ArticleNeuroImage. Clinical2020
Cortical hyperactivation at low working memory load: A primary processing abnormality in people with schizophrenia?
Article in NeuroImage. Clinical, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Visual suppression deficits as a biomarker of working memory impairment in schizophrenia.Schizophrenia research. Cognition · 2026Review
- ERP Decoding Analysis of Visual Working Memory Processes in Schizophrenia.Alpha psychiatry · 2026Article
- Abnormalities in attention and working memory in schizophrenia: The hyperfocusing hypothesis.Current directions in psychological science · 2025Article
- Medial Prefrontal Cortex Dysfunction Mediates Working Memory Deficits in Patients With Schizophrenia.Biological psychiatry global open science · 2023Article
- Working Memory in People with Schizophrenia.Current topics in behavioral neurosciences · 2023Article
- Inefficient white matter activity in Schizophrenia evoked during intra and inter-hemispheric communication.Translational psychiatry · 2022Article
- Impaired Filtering and Hyperfocusing: Neural Evidence for Distinct Selective Attention Abnormalities in People with Schizophrenia.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
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Authors and funding
6 authors.
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Abstract
A frequent finding when studying substrates of working memory (WM) deficits in people with schizophrenia (PSZ) is task-induced hyperactivation relative to healthy control subjects (HCS) when WM load is low. Hyperactivation accompanying similar performance is commonly attributed to cognitive deficits rendering relatively easy operations more resource-consuming. To test if hyperactivation at low load really is secondary to cognitive impairment in PSZ, we re-analyzed functional MRI data showing left posterior parietal cortex (PPC) hyperactivation in PSZ when holding a single color-item in WM. In subgroups matched for the number of items successfully stored in WM (K) by excluding the highest-performing HCS and lowest-performing PSZ, performance was almost identical across all set sizes (1-7). While BOLD activation at the larger set sizes did not differ between groups, PSZ still robustly hyperactivated left PPC when a single item had to be maintained. The same pattern was observed in subgroups matched for model-based estimates of WM capacity or attentional lapse rate. Given that in the K-matched subsamples PSZ performed as well as HCS even in the most challenging load conditions and that no BOLD signal difference was seen at high loads, it is implausible that PSZ over-recruited WM-related neural structures because they were more challenged by maintaining a single item in WM. Instead, the findings are consistent with a primary schizophrenia-related processing abnormality as proposed by the hyperfocusing hypothesis, which suggests that an abnormally narrow but intense focusing of processing resources is central to many aspects of impaired cognition in PSZ.
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