Here/In This Issue and There/Abstract Thinking: Neurosciences and (Child) Psychiatry

Abstract

This issue of the Journal features 3 neuroimaging studies aimed at advancing our understanding of the neurobiological bases of common psychiatric disorders. The first article focuses on the neurodevelopmental underpinnings of schizophrenia and bipolar disorder. There is evidence that the 2 disorders are related to neurodevelopmental abnormalities. However, the timing and impact of such neurodevelopmental alterations might differ in the 2 disorders. To address this hypothesis, Sugranyes and colleagues (p. 677) conducted the first magnetic resonance imaging study comparing gray matter volume in 38 offspring of patients with schizophrenia (SzO), 77 offspring of patients with bipolar disorder (BdO), and 83 offspring of community controls (CcO) who were 6 to 17 years old. As evaluated by clinicians blinded to parental status, none of the SzO or BdO offspring presented with psychosis, bipolar disorder, or prodromal syndrome, although some of them presented with other Axis I disorders. CcO offspring were excluded if they had a personal or first-degree family history of schizophrenia or bipolar spectrum disorders. The investigators found that total cerebral gray volume was significantly reduced in SzO compared with CcO offspring. Compared with BdO and CcO offspring, SzO offspring presented with significantly reduced volume in the left inferior frontal cortex/anterior insula. There were no significant brain volume differences between BdO and CcO offspring. These findings suggest that the neurodevelopmental correlates of premorbid schizophrenia and bipolar disorder are likely to differ. SzO offspring would be characterized by more evident and earlier neurodevelopmental alterations related to genetic and early environmental influences. In contrast, gray matter alterations in BdO offspring might emerge at a later stage. The second study, by Schweren and colleagues (p. 660), was carried out to gain insight into the neurobiology of attention-deficit/hyperactivity disorder (ADHD), in particular, its brain structural correlates. Importantly, the study also addressed the effect of psychostimulants on the brains of children with ADHD, which is not yet fully understood. The investigators compared measurements of brain cortical thickness in 308 youths with ADHD and 184 controls (8–28 years old) from the European NeuroIMAGE sample. Eighty-eight percent of participants with ADHD had received psychostimulants at some point in their lives, on average for approximately 5 years. Of note, the investigators obtained detailed information on type, dose, and duration of treatment with psychostimulants for each participant. They found that, compared with controls, youths with ADHD had significantly decreased cortical thickness in the medial temporal cortex, bilaterally, which persisted even after controlling for psychiatric comorbidities and regardless of the age of the participants. Of note, there were no significant differences in cortical thickness between psychostimulant-treated and psychostimulant-naive participants with ADHD. In addition, neither treatment duration nor mean dose was related to cortical thickness. These findings are in line with recent evidence showing that networks other than the frontostriatal one, classically believed to underpin ADHD, are relevant in the pathophysiology of the disorder. This study does not support previous evidence of brain structural normalization after treatment with psychostimulants. It is worthy of note that, although medication effects would ideally be tested in a long-term controlled trial in which participants are randomly assigned to psychostimulant treatment or placebo, this is clearly unethical. The third study, by Bos and colleagues (p. 668), combined the assessment of 2 different brain features estimated by structural neuroimaging, namely cortical gyrification and white matter structure, to advance our knowledge of the brain structural correlates of autism spectrum disorder (ASD). The study tested the hypothesis that decreased cortical gyrification is related to altered white matter connectivity in a sample of 30 children with ASD and 29 typically developing controls 8 to 18 years of age. Compared with controls, participants with ASD showed a decrease in the gyrification index in the left prefrontal and parietal cortex. Importantly, a similar result was found in the analysis of an independent, free, and publicly released large neuroimaging dataset on ASD, the Autism Brain Imaging Data Exchange (ABIDE). This is a crucial result that is particularly relevant in light of inconsistent findings that characterized the early wave of neuroimaging studies in (child) psychiatry. The use of the ABIDE dataset to replicate study findings highlights the value, for the scientific community, of free data sharing as a way to overcome the challenge of recruiting large samples in neuroimaging research. Consistent with their hypothesis, the investigators also found that radial diffusivity (a diffusion tensor imaging parameter that allows estimation of structural connectivity) in the forceps minor was inversely related to prefrontal gyrification in children with ASD. Overall, this study suggests that, in addition to abnormal brain size, altered gyrification and structural connectivity might be relevant neurobiological correlates of ASD.