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Comparative Study
. 2011 Sep;37(5):950-7.
doi: 10.1093/schbul/sbp164. Epub 2010 Jan 6.

Iconic decay in schizophrenia

Affiliations
Comparative Study

Iconic decay in schizophrenia

Britta Hahn et al. Schizophr Bull. 2011 Sep.

Abstract

Working memory impairment is considered a core deficit in schizophrenia, but the precise nature of this deficit has not been determined. Multiple lines of evidence implicate deficits at the encoding stage. During encoding, information is held in a precategorical sensory store termed iconic memory, a literal image of the stimulus with high capacity but rapid decay. Pathologically increased iconic decay could reduce the number of items that can be transferred into working memory before the information is lost and could thus contribute to the working memory deficit seen in the illness. The current study used a partial report procedure to test the hypothesis that patients with schizophrenia (n = 37) display faster iconic memory decay than matched healthy control participants (n = 28). Six letters, arranged in a circle, were presented for 50 ms. Following a variable delay of 0-1000 ms, a central arrow cue indicated the item to be reported. In both patients and control subjects, recall accuracy decreased with increasing cue delay, reflecting decay of the iconic representation of the stimulus array. Patients displayed impaired memory performance across all cue delays, consistent with an impairment in working memory, but the rate of iconic memory decay did not differ between patients and controls. This provides clear evidence against faster loss of iconic memory representations in schizophrenia, ruling out iconic decay as an underlying source of the working memory impairment in this population. Thus, iconic decay rate can be added to a growing list of unimpaired cognitive building blocks in schizophrenia.

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Figures

Fig. 1.
Fig. 1.
Sequence of Events in the Partial Report Procedure Employed to Estimate Iconic Decay Rates. Participants verbally reported the letter that was cued by the central arrow. SOA = stimulus onset asynchrony.
Fig. 2.
Fig. 2.
Mean Memory Performance, Reflected by Discrimination Index d′, in Patients With Schizophrenia (SZ, n = 37) and Matched Healthy Control Subjects (HC, n = 28) Across a Range of Delay Periods Between Target Array Onset and Cue Onset (Stimulus Onset Asynchrony, SOA). Error bars reflect 95% confidence intervals, adjusted to remove within-group between-subject variability in average d′ scores across SOAs.
Fig. 3.
Fig. 3.
Mean Time Constant Estimates (± SEM) and Overall d′ Scores, Averaged Across Delay Intervals, for Patients With Schizophrenia (SZ) and Healthy Control Subjects (HC).

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