Abstract
BackgroundSchizophrenia shares some genetic risk and clinical symptoms with bipolar disorder. Clinical heterogeneity across subjects is thought to contribute to variable structural imaging findings across studies. The current study investigates cortical thickness in young adults diagnosed with schizophrenia or bipolar I disorder with a history of hyperthymic mania. We hypothesize that cortical thickness will be most similar between SCZ and the psychotic bipolar 1 disorder subtype.MethodsPatients with schizophrenia (n = 52), psychotic bipolar I disorder (PBD; n = 49) and non-psychotic bipolar I disorder (NPBD; n = 24) and healthy controls (n = 40) were scanned in a 3T Trio MRI. The thickness of 34 cortical regions was estimated with FreeSurfer, and analyzed using univariate analyses of variance. Relationships to psychotic (SAPS) and negative (SANS) symptoms were investigated using linear regression.ResultsCortical thickness showed significant group effects, after covarying for sex, age, and intracranial volume (p = 0.001). SCZ subjects had thinner paracentral, inferior parietal, supramarginal and fusiform cortices compared to CON. Caudal anterior cingulate cortical thickness was increased in SCZ, PBD and NPBD. Cortical thickness in PBD and NPBD were not significantly different from controls. Significant partial correlations were observed for SAPS severity with middle temporal (r = − 0.26; p = 0.001) and fusiform (− 0.26; p = 0.001) cortical thickness.ConclusionsIndividuals with SCZ displayed significantly reduced cortical thickness in several cortical regions compared to both CON and bipolar. We found that SCZ participants had significant cortical thinning relative to CON and bipolar disorder most significantly in the frontal (i.e. paracentral), parietal (i.e. inferior parietal, supramarginal), and temporal (i.e. middle temporal, fusiform) cortices.
Highlights
Schizophrenia shares some genetic risk and clinical symptoms with bipolar disorder
Clinical measures Based on multivariate testing, there was a significant main effect of diagnosis (F(6,310) = 20.530, Wilk’s Λ = 0.512, p < 0.001, η2 = 0.284) after controlling for age and sex, indicating a difference in Scale for the Assessment of Positive Symptoms (SAPS) and Scale for the Assessment of Negative Symptoms (SANS) scores between groups
Differences in scores were driven by higher ratings in the SCZ and psychotic bipolar I disorder (PBD) groups relative to controls (CON) in the SAPS data, and SCZ relative to all other groups in the SANS scores (Table 1; Fig. 1)
Summary
Schizophrenia shares some genetic risk and clinical symptoms with bipolar disorder. Clinical heterogeneity across subjects is thought to contribute to variable structural imaging findings across studies. The cortical structure of the brain is commonly quantitatively measured via gray matter volume, a measurement that is dependent on both cortical thickness and surface area of a region. These structural measures are thought to be Godwin et al Int J Bipolar Disord (2018) 6:16 heritable (Panizzon et al 2009) and can provide insight into the genetic differences between patient populations. To the extent abnormal function in cortical and subcortical networks, which are thought to be perturbed in both diseases (Uhlhaas 2013; Hulshoff Pol et al 2012; Menon 2011), can be explained by abnormality of structure, the region-specific nature of cortical thinning could provide insight into differential developmental trajectories of brain disorders (Fischl et al 1999; Fischl and Dale 2000)
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