On neuroimaging correlates of aggression in psychoses

Introduction. Aggressive behaviour in persons with a psychotic disorder is clinically highly relevant because of its impact on patients' families, society and caregivers - also, it increases stigmatization of psychiatric patients in general. The neurobiological processes triggering aggression in psychoses are little known. A comprehension of these underlying mechanisms could enhance the predictability and prevention of violent acts and permit a specialized and more individualized patient treatment - also, this could drastically reduce stigmatization. Here, we investigated the neurobiological underpinnings of aggression in psychoses by means of magnetic resonance imaging.
Methods. We performed two systematic reviews examining results on structural and functional magnetic resonance imaging correlates of aggression in persons with psychoses in order to synthesize the current knowledge in this field. Also, we calculated an effect size analysis on structural correlates of aggression in psychoses. Then, we conducted a voxel-based morphometry (VBM) study investigating correlates of an agitated-aggressive syndrome in early psychoses.
Results. We systematically reviewed twelve studies on structural magnetic resonance imaging correlates of aggression in psychoses including a total of 314 patients and 96 healthy control participants (HC). Qualitative analyses showed lower volumes of whole brain (WB), prefrontal regions, temporal lobe, hippocampus, thalamus, and cerebellum, and larger volumes of the lateral ventricles, amygdala and putamen in violent (VS) as opposed to non-violent schizophrenia persons (NVS). In the quantitative effect size analyses, violent persons with schizophrenia exhibited a significantly lower WB volume than HC (p = 0.004) and than non-violent persons with schizophrenia (p = 0.007).
Our systematic review on functional magnetic resonance imaging correlates of aggression in psychoses included twelve studies with 236 patients and 92 HC. During the n-back tasks, VS as opposed to NVS hypoactivated their inferior parietal lobe. When anticipating shock, VS versus NVS hyperactivated their medial prefrontal gyrus, cuneus, middle temporal gyrus and middle occipital gyrus. When viewing negative emotional pictures, VS versus NVS hyperactivated the middle frontal gyrus, inferior frontal gyrus, anterior cingulate, lingual gyrus, precentral gyrus, globus pallidus, mid-cingulate, and precuneus.
In our study examining VBM correlates in early psychoses we found reduced lingual gyrus volumes in persons with early psychoses with an agitated-aggressive syndrome as opposed to HC.
Conclusion. We found nonsystematic structural and functional correlates of aggression in psychoses. In total, only very little studies on the neurobiological underpinnings of aggression in psychoses have been conducted. There have been no attempts to replicate any of the observed findings in the published literature. Focusing on future directions, we recommend that authors adhere to clear definitions of aggression, measurements of psychopathology, comorbidities and medication. In particular, replication studies would allow for a better synthesis of the findings. Furthermore, there are no studies on affective psychoses or early psychoses. Our pilot study on VBM correlates of aggression in early psychoses provides a first hint towards the hypothesis that the lingual gyrus volume may be inversely correlated with an agitated-aggressive syndrome in early stages of psychoses.