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Background Violence in psychosis has been linked to antisocial behavior and psychopathy traits. Psychopathy comprises aspects of interpersonal, affective, lifestyle, and antisocial traits which may be differently involved in violent offending by persons with psychotic disorders. We explored psychopathy subdomains among violent offenders with and without a psychotic disorder. Methods 46 males, with a history of severe violence, with (n = 26; age 35.85 ± 10.34 years) or without (n = 20; age 39.10 ± 11.63 years) a diagnosis of a psychotic disorder, were assessed with the Psychopathy Checklist-Revised (PCL-R). PCL-R was split into subdomains following the four-facet model. Group differences in total and subdomain scores were analyzed with a general linear model with covariates. Results Total PCL-R scores did not differ between the groups (p = 0.61, Cohen’s d = 0.17). The violent offenders without psychotic disorders had higher facet 2 scores than the patient group with psychotic disorders (p = 0.029, Cohen’s d = 0.77). Facet 1, 3, or 4 scores did not differ between the groups. Controlling for age did not alter the results. Conclusion Patients with a psychotic disorder and a history of severe violence have lower affective psychopathy scores than violent offenders without psychotic disorders. This observation may point toward distinct underlying mechanisms for violence and may provide a target for focused treatment and prevention.

This paper clarifies the conceptual space of discussion of legal insanity by considering the virtues of the ‘medical model’ model that has been used in Norway for almost a century. The medical model identifies insanity exclusively with mental disorder, and especially with psychosis, without any requirement that the disorder causally influenced the commission of the crime. We explore the medical model from a transdisciplinary perspective and show how it can be utilised to systematise and reconsider the central philosophical, legal and medical premises involved in the insanity debate. A key concern is how recent transdiagnostic and dimensional approaches to psychosis can illuminate the law's understanding of insanity and its relation to mental disorder. The authors eventually raise the question whether the medical model can be reconstructed into a unified insanity model that is valid across the related disciplinary perspectives, and that moves beyond current insanity models. publishedVersion

Magnetic resonance imaging (MRI) studies have shown the brains of schizophrenia patients to have smaller hippocampi, larger ventricles, and reduced cortical thickness and regional brain volumes, as compared to the brains of mentally healthy subjects. The abnormal brain morphology may reflect subtle deviances from normal brain development. Early adverse somatic events, in the current thesis studied in the form of obstetric complications (OCs), in the pre-, peri-, or postnatal periods can cause or influence a deviant neurodevelopment. In scientific studies, it has been demonstrated that occurrence of OCs increase the risk of schizophrenia. Moreover, results from experimental animal studies demonstrate that different OCs cause both abnormal changes in brain morphology and behaviour that parallel what is observed in schizophrenia. In humans, OCs have been related to smaller hippocampi, larger lateral ventricles, and reduced cortical volume in schizophrenia patients with as compared to patients without a history of OCs. Taken together, these findings suggest that early somatic trauma such as OCs may exert an influence on neurodevelopment, detectable in the brain decades later. The main aim of this PhD thesis was to investigate the relationship between a history of (OCs) and brain morphology in patients with schizophrenia. The subaims were to study 1) if such a putative effect could explain some of the differences in brain morphology observed between schizophrenia patients and healthy controls, and 2) if the effect of OCs on hippocampal volume, if demonstrated, is modified by genetic variation (allele variation in single nucleotide polymorphisms). The subject sample included in the current four studies comprises 54 schizophrenia patients and 54 healthy control subjects. They all underwent clinical examination, genotyping, and MRI scanning at the Karolinska Institutet and Karolinska University Hospital in Stockholm, Sweden. Automated software tools were used to obtain measures of basal ganglia nuclei and hippocampal volumes, cortical thickness, and cortical folding patterns. Information on OCs was independently collected from original birth records. The main findings were that OCs are not associated with basal ganglia volumes (study I) or cortical thickness (study II), but significantly associated with reduced cortical folding in the left pars triangularis (Broca’s area) (study III) and with altered hippocampal volumes (study IV). The effect of OCs on hippocampal volume appeared to be modulated by allele variation in the hypoxia-regulated GRM3 gene (study IV). Furthermore, schizophrenia patients did not differ from healthy control subjects with respect to the rate or severity of OCs per se; the effects of OCs on basal ganglia volumes, cortical thickness, and cortical gyrification; or the gene*OCs interaction effect on hippocampal volume. In conclusion, while some brain structures (cortical thickness, basal ganglia volumes) were unaffected by a history OCs, OCs influenced other aspects of brain morphology (hippocampal volume, cortical folding) in the same way in both patients with schizophrenia and healthy controls. The differences in brain morphology found between schizophrenia patients and healthy controls were not effects of OCs. Genetic variation may modulate the effect of OCs on hippocampal volume.