Cortical thickness in individuals with non-clinical and clinical psychotic symptoms

Abstract

Symptoms that are linked to psychosis are also experienced by individuals who are not in need of care. In the present study, cortical thickness was investigated in these individuals. Fifty individuals with non-clinical auditory verbal hallucinations (most of them also experienced other non-clinical psychotic symptoms), 50 patients with a psychotic disorder and auditory verbal hallucinations, and 50 healthy control subjects underwent structural magnetic resonance imaging. Data were analysed using FreeSurfer. Cortical thickness in the pars orbitalis, paracentral lobule, fusiform gyrus and inferior temporal gyrus was lowest in patients, intermediate in the non-clinical hallucinating group, and highest in control subjects. The patients also showed thinning in widespread additional areas compared to the two other groups, whereas both hallucinating groups showed similar levels of thinning in the insula. Ranking the levels of cortical thickness per brain region across groups revealed that for 88% of brain regions, cortical thickness was lowest in patients, intermediate in the non-clinical hallucinating group, and highest in controls. These findings show that individuals with non-clinical psychotic symptoms show a similar but less pronounced pattern of cortical thinning as patients with a psychotic disorder, which is suggestive of a similar, but milder underlying pathophysiology in this group compared to the psychosis group.

Partitioning heritability analysis reveals a shared genetic basis of brain anatomy and schizophrenia

“…Neuroimaging studies have reported widespread brain anatomical changes as potential pathogenic features of the disorder(2). Such brain alterations have been linked to various clinical symptoms, encompassing cognitive impairment(3), auditory hallucinations(4–7), and social dysfunction(8). Nevertheless, a major question remains unanswered: which of the structural changes reflect a shared genetic basis with disease etiology – and thus are potential endophenotypes(9), or arise secondary to disease progression or treatment-related mechanisms(10).…”

Early visual processing deficits in patients with schizophrenia during spatial frequency-dependent facial affect processing

“…Therefore, decreased activation of the medial frontal gyrus in the LSF fear condition explains the secondary effect of magnocellular pathway deficiencies affecting the perception of fear emotion. In addition, since studies repeatedly reported reduced gray matter volume (Borgwardt et al, 2010;Hirjak et al, 2014;van Lutterveld et al, 2014) and reduced functional connectivity (Liu et al, 2011) related to paracentral lobule in schizophrenia patients, this area could be an important anatomical region that might reflect a deficit of early visual processing in SPR.…”

Paracingulate sulcus morphology and hallucinations in clinical and non-clinical groups

“…The recruitment procedure for healthy control and non-clinical participants with AVHs has been described previously (e.g. 24,25 Importantly, hallucinating subjects were free of delusions, disorganization, and negative symptoms. Anxiety or depressive disorder in full remission were not considered exclusion criteria.…”