Abstract
Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity. It is unknown whether hallucinations across the psychosis continuum exhibit similar alterations in functional connectivity, suggesting a common neural mechanism, or whether different mechanisms link to hallucinations across phenotypes. We acquired resting-state functional MRI scans of 483 participants, including 40 non-clinical individuals with hallucinations, 99 schizophrenia patients with hallucinations, 74 bipolar-I disorder patients with hallucinations, 42 bipolar-I disorder patients without hallucinations, and 228 healthy controls. The weighted connectivity matrices were compared using network-based statistics. Non-clinical individuals with hallucinations and schizophrenia patients with hallucinations exhibited increased connectivity, mainly among fronto-temporal and fronto-insula/cingulate areas compared to controls (P < 0.001 adjusted). Differential effects were observed for bipolar-I disorder patients with hallucinations versus controls, mainly characterized by decreased connectivity between fronto-temporal and fronto-striatal areas (P = 0.012 adjusted). No connectivity alterations were found between bipolar-I disorder patients without hallucinations and controls. Our results support the notion that hallucinations in non-clinical individuals and schizophrenia patients are related to altered interactions between sensory and higher-order cognitive brain regions. However, a different dysconnectivity pattern was observed for bipolar-I disorder patients with hallucinations, which implies a different neural mechanism across the psychosis continuum.
Highlights
Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity
Patients with bipolar disorder who experience psychotic symptoms may hold a position in between both ends of the spectrum. It remains to be determined if hallucinations in non-clinical individuals, patients with schizophrenia, and patients with bipolar disorder share a common neural mechanism or if hallucinations stem from different neural mechanisms across these three groups
The groups differed in motion parameters (F(4) = 20.3, P < 0.001), with patients with bipolar-I disorder and schizophrenia showing more movement than healthy controls and non-clinical individuals
Summary
Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity. Non-clinical individuals with hallucinations and schizophrenia patients with hallucinations exhibited increased connectivity, mainly among fronto-temporal and fronto-insula/cingulate areas compared to controls (P < 0.001 adjusted). Our results support the notion that hallucinations in non-clinical individuals and schizophrenia patients are related to altered interactions between sensory and higher-order cognitive brain regions. Patients with bipolar disorder who experience psychotic symptoms may hold a position in between both ends of the spectrum It remains to be determined if hallucinations in non-clinical individuals, patients with schizophrenia, and patients with bipolar disorder share a common neural mechanism (and differ mainly in severity) or if hallucinations stem from different neural mechanisms across these three groups. Neuropsychological studies indicate that cognitive control processes, including inhibition and executive functioning, are less altered in bipolar-I patients than in schizophrenia patients and may be used for compensatory strategies[20,21,22]
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