Purpose: To generate a model of chronic glaucoma in rats, by means of a single injection that simulates the pathology that occurs in humans. Methods: A total of 47 Long‐Evans rats of both sexes were used; 30 rats received an intracameral injection of a suspension of fibronectin‐loaded poly‐lactic‐glycolic acid microspheres into the right eye, and the other 17 served as controls. They were followed up for 24 weeks, evaluating intraocular pressure (IOP) with a rebound tonometer, neuro‐retinal structure by optical coherence tomography (OCT) with segmentation protocols for the analysis of the entire retina, the ganglion cell layer (GCL) and the peripapillary retinal nerve fibre layer (pRNFL); as well as retinal functionality by electroretinography (ERG). Results: The IOP of the induced eyes increased progressively and chronically (11.64 ± 1.43 to 21.89 ± 3.94 mmHg) compared to the controls (p = 0.025) and with higher levels than the contralateral eyes (p < 0.05) until week 20, when this trend reversed. The induced eyes showed fluctuations in OCT retinal thickness over time. A trend of less thickness in the retina and GCL was measured in the induced eye and its contralateral eye; but at the end of the study, greater thicknesses were quantified than in the control eyes (p = 0.036). In addition, a lower ERG signal was recorded in the induced eyes. Ganglion cell functionality progressively decreased and was lower than contralateral eyes and control eyes at 12 and 24 weeks (p < 0.05). Males showed higher IOP (p < 0.05), greater thicknesses in the retina and lesser in the GCL and pRNFL (p < 0.05), with decreased functionality at 12 and 24 weeks compared to females. Conclusions: A minimally invasive chronic glaucoma model was obtained using single‐injection by pharmaceutical technology, which produced a progressive increase in intraocular pressure and structural and functional neuro‐retinal damage.
Resumen La hemorragia retrobulbar es un sangrado en la región intraorbitaria retroseptal que genera un síndrome compartimental orbitario. Se presenta el caso de una mujer de 86 años que acudió a Urgencias por dolor ocular y pérdida de visión en ojo izquierdo de seis horas de evolución. Presentaba tratamiento anticoagulante con 300 mg/día de Dabigatrán por fibrilación auricular como único antecedente médico. La exploración clínica fue compatible con hemorragia retrobulbar, diagnóstico confirmado por TAC urgente, realizándose de forma inmediata una cantotomía con cantolisis. Se realizó RMN orbitaria que descartó la existencia de malformaciones arteriovenosas como factor desencadenante, diagnosticándose de hemorragia retrobulbar espontánea asociada a consumo de anticoagulantes. La singularidad de este caso radica en formar parte del pequeño porcentaje de hemorragias retrobulbares que no se asocian a causa traumática ni postquirúrgica así como en ilustrar una localización muy poco frecuente de sangrado asociado a anticoagulación.
Purpose: To evaluate changes in visual function and anatomical structures in the neuroretina of patients diagnosed with Alzheimer's disease (AD) in comparison with healthy controls. Methods: A total of 25 eyes of 13 AD patients and 80 eyes of 40 healthy subjects were analysed. Best corrected visual acuity (BCVA) was assessed in different contrast situations (100%, 2.5%, 1.25%) with ETDRS chart (Early Treatment Diabetic Retinopathy Study). Also, retinal nerve fibre layer (RNFL) and ganglion cell layer (GCL) thickness were analysed using Spectralis and Triton optical coherence tomography (OCT), globally and by sectors, both in peripapillary and macular area. Results: A statistically significant decrease was found in BCVA in AD patients in comparison with controls (p < 0.001), specifically in 100% and 1.25% contrast charts. Regarding structural analysis, a significant reduction in retinal thickness was found in AD patients in comparison with controls. Global thickness was found to be significantly thinner in peripapillary retina in Triton OCT (p < 0.001). In a similar way, macular GCL, both in Triton and Spectralis OCT, showed a significant thinning (p < 0.001) in global and sectorial analysis. RNFL showed a significant tendency towards thinning, but specifically in infero‐temporal sector of macular area in Spectralis OCT (p < 0.001). Conclusions: The neurodegeneration that AD produces to the brain affects the retina in a parallel way, and that can be objectified by measuring BCVA parameters and thickness measurements in OCT. Compared to healthy controls, AD has a significant thinning in several neuroretinal layers, which can be considered a potential diagnostic tool considering that OCT is a quick, reproducible, non‐invasive test.
Purpose: To assess whether the existence of colour vision deficiency or colour blindness involves impairment of visual acuity, contrast sensitivity and colour vision and results in variations in retinal nerve fibre layer (RNFL) thickness, macular area, retinal ganglion cell complex and retinal layers that contain photoreceptors (bastons and cones) versus subjects with normal colour vision within the same age and gender distribution. Methods: Cross‐sectional and observational study including 50 eyes of subjects with colour blindness and 50 eyes of control subjects. Visual function (visual acuity, contrast sensitivity and colour vision) and neuroretinal structure were assessed in all subjects using optical coherence tomography (OCT). Results: Significant thinning of the retinal nerve fibre layer, ganglion cell layer and retina were observed in the colour blindness group. Significant thinning was also recorded in layers that involve photoreceptor nuclei (between the outer limiting layer and the Bruch membrane and between the outer plexiform layer and the outer limiting membrane). Conclusions: Significantly reduced thicknesses in the RNFL and several retinal layers (ganglion cell and photoreceptor layers) were found, demonstrating that colour blindness is associated with thinning in retinal and RNFL thickness, and in the retinal layers that involve photoreceptor nuclei. OCT study with retinal segmentation therefore seems to be a marker of colour blindness of utility in clinical practice in the case of doubt regarding diagnosis. This analysis could be useful in evaluating the effectiveness of potential therapies such as gene treatment.
Purpose: To evaluate the differences in RNFL and GCL between patients with relapsing–remitting multiple sclerosis (RR‐MS), fibromyalgia (FM) and healthy controls, as well as their correlation with disease time and severity. Methods: 94 eyes of RR‐MS patients, 55 eyes of FM patients and 90 eyes of healthy controls were evaluated using the Spectralis OCT Posterior Pole protocol (64‐cell array grid). The thicknesses of both layers were compared for each of the 64 cells between the three groups, the correlation of each layer with the time of the disease was studied, as well as with the EDSS in the case of RR‐MS and with the questionnaires FIQ and EQ‐5D in the case of FM. Results: We observed a significant thinning (p < 0.05) of the GCL in both pathologies compared to healthy subjects, being the damage significantly greater in RR‐MS. Regarding the RNFL, a significant thinning was observed in the RR‐EM but not in the FM. On the other hand, GCL was correlated with the time of evolution in RR‐MS patients, but not in those with FM, and was significantly correlated with a greater impact of FM (FIQ and EQ‐5D), but not with the EDSS in the case of RR‐MS. In addition, it is in the GCL where a high concentration of cells (>50%) which a greater ability to discriminate between healthy and pathological subjects (AUC > 0.5) was found. Conclusions: The GCL damage in FM patients, similar to that in RR‐MS patients, suggests that there is an underlying neurodegenerative process in this pathology. In the absence of other biomarkers, OCT could be postulated as a potential biomarker in FM, since GCL shows significant thinning and correlates with the impact of this disease on quality of life.
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