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A fundamental scheme in the organization of the early visual cortex is the retinotopic representation of the contralateral visual hemifield on each hemisphere. We determined the cortical organization in a novel congenital visual pathway disorder, FHONDA-syndrome, where the axons from the temporal retina abnormally cross to the contralateral hemisphere. Using ultra-high field fMRI at 7 T, the population receptive field (pRF) properties of the primary visual cortex were modeled for two affected individuals and two controls. The cortical activation in FHONDA was confined to the hemisphere contralateral to the stimulated eye. Each cortical location was found to contain a pRF in each visual hemifeld and opposing hemifields were represented as retinotopic cortical overlays of mirror-symmetrical locations across the vertical meridian. Since, the enhanced crossing of the retinal fibers at the optic chiasm observed in FHONDA has been previously assumed to be exclusive to the pigment-deficiency in albinism, our direct evidence of abnormal mapping in FHONDA highlights the independence of pigmentation and development of the visual cortex. These findings thus provide fundamental insights into the developmental mechanisms of the human visual system and underline the general relevance of the interplay of subcortical stability and cortical plasticity.

Background and Objective: Alzheimer's disease (AD) has been shown to affect vision in human patients and animal models. This study was conducted to explore ocular abnormalities in the primary visual pathway and their relationship with hippocampal atrophy in patients with AD and mild cognitive impairment (MCI). The aim of this study was to investigate the potential value of ocular examinations as a biomarker during the AD progression. Methods: Patients with MCI ( n = 23) or AD ( n = 17) and age-matched cognitively normal controls (NC; n = 19) were enrolled. Pattern visual-evoked potentials (PVEP), flash electroretinogram (FERG) recordings and optical coherence tomography (OCT) were performed for all participants. Hippocampal volumes were measured by 3T magnetic resonance imaging. Cognitive function was assessed by Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog). Pearson correlation was employed to analyze the potential associations between ocular abnormalities and hippocampal volumes. Hierarchical regression models were conducted to determine associations between cognitive performances and ocular abnormalities as well as hippocampal volumes after adjusting for confounding factors including age, sex, cognitive reserve, and APOE4 status. Results: PVEP amplitude of P100 waveform was significantly decreased in AD patients compared to MCI and normal individuals. In FERG test, delayed latencies of rod response, rod cone response and 3.0 flicker time were found in cognitively impaired groups, indicating dysfunctions of both the rod and cone systems in the disease progression. OCT test revealed reduced macular retinal nerve fiber layer (m-RNFL) thickness in MCI and AD patients, which significantly correlated with brain structure of hippocampus particularly vulnerable during the progression of AD. Interestingly, P100 amplitude showed a significant association with hippocampal volumes even after adjusting confounding factors including age, sex, and cognitive reserve. Hierarchical regression analysis further demonstrated that m-RNFL thickness, as well as hippocampal volumes, significantly associated with ADAS-cog scores. Conclusion: P100 amplitude and m-RNFL thickness showed significant correlations with brain structure involved in AD-related neurodegeneration, and therefore proved to be potential indicators of brain imaging pathologies.

Increasing evidence of ocular impairments in Alzheimer’s disease (AD) has drawn the attention of researchers worldwide towards retinal neurodegeneration in AD. The AD-associated changes observed in the retina include visual discrepancies, pupil size modulations, retinal nerve layer changes, retinal blood flow alterations and histopathological changes. The brain cells that act as pathological triggers for the progression of retinal neurodegeneration associated with AD are microglia, astrocytes and neurons. Various molecular pathways lead to structural and functional abnormalities in the retina, significantly affecting the brain including Aβ accumulation, apoptosis, inflammation and oxidative stress. Therapeutic agents under development that ameliorate disease conditions by targeting retinal anomalies include mesenchymal stem cell-conditioned media, BDNF, glatiramer acetate, salvianolic acid B, Lycium barbarum extract and exosomes. Investigating real-time alterations in the retina in AD may not only affect diagnostic approaches but also help to clarify neuropathological pathways and offer helpful measurements for assessing novel therapeutic approaches for AD.

Vision has a crucial role to play in human development and functioning. It is, therefore, not surprising that vision plays a fundamental role in the development of the child. As a consequence, an alteration in visual function is, therefore, likely to hinder the child’s development. Although ocular disorders are well known, diagnosed and taken into account, cerebral visual impairments (CVI) resulting from post-chiasmatic damage are largely underdiagnosed. However, among the disorders resulting from an episode of perinatal asphyxia and/or associated with prematurity, or neonatal hypoglycaemia, CVIs are prominent. In this article, we focus on the role of the possible effects of CVI on a child’s learning abilities, leading to major difficulty in disentangling the consequences of CVI from other neurodevelopmental disorders (NDD) such as dyslexia, dyscalculia, dysgraphia, attention-deficit/hyperactivity disorder (ADHD), developmental coordination disorder (DCD) and autism spectrum disorders (ASD). Although we focus here on the possible overlap between children with CVI and children with other NDD, De Witt et al. (Wit et al. Ear Hear 39:1–19, 2018) have raised exactly the same question regarding children with auditory processing disorders (the equivalent of CVI in the auditory modality). We underline how motor, social and cognitive development as well as academic success can be impaired by CVI and raise the question of the need for systematic evaluation for disorders of vision, visual perception and cognition in all children presenting with a NDD and/or previously born under adverse neurological conditions.

We report a case of voriconazole-induced visual abnormality based on drug interaction of voriconazole and esomeprazole, therapeutic drug monitoring, and optimal therapy. An 81-year-old male developed visual abnormality after the blood concentration of voriconazole was up to 6.47 mg/L induced by coadministration with esomeprazole. Voriconazole is a substrate of multiple CYP450 isoenzymes including CYP2C19 (the major route), CYP3A4, and CYP2C9. Esomeprazole, a proton pump inhibitor (PPI), is also converted to inactive metabolites through CYP3A4 and CYP2C19-mediated metabolism, and is also a CYP2C19 inhibitor. The coadministration with esomeprazole inhibited the metabolism of voriconazole via CYP2C19 and promoted the elevation of voriconazole blood concentration beyond the minimum toxic level (5.5 mg/L). According to the pharmacist's advice, the adverse effects of visual abnormalities in the patient disappeared after the clinician reduced voriconazole dosage by 50% when other medication schedules remained unchanged. Therefore, therapeutic drug monitoring of voriconazole should be considered in patients receiving PPIs, especially esomeprazole, in order to adjust the dosage in time and achieve optimal therapeutic response and minimal adverse reaction.

The albino visual pathway is abnormal in that many fibres from the temporal retina project to the contralateral visual cortex. The visual projections in a human albino and a control have been investigated with fMRI and VEP during independent visual stimulation of both hemifields. Activity in the occipital cortex in the normal was contralateral to the stimulated visual field, whereas it was contralateral to the stimulated eye in the albino, independent of the stimulated visual field. Thus, the albino visual cortex is activated not only by stimulation in the contralateral visual field, but also by abnormal input representing the ipsilateral visual field. These novel findings help elucidate the nature of albino misrouting.

Non-motor symptoms in Parkinson’s disease are an important cause of morbidity and may even precede the onset of the motor features of the disease. Visual abnormalities are among the most frequent non-motor symptoms observed during the early stages of the disease. Some of the visual symptoms of Parkinson’s disease can likely be explained by the presence of dopaminergic neurons within the retina, where the progressive loss of dopamine and the accumulation of α-synuclein within the retinal layers leads to visual dysfunction, while some are caused by abnormalities in cortical visual processing. Many of these visual symptoms can be overlooked or go unrecognized. We review the visual symptoms in Parkinson’s disease, including visual-processing and ocular motility abnormalities, stereopsis deficits, and visual hallucinations, focusing on the early stages of the disease. We focus on the reciprocal influence between the visual symptoms and the progression of the disease, analyzing the influence of dopaminergic therapy on the visual abnormalities. Finally, we discuss the possible role of some of these visual symptoms as possible markers or early diagnostic signs of the disease.

Background Visual abnormality is a common sensory impairment in autism spectrum disorder (ASD), which may cause behavioral problems. However, only a few studies exist on the neural features corresponding to the visual symptoms in ASD. The purpose of this study was to investigate the relationship between cortical responses to visual stimuli and visual abnormality to examine the neurophysiological mechanisms of the visual abnormality in ASD. Methods Twenty-two high-functioning children with ASD (10.95 ± 2.01 years old) and 23 age-matched typically developing (TD) children (10.13 ± 2.80 years old) participated in this study. We measured the cortical responses (i.e., activated intensity and attenuation ratio) elicited by the Original visual image and other two types of bright images (the Dot noise or Blind image, which includes overlapped particles onto the Original image or the enhanced-brightness version of the Original image, respectively) using magnetoencephalography. Results The severity of visual abnormalities was significantly associated with behavioral problems in children with ASD. In addition, we found the increased cortical activation in response to the Original image in the left supramarginal gyrus (SMG) and middle temporal gyrus in children with ASD. However, there were no inter-group differences in the primary visual and medial orbitofrontal cortices. Furthermore, when we compared cortical responses according to the type of images, children with ASD showed lesser attenuation of the activated intensities than children with TD in response to the bright images compared with the Original image in the right SMG. These attenuation ratios (Dot noise/Original and Blind/Original) were also associated with the severity of visual abnormalities. Conclusions Our results show that dysfunction of stimulus-driven neural suppression plays a crucial role in the neural mechanism of visual abnormality in children with ASD. To the best of our knowledge, this is the first magnetoencephalography study to demonstrate the association between the severity of visual abnormality and lower attenuation ratios in children with ASD. Our results contribute to the knowledge of the mechanisms underlying visual abnormality in children with ASD, and may therefore lead to more effective diagnosis and earlier intervention.

Background: This retrospective cohort study primarily aimed to investigate the possible association of computer use with visual field abnormalities (VFA) among Japanese workers. Methods: The study included 2,377 workers (mean age 45.7 [standard deviation, 8.3] years; 2,229 men and 148 women) who initially exhibited no VFA during frequency doubling technology perimetry (FDT) testing. Subjects then underwent annual follow-up FDT testing for 7 years, and VFA were determined using a FDT-test protocol (FDT-VFA). Subjects with FDT-VFA were examined by ophthalmologists. Baseline data about the mean duration of computer use during a 5-year period and refractive errors were obtained via self-administered questionnaire and evaluations for refractive errors (use of eyeglasses or contact lenses), respectively. Results: A Cox proportional hazard analysis demonstrated that heavy computer users (>8 hr/day) had a significantly increased risk of FDT-VFA (hazard ratio [HR] 2.85; 95% confidence interval [CI], 1.26–6.48) relative to light users (<4 hr/day), and this association was strengthened among subjects with refractive errors (HR 4.48; 95% CI, 1.87–10.74). The computer usage history also significantly correlated with FDT-VFA among subject with refractive errors (P < 0.05), and 73.1% of subjects with FDT-VFA and refractive errors were diagnosed with glaucoma or ocular hypertension. Conclusions: The incidence of FDT-VFA appears to be increased among Japanese workers who are heavy computer users, particularly if they have refractive errors. Further investigations of epidemiology and causality are warranted.

Study objective: To study the association between computer use and visual field abnormalities (VFA) and to assess whether heavy computer users have an increased risk of glaucoma. Design: Cross sectional multicentre study. Subjects and observation procedures: A total of 10 202 randomly selected Japanese workers (mean (SD) age 43.2 (9.8) years) were screened for VFA using the frequency doubling technology perimetry (FDT-VFA), in addition to undergoing a general medical check up, and then ophthalmologically examined. Information about their computer use and refractive errors was obtained from a questionnaire and interview, respectively. Main results: As a result of FDT test, 522 and 8602 subjects were positive and negative for FDT-VFA, respectively. A significant (p = 0.004) interaction was found between computer use and refractive errors regarding the risk of FDT-VFA. In stratified analysis, heavy computer users with refractive errors showed a significant positive association with FDT-VFA (odds ratio (OR)  = 1.74, 95% confidence interval (CI) 1.28 to 2.37), while those without refractive errors did not. Comparison of 165 subjects with an ophthalmological diagnosis of glaucoma and 2918 controls showed that the OR for glaucoma of heavy computer users with refractive errors was 1.82 (95% CI 1.06 to 3.12). Of 165 subjects with glaucoma, 141 had refractive errors, especially myopia (96.4%, 136 of 141). Conclusions: Although there are limitations to this study, such as its cross sectional design, heavy computer users with refractive errors seem to have an increased risk of FDT-VFA. Glaucoma might be involved in an underlying disease and myopia in a risk factor for FDT-VFA.