Eye and Brain最新文献

Purpose: We improve pupillary responses and diagnostic performance of flicker pupil perimetry through alterations in global and local color contrast and luminance contrast in adult patients suffering from visual field defects due to cerebral visual impairment (CVI).

Methods: Two experiments were conducted on patients with CVI (Experiment 1: 19 subjects, age M and SD 57.9 ± 14.0; Experiment 2: 16 subjects, age M and SD 57.3 ± 14.7) suffering from absolute homonymous visual field (VF) defects. We altered global color contrast (stimuli consisted of white, yellow, cyan and yellow-equiluminant-to-cyan colored wedges) in Experiment 1, and we manipulated luminance and local color contrast with bright and dark yellow and multicolor wedges in a 2-by-2 design in Experiment 2. Stimuli consecutively flickered across 44 stimulus locations within the inner 60 degrees of the VF and were offset to a contrasting (opponency colored) dark background. Pupil perimetry results were compared to standard automated perimetry (SAP) to assess diagnostic accuracy.

Results: A bright stimulus with global color contrast using yellow (p= 0.009) or white (p= 0.006) evoked strongest pupillary responses as opposed to stimuli containing local color contrast and lower brightness. Diagnostic accuracy, however, was similar across global color contrast conditions in Experiment 1 (p= 0.27) and decreased when local color contrast and less luminance contrast was introduced in Experiment 2 (p= 0.02). The bright yellow condition resulted in highest performance (AUC M = 0.85 ± 0.10, Mdn = 0.85).

Conclusion: Pupillary responses and pupil perimetry's diagnostic accuracy both benefit from high luminance contrast and global but not local color contrast.

Purpose: To investigate the impact of attention orientation in young myopic adults with astigmatism.

Methods: The effect of attention on foveal meridional performance and anisotropy was measured in corrected myopes with various levels of astigmatism (with-the-rule astigmatism ≤ -0.75D, Axis: 180 ± 20) using orientation-based attention. Attention was manipulated by instructing subjects to attend to either the horizontal or the vertical line of a central pre-stimulus (a pulsed cross) along separate blocks of trials. For each attention condition, meridional acuity and reaction times were measured via an annulus Gabor target situated remotely from the cross and presented at random horizontally and vertically in a two-alternative forced-choice employing two interleaved staircase procedures (one-up/one-down). Attention modulations were estimated by the difference in performance between horizontal and vertical attention.

Results: Foveal meridional performance and anisotropy were strongly affected by the orientation of attention, which appeared critical for the enhancement of reaction times and resolution. Under congruent orienting of attention, foveal meridional anisotropy was correlated with the amount of defocus for both reaction time and resolution, demonstrating greater vertical performance than horizontal performance as myopia increased. Compatible with an attentional compensation of blur through optimal orienting of attention, vertical attention enhanced reaction times compared to horizontal attention and was accompanied by an increase in overall acuity when myopia increased. Increased astigmatism was associated with smaller attention effects and asymmetry, suggesting potential deficits in the compensation of blur in astigmatic eyes.

Conclusion: Collectively, attention to orientation plays a significant role in horizontal-vertical foveal meridional anisotropy and can modulate the asymmetry of foveal perception imposed by the optics of the eye in episodes of uncorrected vision. Further work is necessary to understand how attention and refractive errors interact during visual development. These results may have practical implications for methods to enhance vision with attention training in myopic astigmats.

Introduction: Previous works on experience-dependent brain plasticity have been limited to the cortical structures, overlooking subcortical visual structures such as the lateral geniculate nucleus (LGN). Animal studies have shown substantial experience dependent plasticity and using fMRI, human studies have demonstrated similar properties in patients with cataract surgery. However, in neither animal nor human studies LGN has not been directly assessed, mainly due to its small size, tissue heterogeneity, low contrast/noise ratio, and low spatial resolution.

Methods: Utilizing a new algorithm that markedly improves the LGN visibility, LGN was evaluated in a group of low vision patients before and after retinal intervention to reinstate vision and normal sighted matched controls.

Results: Between and within groups comparisons showed that patients had significantly smaller left (p< 0.0001) and right (p < 0.00002) LGN volumes at baseline as compared to the one-year follow-up volumes. The same baseline and one year comparison in controls was not significant. Significant positive correlations were observed between the incremental volume increase after gene therapy of the left LGN and the incremental increase in the right (r = 0.71, p < 0.02) and left (r = 0.72, p = 0.018) visual fields. Incremental volume increase of the right LGN also showed a similar positive slope but did not reach significance.

Discussion: These results show that despite significantly less volume at baseline, retinal gene therapy promotes robust expansion and increase in LGN volume. Reinstating vision may have facilitated the establishment of new connections between the retina and the LGN and/or unmasking of the dormant connections. The exact trajectory of the structural changes taking place in LGN is unclear but our data shows that even after years of low vision, the LGN in RPE65 patients has the potential for plasticity and expansion to a nearly normal volume one year after gene therapy administration.

Introduction: Diabetic patients routinely have high levels of high mobility group box 1 (HMGB1) protein in their plasma, vitreous and ocular membranes, which is strongly correlated with subclinical chronic inflammation in the eye. Our previous work has suggested that high HMGB1 in diabetes plays a role in retinal inflammation and angiogenesis, but its role in the optic nerve damage is unclear. Therefore, our goal is to examine the role of HMGB1 in optic nerve damage in diabetes.

Methods: Gene expression of HMGB1 was quantified in the optic nerve from streptozotocin-induced diabetic mice by qRT-PCR, and their protein expressions by Western blot analysis and immunofluorescence staining. Using immunohistochemical technique, expression of reactive astrogliosis (indicator of neuroinflammation) and nerve demyelination/damage were determined by quantifying glial fibrillary acid protein (GFAP) and myelin basic protein (MBP), respectively. The role of HMGB1 in the optic nerve damage and alteration visual pathways was confirmed in mice receiving glycyrrhizin, a HMGB1 inhibitor. Similar parameters were measured in the optic nerve from human donors with diabetes.

Results: Compared to normal mice, diabetic mice exhibited increased levels of HMGB1, higher GFAP expression, and decreased MBP in the optic nerve. Double immunofluorescence microscopy revealed that diabetes induced increased HMGB1 immunoreactivities were significantly colocalized with GFAP in the optic nerve. Glycyrrhizin supplementation effectively reduced HMGB1 and maintained normal axonal myelination and visual conduction. Results from mice optic nerve confirmed the results obtained from human donors with diabetes.

Discussions: Thus, diabetes-induced HMGB1 upregulation promotes optic nerve demyelination and inflammation. The regulation of HMGB1 activation has potential to protect optic nerve damage and the abnormalities of visual pathways in diabetic patients.

Optic nerve cupping or enlargement of the cup-to-disc ratio is widely recognized as a feature of glaucoma, however it may also occur in non-glaucomatous optic neuropathies. The most well-recognized non-glaucomatous optic neuropathies that cause cupping include compressive optic neuropathies, arteritic anterior ischemic optic neuropathies, hereditary optic neuropathies, and optic neuritis. Cupping is thought to consist of two main components: prelaminar and laminar thinning. The former is a shallow form of cupping and related to loss of retinal ganglion cells, whereas the latter involves damage to the lamina cribrosa and peripapillary scleral connective tissue. Differentiating glaucomatous and non-glaucomatous optic nerve cupping remains challenging even for experienced observers. Classically, the optic nerve in non-glaucomatous causes has pallor of the neuroretinal rim, but the optic nerve should not be examined in isolation. The patient's medical history, history of presenting illness, visual function (visual acuity, color vision and visual field testing) and ocular examination also need to be considered. Ancillary testing such as optical coherence tomography of the retinal nerve fiber layer and ganglion cell layer-inner plexiform layer may also be helpful in localizing the disease. In this review, we review the non-glaucomatous causes of cupping and provide an approach to evaluating a patient that presents with an enlarged cup-to-disc ratio.

Vestibular schwannomas (VSs), also called acoustic neuromas, are benign intracranial neoplasms of the vestibulocochlear (VIII) cranial nerve. Management options include "wait-and-scan," stereotactic radiosurgery and surgical resection. Due to the proximity of the VIII nerve to the facial (VII) nerve in the cerebello-pontine angle, the VII nerve is particularly vulnerable to the effects of surgical resection. This can result in poor eye closure, lagophthalmos and resultant corneal exposure post VS resection. Additionally, compression from the tumor or resection can cause trigeminal (V) nerve damage and a desensate cornea. The combination of an exposed and desensate cornea puts the eye at risk of serious ocular complications including persistent epithelial defects, corneal ulceration, corneal vascularization, corneal melting and potential perforation. The abducens (VI) nerve can be affected by a large intracranial VS causing raised intracranial pressure (a false localizing sign) or as a result of damage to the VI nerve at the time of resection. Other types of neurogenic strabismus are rare and typically transient. Contralaterally beating nystagmus as a consequence of vestibular dysfunction is common post-operatively. This generally settles to pre-operative levels as central compensation occurs. Ipsilaterally beating nystagmus post-operatively should prompt investigation for post-operative cerebrovascular complications. Papilledema (and subsequent optic atrophy) can occur as a result of a large VS causing raised intracranial pressure. Where papilledema follows surgical resection of a VS, it can indicate that cerebral venous sinus thrombosis has occurred. Poor visual function following VS resection can result as a combination of all these potential complications and is more likely with larger tumors.

Purpose: To assess the diagnostic accuracy of visual field results generated by the newly developed software (CU-VF) and the standard automated perimetry (SAP) for detecting hemianopia.

Patients and methods: Forty-three subjects with hemianopia and 33 controls were tested with the CU-VF software on a personal computer and SAP. Hemianopia was defined as the presence of a hemianopic field respecting the vertical meridian on SAP with the corresponding neuroimaging pathology as evaluated by 2 neuro-ophthalmologists. Results of CU-VF were independently evaluated by 2 neuro-ophthalmologists, 1 general ophthalmologist, and 1 general practitioner in terms of the presence of hemianopia. Sensitivity, specificity, and kappa coefficient for inter-observer reliability were calculated. Satisfaction and ease of use were evaluated with a visual analog-scale questionnaire and analyzed using paired t-test.

Results: The sensitivity (95% CI) and specificity (95% CI) of the CU-VF to detect hemianopia was 74.42% (58.53-85.96) and 93.94% (78.38-99.94). Kappa coefficient between neuro-ophthalmologists versus general ophthalmologist and general practitioner were 0.71 and 0.84, respectively. The mean (SD) test duration was 2.25 (0.002) minutes for the CU-VF and 5.38 (1.34) minutes for SAP (p < 0.001). Subjects reported significantly higher satisfaction and comfort using the CU-VF software compared to SAP.

Conclusion: The CU-VF screening software showed good validity and reliability to detect hemianopia, with shorter test duration and higher subject satisfaction compared to SAP.