Central nervous system vascular disease can be combined with a variety of ocular signs, such as orbital pain, flash, visual field defects, vision loss, eye muscle paralysis. Therefore, some patients were first diagnosed in ophthalmology, including aneurysm rupture, arterial dissection, cerebral apoplexy and other critical nervous system diseases that need rapid treatment. If the doctors didn't know enough, the diagnosis and treatment might be delayed. Most of the vascular diseases of the central nervous system related to ophthalmology have clinical manifestations that cannot be explained by ophthalmology. In the face of chronic conjunctivitis, unexplained visual field defect or cranial nerve paralysis with local ineffective treatment, it is necessary to broaden the thinking of differential diagnosis. To understand the characteristics of vascular diseases of the central nervous system that are prone to ocular manifestations can provide references for the clinical diagnosis and treatment of ophthalmology.
Primary or secondary death of retinal ganglion cells (RGC) is a common outcome in various optic neuropathies, often resulting in severe visual damage. The inherent characteristics of RGC include the continuous upregulation of intracellular growth-inhibitory transcription factors and the downregulation of growth-inducing transcription factors during cell differentiation. Additionally, the external inhibitory microenvironment following RGC damage, including oxidative stress, chronic inflammation, lack of neurotrophic factors, high expression of myelin proteins, and the formation of glial scars, all restrict axonal regeneration. Both intrinsic and extrinsic factors lead to the death of damaged RGC and hinder axonal regeneration. Various neuroprotective agents and methods attempt to promote neuroprotection and axonal regeneration from both intrinsic and extrinsic aspects, and well knowledge of these neuroprotective strategies is of significant importance for promoting the neuroprotective experimental research and facilitating its translation into clinical practice.
Objective To establish and evaluate a rat model of nonarteritic anterior ischemic optic neuropathy (NAION). Methods The rats were randomly divided into control group (n=13), sham laser group (n=11) and NAION group (n=23). The right eye was set as the experimental eye. NAION model was induced by directly illuminating the optic nerve (ON) of the right eye with 532 nm green laser, after intravenous infusion with the photosensitizing agent Rose Bengal. Sham laser treatment consisted of illuminating the ON region with 532 nm laser without Rose Bengal injection. Rats in control group underwent no intervention. The appearance of optic disc was observed with funduscope at 12 hours, 1, 3, 7, 28 days post-illumination. The histologic changes in the retina and ON of the NAION model were evaluated qualitatively with hematoxylin and eosin (HE) staining and transmission electron microscopy. The retrograde-labeled retinal ganglion cells (RGC) were counted on photographs taken from retinal flat mounts in a masked fashion. Results The optic disc in NAION eyes were swollen 3 days after photodynamic treatment. HE-stained longitudinal ON sections of NAION revealed vacuolar degeneration on day 3 after induction. Besides, ultrastructural study showed axonal edema and collapsed sheaths in the ischemic optic nerve at the same time point after modeling. ON edema resolved 7 days after induction. The final results revealed optic disc atrophy, extensive axonal loss, severe glial scar, and RGC death in large numbers 4 weeks after modeling. There were no aforementioned manifestations in control and sham laser group. The RGC density of the right eyes was statistically significantly lower in NAION group than that in control group and in sham laser group (t=−14.142, −14.088; P=0.000, 0.000). The survival rate of RGC was statistically significantly lower in NAION group than in control group and in sham laser group (t=−17.048, −16.667; P=0.000, 0.000). There was no difference of RGC density and survival rate of RGC between control and sham laser group (t=0.050, 0.348; P=0.961, 0.731). Conclusion A rat model of NAION was established successfully by photodynamic treatments with Rose Bengal, which induce optic nerve damage and RGC death.
ObjectiveTo observe the changes in subfoveal choroidal thickness (SFCT) and peripapillary choroidal thickness (pCT) in nonarteritic anterior ischemic optic neuropathy (NAION).MethodsNineteen newly occurred NAION patients were included. The patients were divided into group A (20 affected eyes of 19 patients) and B (18 fellow eyes of 18 patients). Twenty eyes of 20 age, gender, intraocular pressure and axial length-matched healthy volunteers (group C) were enrolled in this study. The differences of age (t=1.58), gender ratios (χ2=0.107), intraocular pressure (t=0.092) and axial length (t=0.148) between 3 groups were not significant (P＞0.05). SFCT, pCT were measured at first visit, 1 month and 3 months after treatment using enhanced deep imaging technique of spectral domain optical coherence tomography. The correlation of best corrected visual acuity (BCVA) and the choroidal thickness was investigated.ResultsAt the first visit, the mean SFCT and pCT in group A were significant thicker than group C (t=2.957, 2.844; P=0.006, 0.009). There was no difference of SFCT and pCT between group B and C (t=2.019, 2.024; P=0.053, 0.057). There was no correlation between BCVA and SFCT, pCT (F=0.161, 0.033; P=0.695, 0.859). One month after treatment, SFCT in group A was still thicker than group C (t=2.803, P=0.009); while pCT was decreased in group A when compared to group C, but the difference was not significant (t=1.871, P=0.084). Three months after treatment, the differences of SFCT and pCT were not significant between group A and C (t=1.223, 1.105; P=0.236, 0.282).ConclusionsAt first visit, SFCT and pCT in NAION eyes showed a significant increase when compared to normal eyes. One month later, pCT in NAION eyes decreased to normal. Three months later, both SFCT and pCT decreased. These findings may suggest that a thickened choroid is a clinical characteristic at acute stage in NAION eyes.
ObjectiveTo investigate the neuroprotective effect of Benztropine on retinal ganglion cells (RGCs) death and optic nerve injury in rats model of non-arteritis anterior ischemic optic neuropathy (rNAION).MethodsA total of 25 Sprague-Dawley rats were randomly divided into Benztropine treatment group (n=13) and PBS control group (n=12). The right eye was set as the experimental eye. rNAION model was established by using rose Bengal combined with laser photodynamic method. The rats in the Benztropine treatment group were received intraperitoneal injection with Benztropine 10 mg/kg (0.2 ml) daily for 3 weeks, while the rats in the PBS control group were received intraperitoneal injection with an equal volume of PBS. At 1, 3 and 7 days after modeling, the retinal and optic disc conditions of the rats were observed by direct ophthalmoscopy. Retrograde labeling, fluorescence microscopy and transmission electron microscopy were used to observe the survival of RGCs and the damage of the optic nerve myelin and axon at 4 weeks after modeling. The RGCs density and survival rate of the two groups were compared by One-Way Anova.ResultsAt 1 and 3 days after modeling, the optic disc edema was observed in the rats of rNAION model group. At 7 days after modeling, the optic disc edema decreased and the boundary was blurred compared with 3 days after modeling.After 4 weeks, the RGCs density in the PBS group was 308±194/mm2 and the survival rate was 13.7%. The density of RGCs in the Benztropine group was 1173+868/mm2 and the survival rate was 47.6%. The differences of RGCs density and survival rate were significant between the two groups (F=7.552, 8.184; P=0.015, 0.012). Myelin disintegration, axon degeneration, onion-like body and gliosis were observed in the optic nerve sections of rNIAON in the PBS group, while the damage of axon and myelin structure in the Benztropine group was significantly less than that in the PBS group.ConclusionsBenztropine group showed higher RGC survival rate, less damage of axon and myelin structure on rNAION model. This study explored the potential neuroprotective effect of Benztropine.