Interocular transfer of movement after‐effects in schizophrenia

Tress, Kathleen H.; Kugler, Barbara T.

doi:10.1111/j.2044-8295.1979.tb01708.x

Cited by 7 publications

(6 citation statements)

References 2 publications

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“…Few studies have manipulated these parameters within a single experiment; however, differences in parameter values may explain discrepancies across studies. Of those studies comparing the duration of movement aftereffects between schizophrenia and healthy controls, two studies reported longer aftereffect durations in schizophrenia (Abraham and McCallum, 1973;Claridge, 1960), five studies reported null findings (Herrington and Claridge, 1965;Hersen et al, 1972;Krishnamoorti and Shagass, 1963;Schein, 1960;Tress and Kugler, 1979), and no studies observed longer durations in controls. With the aforementioned caveat regarding null findings in mind, it is nevertheless interesting that those studies reporting greater duration of the movement aftereffect in patients used relatively long adapter durations (1 minute), whereas those that reported null results used shorter adapter durations (15-30 seconds).…”

Section: Critical Review Of Findings In Schizophreniamentioning

confidence: 99%

A review of visual aftereffects in schizophrenia

Thakkar

Silverstein

Brascamp

2019

Neuroscience & Biobehavioral Reviews

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Psychosis-a cardinal symptom of schizophrenia-has been associated with a failure to appropriately create or use stored regularities about past states of the world to guide the interpretation of incoming information, which leads to abnormal perceptions and beliefs. The visual system provides a test bed for investigating the role of prior experience and prediction, as accumulated knowledge of the world informs our current perception. More specifically, the strength of visual aftereffects, illusory percepts that arise after prolonged viewing of a visual stimulus, can serve as a valuable measure of the influence of prior experience on current visual processing. In this paper, we review findings from a largely older body of work on visual aftereffects in schizophrenia, attempt to reconcile discrepant findings, highlight the role of antipsychotic medication, consider mechanistic interpretations for behavioral effects, and propose directions for future research.

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Section: Critical Review Of Findings In Schizophreniamentioning

confidence: 99%

A review of visual aftereffects in schizophrenia

Thakkar

Silverstein

Brascamp

2019

Neuroscience & Biobehavioral Reviews

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“…A handful of early studies measuring the duration or strength of these aftereffects in patients with schizophrenia (reviewed in Harris, 1994), have yielded conflicting findings. These include slower aftereffect build-up (Abraham and McCallum, 1973;Claridge, 1960;Herrington and Claridge, 1965), no difference in aftereffect duration (Tress and Kugler, 1979), and reduced aftereffect strength (Kelm, 1962(Kelm, , 1968Wertheimer, 1954;Wertheimer and Jackson, 1957). Discrepant findings across studies have been attributed to a combination of medication use, as antipsychotics reduce visual aftereffect duration in healthy individuals (Harris et al, 1986;Harris et al, 1983), clinical status, and mode of measuring aftereffects (Harris, 1994).…”

Section: Introductionmentioning

confidence: 99%

Altered short-term neural plasticity related to schizotypal traits: Evidence from visual adaptation

Thakkar

Antinori

Carter

et al. 2019

Schizophrenia Research

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Abnormalities in synaptic plasticity are argued to underlie the neural dysconnectivity observed in schizophrenia. One way to measure synaptic plasticity is through sensory adaptation, whereby sensory neurons exhibit reduced sensitivity after sustained stimulus exposure. Evidence for decreased adaptation in individuals with schizophrenia is currently inconclusive, possibly due to heterogeneity in clinical and medication status across samples. Here we circumvent these confounds by examining whether altered adaptation is represented sub-clinically in the general population. To test this we used three paradigms from visual perception research that provide a precise and non-invasive index of adaptation in the visual system. Two paradigms involve a class of illusory percepts termed visual aftereffects. The third relies on a visual phenomenon termed binocular rivalry, where incompatible stimuli are presented to the two eyes and observers alternate between perceiving exclusively one stimulus or a combination of the two (i.e. mixed perception). We analyzed the strength and dynamics of visual adaptation in these paradigms, in relation to schizotypy. Our results showed that increased schizotypal traits were related to reduced orientation, but not luminance, aftereffect strength (Exp. 1). Further, increased schizotypy was related to a greater proportion of mixed perception during binocular rivalry (Exp. 1 and 2). Given that visual adaption is well understood at cellular and computational levels, our data suggest that short-term plasticity in the visual system can provide important information about the disease mechanisms of schizophrenia.

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“…As noted earlier, Gulman et al (1982) found that SEP transmission time was decreased from left to right hemisphere, suggesting directional loss of inhibition. Similarly, Tress et al (1979) found a large discrepancy between left ipsilateral and contralateral SEPs present in normal subjects, but not in schizophrenics. Both of these findings are consistent with the relative increase in right-to-left-hand transfer errors in the schizophrenic subjects of the present study.…”

Section: Discussionmentioning

confidence: 75%

“…The basic procedure for this test has been described in Tress and Kugler (1979). The stimulus disc was 24 in.…”

Section: Methodsmentioning

confidence: 99%

“…Although the neural substrate for the aftereffect has not been demonstrated conclusively, it is now believed that transfer depends on communication between the two visual association cortices, so the absence of callosal connections between these areas may account for the lack of transfer (Dixon & Jeeves, 1970). Tress and Kugler (1979) examined this phenomenon in 16 chronic schizophrenics and found greater transfer compared with normal controls, implying callosal dysfunction in the form of lack of inhibition. Although these results are theoretically provocative, the failure to include a psychiatric control group makes interpretation of the data difficult.…”

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confidence: 99%

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Callosal dysfunction in schizophrenia and schizo-affective disorder.

Craft¹,

Willerman²,

Bigler³

1987

Journal of Abnormal Psychology

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at Austin and the Austin Neurological Clinic Studies of corpus callosum dysfunction in schizophrenia have typically relied on measures that reveal impairment in commissurotomy patients, but measures that distinguish people with callosal agenesis may be more appropriate. Four of these indexes were included in the present study. Tests of associated movements, cross-localization of touch, interocular transfer of spiral aftereffect, and transfer of blind formboard learning were administered to 18 chronic schizophrenics, 19 schizoaffectives, and 20 normal volunteers. Both schizophrenics and schizo-affectives were impaired on all measures except transfer of blind formboard learning. Schizophrenics also made significantly more associated movements than schizo-affectives and exhibited a different pattern of cross-localization deficit. These results support the hypothesis of developmental callosal dysfunction in schizophrenia and schizo-affective disorder, although the nature of this dysfunction differs in part from that exhibited by acallosals.Several studies have indicated that two related functions of the corpus callosum, conduction and inhibition of nerve impulses, may be disrupted in schizophrenics. Tress, Kugler, and Caudrey (1979) and Jones and Miller (1981) compared contralateral and ipsilateral somatosensory-evoked potentials (SEPs) in schizophrenics and in normal people (normals). Normals' SEPs from the ipsilateral cortex were delayed relative to their contralateral responses. Jones and Miller attributed this delay to the predominance of contralateral pathways in the normal brain, which cause ipsilateral potentials to be produced by crossing over the callosum and then back to the original hemisphere. Because only one crossing is required for contralateral SEPs, they show a reduced latency relative to ipsilateral responses in normals. In contrast to the normal pattern, both of the aforementioned studies found that schizophrenics' ipsilateral and contralateral SEP latencies were identical, implying that ipsilateral responses were being produced by ipsilateral pathways. Absence of an ipsilateral latency delay may thus be secondary to impaired callosal conduction in the schizophrenic subjects, which in turn may be related to failure of ipsilateral pathway inhibition.Gulman, Wildschiodtz, and Orbaek (1982) also found a significantly reduced latency delay between contralateral and ipsi-This study was completed in partial fulfillment of the requirements for Suzanne Craft's doctoral degree from the University of Texas at Austin.

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Interocular transfer of movement after‐effects in schizophrenia

Cited by 7 publications

References 2 publications

A review of visual aftereffects in schizophrenia

A review of visual aftereffects in schizophrenia

Altered short-term neural plasticity related to schizotypal traits: Evidence from visual adaptation

Callosal dysfunction in schizophrenia and schizo-affective disorder.

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