of these projection neurons is reduced in Tag1-deficient mice as a result of impaired migration. We demonstrate that the detected alterations in the number of mitral cells are well correlated with diminished odor discrimination ability and social long-term memory formation. Reduced neuronal activation in the olfactory bulb and the corresponding olfactory cortex suggest that Tag1 is crucial for the olfactory circuit formation in mice. Our results underpin the significance of a numerical defect in the mitral cell layer in the processing and integration of odorant information and subsequently in animal behavior.

We present a case of acute endophthalmitis after intravitreal dexamethasone implant injection and discuss the management of this rare and challenging case in which the implant could not be removed. A 50-year-old woman with a history of branch retinal vein occlusion in the right eye was treated with intravitreal dexamethasone implant injection for macular oedema. Four days after injection, the patient was admitted to the department with acute pain, decreased vision, and redness. A diagnosis of acute post-intravitreal injection endophthalmitis was made. A 23-guage (23G) vitrectomy was performed immediately to remove the implant, and a vitreous tap for culture and polymerase chain reaction was acquired during the procedure. We were unable to remove the dexamethasone implant during the vitrectomy because of dense membrane formation. At the end of the procedure, we injected intravitreal antibiotics (vancomycin and amikacin), and the patient was treated with fortified topical antibiotics and steroids. At the time of writing, 5 years later, the patient retains a best corrected visual acuity of 10/10 (6/6) with dexamethasone implant therapy maintenance. Intravitreal dexamethasone implant-associated endophthalmitis is a rare and challenging condition. Immediate 23G pars plana vitrectomy, even without removal of the implant, can lead to favourable visual results.

The vitreous body occupies nearly 80% of the total ocular volume. It constitutes a dynamic structure that normally changes composition and formation through time. Vitreous characteristics can also change owing trauma, metabolic or oxidative factors. Physiologically, the process of gradual vitreous liquefaction (synchysis) comes along with the progressive vitreous collagen fibrils packing and aggregation (syneresis). Both synchysis and syneresis can lead to posterior vitreous detachment (PVD) after normal cortex dehiscence from the underlying retina tissue (vitreoretinal interface). In contrast, when the dehiscence process is abnormal (anomalous, incomplete or partial), various pathological conditions can be created on the retina. The pathologies formed specifically on the macular region from the above conditions are named vitreomacular interface diseases (VMID). In this presentation, we will analyse the pathophysiological mechanisms of different VMID like a macular hole (MH), vitreomacular traction syndrome (VTS) and epiretinal membrane (ERM). Moreover, we will present different molecular and cellular components mentioned in the literature and implicated in VMID formation, and we will try to highlight potential future treatment options for the diseases.