Revisiting the Backward Masking Deficit in Schizophrenia: Individual Differences in Performance and Modeling With Transcranial Magnetic Stimulation

Luber, Bruce; Stanford, Arielle D.; Malaspina, Dolores; Lisanby, Sarah H.

doi:10.1016/j.biopsych.2006.10.007

Cited by 17 publications

(9 citation statements)

References 42 publications

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“…40 Interestingly, when transcranial magnetic stimulation is used to interrupt processes of the occipital lobe, similar impairments in task performance are seen in schizophrenia patients and healthy control participants. 41 It may be that anomalies in gamma oscillations and lateral occipital hemodynamic response reflect the more generalized impairment in perceiving masked visual stimuli observed in schizophrenia rather than the specific early perceptual abnormalities noted in the present study and by other researchers. 8,11 Indeed, abnormal lateral occipital complex function during masking paradigms appears not to mark genetic liability for the disorder.…”

Section: Discussioncontrasting

confidence: 47%

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Sponheim

Sass

Noukki

et al. 2012

Schizophrenia Bulletin

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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.

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Section: Discussioncontrasting

confidence: 47%

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Sponheim

Sass

Noukki

et al. 2012

Schizophrenia Bulletin

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“…This interval was chosen based on a number of previous studies that found that TMS had maximum effect on visual perception between 80 and 120 ms after stimulus onset (Amassian et al 1989;Boyer et al 2005;Corthout et al 1999;Kammer 2007;Kastner et al 1998;Luber et al 2007;Maccabee et al 1991;Miller et al 1996). In one-half of the blocks, subjects received a TMS pulse to the occipital cortex; in the other one-half of the blocks, the subjects received a pulse at the same stimulus intensity to the vertex of the head.…”

Section: Methodsmentioning

confidence: 99%

Direct injection of noise to the visual cortex decreases accuracy but increases decision confidence

Rahnev

Maniscalco

Luber

et al. 2012

Journal of Neurophysiology

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131

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Rahnev DA, Maniscalco B, Luber B, Lau H, Lisanby SH. Direct injection of noise to the visual cortex decreases accuracy but increases decision confidence. J Neurophysiol 107: 1556 -1563, 2012. First published December 14, 2011 doi:10.1152/jn.00985.2011The relationship between accuracy and confidence in psychophysical tasks traditionally has been assumed to be mainly positive, i.e., the two typically increase or decrease together. However, recent studies have reported examples of exceptions, where confidence and accuracy dissociate from each other. Explanations for such dissociations often involve dual-channel models, in which a cortical channel contributes to both accuracy and confidence, whereas a subcortical channel only contributes to accuracy. Here, we show that a single-channel model derived from signal detection theory (SDT) can also account for such dissociations. We applied transcranial magnetic stimulation (TMS) to the occipital cortex to disrupt the internal representation of a visual stimulus. The results showed that consistent with previous research, occipital TMS decreased accuracy. However, counterintuitively, it also led to an increase in confidence ratings. The data were predicted well by a single-channel SDT model, which posits that occipital TMS increased the variance of the internal stimulus distributions. A formal model comparison analysis that used information theoretic methods confirmed that this model was preferred over single-channel models, in which occipital TMS changed the signal strength or dual-channel models, which assume two different processing routes. Thus our results show that dissociations between accuracy and confidence can, at least in some cases, be accounted for by a single-channel model.

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“…But this was only detected for one group, that of ''non-schizophrenic psychotics'', and all the other data in this study were of the Type-A kind. Luber et al (2007) detected a number of ripples in their masking functions (see their Figure 1). However the overall trend is that of Type-A masking.…”

Section: Type-a Masking In Schizophreniamentioning

confidence: 96%

“…Of these studies, the majority have uncovered abnormal masking on the part of the schizophrenic subjects: Braff (1989); Braff and Saccuzzo (1985); Butler et al (1996Butler et al ( , 2002, this latter study found abnormalities both under Type-A and Type-B masking, see below); Cadenhead et al (1997); Goghari and Sponheim (2008); Granholm and Verney (2004); Green et al (1994aGreen et al ( , 1994bGreen et al ( , 2003a in the case of target location and target identification with a high energy mask, 2003b); Harvey et al (1990); Keri et al (2000Keri et al ( , 2001; Knight et al (1985); Koelkebeck et al (2005); Rund (1993); Rund et al (1993); Saccuzzo et al (1974Saccuzzo et al ( , 1996; Saccuzzo and Michael (1984); Saccuzzo and Schubert (1981); Schechter et al (2003); Schü tze et al (2007); Slaghuis (2004); Slaghuis and Bakker (1995, mainly in the case of the subjects with negative-symptom schizophrenia); Slaghuis and Curran (1999); Suslow and Arolt (1997); Weiner et al (1990);and Wynn et al (2005) all found some degree of abnormal masking on the part of the schizophrenic subjects in the case of Type-A masking. Luber et al (2007) divided their schizophrenic subjects into ''good performers'' and ''unresponsive subjects'', and reported substantially abnormal masking in the latter group. Also, Braff (1981) identified deficits in schizophrenic individuals relative to depressed subjects, Braff and Saccuzzo (1981) detected abnormal masking in paranoid schizophrenic patients relative to depressed patients, …”

Section: Type-amentioning

confidence: 98%

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Are masking abnormalities in schizophrenia specific to type-B masking?

Skottun¹,

Skoyles

2009

The World Journal of Biological Psychiatry

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The abnormal visual masking in those with schizophrenia, it has been proposed, arises from a deficiency in their magnocellular system. Two kinds of masking exist: Type-A and Type-B. Type-A masking is characterized by the masking being strongest when target and mask are presented simultaneously. Type-B masking is characterized by a non-monotonic masking curve, i.e. the masking is largest when the mask is presented at some time after the target. The proposed link between masking and magnocellular activity applies mainly to Type-B masking. Thus, a magnocellular deficiency, if it exists, should effect Type-B masking more prominently than Type-A masking. Here we review the relevant literature. The majority of studies of masking in those with schizophrenia, it is found, have examined only Type-A masking. These find substantial evidence for abnormal masking. Where Type-B masking has been obtained, evidence also exists for abnormalities. However, the abnormal masking in these cases is largely unrelated to the defining characteristic of Type-B masking (i.e. to the non-monotonic masking function). It is concluded that the evidence for linking masking abnormalities in schizophrenia specifically to Type-B masking is weak. This undermines the proposal that masking abnormalities in schizophrenia have a magnocellular origin.

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Revisiting the Backward Masking Deficit in Schizophrenia: Individual Differences in Performance and Modeling With Transcranial Magnetic Stimulation

Cited by 17 publications

References 42 publications

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Fragile Early Visual Percepts Mark Genetic Liability Specific to Schizophrenia

Direct injection of noise to the visual cortex decreases accuracy but increases decision confidence

Are masking abnormalities in schizophrenia specific to type-B masking?

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