Eye and Brain最新文献

Purpose: Visual impairment is a major cause of disability and impairment of cognitive function in older people. Brain structural changes associated with visual function impairment are not well understood. The objective of this study was to assess the association between visual function and cortical thickness in older adults.

Methods: Participants were selected from the French population-based ESPRIT cohort of 2259 community-dwelling adults ≥65 years old enrolled between 1999 and 2001. We considered visual function and brain MRI images at the 12-year follow-up in participants who were right-handed and free of dementia and/or stroke, randomly selected from the whole cohort. High-resolution structural T1-weighted brain scans acquired with a 3-Tesla scanner. Regional reconstruction and segmentation involved using the FreeSurfer image-analysis suite.

Results: A total of 215 participants were included (mean [SD] age 81.8 [3.7] years; 53.0% women): 30 (14.0%) had central vision loss and 185 (86.0%) normal central vision. Vision loss was associated with thinner cortical thickness in the right insula (within the lateral sulcus of the brain) as compared with the control group (mean thickness 2.38 [0.04] vs 2.50 [0.03] mm, 4.8% thinning, p_corrected= 0.04) after adjustment for age, sex, lifetime depression and cardiovascular disease.

Conclusion: The present study describes a significant thinning of the right insular cortex in older adults with vision loss. The insula subserves a wide variety of functions in humans ranging from sensory and affective processing to high-level cognitive processing. Reduced insula thickness associated with vision loss may increase cognitive burden in the ageing brain.

Purpose: Transcranial alternating current stimulation (tACS) is a stimulation protocol used for learning enhancement and mitigation of cognitive dysfunction. Correlated firing has been postulated to be a meta-code that links neuronal spike responses associated with a single entity and may be an important component of high-level cognitive functions. Thus, changes in the covariance firing structure of CNS neurons such as retinal ganglion cells are one potential mechanism by which tACS can exert its effects.

Materials and methods: We used microelectrode arrays to record light-evoked spike responses of 24 retinal ganglion cells in 7 rabbit eyecup preparations and analyzed the covariance between 30 pairs of neighboring retinal ganglion cells before, during, and after 10-minute application of alternating currents of 1 microampere at 10 or 20 Hz.

Results: tACS stimulation significantly changed the covariance structure of correlated firing in 60% of simultaneously recorded retinal ganglion cells. Application of tACS in the retinal preparation increased cross-covariance in 26% of cell pairs, an effect usually associated with increased light-evoked ganglion cell firing. tACS associated decreases in cross-covariance occurred in 37% of cell pairs. Increased covariance was more common in response to the first, 10-minute application of tACS in isolated retina preparation. Changes in covariance were rare after repeated stimulation, and more likely to result in decreased covariance.

Conclusion: Retinal ganglion cell correlated firing is modulated by 1 microampere tACS currents showing that electrical stimulation can significantly and persistently change the structure of the correlated firing of simultaneously recorded rabbit retinal ganglion cells.

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.