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Fragile early visual percepts mark genetic liability specific to schizophrenia.

ABSTRACT: Disruption of visual percepts by a subsequent stimulus (ie, backward masking) has been consistently noted in schizophrenia, with some evidence that this fragility in early perception is present in people with genetic liability for the disorder. Given the potential of backward masking paradigms to mark neural processes that confer risk for schizophrenia, it is important to test the diagnostic specificity of abnormalities in visual perception. To more fully assess whether masking visual stimuli reveals a marker of genetic liability (ie, endophenotype) specific to schizophrenia, we tested 44 people with the disorder, 29 people with bipolar disorder, 56 first-degree biological relatives of people with schizophrenia, 26 first-degree biological relatives of people with bipolar disorder, and 43 nonpsychiatric control participants using a magnocellular-biased visual backward masking procedure that included target-to-mask onset asynchronies ranging from 0 to 80 ms. Relatives of people with schizophrenia who were without schizophrenia spectrum disorders exhibited impaired performance compared with nonpsychiatric control participants and relatives of people with bipolar disorder when a visual mask interrupted early perception (eg, 27 ms). A similar vulnerability of early processes was noted in people with schizophrenia, yet they also had impaired performance when masks occurred at later time points (ie, 80 ms). Performance deficits were not attributable to intellectual function, measures of attention and memory, symptomatology, or medication dosage. Bipolar patients and their relatives failed to exhibit deficits on the backward masking task. Fragility of early visual percepts appears to mark genetic liability specific to schizophrenia and may serve as an endophenotype for the disorder.

SUBMITTER: Sponheim SR

PROVIDER: S-EPMC3686444 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature

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Fragile early visual percepts mark genetic liability specific to schizophrenia.

Sponheim Scott R SR Sass Sarah M SM Noukki Althea L AL Hegeman Bridget M BM

Schizophrenia bulletin 20120323 4

Disruption of visual percepts by a subsequent stimulus (ie, backward masking) has been consistently noted in schizophrenia, with some evidence that this fragility in early perception is present in people with genetic liability for the disorder. Given the potential of backward masking paradigms to mark neural processes that confer risk for schizophrenia, it is important to test the diagnostic specificity of abnormalities in visual perception. To more fully assess whether masking visual stimuli re ...[more]

PMID: 22446567

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Project description:Pioneering studies demonstrating that the contents of visual working memory (WM) can be decoded from the patterns of multivoxel activity in early visual cortex transformed not only how we study WM, but theories of how memories are stored. For instance, the ability to decode the orientation of memorized gratings is hypothesized to depend on the recruitment of the same neural encoding machinery used for perceiving orientations. However, decoding evidence cannot be used to test the so-called sensory recruitment hypothesis without understanding the underlying nature of what is being decoded. Although unknown during WM, during perception decoding the orientation of gratings does not simply depend on activities of orientation tuned neurons. Rather, it depends on complex interactions between the orientation of the grating, the aperture edges, and the topographic structure of the visual map. Here, our goals are to 1) test how these aperture biases described during perception may affect WM decoding, and 2) leverage carefully manipulated visual stimulus properties of gratings to test how sensory-like are WM codes. For memoranda, we used gratings multiplied by radial and angular modulators to generate orthogonal aperture biases despite having identical orientations. Therefore, if WM representations are simply maintained sensory representations, they would have similar aperture biases. If they are abstractions of sensory features, they would be unbiased and the modulator would have no effect on orientation decoding. Results indicated that fMRI patterns of delay period activity while maintaining the orientation of a grating with one modulator (eg, radial) were interchangeable with patterns while maintaining a grating with the other modulator (eg, angular). We found significant cross-classification in visual and parietal cortex, suggesting that WM representations are insensitive to aperture biases during perception. Then, we visualized memory abstractions of stimuli using a population receptive field model of the visual field maps. Regardless of aperture biases, WM representations of both modulated gratings were recoded into a single oriented line. These results provide strong evidence that visual WM representations are abstractions of percepts, immune to perceptual aperture biases, and compel revisions of WM theory.

Project description:BackgroundIndividuals with schizophrenia are at higher risk of physical illnesses, which are a major contributor to their 20-year reduced life expectancy. It is currently unknown what causes the increased risk of physical illness in schizophrenia.AimsTo link genetic data from a clinically ascertained sample of individuals with schizophrenia to anonymised National Health Service (NHS) records. To assess (a) rates of physical illness in those with schizophrenia, and (b) whether physical illness in schizophrenia is associated with genetic liability.MethodWe linked genetic data from a clinically ascertained sample of individuals with schizophrenia (Cardiff Cognition in Schizophrenia participants, n = 896) to anonymised NHS records held in the Secure Anonymised Information Linkage (SAIL) databank. Physical illnesses were defined from the General Practice Database and Patient Episode Database for Wales. Genetic liability for schizophrenia was indexed by (a) rare copy number variants (CNVs), and (b) polygenic risk scores.ResultsIndividuals with schizophrenia in SAIL had increased rates of epilepsy (standardised rate ratio (SRR) = 5.34), intellectual disability (SRR = 3.11), type 2 diabetes (SRR = 2.45), congenital disorders (SRR = 1.77), ischaemic heart disease (SRR = 1.57) and smoking (SRR = 1.44) in comparison with the general SAIL population. In those with schizophrenia, carrier status for schizophrenia-associated CNVs and neurodevelopmental disorder-associated CNVs was associated with height (P = 0.015-0.017), with carriers being 7.5-7.7 cm shorter than non-carriers. We did not find evidence that the increased rates of poor physical health outcomes in schizophrenia were associated with genetic liability for the disorder.ConclusionsThis study demonstrates the value of and potential for linking genetic data from clinically ascertained research studies to anonymised health records. The increased risk for physical illness in schizophrenia is not caused by genetic liability for the disorder.

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Fragile early visual percepts mark genetic liability specific to schizophrenia.

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Fragile early visual percepts mark genetic liability specific to schizophrenia.

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