Visual Processing Deficits Research Articles

Disorders of Movement due to Acquired and Traumatic Brain Injury.

Purpose of Review Both traumatic and acquired brain injury can result in diffuse multifocal injury affecting both the pyramidal and extrapyramidal tracts. Thus, these patients may exhibit signs of both upper motor neuron syndrome and movement disorder simultaneously which can further complicate diagnosis and management. We will be discussing movement disorders following acquired and traumatic brain injury.Recent FindingsMultiple functions including speech, swallowing, posture, mobility, and activities of daily living can all be affected. Medical treatment and rehabilitation-based therapy can be especially challenging due to accompanying cognitive deficits and severity of the disorder which can involve multiple limbs in addition to muscles of the face and axial skeleton. Tremor and dystonia are the most reported movement disorders following traumatic brain injury. Dystonia and myoclonus are well documented following hypoxic ischemic brain injuries. Electrophysiological studies such as dynamic surface poly-electromyography can assist with identifying phenomenology, especially differentiating between jerk-like phenomenon and help guide further work up and management. Management with medications remains challenging due to potential adverse effects. Surgical interventions including stereotactic surgery, deep brain stimulation, and intrathecal baclofen pumps have been reported, but most of the evidence supporting them has been limited to primarily case reports except for post-traumatic tremor.SummaryBrain injury can lead to motor disorders, movement disorders, visual (processing) deficits, and vestibular deficits which often coexist with cognitive deficits making it challenging to treat and rehabilitate these patients. Unfortunately, the evidence regarding the medical management and rehabilitation of brain injury patients with movement disorders is sparse and leaves much to be desired.

Age and Sex-Related Changes in Retinal Function in the Vervet Monkey.

Among the deficits in visual processing that accompany healthy aging, the earliest originate in the retina. Moreover, sex-related differences in retinal function have been increasingly recognized. To better understand the dynamics of the retinal aging trajectory, we used the light-adapted flicker electroretinogram (ERG) to functionally assess the state of the neuroretina in a large cohort of age- and sex-matched vervet monkeys (N = 35), aged 9 to 28 years old, with no signs of obvious ocular pathology. We primarily isolated the cone–bipolar axis by stimulating the retina with a standard intensity light flash (2.57 cd/s/m2) at eight different frequencies, ranging from 5 to 40 Hz. Sex-specific changes in the voltage and temporal characteristics of the flicker waveform were found in older individuals (21–28 years-old, N = 16), when compared to younger monkeys (9–20 years-old, N = 19), across all stimulus frequencies tested. Specifically, significantly prolonged implicit times were observed in older monkeys (p < 0.05), but a significant reduction of the amplitude of the response was only found in old male monkeys (p < 0.05). These changes might reflect ongoing degenerative processes targeting the retinal circuitry and the cone subsystem in particular. Altogether, our findings corroborate the existing literature in humans and other species, where aging detrimentally affects photopic retinal responses, and draw attention to the potential contribution of different hormonal environments.

The Hermann grid illusion fails to fool patients with schizophrenia: Experimental support for a reduced lateral inhibition hypothesis

A large body of evidence indicated that patients with schizophrenia spectrum disorders show deficit in perceptual and visual processing, but little is known about the origin of this defect. One of the strategies used to reveal the origin of such defects is to use tests that have a strong neuropsychological basis in normal individuals. In this study, we used the Hermann grid task to reveal the source of visual deficit in patients with schizophrenia. Several findings have shown that the Hermann grid illusion results from lateral inhibition of neuro-visual pathway cells. We compared 26 patients with schizophrenia to 26 participants with high schizotypy traits and 26 normal controls in a computer test we designed for the Hermann grid illusion. Chi-square analysis revealed that the patients with schizophrenia and the participants with high schizotypy traits reported significantly less the Hermann grid illusion than healthy controls. Therefore, the results support the hypothesis of a defect in lateral inhibition of patients with schizophrenia. This might suggest that the visual pathway cells in schizophrenic patients failed to properly combine the data from the visual receptors as they do in healthy people. • The Hermann grid illusion has wealthy neuropsychological background. • Visual perception difficulties in schizophrenia have been always reported. • Patients with schizophrenia do not report the Hermann grid illusion. • Evidence show that lateral inhibition contributes in the Hermann grid illusion. • Lack of Hermann grid illusion support a lateral inhibition defect in schizophrenia.

Alterations in Retinal Signaling Across Age and Sex in 3xTg Alzheimer's Disease Mice.

Background:Visual disturbances often precede cognitive dysfunction in patients with Alzheimer’s disease (AD) and may coincide with early accumulation of amyloid-β (Aβ) protein in the retina. These findings have inspired critical research on in vivo ophthalmic Aβ imaging for disease biomarker detection but have not fully answered mechanistic questions on how retinal pathology affects visual signaling between the eye and brain.Objective:The goal of this study was to provide a functional and structural assessment of eye-brain communication between retinal ganglion cells (RGCs) and their primary projection target, the superior colliculus, in female and male 3xTg-AD mice across disease stages.Methods:Retinal electrophysiology, axonal transport, and immunofluorescence were used to determine RGC projection integrity, and retinal and collicular Aβ levels were assessed with advanced protein quantitation techniques.Results:3xTg mice exhibited nuanced deficits in RGC electrical signaling, axonal transport, and synaptic integrity that exceeded normal age-related decrements in RGC function in age- and sex-matched healthy control mice. These deficits presented in sex-specific patterns among 3xTg mice, differing in the timing and severity of changes.Conclusion:These data support the premise that retinal Aβ is not just a benign biomarker in the eye, but may contribute to subtle, nuanced visual processing deficits. Such disruptions might enhance the biomarker potential of ocular amyloid and differentiate patients with incipient AD from patients experiencing normal age-related decrements in visual function.

Probabilistic Decision-Making in Children With Dyslexia.

BackgroundNeurocognitive mechanisms underlying developmental dyslexia (dD) remain poorly characterized apart from phonological and/or visual processing deficits. Assuming such deficits, the process of learning complex tasks like reading requires the learner to make decisions (i.e., word pronunciation) based on uncertain information (e.g., aberrant phonological percepts)—a cognitive process known as probabilistic decision making, which has been linked to the striatum. We investigate (1) the relationship between dD and probabilistic decision-making and (2) the association between the volume of striatal structures and probabilistic decision-making in dD and typical readers.MethodsTwenty four children diagnosed with dD underwent a comprehensive evaluation and MRI scanning (3T). Children with dD were compared to age-matched typical readers (n = 11) on a probabilistic, risk/reward fishing task that utilized a Bayesian cognitive model with game parameters of risk propensity (γ+) and behavioral consistency (β), as well as an overall adjusted score (average number of casts, excluding forced-fail trials). Volumes of striatal structures (caudate, putamen, and nucleus accumbens) were analyzed between groups and associated with game parameters.ResultsdD was associated with greater risk propensity and decreased behavioral consistency estimates compared to typical readers. Cognitive model parameters associated with timed pseudoword reading across groups. Risk propensity related to caudate volumes, particularly in the dD group.ConclusionDecision-making processes differentiate dD, associate with the caudate, and may impact learning mechanisms. This study suggests the need for further research into domain-general probabilistic decision-making in dD, neurocognitive mechanisms, and targeted interventions in dD.

EEG Global Coherence in Scholar ADHD Children during Visual Object Processing.

Among neurodevelopmental disorders, attention deficit hyperactivity disorder (ADHD) is the main cause of school failure in children. Notably, visuospatial dysfunction has also been emphasized as a leading cause of low cognitive performance in children with ADHD. Consequently, the present study aimed to identify ADHD-related changes in electroencephalography (EEG) characteristics, associated with visual object processing in school-aged children. We performed Multichannel EEG recordings in 16-year-old children undergoing Navon’s visual object processing paradigm. We mapped global coherence during the processing of local and global visual stimuli that were consistent, inconsistent, or neutral. We found that Children with ADHD showed significant differences in global weighted coherence during the processing of local and global inconsistent visual stimuli and longer response times in comparison to the control group. Delta and theta EEG bands highlighted important features for classification in both groups. Thus, we advocate EEG coherence and low-frequency EEG spectral power as prospective markers of visual processing deficit in ADHD. Our results have implications for the development of diagnostic interventions in ADHD and provide a deeper understanding of the factors leading to low performance in school-aged children.

Large-conductance calcium-activated potassium channel haploinsufficiency leads to sensory deficits in the visual system: a case report

BackgroundMutations in the genes encoding the large-conductance calcium-activated potassium channel, especially KCNMA1 encoding its α-subunit, have been linked to several neurological features, including intellectual disability or autism. Associated with neurodevelopmental phenotypes, sensory function disturbances are considered to be important clinical features contributing to a variety of behavioral impairments. Large-conductance calcium-activated potassium channels are important in regulating neurotransmission in sensory circuits, including visual pathways. Deficits in visual function can contribute substantially to poor quality of life, while therapeutic approaches aimed at addressing such visual deficits represent opportunities to improve neurocognitive and neurobehavioral outcomes.Case presentationWe describe the case of a 25-year-old Caucasian male with autism spectrum disorder and severe intellectual disability presenting large-conductance calcium-activated potassium channel haploinsufficiency due to a de novo balanced translocation (46, XY, t [9; 10] [q23;q22]) disrupting the KCNMA1 gene. The visual processing pathway of the subject was evaluated using both electroretinography and visual contrast sensitivity, indicating that both retinal bipolar cell function and contrast discrimination performance were reduced by approximately 60% compared with normative control values. These findings imply a direct link between KCNMA1 gene disruption and visual dysfunction in humans. In addition, the subject reported photophobia but did not exhibit strabismus, nystagmus, or other visual findings on physical examination.ConclusionsThis case study of a subject with large-conductance calcium-activated potassium channel haploinsufficiency and photophobia revealed a visual pathway deficit at least at the retinal level, with diminished retinal light capture likely due to bipolar cell dysfunction and an associated loss of contrast sensitivity. The data suggest that large-conductance calcium-activated potassium channels play an important role in the normal functioning of the visual pathway in humans, and that their disruption may play a role in visual and other sensory system symptomatology in large-conductance calcium-activated potassium channelopathies or conditions where disruption of large-conductance calcium-activated potassium channel function is a relevant feature of the pathophysiology, such as fragile X syndrome. This work suggests that the combined use of physiological (electroretinography) and functional (contrast sensitivity) approaches may have utility as a biomarker strategy for identifying and characterizing visual processing deficits in individuals with large-conductance calcium-activated potassium channelopathy.Trial registration ID-RCB number 2019-A01015-52, registered 17/05/2019.

Impaired Affordance Perception as the Basis of Tool Use Deficiency in Alzheimer's Disease.

The present study investigated whether defective affordance perception capacity underpins tool use deficits in patients with Alzheimer’s disease (AD). An affordance, a concept James Gibson introduced, scales environmental objects to an animal’s action capabilities, thus offering opportunities for action. Each man-made artifact carries both a primary affordance (its designed function) and secondary affordances. In Experiment 1, participants identified secondary affordances of objects as a measure of their ability to identify alternative uses of familiar tools. A single response Go/No-Go task was administered to 4 groups: AD, mild cognitive impairment (MCI), Parkinson’s disease (PD), and elderly controls (EC). Groups were matched for age and years of education. The AD group performed poorest, followed by MCI, and PD and EC. EC and PD groups’ results failed to reach statistical significance, and the AD group performed at chance. In Experiment 2, participants judged the physical properties of the same objects used in Experiment 1. Even AD patients performed reliably, ruling out a visual processing deficit as the basis for their poor performance in Experiment 1. Results suggest that degraded affordance detection capacity can differentiate AD from normal aging and other neurodegenerative disorders and could be an affordable marker for AD, even in the early stages of AD.

Visual-processing deficits in children with neurofibromatosis type 1: A clinical marker of reading difficulties.

Today's estimates indicate that nearly 50% of children with Neurofibromatosis type 1 (NF1) suffer from reading disabilities, with a high impact on their academic achievement. In addition to the well-documented importance of phonological skills in reading acquisition and neurodevelopmental disorders, visual-attention processes also appear as important factors in learning to read. The present study aimed at assessing the role of visual-processing dysfunction in the high prevalence of reading disabilities in NF1 children and providing a useful tool for clinician in the early detection of reading impairment in this neurogenetic disorder. Forty-two children with NF1 and 42 typically developing children (TD) participated in the study. All were right-handed and did not present intellectual disability or attention deficit hyperactivity disorder. Visual-attention processes were assessed with the Developmental Eye Movement (DEM) test, together with the NF1 children's reading level. NF1 children with and without reading disabilities were then compared. The results showed that visual-processing deficits were highly present among the NF1 children included in our study. Furthermore, poor readers with NF1 presented an increased risk of visual-processing deficits compared to peers. This finding supports the role of visual-processing deficits in the reading difficulties encountered in nearly half of children with NF1. Finally, in NF1 children without intellectual or attention disability, visual-processing deficits emerge as one of the clinical markers of reading disabilities. The study holds important clinical implications both for the identification, by providing a useful screening tool, and the management of reading disabilities in NF1 children.

Effects of Acute Hypoxia on Early Visual and Auditory Evoked Potentials.

Reduced levels of environmental oxygen lead to hypoxic hypoxia and are a primary threat in tactical aviation. The visual system is particularly vulnerable to hypoxia, and its impairment can severely impact performance. The auditory system is relatively spared by hypoxia, although which stages of auditory processing are most impacted by hypoxia remains unclear. Previous work has used electroencephalography (EEG) to assess neural markers of cognitive processing for visual and auditory stimuli and found that these markers were sensitive to a normobaric hypoxic exposure. In the current study, we assessed whether early sensory evoked potentials, that precede cognitive activity, are also impaired by normobaric hypoxia. In a within-subjects design, we compared visual (P100) and auditory evoked potentials (sensory gating for the P50, N100, and P200) in 34 healthy adults during normoxic (21% O2) and two separate hypoxic (9.7% O2) exposures. Self-reported symptoms of hypoxia were also assessed using the Hypoxia Symptom Questionnaire (HSQ). We found that P100 mean amplitude was not reduced under hypoxic compared to normoxic conditions, suggesting no statistically significant impairment of early visual processing. The sensory gating ratio for auditory stimuli was intact for paired responses of the P50 and N100. However, the P200 sensory gating ratio was attenuated under hypoxic compared to normoxic conditions, suggesting disruption of the auditory system specific to the level of allocating attention that follows basic auditory processing. Exploratory analyses of HSQ scores identified a robust effect of hypoxia. However, consistency of symptoms reported between the two hypoxia exposures exhibited high intra-individual variability, which may have implications for the theory that individuals have a consistent hypoxia signature or reliable constellation of responses to hypoxia. These findings suggest that early sensory processing is not impaired during hypoxia, but for the auditory system there is impairment at the level of attentional processing. Given the previous findings of impaired visual performance under hypoxia, these results suggest that this impairment does not stem from early visual processing deficits in visual cortex. Together these findings help focus the search on when and where hypoxia-induced deficits occur and may guide the development of countermeasures for hypoxia in tactical aviation.

Processing of Spoken Emotions in Schizophrenia: Forensic and Non-forensic Patients Differ in Emotional Identification and Integration but Not in Selective Attention.

Patients with schizophrenia (PwS) typically demonstrate deficits in visual processing of emotions. Less is known about auditory processing of spoken-emotions, as conveyed by the prosodic (tone) and semantics (words) channels. In a previous study, forensic PwS (who committed violent offenses) identified spoken-emotions and integrated the emotional information from both channels similarly to controls. However, their performance indicated larger failures of selective-attention, and lower discrimination between spoken-emotions, than controls. Given that forensic schizophrenia represents a special subgroup, the current study compared forensic and non-forensic PwS. Forty-five PwS listened to sentences conveying four basic emotions presented in semantic or prosodic channels, in different combinations. They were asked to rate how much they agreed that the sentences conveyed a predefined emotion, focusing on one channel or on the sentence as a whole. Their performance was compared to that of 21 forensic PwS (previous study). The two groups did not differ in selective-attention. However, better emotional identification and discrimination, as well as better channel integration were found for the forensic PwS. Results have several clinical implications: difficulties in spoken-emotions processing might not necessarily relate to schizophrenia; attentional deficits might not be a risk factor for aggression in schizophrenia; and forensic schizophrenia might have unique characteristics as related to spoken-emotions processing (motivation, stimulation).

Classification of EEG signals from young adults with dyslexia combining a Brain Computer Interface device and an Interactive Linguistic Software Tool

The magnocellular pathway deficit theory has long been considered to be a possible cause for dyslexia, providing an alternative method to explain auditory and visual processing deficits. Several studies have attempted to classify these deficits with the application of machine learning in anatomical brain imaging, rendering the classification techniques using EEG graph measures both robust and reliable. In this paper, a classification of university students with and without dyslexia is attempted with the use of a Brain Computer Interface (BCI) Device and an Interactive Linguistic Software Tool in order to validate the application of such a device in classifying dyslexia in a higher education population. EEG signals acquired from a wearable, sensory EEG recording device from 12 university students with dyslexia along with 14 typically developed, age matched individuals are recorded, while participants were examined in three different experimental conditions: a) auditory discrimination, b) visual recognition c) visual recognition with background music. Spectral features extracted from each EEG rhythm (δ, θ, α, β, γ) are used to train a Random Forests classifier, aiming to identify quantitative EEG features that characterize dyslexia in different brain regions. Results show high levels of accuracy, sensitivity and specificity (above 95%) in the entire brain, followed by the left and right hemisphere, with the highest discrimination performance reported during the third experimental condition with the presence of background music. Different experimental conditions provide high classification accuracy that results in correct discrimination between higher education students with and without dyslexia.

Shallow or deep? The impact of orthographic depth on visual processing impairments in developmental dyslexia

The extent to which impaired visual and phonological mechanisms may contribute to the manifestation of developmental dyslexia across orthographies of varying depth has yet to be fully established. By adopting a cross-linguistic approach, the current study aimed to explore the nature of visual and phonological processing in developmental dyslexic readers of shallow (Italian) and deep (English) orthographies, and specifically the characterisation of visual processing deficits in relation to orthographic depth. To achieve this aim, we administered a battery of non-reading visual and phonological tasks. Developmental dyslexics performed worse than typically developing readers on all visual and phonological tasks. Critically, readers of the shallow orthography were disproportionately impaired on visual processing tasks. Our results suggest that the impaired reading and associated deficits observed in developmental dyslexia are anchored by dual impairments to visual and phonological mechanisms that underpin reading, with the magnitude of the visual deficit varying according to orthographic depth.

Invited Session V: GABAergic function and dysfunction in visual perception: Abnormal processing of visual context in schizophrenia

People with schizophrenia (SZ) exhibit persistent deficits in visual processing including reduced contrast sensitivity and poor detection of complex image structure, such as contours. Over recent years accumulating psychophysical evidence indicates that vision in SZ is associated with a reduced influence of spatial context which in turn has been attributed to reduced spatial suppression in visual cortex. Compared to controls, people with SZ do not experience the same reduction in perceived contrast that occurs when targets are embedded in a high contrast background. This appears to be a cortical phenomenon: reduced influence of context is not limited to contrast but carries over to other image attributes (such as orientation) but not others (such as luminance). Finally, although patients poor processing of higher-order image structure has been attributed to differences in perceptual grouping, work from my lab indicates that abnormal processing of context may also contribute to patients' poor sensitivity for contours. It does this by (a) reducing their sensitivity to local orientation and (b) reducing their ability to discount irrelevant background structure. Taken together these results suggest that abnormal processing of context contributes to a range of visual processing deficits in SZ.

Chapter 10 - Visual objects and their colors

The ventral temporal cortex hosts key regions for the high-level visual processing of object shape and color. These areas represent nodes of large-scale neural circuits dedicated to object recognition. In the language-dominant hemisphere, some of these regions communicate with the language systems; by assigning verbal labels to percepts, these circuits speedup stimulus categorization, and permit fast and accurate interindividual communication. By impairing the functioning of these circuits, neurological damage may provoke disabling disorders of the processing of visual objects and of their colors. Brain damage of vascular, degenerative, toxic, or traumatic origin can induce deficits at different levels of visual processing, from the building of shape- or wavelength-invariant percepts, to their connections with semantic knowledge and with the appropriate lexical entry. After an overview of the neuroimaging of domain-preferring regions for object shape and color in the ventral temporal cortex, this chapter reviews evidence from historical and recent cases of acquired visual agnosia and color processing deficits. A recurrent motif emerging from patients' patterns of performance and lesion locations is the existence of caudo-rostral gradients in the ventral occipito-temporal cortex, spanning from more perceptual to more cognitive stages of processing.

Spatial Frequency Discrimination in Patients with Schizophrenia Spectrum and Bipolar Disorders: Evidence of Early Visual Processing Deficits and Associations with Intellectual Abilities

Spatial Frequency Discrimination in Patients with Schizophrenia Spectrum and Bipolar Disorders: Evidence of Early Visual Processing Deficits and Associations with Intellectual Abilities

Restoration of FMRP expression in adult V1 neurons rescues visual deficits in a mouse model of fragile X syndrome

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABAA receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.

Cognitive function mediates the relationship between visual contrast sensitivity and functional outcome in schizophrenia

BackgroundIndividuals with schizophrenia exhibit deficits in visual contrast processing, though less is known about how these deficits impact neurocognition and functional outcomes. This study investigated effects of contrast sensitivity (CS) on cognition and capacity for independent living in schizophrenia. Methods: Participants were 58 patients with schizophrenia (n = 49) and schizoaffective disorder (n = 9). Patients completed a psychophysical paradigm to obtain CS with stimuli consisting of grating patterns of low (0.5 and 1 cycles/degree) and high spatial frequencies (4, 7, 21 cycles/degree). Patients completed the MATRICS Consensus Cognitive Battery and Wechsler Adult Intelligence Scales, Third Edition to assess cognition, and the problem-solving factor of the Independent Living Scales to assess functional capacity. We computed bivariate correlation coefficients for all pairs of variables and tested mediation models with CS to low (CS–LSF) and high spatial frequencies (CS–HSF) as predictors, cognitive measures as mediators, and capacity for independent living as an outcome. Results: Cognition mediated the relationship between CS and independent living with CS–LSF a stronger predictor than CS–HSF. Mediation effects were strongest for perceptual organization and memory-related domains. In an expanded moderated mediation model, CS–HSF was found to be a significant predictor of independent living through perceptual organization as a mediator and CS–LSF as a moderator of this relationship. Conclusion: CS relates to functional capacity in schizophrenia through neurocognition. These relationships may inform novel visual remediation interventions.

Binocular Interactions in Glaucoma Patients With Nonoverlapping Visual Field Defects: Contrast Summation, Rivalry, and Phase Combination.

PurposeIn glaucoma, visual field defects in the left and right eye may be non-overlapping, resulting in an intact binocular visual field. In clinical management, these patients are often considered to have normal vision. However, visual performance also relies on binocular processing. The aim of this study was to evaluate binocular visual functions in glaucoma patients with intact binocular visual field, normal visual acuity, and stereoscopy.MethodsWe measured in 10 glaucoma patients and 12 age-similar controls: (1) monocular and binocular contrast sensitivity functions (CSF) using a modified quick CSF test to assess binocular contrast summation, (2) dominance during rivalry, and (3) contrast ratio at balance point with a binocular phase combination test. A mirror stereoscope was used to combine the left and right eye image (each 10° horizontally by 12° vertically) on a display.ResultsArea under the monocular and binocular CSF was lower in glaucoma compared to healthy (P < 0.001), but the binocular contrast summation ratio did not differ (P = 0.30). For rivalry, the percentage of time of mixed percept was 9% versus 18% (P = 0.056), the absolute difference of the percentage of time of dominance between the two eyes 19% versus 10% (P = 0.075), and the rivalry rate 8.2 versus 12.1 switches per minute (P = 0.017) for glaucoma and healthy, respectively. Median contrast ratio at balance point was 0.66 in glaucoma and 1.03 in controls (P = 0.011).ConclusionsBinocular visual information processing deficits can be found in glaucoma patients with intact binocular visual field, normal visual acuity, and stereoscopy.

Visual processing and BDNF levels in first-episode schizophrenia

Previous studies have shown that patients diagnosed with schizophrenia (SCZ) have deficits in early visual processing, namely contrast processing. The brain-derived neurotropic factor (BDNF) is an important measure to investigate neuroplasticity in some visual functions like visual perception. In this study, we investigated the relationship between visual processing and BDNF levels in first-episode SCZ patients. Thirty-nine healthy controls and 43 first-episode SCZ patients were enrolled. Contrast sensitivity measurements were conducted using low, mid- and high spatial frequencies. First-episode SCZ patients had higher contrast sensitivity than healthy controls for all frequencies, except for the middle spatial frequency. Negative correlations were found between BDNF, contrast sensitivity and clinical variables, mostly for middle and high spatial frequencies among females. Our results provide support for (i) the association of SCZ with alterations of magno- and parvocellular pathway functioning and (ii) decreased BDNF levels in first-episode SCZ patients. This study highlights the importance of using biomarkers along with other measures to investigate visual processing in SCZ and other disorders.