Neural basis of the visual working memory deficit in schizophrenia: Merging evidence from fMRI and EEG

Although people with schizophrenia (PSZ) exhibit robust and reliable deficits in working memory (WM) capacity, the neural processes that give rise to this impairment remain poorly understood. One reason for this lack of clarity is that most studies employ a single neural recording modality-each with strengths and weaknesses-with few examples of integrating results across modalities. To address this gap, we conducted a secondary analysis that combined data from an overlapping set of subjects in previously published electroencephalographic and functional magnetic resonance imaging studies that used nearly identical working memory tasks (visual change detection). The prior studies found similar patterns of results for both posterior parietal BOLD activation and suppression of the alpha frequency band within the EEG. Specifically, both signals exhibited abnormally shallow modulation as a function of the amount of information being stored in WM in PSZ. In the present study, both alpha suppression and posterior parietal BOLD activity increased as the number of items stored in WM increased. The magnitude of alpha suppression modulation was correlated with the magnitude of BOLD signal modulation in PSZ, but not in HCS. This finding suggests that the same illness-related biological processes constrain both alpha suppression and BOLD signal modulation as a function of WM storage in PSZ. The complementary strengths of these two techniques may thus combine to advance the identification of the processes underlying WM deficits in PSZ.

Automated summary

Research has found that individuals with schizophrenia exhibit shallow modulation patterns in working memory tasks, with both alpha suppression and posterior parietal BOLD activity increasing as the number of items stored in working memory increases. In individuals with schizophrenia, the magnitude of alpha suppression modulation is correlated with the magnitude of BOLD signal modulation.