Search

Background : Glaucoma is a chronic, vision-threatening disease, and a major cause of legal blindness. The current view is no longer limited to the progressive optic nerve injury, since growing evidence strongly support the interpretation of glaucoma as a complex neurodegenerative disease. However, the precise pathogenic mechanisms leading to the onset and progression of central nervous system (CNS) impairment, and the functional consequences of this damage, are still partially understood. The main aim of this review is to provide a complete and updated overview of the current knowledge regarding the CNS involvement in glaucoma, and the possible therapeutic perspectives. Methods : We made a careful survey of the current literature reporting all the relevant findings related to the cognitive dysfunctions occurring in glaucoma, with specific remarks dedicated on the higher-order visual function impairment and the possible employment of neuroprotective agents. Results : The current literature strongly support the interpretation of glaucoma as a multifaceted chronic neurodegenerative disease, widely affecting the CNS. The cognitive impairment may vary in terms of higher-order functions involvement and in the severity of the degeneration. Although several neuroprotective agents are currently available, the development of new molecules represents a major topic of investigation for future clinical trials. Conclusions : Glaucoma earned the right to be fully considered a neurodegenerative disease. Glaucomatous patients may experience a heterogeneous set of visual and cognitive symptoms, progressively deteriorating the quality of life. Neuroprotection is nowadays a necessary therapeutic goal and a future promising way to preserve visual and cognitive functions, thus improving patients' quality of life. [ABSTRACT FROM AUTHOR]

Background: Carotid artery stenosis (CAS) is a multifaceted disease characterized by possible ocular involvement. Treatment with carotid endarterectomy helps to restore cerebral perfusion, which may prevent ocular and cerebral complications. The main aim was to assess retinal and choroidal vascular perfusion changes before and after endarterectomy in patients affected by CAS. Methods: The design of the study was prospective and observational, including patients affected by CAS and healthy controls. The follow-up was 3 months. We performed quantitative optical coherence tomography (OCT) angiography (OCTA) analyses of retinal perfusion changes, before and after endarterectomy. The main outcome measures were the quantitative changes of choroidal thickness (CT), retinal nerve fiber layer (RNFL), and ganglion cell layer (GCL); vessel density (VD); and vessel tortuosity (VT) OCTA metrics were also measured. Results: Sixty eyes of 30 patients affected by CAS and 30 eyes of 30 controls were included. We separately considered the ipsilateral eyes to CAS, the contralateral eyes to CAS, and the healthy eyes. Visual symptoms were absent in all the patients. RNFL and GCL resulted similar between patients and controls (p > 0.05). CT was significantly thinner in ipsilateral eyes than controls (p < 0.01), and it resulted unchanged after surgery (p > 0.05). VD resulted significantly altered only in some plexa of the ipsilateral eyes (p < 0.01), whereas VT disclosed decreased values of the entire retinal vascular network, both in ipsilateral and contralateral eyes (p < 0.05). Endarterectomy was followed by statistically significant improvement of retinal perfusion (p < 0.05). Conclusion: Optical coherence tomography angiography can noninvasively detect postendarterectomy retinal perfusion improvements in CAS patients with baseline diabetes and hypertension as a systemic risk factor. [ABSTRACT FROM AUTHOR]

Background: Retinitis Pigmentosa (RP) represents a retinal dystrophy with an extremely complex pathogenesis further worsened by the impairment of the retinal vascular supply. The main goal of this study was to identify different vascular patterns in RP, by means of optical coherence tomography angiography (OCTA). Methods: A total of 32 RP patients (16 males, 50%; mean age 45.93 ± 11.4) and 32 healthy age-matched controls (16 males, 50%; age 42.8 ± 11.2). High resolution OCT and OCTA images were obtained from all participants. Several quantitative parameters were extracted both from structural OCT and OCTA images. A post-hoc analysis assessed the relationship between the quantitative OCTA parameters adopted and the following measures: best corrected visual acuity (BCVA), central macular thickness (CMT) and retinal nerve fiber layer (RNFL). Results: Mean LogMAR BCVA was 0.24 ± 0.32 for RP patients and 0.0 ± 0.0 for controls (p < 0.01). CMT, choroidal thickness and RNFL were statistically different between RP and controls (p < 0.01). OCTA parameters showed strong alterations of the retinal vascular network in RP (all p < 0.01). Several statistically significant correlations were also found. Furthermore, a vessel tortuosity cut-off of 4.80 and a vessel rarefaction cut-off of 0.62 enabled the RP cohort to be divided into two significantly different sub-groups in terms of BCVA, RNFL and CMT. Conclusions: Quantitative OCTA parameters help identify vascular abnormalities in RP, separating two different vascular patterns. [ABSTRACT FROM AUTHOR]

Background: To identify different choroidal patterns in Stargardt disease (STGD) and to assess their clinical correlates. Methods: 100 STGD eyes (29 males; mean age 42.6 ± 16.5 years) and 100 control eyes (29 males; mean age 43.2 ± 8.5 years) were included. Optical coherence tomography (OCT) and OCT angiography (OCTA) images were obtained. Four different choroidal patterns, quantitative OCT and OCTA parameters were assessed and statistically analyzed. The main outcome was the correlation between each choroidal pattern and anatomical and functional retinal status. Furthermore, we assessed structural and best corrected visual acuity (BCVA) changes of each STGD subgroup after one-year. Results: Mean BCVA was 0.63 ± 0.44 LogMAR for STGD patients and 0.0 ± 0.0 LogMAR for controls (p < 0.01). All quantitative parameters appeared deteriorated in STGD compared to controls (p < 0.01). Choroidal patterns were distributed as follows: Pattern 1 (normal appearing choroid) (15%), Pattern 2 (reduced Sattler or Haller layer) (29%), Pattern 3 (reduced Sattler and Haller layers) (26%), Pattern 4 (Pattern 3 + choroidal caverns) (30%). More advanced patterns significantly correlated with a more severe loss of retinal structural integrity. Furthermore, only Pattern 3 and Pattern 4 showed remarkable signs of progression after one year. Conclusions: Choroidal patterns were related with retinal structural status and BCVA loss, and with different disease progression. [ABSTRACT FROM AUTHOR]