Chronic tinnitus has been associated with brain structural changes in both the auditory system as well as limbic system. While there is considerable inconsistency across brain structural findings, growing evidence suggests that distress and other non-auditory symptoms modulate effects. In this study we addressed this issue, testing the hypothesis that limbic changes in tinnitus relate to both disease-related distress as well as co-morbid psychopathology. We obtained high-resolution structural magnetic resonance imaging (MRI) scans from a total of 125 subjects: 59 patients with bilateral chronic tinnitus (29 with a co-morbid psychiatric condition, 30 without), 40 healthy controls and 26 psychiatric controls with depression/anxiety disorders (without tinnitus). Voxel-based morphometry with the CAT12 software package was used to analyse data. First, we analysed data based on a 2 × 2 factorial design (tinnitus; psychiatric co-morbidity), showing trend-level effects for tinnitus in ROI analyses of the anterior cingulate cortex and superior/transverse temporal gyri, and for voxel-based analysis in the left parahippocampal cortex. Multiple regression analyses showed that the parahippocampal finding was mostly predicted by tinnitus rather than (dimensional) psychopathology ratings. Comparing only low-distress tinnitus patients (independent of co-morbid conditions) with healthy controls also showed reduced left parahippocampal grey matter. Our findings demonstrate that depression and anxiety (not only subjective distress) are major modulators of brain structural effects in tinnitus, calling for a stronger consideration of psychopathology in future neurobiological and clinical studies of tinnitus.

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Human psychopathology is the result of complex and subtle neurobiological alterations. Categorial DSM or ICD diagnoses do not allow a biologically founded and differentiated description of these diverse processes across a spectrum or continuum, emphasising the need for a scientific and clinical paradigm shift towards a dimensional psychiatric nosology. The subclinical part of the spectrum is, however, of special interest for early detection of mental disorders. We review the current evidence of brain structural correlates (grey matter volume, cortical thickness, and gyrification) in non-clinical (psychiatrically healthy) subjects with minor depressive and anxiety symptoms. We identified 16 studies in the depressive spectrum and 20 studies in the anxiety spectrum. These studies show effects associated with subclinical symptoms in the hippocampus, anterior cingulate cortex, and anterior insula similar to major depression and changes in amygdala similar to anxiety disorders. Precuneus and temporal areas as parts of the default mode network were affected specifically in the subclinical studies. We derive several methodical considerations crucial to investigations of brain structural correlates of minor psycho(patho)logical symptoms in healthy participants. And we discuss neurobiological overlaps with findings in patients as well as distinct findings, e.g. in areas involved in the default mode network. These results might lead to more insight into the early pathogenesis of clinical significant depression or anxiety and need to be enhanced by multi-centre and longitudinal studies.

Irritability and nonviolent aggression are common behavioral features across the population, yet there is limited neurobiological research into subclinical phenotypes representing the lower edge of a symptom continuum ranging from slight irritability to criminal violence. We studied brain structural correlates of irritability in a large healthy cohort to test the hypothesis of associations with fronto-limbic brain structures implicated in mood regulation. In a large multicenter effort, we recruited 409 mentally healthy adults from the community, who received T1-weighted high-resolution 3 T MRI scans. These structural scans were automatically preprocessed for voxel- and surface-based morphometry measurements with the CAT 12 toolbox implemented in SPM 12. Subclinical aggressive symptoms were assessed using the SCL-90-R aggression/hostility subscale and then correlated with cortical volume (VBM), and cortical thickness and gyrification. VBM analysis showed significant (P < 0.05, FDR-corrected at peak-level) positive correlations of cortical volume with SCL-90-R aggression subscale values in large clusters spanning bilateral anterior cingulate and orbitofrontal cortices and left lingual and postcentral gyri. Surface-based morphometry yielded mostly uncorrected positive correlations with cortical thickness in bilateral precentral gyri and with gyrification in left insula and superior temporal gyrus. Our findings imply an association of subclinical aggressive symptoms with cortical volume in areas important for emotion awareness and regulation, which might also be related to cortical adaptation to mental stress. These results overlap with several findings on impulsive aggression in patients suffering from affective and disruptive behavior disorders. They also suggest a biological symptom continuum manifesting in these brain areas. Hum Brain Mapp 38:6230-6238, 2017. © 2017 Wiley Periodicals, Inc.

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