Toward the neural mechanisms of reduced working memory capacity in schizophrenia

Abstract

People with schizophrenia (PSZ) demonstrate reliable reductions in working memory (WM) capacity (i.e., the number of objects that can be held in memory). The present study asked whether WM impairments in PSZ can be explained by the same neural mechanisms that underlie individual differences in WM capacity among healthy individuals. Specifically, we examined event-related potentials in PSZ and healthy matched controls during a change detection task that required the storage of multiple objects in WM. The amplitude of contralateral delay activity (CDA), which correlates with WM capacity in healthy individuals, was larger in controls than in PSZ for memory loads of 3 and 5 objects, but larger in PSZ than in controls for a memory load of 1. This same pattern was found in the subgroups of PSZ and controls with an equivalent WM capacity. Moreover, the increase in CDA amplitude was correlated with individual differences in capacity in controls, but not in PSZ. These results demonstrate that WM impairment in PSZ is not associated with the same patterns of neural activity that characterize low WM capacity in healthy individuals. We propose that WM impairment in PSZ instead reflects a specific impairment in the ability to distribute attention broadly.

Keywords: CDA; event-related potentials; visual short-term memory.

Figure 1.

(A) A no-change trial with memory load 3 in a block in which circles are to be remembered (as indicated by the outline shape at fixation). (B) K-score at each memory load. Group means with error bars representing the standard error are presented and values for individual participants in each group are plotted alongside the group means. Oval indicates those control participants included in the matched-group analysis that contained all PSZ. Box indicates those individuals included in the matched-group analysis that eliminated extreme participants from both groups. (C) Grand-average ERP waveforms time-locked to encoding array onset for HCS and PSZ groups, averaged across memory load. CDA is the differential activity between the contralateral and ipsilateral waveforms (shown filled in gray).

Figure 2.

(A) Grand-average ERP waveforms time-locked to encoding array onset showing the CDA difference waves (computed by subtracting the ipsilateral from the contralateral waveforms seen in Fig. 1C). (B) The mean amplitude of CDA between 400 and 1000 post-stimulus.

Figure 3.

(A) K scores for groups containing all PSZ, with the best performing HCS eliminated. (B) The mean amplitude of CDA between 400 and 1000 post-stimulus for the group in (A). (C) K scores for groups matched by eliminating participants from both groups that had extreme K-scores at memory load 3. (D) The mean amplitude of CDA between 400 and 1000 post-stimulus for the groups shown in (C).

Figure 4.

A scatter plot showing each participant's K score at memory load 3 against the increase in CDA amplitude between memory loads 1 and 3 for the HCS and PSZ groups.

Figure 5.

A scatter plot showing each participant's K score between memory loads 3 and 5 against the CDA amplitude at memory load 1.