Early Visual Processing Deficits Research Articles

Association between retinal and cortical visual electrophysiological impairments in schizophrenia.

Electrophysiological impairments in the magnocellular visual system have been reported among patients with schizophrenia, but previous theories proposed that these deficits may begin in the retina. We therefore sought to evaluate the potential contribution of the retina by comparing retinal and cortical visual electrophysiological impairments between patients with schizophrenia and healthy controls. We recruited patients with schizophrenia and age- and sex-matched healthy controls. We recorded the P100 amplitude and latency using electroencephalography (EEG) while projecting low (0.5 cycles/degree) or high (15 cycles/degree) spatial frequency gratings at a temporal frequency of 0 Hz or 8 Hz. We compared the P100 results with previous results for retinal ganglion cell activity (N95) in these participants. We analyzed data using repeated-measures analysis of variance and correlation analyses. We recruited 21 patients with schizophrenia and 29 age- and sex-matched healthy controls. Results showed decreased P100 amplitude and increased P100 latency among patients with schizophrenia compared with healthy controls (p < 0.05). Analyses reported the main effects of spatial and temporal frequency but no interaction effects of spatial or temporal frequency by group. Moreover, correlation analysis indicated a positive association between P100 latency and previous retinal results for N95 latency in the schizophrenia group (p < 0.05). Alterations in the P100 wave among patients with schizophrenia are consistent with the deficits in early visual cortical processing shown in the literature. These deficits do not seem to correspond to an isolated magnocellular deficit but appear to be associated with previous retinal measurements. Such an association emphasizes the role of the retina in the occurrence of visual cortical abnormalities in schizophrenia. Studies with coupled electroretinography-EEG measurements are now required to further explore these findings. https://clinicaltrials.gov/ct2/show/NCT02864680.

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.

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

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.

An Event-Related Potential Investigation of Early Visual Processing Deficits During Face Perception in Youth at Clinical High Risk for Psychosis.

Impairments in early visual face perception are well documented in patients with schizophrenia. Specifically, event-related potential (ERP) research in patients with schizophrenia has demonstrated deficits in early sensory processing of stimulus properties (P1 component) and the structural encoding of faces (N170 component). However, it is not well understood if similar impairments are present in individuals at clinical high risk (CHR) for psychosis (ie, those in the putative prodromal stage of the illness). Thus, it is unknown if face perception deficits are the result of illness onset or are present in the high-risk period for the illness. The present study used the ERP technique to examine neural activation when viewing facial emotion expressions and objects in 44 CHR and 47 control adolescents and young adults (N = 91). P1 amplitude was similar across groups, indicating that early sensory processing impairments did not substantially contribute to face perception deficits in CHR youth. CHR youth exhibited reduced N170 amplitude compared to controls when viewing faces but not objects, implicating a specific deficit in the structural encoding of faces rather than a general perceptual deficit. Further, whereas controls demonstrated the expected face-selective N170 effect (ie, larger amplitude for faces than objects), CHR youth did not, which suggests that facial emotion expressions do not elicit the expected preferential perceptual processing for critical social information in individuals at CHR for psychosis. Together, these findings provide valuable information regarding the specific impairments contributing to face perception deficits in the high-risk period where treatment stands to aid in preventing illness progression.

129 Pilot study: the validity of the queens square screening test for visual deficits in a cohort of patients with dementia

IntroductionThere is limited research on the visual deficits found in dementia. The Queens Square Screening Test for Visual Deficits (QS test) is designed to screen for changes in visual processing. Our study aimed to validate this test and examine the types of visual processing deficits found in dementia.MethodsWe assessed the QS test in participants with dementia, mild cognitive impairment (MCI), and healthy controls. Participants were recruited from the Neurology and Geriatrics departments of a tertiary hospital over 3-months. Cognitive impairment was measured using the Rowland Universal Dementia Assessment Scale (RUDAS).ResultsTwenty-six patients were examined. There were no statistically significant differences in age, gender, English fluency, and education between the three groups. Participants with dementia (n=8, mean RUDAS 17.5/30) scored 51.4/71 on the QS test, compared to 60.7/71 in MCI (n=7, mean RUDAS 25.0/30) and 64.6/71 in controls (n=11, mean RUDAS 27.4/30). The mean scores for each subset of the QS test for dementia, MCI and normal cognition, respectively, were: early visual processing – 19.6/25, 22.4/25, 23.7/25; object perception – 5.6/11, 7.9/11, 8.7/11; space perception – 11.4/14, 11.1/14, 12.4/14; face perception – 4.4/8, 6.4/8, 7.0/8; reading – 10.4/13, 12.9/13, 12.8/13.ConclusionIn this pilot study, the QS test was markedly abnormal in dementia but did not differentiate between MCI and normal cognition. Our findings suggest that deficits in early visual processing, reading, and the perception of objects and faces are common in dementia. Understanding the types of visual difficulties may improve the care of patients with dementia.

Visuospatial neglect is more severe when stimulus density is large

ABSTRACTPatients with visuospatial neglect (VSN) suffer from an imbalance in visual attention between their left and right (egocentric or allocentric) hemispace. The view of VSN as an attentional imbalance between two hemispaces ignores the fact that—in our daily life—we are presented with varying levels of stimulus density, within but also across hemispaces. Therefore, we developed a novel experimental paradigm in which stroke patients (n = 207) were presented with a different number of simple objects in the left and right (egocentric) hemispaces and were asked to indicate whether there were more objects in the left or the right hemispace. We systematically varied the density of visual stimuli to investigate whether a high level of stimulus density impairs task performance of patients with VSN to a larger degree than it does for patients without VSN. Error rate increased when more objects were presented in the display, but this effect was most pronounced in patients with VSN, especially when more objects were presented in their contralesional than in their ipsilesional hemispace. Our findings reveal that deficits in early visual processing in patients with VSN become especially apparent when overall stimulus density is high. The degree of stimulus density should therefore be taken into account when considering the impact of attentional deficits on activities in daily life.

Psychophysical evaluation of contrast sensitivity using Gabor patches in tobacco addiction

This study, an extension of Fernandes et al. (2017), provided consistent contrast sensitivity function (CSF) measurements in a large sample. CSF was assessed for luminance stimuli in different 48 chronic smokers and 50 healthy nonsmokers. Stimuli for the CSF were Gabor patches with spatial frequencies of .2, 2.5, 5.0, 10.0, and 20.0 cycles per degree (cpd). The use of Gabor patches minimizes uncertainty in spatial position and detection of frequencies. The Gabor patches consisted of vertical gratings that were multiplied by a two-dimensional spatial Gaussian envelope. All of the groups were matched for gender and level of education. All of the participants were free from any neurological disorder, cardiovascular disease, and identifiable ocular disease, and they had normal or corrected-to-normal visual acuity. No abnormalities were detected on the fundoscopic examination or optical coherence tomographic examination. The smoker group had a lower CSF compared with healthy nonsmokers at all spatial frequencies. These results indicate that cigarette smoking or chronic exposure to its constituent compounds affects early-stage visual discrimination, suggesting the existence of deficits in early visual spatial processing in smokers.

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

BackgroundWorking memory (WM) deficits are a core feature of schizophrenia. Electrophysiological studies suggest that impaired early visual processing may contribute to impaired WM in the visual domain. Abnormal N-methyl-D-aspartate (NMDA) receptor function has been implicated both in WM and in early visual processing deficits in schizophrenia. We investigated whether ketamine, a noncompetitive NMDA antagonist, would replicate in healthy volunteers the WM performance and early visual processing abnormalities we and others have reported in patients with schizophrenia. MethodsForty-four healthy volunteers were randomly assigned to receive intravenous ketamine or placebo. During infusion, the effects of ketamine were recorded using standardized psychiatric scales. Visual evoked potentials (P100 and P300 components) were recorded during performance of a delayed matching to sample task. ResultsKetamine induced mild psychosis-like symptoms and impaired WM performance. It also significantly increased the P100 amplitude, while P300 amplitude decreased in a load-dependent manner. Amplitudes of P100 during retrieval correlated with cognitive performance only in the placebo group. ConclusionsWe confirmed previous studies showing that ketamine reproduces the impairment of WM performance and smaller P300 amplitudes observed in schizophrenia. However, ketamine increased visual P100 amplitude in contrast to our observation of reduced P100 amplitudes in established schizophrenia. The effects of ketamine on WM and P300 are likely to involve impaired NMDA function, as these receptors are implicated in changes of synaptic strength underlying associative learning and memory. Increased P100 amplitude may reflect the secondary disinhibition of cortical glutamate release that occurs after NMDA blockade.

Neural oscillatory deficits in schizophrenia predict behavioral and neurocognitive impairments.

Paying attention to visual stimuli is typically accompanied by event-related desynchronizations (ERD) of ongoing alpha (7–14 Hz) activity in visual cortex. The present study used time-frequency based analyses to investigate the role of impaired alpha ERD in visual processing deficits in schizophrenia (Sz). Subjects viewed sinusoidal gratings of high (HSF) and low (LSF) spatial frequency (SF) designed to test functioning of the parvo- vs. magnocellular pathways, respectively. Patients with Sz and healthy controls paid attention selectively to either the LSF or HSF gratings which were presented in random order. Event-related brain potentials (ERPs) were recorded to all stimuli. As in our previous study, it was found that Sz patients were selectively impaired at detecting LSF target stimuli and that ERP amplitudes to LSF stimuli were diminished, both for the early sensory-evoked components and for the attend minus unattend difference component (the Selection Negativity), which is generally regarded as a specific index of feature-selective attention. In the time-frequency domain, the differential ERP deficits to LSF stimuli were echoed in a virtually absent theta-band phase locked response to both unattended and attended LSF stimuli (along with relatively intact theta-band activity for HSF stimuli). In contrast to the theta-band evoked responses which were tightly stimulus locked, stimulus-induced desynchronizations of ongoing alpha activity were not tightly stimulus locked and were apparent only in induced power analyses. Sz patients were significantly impaired in the attention-related modulation of ongoing alpha activity for both HSF and LSF stimuli. These deficits correlated with patients’ behavioral deficits in visual information processing as well as with visually based neurocognitive deficits. These findings suggest an additional, pathway-independent, mechanism by which deficits in early visual processing contribute to overall cognitive impairment in Sz.

Visual Evoked Potentials as a Readout of Cortical Function in Infants With Tuberous Sclerosis Complex.

Tuberous sclerosis complex is an autosomal dominant genetic disorder that confers a high risk for neurodevelopmental disorders, such as autism spectrum disorder and intellectual disability. Studies have demonstrated specific delays in visual reception skills that may predict the development of autism spectrum disorder and intellectual disability. Based on evidence for alterations in the retinogeniculate pathway in animal models of tuberous sclerosis complex, we asked whether children with tuberous sclerosis complex demonstrate alterations in early visual processing that may undermine the development of higher-level visual behaviors. Pattern-reversal visual evoked potentials were recorded in infants with tuberous sclerosis complex (n = 16) and typically developing infants (n = 18) at 12 months of age. Infants with tuberous sclerosis complex demonstrated remarkably intact visual evoked potentials even within the context of intellectual disability and epilepsy. Infants with tuberous sclerosis complex show intact visual cortical processing, suggesting that delays in visually mediated behaviors in tuberous sclerosis complex may not be rooted in early visual processing deficits.

Early visual processing deficits in patients with schizophrenia during spatial frequency-dependent facial affect processing

Abnormal facial emotion recognition is considered as one of the key symptoms of schizophrenia. Only few studies have considered deficits in the spatial frequency (SF)-dependent visual pathway leading to abnormal facial emotion recognition in schizophrenia. Twenty-one patients with schizophrenia and 19 matched healthy controls (HC) were recruited for this study. Event-related potentials (ERP) were measured during presentation of SF-modulated face stimuli and their source imaging was analyzed. The patients showed reduced P100 amplitude for low-spatial frequency (LSF) pictures of fearful faces compared with the HC group. The P100 amplitude for high-spatial frequency (HSF) pictures of neutral faces was increased in the schizophrenia group, but not in the HC group. The neural source activities of the LSF fearful faces and HSF neutral faces led to hypo- and hyperactivation of the frontal lobe of subjects from the schizophrenia group and HC group, respectively. In addition, patients with schizophrenia showed enhanced N170 activation in the right hemisphere in the LSF condition, while the HC group did not. Our results suggest that deficits in the LSF-dependent visual pathway, which involves magnocellular neurons, impair early visual processing leading to dysfunctional facial emotion recognition in schizophrenia. Moreover, it suggests impaired bottom-up processing rather than top-down dysfunction for facial emotion recognition in these patients.

Binocular depth perception in individuals at clinical high risk for psychosis: No evidence of dysfunction.

In the last decade the interest in the role of the visual system in schizophrenia has grown, with evidence pointing to dysfunction in bottom-up visual processing that leads to early visual processing deficits. A fundamental component of visual perception is binocular depth perception (BDP), that is, depth perception derived by the difference between the images impressed upon the left and right retina. Two studies reported impaired BDP in schizophrenia and suggested a possible developmental deficit of brain structures involved in early visual processing. The aim of this study was to examine BDP in a young population at clinical high risk (CHR) of developing psychosis to determine whether this dysfunction is present in this potentially prepsychotic period. Forty-two CHR participants and 44 healthy controls were assessed using a computerized test of depth perception; a subsample completed a test of stereopsis. The computerized test comprised two trial blocks, with four conditions at increasing level of difficulty, in which participants were asked to discriminate the relative depth of two stimuli simultaneously presented on the screen. BDP was not impaired in the CHR group, whose performance was similar to that of the control group on both measures. For the CHR group performance in both tests was not correlated to positive symptoms. These results indicate that BDP is preserved in individuals at CHR for psychosis, and impaired BDP should not be considered a vulnerability marker for schizophrenia. Nevertheless future studies should verify BDP's potential power in predicting schizophrenia.

Modulation of affective face processing deficits in Schizophrenia by congruent emotional sounds

Schizophrenia is a psychiatric disorder resulting in prominent impairments in social functioning. Thus, clinical research has focused on underlying deficits of emotion processing and their linkage to specific symptoms and neurobiological dysfunctions. Although there is substantial research investigating impairments in unimodal affect recognition, studies in schizophrenia exploring crossmodal emotion processing are rare. Therefore, event-related potentials were measured in 15 patients with schizophrenia and 15 healthy controls while rating the expression of happy, fearful and neutral faces and concurrently being distracted by emotional or neutral sounds. Compared with controls, patients with schizophrenia revealed significantly decreased P1 and increased P2 amplitudes in response to all faces, independent of emotion or concurrent sound. Analyzing these effects with regard to audiovisual (in)congruence revealed that P1 amplitudes in patients were only reduced in response to emotionally incongruent stimulus pairs, whereas similar amplitudes between groups could be observed for congruent conditions. Correlation analyses revealed a significant negative correlation between general symptom severity (Brief Psychiatric Rating Scale-V4) and P1 amplitudes in response to congruent audiovisual stimulus pairs. These results indicate that early visual processing deficits in schizophrenia are apparent during emotion processing but, depending on symptom severity, these deficits can be restored by presenting concurrent emotionally congruent sounds.

A neurophysiological deficit in early visual processing in schizophrenia patients with auditory hallucinations

Existing 67-channel event-related potentials, obtained during recognition and working memory paradigms with words or faces, were used to examine early visual processing in schizophrenia patients prone to auditory hallucinations (AH, n = 26) or not (NH, n = 49) and healthy controls (HC, n = 46). Current source density (CSD) transforms revealed distinct, strongly left- (words) or right-lateralized (faces; N170) inferior-temporal N1 sinks (150 ms) in each group. N1 was quantified by temporal PCA of peak-adjusted CSDs. For words and faces in both paradigms, N1 was substantially reduced in AH compared with NH and HC, who did not differ from each other. The difference in N1 between AH and NH was not due to overall symptom severity or performance accuracy, with both groups showing comparable memory deficits. Our findings extend prior reports of reduced auditory N1 in AH, suggesting a broader early perceptual integration deficit that is not limited to the auditory modality.

Delayed early face processing in bipolar disorder

Bipolar disorder primarily encompasses mood symptom states of depression and mania separated by symptom-free euthymia, and patients also exhibit cognitive deficits that include face processing. However, there is minimal extant event-related potential (ERP) research investigating the time course of these impairments. The aim of the present study was to contribute to a greater understanding of the specific stages of face processing that are impaired in bipolar disorder. Bipolar and age-matched and sex-matched control individuals completed an emotional go/no-go paradigm involving happy and sad face stimuli during ERP acquisition. Amplitudes and latencies of frontocentral P80, N120 and vertex positive potential (VPP) ERP components were analysed in response to 'go' stimuli. Across groups, VPP latencies were reduced in response to sad compared with happy face stimuli. Between groups, individuals with bipolar disorder demonstrated overall increased latencies in P80 and VPP ERP components. Current and previous studies suggest that patients with bipolar disorder exhibit early visual processing deficits, but the present study contributes new evidence of a deficit in the visual P80 ERP. Delayed neural responses may be an ERP correlate of white matter deficits that have previously been identified. Furthermore, implications for early visual impairments may involve behavioural symptoms downstream.

Backward masking reveals different visual processing of schizophrenic and depressive patients

Visual backward masking is a very sensitive tool for studying early visual processing deficits and a reliable endophenotype of schizophrenia. Mental diseases strongly overlap in many aspects, for example, in psychopathology, cognition, and genetics. Here, we show that strong masking deficits are found in patients with functional psychoses but not in non-psychotic patients, namely, depressive patients and abstinent alcoholics. We tested 28 schizophrenic, 22 schizoaffective, 20 bipolar patients, 26 major depressive patients, 23 abstinent alcoholics, and 24 healthy control subjects with various variants of the shine-through masking paradigm. Patients with schizophrenia, schizoaffective disorder, and bipolar disorder, show strongly prolonged SOAs compared to controls. Patients with unipolar major depression and abstinent alcoholics, however, perform like healthy controls. We suggest that patients with functional psychoses suffer from similar visual dysfunctions whereas visual processing of depressive patients seems to differ. [The work was supported by the Volkswagen Foundation.]

Proline and COMT Status Affect Visual Connectivity in Children with 22q11.2 Deletion Syndrome

BackgroundIndividuals with the 22q11.2 deletion syndrome (22q11DS) are at increased risk for schizophrenia and Autism Spectrum Disorders (ASDs). Given the prevalence of visual processing deficits in these three disorders, a causal relationship between genes in the deleted region of chromosome 22 and visual processing is likely. Therefore, 22q11DS may represent a unique model to understand the neurobiology of visual processing deficits related with ASD and psychosis.MethodologyWe measured Event-Related Potentials (ERPs) during a texture segregation task in 58 children with 22q11DS and 100 age-matched controls. The C1 component was used to index afferent activity of visual cortex area V1; the texture negativity wave provided a measure for the integrity of recurrent connections in the visual cortical system. COMT genotype and plasma proline levels were assessed in 22q11DS individuals.Principal FindingsChildren with 22q11DS showed enhanced feedforward activity starting from 70 ms after visual presentation. ERP activity related to visual feedback activity was reduced in the 22q11DS group, which was seen as less texture negativity around 150 ms post presentation. Within the 22q11DS group we further demonstrated an association between high plasma proline levels and aberrant feedback/feedforward ratios, which was moderated by the COMT 158 genotype.ConclusionsThese findings confirm the presence of early visual processing deficits in 22q11DS. We discuss these in terms of dysfunctional synaptic plasticity in early visual processing areas, possibly associated with deviant dopaminergic and glutamatergic transmission. As such, our findings may serve as a promising biomarker related to the development of schizophrenia among 22q11DS individuals.

Sustained versus transient brain responses in schizophrenia: the role of intrinsic neural activity

Schizophrenia patients (SZ) show early visual processing deficits in many, but not all, tasks. These deficits may be associated with dysregulation of intrinsic oscillatory activity that compromises signal-to-noise in the SZ brain. This question was studied using visual steady-state stimulation and post-steady-state presentation of transient visual stimuli. SZ had higher intrinsic oscillatory activity at the steady-state stimulation frequency (12.5Hz) and at the 6.25Hz subharmonic, showed a significant decrease in visual steady-state magnitude over 2s of stimulation, and were unable to promptly terminate the steady-state response following stimulation offset. If adjustment for levels of intrinsic brain activity were made, however, it would have appeared that SZ had activity of similar magnitude as healthy subjects following steady-state stimulus termination, indicating that such adjustments could substantially alter theoretical interpretations. Visual evoked potential abnormalities (N1/P2 amplitudes) present among SZ at the initiation of steady-state stimulation were less apparent in the 750ms immediately following steady-state stimulation offset. Higher intrinsic oscillatory brain activity may be a fundamental characteristic of SZ that merits further evaluation for understanding this disorder's neuropathological correlates and associated symptomatology.

The McCollough Effect and Facial Emotion Discrimination in Patients With Schizophrenia and Their Unaffected Relatives

Abnormalities in visual processing have been found consistently in schizophrenia patients, including deficits in early visual processing, perceptual organization, and facial emotion recognition. There is however no consensus as to whether these abnormalities represent heritable illness traits and what their contribution is to psychopathology. Fifty patients with schizophrenia, 61 of their first-degree healthy relatives, and 50 psychiatrically healthy volunteers were tested with regard to facial affect (FA) discrimination and susceptibility to develop the color-contingent illusion [the McCollough Effect (ME)]. Both patients and relatives demonstrated significantly lower accuracy in FA discrimination compared with controls. There was also a significant effect of familiality: Participants from the same families had more similar accuracy scores than those who belonged to different families. Experiments with the ME showed that schizophrenia patients required longer time to develop the illusion than relatives and controls, which indicated poor visual adaptation in schizophrenia. Relatives were marginally slower than controls. There was no significant association between the measures of FA discrimination accuracy and ME in any of the participant groups. Facial emotion discrimination was associated with the degree of interpersonal problems, as measured by the Schizotypal Personality Questionnaire in relatives and healthy volunteers, whereas the ME was associated with the perceptual-cognitive symptoms of schizotypy and positive symptoms of schizophrenia. Our results support the heritability of FA discrimination deficits as a trait and indicate visual adaptation abnormalities in schizophrenia, which are symptom related.