Loss Of Visual Input Research Articles

Effect of Vision and Surface Slope on Postural Sway in Healthy Adults: A Prospective Cohort Study.

Postural stability requires an interaction between cognitive, perceptual, sensory, and motor functions. Thus, impairment in any of these systems may affect postural balance. This study assessed the effect of visual input and surface slope on postural stability. The study was conducted on healthy participants, 11 females and 11 males who were 24-34 years of age. They were asked to perform still upright bipedal standing on flat and +/-20° sloped surfaces with eyes open (EO) and closed (EC). Six center of pressure (COP) parameters were measured by posturography. A significant relationship was observed between COP parameters, standing conditions, and body mass index. Gender had no significant effect on the COP. The loss of visual input within each standing condition did not affect the COP parameters. In contrast, differences were observed between standing on a flat surface and uphill with EC and between standing on a flat surface and downhill with EC and EO. When the participants were standing on inclined surfaces, the loss of vision significantly increased the postural instability. Young healthy adults demonstrated the greatest difficulty in standing uphill with EC. This was followed by standing downhill with EC and standing downhill with EO.

Structural and Functional Plasticity in the Dorsolateral Geniculate Nucleus of Mice following Bilateral Enucleation

Within the nervous system, plasticity mechanisms attempt to stabilize network activity following disruption by injury, disease, or degeneration. Optic nerve injury and age-related diseases can induce homeostatic-like responses in adulthood. We tested this possibility in the thalamocortical (TC) neurons in the dorsolateral geniculate nucleus (dLGN) using patch-clamp electrophysiology, optogenetics, immunostaining, and single-cell dendritic analysis following loss of visual input via bilateral enucleation. We observed progressive loss of vGlut2-positive retinal terminals in the dLGN indicating degeneration post-enucleation that was coincident with changes in microglial morphology indicative of microglial activation. Consistent with the decline of vGlut2 puncta, we also observed loss of retinogeniculate (RG) synaptic function assessed using optogenetic activation of RG axons while performing whole-cell voltage clamp recordings from TC neurons in brain slices. Surprisingly, we did not detect any significant changes in the frequency of miniature post-synaptic currents (mEPSCs) or corticothalamic feedback synapses. Analysis of TC neuron dendritic structure from single-cell dye fills revealed a gradual loss of dendrites proximal to the soma, where TC neurons receive the bulk of RG inputs. Finally, analysis of action potential firing demonstrated that TC neurons have increased excitability following enucleation, firing more action potentials in response to depolarizing current injections. Our findings show that degeneration of the retinal axons/optic nerve and loss of RG synaptic inputs induces structural and functional changes in TC neurons, consistent with neuronal attempts at compensatory plasticity in the dLGN.

An architectonic type principle in the development of laminar patterns of cortico-cortical connections

Structural connections between cortical areas form an intricate network with a high degree of specificity. Many aspects of this complex network organization in the adult mammalian cortex are captured by an architectonic type principle, which relates structural connections to the architectonic differentiation of brain regions. In particular, the laminar patterns of projection origins are a prominent feature of structural connections that varies in a graded manner with the relative architectonic differentiation of connected areas in the adult brain. Here we show that the architectonic type principle is already apparent for the laminar origins of cortico-cortical projections in the immature cortex of the macaque monkey. We find that prenatal and neonatal laminar patterns correlate with cortical architectonic differentiation, and that the relation of laminar patterns to architectonic differences between connected areas is not substantially altered by the complete loss of visual input. Moreover, we find that the degree of change in laminar patterns that projections undergo during development varies in proportion to the relative architectonic differentiation of the connected areas. Hence, it appears that initial biases in laminar projection patterns become progressively strengthened by later developmental processes. These findings suggest that early neurogenetic processes during the formation of the brain are sufficient to establish the characteristic laminar projection patterns. This conclusion is in line with previously suggested mechanistic explanations underlying the emergence of the architectonic type principle and provides further constraints for exploring the fundamental factors that shape structural connectivity in the mammalian brain.

Postural Stability in Older Adults With Alzheimer Disease.

The prevalence of adults with Alzheimer disease (AD) aged >65 years is increasing and estimated to quadruple by 2051. The aim of this study was to investigate postural stability in people with mild to moderate AD and factors contributing to postural instability compared with healthy peers (controls). A computerized systematic search of databases and a hand search of reference lists for articles published from 1984 onward (English-language articles only) were conducted on June 2, 2015, using the main key words "postural stability" and "Alzheimer's disease." Sixty-seven studies were assessed for eligibility (a confirmed diagnosis of AD, comparison of measured postural stability between participants with AD and controls, measured factors potentially contributing to postural instability). Data were extracted, and Downs and Black criteria were applied to evaluate study quality. Eighteen articles were analyzed using qualitative synthesis and reported based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Strength of evidence was guided by the Grading of Recommendations Assessment, Development and Evaluation. Strong evidence was found that: (1) older adults with mild to moderate AD have reduced static and functional postural stability compared with healthy peers (controls) and (2) attentional demand during dual-task activity and loss of visual input were key factors contributing to postural instability. Deta-analysis was not possible due to heterogeneity of the data. Postural stability is impaired in older adults with mild to moderate AD. Decreasing visual input and concentrating on multiple tasks decrease postural stability. To reduce falls risk, more research discerning appropriate strategies for the early identification of impairment of postural stability is needed. Standardization of population description and consensus on outcome measures and the variables used to measure postural -instability and its contributing factors are necessary to ensure meaningful synthesis of data.

Two distinct mechanisms for experience-dependent homeostasis.

Models of firing rate homeostasis such as synaptic scaling and the sliding synaptic plasticity modification threshold predict that decreasing neuronal activity (e.g. by sensory deprivation) will enhance synaptic function. Manipulations of cortical activity during two forms of visual deprivation (dark exposure (DE) and binocular lid suture (BS)) revealed that, contrary to expectations, spontaneous firing in conjunction with loss of visual input is necessary to lower the threshold for Hebbian plasticity and increases mEPSC amplitude. Blocking activation of GluN2B receptors, which are up-regulated by DE, also prevents the increase in mEPSC amplitude, suggesting that DE potentiates mEPSCs primarily through a Hebbian mechanism, not through synaptic scaling. Nevertheless, NMDAR-independent changes in mEPSC amplitude consistent with synaptic scaling could be induced by extreme reductions of activity. Therefore, two distinct mechanisms operate within different ranges of neuronal activity to homeostatically regulate synaptic strength.

Quantitative Romberg's test in acute carbon monoxide poisoning treated by hyperbaric oxygen.

The aim of this study was to evaluate whether monitoring of acute carbon monoxide-poisoned (COP) patients by means of quantitative Romberg's test (QR-test) during a hyperbaric oxygen (HBO₂) therapy regimen could be a useful supplement in the evaluation of neurological status. We conducted a retrospective study (2000-2014) in which we evaluated data containing quantitative sway measurements of acute COP patients (n = 58) treated in an HBO₂ regimen. Each patient was tested using QR-test before and after each HBO₂ treatment. Data were analyzed using linear mixed models (LMM). In each LMM, sway prior to HBO₂ therapy was set as the fixed effect and change in sway after HBO₂ therapy was set as the response variable. Patient, treatment number, weight and age were set as random effects for all LMMs. From the LMMs we found that larger values of sway prior to HBO₂ produced a negative change in sway. We found no correlation between CO level and sway (P=0.1028; P=0.8764; P=0.4749; P=0.5883). Results showed that loss of visual input caused a significant increase in mean sway (P=0.028) and sway velocity (P⟨0.0001). The Quantitative Romberg's test is a fast, useful supplement to neurological evaluation and a potential valuable tool for monitoring postural stability during the course of treatment in acute COP patients.

Perceiving a continuous visual world across voluntary eye blinks.

People blink their eyes every few seconds, but the changes in retinal illumination that accompany eyeblinks are hardly noticed. Furthermore, despite the loss of visual input, visual experience remains continuous across eyeblinks. Two hypotheses were investigated to account for these phenomena. The first proposes that perceptual information is maintained across a blink whereas the second proposes that perceptual information is not maintained but rather postblink perceptual experience is antedated to the beginning of the blink. Two experiments found no evidence for temporal antedating of a stimulus presented during a voluntary eyeblink. In a third experiment subjects judged the temporal duration of a stimulus that was interrupted by a voluntary eyeblink with that of a stimulus presented while the eyes were open. The duration of stimuli that were interrupted by eyeblinks was judged to be 117 ms shorter than that of stimuli presented while the eyes remained open, indicating that blink duration was not accounted for in the perception of stimulus duration. This suggests that perceptual experience is neither maintained nor antedated across eyeblinks, but rather is ignored, perhaps in response to the extraretinal signal that accompanies the eyeblink. (PsycINFO Database Record

Structural brain MRI studies in eye diseases: are they clinically relevant? A review of current findings.

Many eye diseases reduce visual acuity or are associated with visual field defects. Because of the well-defined retinotopic organization of the connections of the visual pathways, this may affect specific parts of the visual pathways and cortex, as a result of either deprivation or transsynaptic degeneration. For this reason, over the past several years, numerous structural magnetic resonance imaging (MRI) studies have examined the association of eye diseases with pathway and brain changes. Here, we review structural MRI studies performed in human patients with the eye diseases albinism, amblyopia, hereditary retinal dystrophies, age-related macular degeneration (AMD) and glaucoma. We focus on two main questions. First, what have these studies revealed? Second, what is the potential clinical relevance of their findings? We find that all the aforementioned eye diseases are indeed associated with structural changes in the visual pathways and brain. As such changes have been described in very different eye diseases, in our view the most parsimonious explanation is that these are caused by the loss of visual input and the subsequent deprivation of the visual pathways and brain regions, rather than by transsynaptic degeneration. Moreover, and of clinical relevance, for some of the diseases - in particular glaucoma and AMD - present results are compatible with the view that the eye disease is part of a more general neurological or neurodegenerative disorder that also affects the brain. Finally, establishing structural changes of the visual pathways has been relevant in the context of new therapeutic strategies to restore retinal function: it implies that restoring retinal function may not suffice to also effectively restore vision. Future structural MRI studies can contribute to (i) further establish relationships between ocular and neurological neurodegenerative disorders, (ii) investigate whether brain degeneration in eye diseases is reversible, (iii) evaluate the use of neuroprotective medication in ocular disease, (iv) determine optimal timing for retinal implant insertion and (v) establish structural MRI examination as a diagnostic tool in ophthalmology.

In vivo visuotopic brain mapping with manganese-enhanced MRI and resting-state functional connectivity MRI

The rodents are an increasingly important model for understanding the mechanisms of development, plasticity, functional specialization and disease in the visual system. However, limited tools have been available for assessing the structural and functional connectivity of the visual brain network globally, in vivo and longitudinally. There are also ongoing debates on whether functional brain connectivity directly reflects structural brain connectivity. In this study, we explored the feasibility of manganese-enhanced MRI (MEMRI) via 3 different routes of Mn2+ administration for visuotopic brain mapping and understanding of physiological transport in normal and visually deprived adult rats. In addition, resting-state functional connectivity MRI (RSfcMRI) was performed to evaluate the intrinsic functional network and structural–functional relationships in the corresponding anatomical visual brain connections traced by MEMRI. Upon intravitreal, subcortical, and intracortical Mn2+ injection, different topographic and layer-specific Mn enhancement patterns could be revealed in the visual cortex and subcortical visual nuclei along retinal, callosal, cortico-subcortical, transsynaptic and intracortical horizontal connections. Loss of visual input upon monocular enucleation to adult rats appeared to reduce interhemispheric polysynaptic Mn2+ transfer but not intra- or inter-hemispheric monosynaptic Mn2+ transport after Mn2+ injection into visual cortex. In normal adults, both structural and functional connectivity by MEMRI and RSfcMRI was stronger interhemispherically between bilateral primary/secondary visual cortex (V1/V2) transition zones (TZ) than between V1/V2 TZ and other cortical nuclei. Intrahemispherically, structural and functional connectivity was stronger between visual cortex and subcortical visual nuclei than between visual cortex and other subcortical nuclei. The current results demonstrated the sensitivity of MEMRI and RSfcMRI for assessing the neuroarchitecture, neurophysiology and structural–functional relationships of the visual brains in vivo. These may possess great potentials for effective monitoring and understanding of the basic anatomical and functional connections in the visual system during development, plasticity, disease, pharmacological interventions and genetic modifications in future studies.

Cross-modal plasticity within the occipital cortex of early blind subjects is driven by loss of visual input rather than by unmasking of existing cross-modal responses

Cross-modal plasticity within the occipital cortex of early blind subjects is driven by loss of visual input rather than by unmasking of existing cross-modal responses

Looking After Polysialic Acid

STKE In some cases, the effects of neuronal activity are restricted to particular developmental stages. For instance, the loss of visual input from one eye early in life leads to a shift in the responsiveness of neurons in the visual cortex toward the functional eye. The onset and time course of

Looking After Polysialic Acid

Many aspects of brain function are modulated by neuronal activity; in some cases, the effects of activity are restricted to particular developmental stages, or critical periods. For instance, loss of visual input from one eye early in life leads to a shift in the responsiveness of neurons in the visual cortex toward the functional eye. The onset and time course of this critical period for ocular dominance plasticity is influenced by the maturation of GABAergic innervation, which is itself regulated by visual input and neuronal activity. But how? Di Cristo et al . found that polysialic acid [PSA, a homopolymer of sialic acid that attaches to neural cell adhesion molecules (NCAMs) and modulates intercellular bonds] and NCAMs were abundant in the neonatal mouse visual cortex but that PSA underwent a steep decline after eye opening. Pups reared in the dark showed increased PSA compared with pups reared under conventional light/dark cycles, and pharmacological suppression of visual signals suppressed the decline. In organotypic cortical cultures, enzymatic removal of PSA with endoneuramidase led to premature maturation of the innervation of pyramidal cell somata by GABAergic basket interneurons. Similarly, endoneuramidase injection into the visual cortex promoted both perisomatic GABAergic innervation and the frequency of miniature inhibitory postsynaptic currents. Moreover, it stimulated the early onset of the critical period for ocular dominance plasticity. Thus, the authors conclude that maturation of GABAergic inhibition--and thereby the initiation of ocular dominance plasticity--is regulated by an activity-dependent decrease in PSA. G. Di Cristo, B. Chattopadhyaya, S. J. Kuhlman, Y. Fu, M.-C. Bélanger, C. Z. Wu, U. Rutishauser, L. Maffei, Z. J. Huang, Activity-dependent PSA expression regulates inhibitory maturation and onset of critical period plasticity. Nat. Neurosci . 10 , 1569-1577 (2007). [PubMed]

Potential Role of Endogenous Brain-Derived Neurotrophic Factor in Long-Term Neuronal Reorganization of the Superior Colliculus after Bilateral Visual Deprivation

The role of the brain-derived neurotrophic factor (BDNF), the BDNF receptor (TrkB), and the glutamic acid decarboxylase (GAD67) after neonatal, bilateral nerve deafferentiation during postnatal development was investigated in the rat superior colliculus (SC). BDNF and GAD67 mRNA expression were significantly increased in optic (Op) and intermediate gray (InG) layers at 5, 8, 15, and 21 days after birth, but not in adult animals. However, TrkB mRNA expression was not modified at any time tested. At 15 days, where changes in BDNF and GAD67 mRNAs were more evident, an upregulation of the NMDAR1A mRNA glutamate receptor in the Op and InG, a modification in the pattern of synaptic zinc in the superficial layers of SC, and an increased synaptophysin immunoreactivity in the Op was found. This indicates the existence of a synergic mechanism between BDNF and NMDA to determine refinement of connections after the loss of visual input in SC.