Measuring visual evoked potentials (VEP) by means of EEG allows the quasi non-invasive assessment of visual function in mice. Such sensory phenotyping is important to screen for genetic or aging effects on vision in preclinical mouse models. Thus, a standardized EEG-like approach for the assessment of sensory evoked potentials in mice is desirable.

We report on a unique electrocorticography (ECoG) experiment in which Steady-State Visual Evoked Potentials (SSVEPs) to frequency- and phase-tagged stimuli were recorded from a large subdural grid covering the entire right occipital cortex of a human subject. The paradigm is popular in EEG-based Brain Computer Interfacing where selectable targets are encoded by different frequency- and/or phase-tagged stimuli. We compare the performance of two state-of-the-art SSVEP decoders on both ECoG- and scalp-recorded EEG signals, and show that ECoG-based decoding is more accurate for very short stimulation lengths (i.e., less than 1 s). Furthermore, whereas the accuracy of scalp-EEG decoding benefits from a multi-electrode approach, to address interfering EEG responses and noise, ECoG decoding enjoys only a marginal improvement as even a single electrode, placed over the posterior part of the primary visual cortex, seems to suffice. This study shows, for the first time, that EEG-based SSVEP decoders can in principle be applied to ECoG, and can be expected to yield faster decoding speeds using less electrodes.

Visually Evoked Potentials (VEPs) were recorded in response to the onset of chromatic and luminance motion gratings of 1 cpd and luminance 40 cd m(-2) subtending a 7 degrees field. At slow speeds (< or =2 cycles s(-1)) the motion onset response exhibits a clear amplitude minimum at isoluminance. Over the Michelson contrast range tested (0.05-0.75) the chromatic response at 2 cycles s(-1) possesses a linear response function compared to the saturating function of the luminance response and the contrast dependency of the former is a factor of 5-6 times greater than for the latter. These differences are suggestive of different neural substrates for the chromatic and luminance motion VEPs at slow speeds. At 10 cycles s(-1) the chromatic motion onset VEP exhibits no amplitude minimum at isoluminance and becomes more like its luminance counterpart in terms of its saturating contrast response function. Furthermore, the contrast dependency of the chromatic and luminance responses differs by only a factor of 1.6 at this faster rate. These findings are consistent with the idea of separate motion mechanisms that operate at fast and slow speeds, the latter having separate channels for colour and luminance motion.

Over the past decades, researchers have explored altered rhythmic responses to visual stimulation in people with schizophrenia using steady state visual evoked potentials (SSVEPs). Here we systematically review studies performed between 1954 and 2021, as identified on PubMed. We included studies if they included people with schizophrenia, a control group, reported SSVEPs as their primary outcome, and used quantitative analyses in the frequency domain. We excluded studies that used SSVEPs to primarily quantify cognitive processes (e.g., attention). Fifteen studies met these criteria. These studies reported decreased SSVEPs across a range of frequencies and electrode locations in people living with schizophrenia compared to controls; none reported increases. Null results, however, were common. Given the typically modest number of subjects in these studies, this is consistent with a moderate effect size. It is notable that most studies targeted frequencies that fall within the alpha and beta band, and investigations of frequencies in the gamma band have been rare. We group test frequencies in frequency bands and summarize the results in topographic plots. From the wide range of approaches in these studies, we distill suggested experimental designs and analysis choices for future experiments. This will increase the value of SSVEP studies, improve our understanding of the mechanisms that result in altered rhythmic responses to visual stimulation in schizophrenia, and potentially further the development of diagnostic tools.

Studies using conventional full-field visual evoked potentials (ffVEP) have reported subtle abnormalities in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). We hypothesize that these abnormalities can be detected in the majority of CIDP patients using enhanced methods.

This paper investigates controlling humanoid robot behavior via motion-onset specific N200 potentials. In this study, N200 potentials are induced by moving a blue bar through robot images intuitively representing robot behaviors to be controlled with mind. We present the individual impact of each subject on N200 potentials and discuss how to deal with individuality to obtain a high accuracy. The study results document the off-line average accuracy of 93% for hitting targets across over five subjects, so we use this major component of the motion-onset visual evoked potential (mVEP) to code people's mental activities and to perform two types of on-line operation tasks: navigating a humanoid robot in an office environment with an obstacle and picking-up an object. We discuss the factors that affect the on-line control success rate and the total time for completing an on-line operation task.

Excitotoxic oligodendroglial death is one of the mechanisms which has been proposed to underlie demyelinating diseases of the CNS. We describe here functional consequences of excitotoxic lesions to the rabbit optic nerve by studying the visual evoked potentials (VEPs) measured in the visual cortex. Nerves were slowly infused with the excitotoxin kainate a subcutaneously implanted osmotic pump which delivered the toxin through a cannula onto the optic nerve. Records of VEPs were obtained before pump implantation and at 1, 3 and 7 days post-implantation, and weekly evaluated thereafter for up to 4 months. We observed that the VEPs generated by light stimuli progressively changed in both amplitude and profile after the lesion as well as in comparison to those generated in control animals infused with vehicle. Histological examination of the damage caused by the excitotoxic insult showed that large areas of the optic nerve were demyelinated and their axons distorted. These observations were confirmed and extended by immunohistochemical analyses using markers to neurofilaments, myelin basic protein and the oligodendrocyte marker APC. The results of the present paper indicate that the consequences of excitotoxicity in the optic nerve share functional and morphological alterations which are found in demyelinating disorders. In addition, this experimental paradigm may be useful to evaluate the functional recovery of demyelinated optic nerves following various repair strategies.

The visual system is one of the most accessible routes to study the central nervous system under pathological conditions, such as in multiple sclerosis (MS). Non-invasive visual evoked potential (VEP) and optical coherence tomography (OCT) were used to assess visual function and neuroretinal thickness in C57BL/6 taking 0.2% cuprizone for 7 weeks and at 5, 8, 12, and 15 days after returning to a normal diet. VEPs were significantly delayed starting from 4 weeks on cuprizone, with progressive recovery off cuprizone, becoming significant at day 8, complete at day 15. In contrast, OCT and neurofilament staining showed no significant axonal thinning. Optic nerve histology indicated that whilst there was significant myelin loss at 7 weeks on the cuprizone diet compared with healthy mice, at 15 days off cuprizone diet demyelination was significantly less severe. The number of Iba 1+ cells was found increased in cuprizone mice at 7 weeks on and 15 days off cuprizone. The combined use of VEPs and OCT allowed us to characterize non-invasively, in vivo, the functional and structural changes associated with demyelination and remyelination in a preclinical model of MS. This approach contributes to the non-invasive study of possible effective treatments to promote remyelination in demyelinating pathologies.

Visual evoked potentials (VEPs) provide important diagnostic information related to the functional integrity of the visual pathways. The aim of this study was to establish normative values of different components of pattern reversal VEPs on Iranian normal adult subjects.

Transcranial magnetic stimulation (TMS) can non-invasively modify cortical neural activity by means of a time-varying magnetic field. For example, in cognitive neuroscience, it is applied to create reversible "virtual lesions" in healthy humans (usually assessed as diminished performance in a behavioral task), thereby helping to establish causal structure-function relationships. Despite its widespread use, it is still rather unclear how TMS acts on existing, task-related neural activity, potentially resulting in a measurable effect on the behavioral level. Here, we deliver TMS to early visual areas while recording EEG in order to directly characterize the interaction between TMS-evoked (TEPs) and visual-evoked potentials (VEPs). Simultaneously, the subjects' performance is assessed in a visual forced-choice task. This allows us to compare the TMS effects on the VEPs across different levels of behavioral impairment. By systematically varying the stimulation intensity, we demonstrate that TMS strongly enhances the overall visual stimulus-related activity (rather than disrupting it). This enhancement effect saturates when behavior is impaired. This might indicate that the neural coding of the visual stimulus is robust to noise within a certain dynamic range (as indexed by the enhancement). Strong disturbances might saturate this range, causing behavioral impairment. Variation of the timing between the visual stimulus and the magnetic pulse reveals a "constructive interference" between the TEPs and VEPs: The better the overlap between both evoked potentials, the stronger the interaction effect when TMS and visual stimulation are combined. Importantly, however, this effect is uncorrelated with the strength of behavioral impairment.

The involvement of the central nervous system is a frequent yet underestimated complication of diabetes mellitus. Visual evoked potentials (VEP) are a simple, sensitive, and noninvasive method for detecting early alterations in central optic pathways. The objective of this paralleled randomized controlled trial was to evaluate the impact of ozone therapy on visual pathways in diabetic patients.

Acetylcholine (ACh) contributes to learning processes by modulating cortical plasticity in terms of intensity of neuronal activity and selectivity properties of cortical neurons. However, it is not known if ACh induces long term effects within the primary visual cortex (V1) that could sustain visual learning mechanisms. In the present study we analyzed visual evoked potentials (VEPs) in V1 of rats during a 4-8 h period after coupling visual stimulation to an intracortical injection of ACh analog carbachol or stimulation of basal forebrain. To clarify the action of ACh on VEP activity in V1, we individually pre-injected muscarinic (scopolamine), nicotinic (mecamylamine), alpha7 (methyllycaconitine), and NMDA (CPP) receptor antagonists before carbachol infusion. Stimulation of the cholinergic system paired with visual stimulation significantly increased VEP amplitude (56%) during a 6 h period. Pre-treatment with scopolamine, mecamylamine and CPP completely abolished this long-term enhancement, while alpha7 inhibition induced an instant increase of VEP amplitude. This suggests a role of ACh in facilitating visual stimuli responsiveness through mechanisms comparable to LTP which involve nicotinic and muscarinic receptors with an interaction of NMDA transmission in the visual cortex.

In our previous study we found that it takes less time to detect coloration change in a moving object compared to coloration change in a stationary one (Kreegipuu etal., 2006). Here, we replicated the experiment, but in addition to reaction times (RTs) we measured visual evoked potentials (VEPs), to see whether this effect of motion is revealed at the cortical level of information processing. We asked our subjects to detect changes in coloration of stationary (0(°)/s) and moving bars (4.4 and 17.6(°)/s). Psychophysical results replicate the findings from the previous study showing decreased RTs to coloration changes with increase of velocity of the color changing stimulus. The effect of velocity on VEPs was opposite to the one found on RTs. Except for component N1, the amplitudes of VEPs elicited by the coloration change of faster moving objects were reduced than those elicited by the coloration change of slower moving or stationary objects. The only significant effect of velocity on latency of peaks was found for P2 in frontal region. The results are discussed in the light of change-to-change interval and the two methods reflecting different processing mechanisms.

Studies of visual cortical responses following visual perceptual learning (VPL) have produced diverse results, revealing neural changes in early and/or higher-level visual cortex as well as changes in regions responsible for higher cognitive processes such as attentional control. In this study, we investigated substrates of VPL in the human brain by recording visual evoked potentials with high-density electroencephalography (hdEEG) before (Session 1) and after (Session 2) training on a texture discrimination task (TDT), with two full nights of sleep between sessions. We studied the following event-related potential (ERP) components: C1 (early sensory processing), P1 and N1 (later sensory processing, modulated by top-down spatial attention), and P3 (cognitive processing). Our results showed a significant decrease in C1 amplitude at Session 2 relative to Session 1 that was positively correlated with the magnitude of improvement in behavioral performance. Although we observed no significant changes in P1 amplitude with VPL, both N1 amplitude and latency were significantly decreased in Session 2. Moreover, the difference in N1 latency between Session 1 and Session 2 was negatively correlated with behavioral improvement. We also found a significant increase in P3 amplitude following training. Our results suggest that VPL of the TDT task may be due to plasticity in early visual cortical areas as well as changes in top-down attentional control and cognitive processing.

The primate visual system analyzes statistical information in natural images and uses it for the immediate perception of scenes, objects, and surface materials. To investigate the dynamical encoding of image statistics in the human brain, we measured visual evoked potentials (VEPs) for 166 natural textures and their synthetic versions, and performed a reverse-correlation analysis of the VEPs and representative texture statistics of the image. The analysis revealed occipital VEP components strongly correlated with particular texture statistics. VEPs correlated with low-level statistics, such as subband SDs, emerged rapidly from 100 to 250 ms in a spatial frequency dependent manner. VEPs correlated with higher-order statistics, such as subband kurtosis and cross-band correlations, were observed at slightly later times. Moreover, these robust correlations enabled us to inversely estimate texture statistics from VEP signals via linear regression and to reconstruct texture images that appear similar to those synthesized with the original statistics. Additionally, we found significant differences in VEPs at 200-300 ms between some natural textures and their Portilla-Simoncelli (PS) synthesized versions, even though they shared almost identical texture statistics. This differential VEP was related to the perceptual "unnaturalness" of PS-synthesized textures. These results suggest that the visual cortex rapidly encodes image statistics hidden in natural textures specifically enough to predict the visual appearance of a texture, while it also represents high-level information beyond image statistics, and that electroencephalography can be used to decode these cortical signals.

Short-term monocular deprivation in adult humans produces a perceptual boost of the deprived eye reflecting homeostatic plasticity. Visual evoked potentials (VEPs) to transient stimuli change after 150 min of monocular deprivation in adult humans. The amplitude of the C1 component of the VEP at a latency of about 100 ms increases for the deprived eye and decreases for the non-deprived eye after deprivation, the two effects being highly negatively correlated. Similarly, the evoked alpha rhythm increases after deprivation for the deprived eye and decreases for the non-deprived eye. The data demonstrate that primary visual cortex excitability is altered by a short period of monocular deprivation, reflecting homeostatic plasticity.

To refine a reliable and reproducible intraoperative visual evoked potentials (iVEPs) monitoring protocol during endoscopic transsphenoidal surgery. To assess the reliability of baseline iVEPs in predicting preoperative visual status and perioperative iVEP variation in predicting postoperative visual outcome.

Visual Evoked Potential (VEP) quantifies electrical signals produced in visual cortex in response to visual stimuli. VEP elicited by light flashes is a useful biomarker to evaluate visual function in preclinical models and it can be recorded in awake or anaesthetised state. Different types of anaesthesia influence VEP properties, such as latency, which measures the propagation speed along nerve fibers, and amplitude that quantifies the power of electrical signal.

Intrinsically photosensitive retinal ganglion cells (ipRGCs) express the photopigment melanopsin, imparting to themselves the ability to respond to light in the absence of input from rod or cone photoreceptors. Since their discovery ipRGCs have been found to play a significant role in non-image-forming aspects of vision, including circadian photoentrainment, neuroendocrine regulation, and pupillary control. In the past decade it has become increasingly clear that some ipRGCs also contribute directly to pattern-forming vision, the ability to discriminate shapes and objects. However, the degree to which melanopsin-mediated phototransduction, versus that of rods and cones, contributes to this function is still largely unknown. Earlier attempts to quantify this contribution have relied on genetic knockout models that target key phototransductive proteins in rod and cone photoreceptors, ideally to isolate melanopsin-mediated responses. In this study we used the Gnat1-/-; Gnat2cpfl3/cpfl3 mouse model, which have global knockouts for the rod and cone α-transducin proteins. These genetic modifications completely abolish rod and cone photoresponses under light-adapted conditions, locking these cells into a "dark" state. We recorded visually evoked potentials in these animals and found that they still showed robust light responses, albeit with reduced light sensitivity, with similar magnitudes to control mice. These responses had characteristics that were in line with a melanopsin-mediated signal, including delayed kinetics and increased saturability. Additionally, we recorded electroretinograms in a sub-sample of these mice and were unable to find any characteristic waveform related the activation of photoreceptors or second-order retinal neurons, suggesting ipRGCs as the origin of light responses. Our results show a profound ability for melanopsin phototransduction to directly contribute to the primary pattern-forming visual pathway.

To identify mechanisms of cortical plasticity of the visual cortex and to quantify their significance, sensitive parameters are warranted. In this context, multifocal visual evoked potentials (mfVEPs) can make a valuable contribution as they are not associated with cancellation artifacts and include also the peripheral visual field.