Physical violence is a frequent occurrence in acute community psychiatry units worldwide. Violent acts by patients cause many direct injuries and significantly degrade quality of care. The most accurate tools for predicting near-term violence on acute units rely on current clinical features rather than demographic risk factors. The efficacy of risk assessment strategies to lower incidence of violence on acute units is unknown. A range of behavioral and psychopharmacologic treatments have been shown to reduce violence among psychiatric inpatients.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder that has a strong genetic basis, and is heterogeneous in its etiopathogenesis and clinical presentation. Neuroimaging studies, in concert with neuropathological and clinical research, have been instrumental in delineating trajectories of development in children with ASD. Structural neuroimaging has revealed ASD to be a disorder with general and regional brain enlargement, especially in the frontotemporal cortices, while functional neuroimaging studies have highlighted diminished connectivity, especially between frontal-posterior regions. The diverse and specific neuroimaging findings may represent potential neuroendophenotypes, and may offer opportunities to further understand the etiopathogenesis of ASD, predict treatment response, and lead to the development of new therapies.

The relationship between mental illness, violence, and criminal behavior is complex, and involves a multifaceted interaction of biological, psychological, and social processes. In this article, we review the emerging research that examines the neurobiological and psychological factors that distinguish between persons with mental illness who do and who do not engage in crime and violence. Additionally, a novel model for understanding the interaction between mental illness and criminalness is proposed. (As defined by Morgan and colleagues, criminalness is defined as behavior that breaks laws and social conventions and/or violates the rights and wellbeing of others.) Stemming from this model and outlined research, we argue that management and treatment approaches should target the co-occurring domains of mental illness and criminalness to improve criminal and psychiatric outcomes. Specifically, we discuss and propose effective housing (management) and biopsychosocial intervention strategies for improving outcomes.

Adolescence is characterized by heightened risk-taking, including substance misuse. These behavioral patterns are influenced by ontogenic changes in neurotransmitter systems, particularly the dopamine system, which is fundamentally involved in the neural coding of reward and motivated approach behavior. During adolescence, this system evidences a peak in activity. At the same time, the dopamine (DA) system is neuroplastically altered by substance abuse, impacting subsequent function. Here, we describe properties of the dopamine system that change with typical adolescent development and that are altered with substance abuse. Much of this work has been gleaned from animal models due to limitations in measuring dopamine in pediatric samples. Structural and functional neuroimaging techniques have been used to examine structures that are heavily DA-innervated; they measure morphological and functional changes with age and with drug exposure. Presenting marijuana abuse as an exemplar, we consider recent findings that support an adolescent peak in DA-driven reward-seeking behavior and related deviations in motivational systems that are associated with marijuana abuse/dependence. Clinicians are advised that (1) chronic adolescent marijuana use may lead to deficiencies in incentive motivation, (2) that this state is due to marijuana’s interactions with the developing DA system, and (3) that treatment strategies should be directed to remediating resultant deficiencies in goal-directed activity.

Childhood-onset schizophrenia is a rare pediatric onset psychiatric disorder continuous with and typically more severe than its adult counterpart. Neuroimaging research conducted on this population has revealed similarly severe neural abnormalities. When taken as a whole, neuroimaging research in this population shows generally decreased cortical gray matter coupled with white matter connectivity abnormalities, suggesting an anatomical basis for deficits in executive function. Subcortical abnormalities are pronounced in limbic structures, where volumetric deficits are likely related to social skill deficits, and cerebellar deficits that have been correlated to cognitive abnormalities. Structures relevant to motor processing also show a significant alteration, with volumetric increase in basal ganglia structures likely due to antipsychotic administration. Neuroimaging of this disorder shows an important clinical image of exaggerated cortical loss, altered white matter connectivity, and differences in structural development of subcortical areas during the course of development and provides important background to the disease state.

Criminal conduct is not always violent, and violence does not always lead to criminal charges. Moreover, crime and violence have multifaceted etiologies. Most violence in society is not attributable to mental illness. Where there is a small relationship between violence and mental illness, the risk of violence increases for individuals with substance use histories. Underlying trauma can also play a role. Antisocial attitudes, behaviors, and peer groups further increase the risk that individuals, including those with mental illness, will find themselves at risk of criminal recidivism. Criminal histories among public mental health populations, and mental health and substance use disorders among criminal populations are each higher than general population comparisons. Care within behavioral health settings should therefore target decreased criminal recidivism and decreased violence as part of recovery for those individuals at risk, using trauma-informed approaches and peer supports. Interventions that show promise bring criminal justice and behavioral health systems together, and include police-based diversion, specialty courts, court-based alternatives to incarceration, and coordinated re-entry programs. This article reviews these options along with specific risk management strategies, such as using risk, needs, and responsivity factors as a means of improving overall outcomes for persons with mental illness, while minimizing their risk of further criminalization and victimization.

Almost no literature addresses treatment planning for the forensic psychiatric patient. In the absence of such guidance, recovery-oriented multifocal treatment planning has been imported into forensic mental health systems from community psychiatric settings, despite the fact that conditions of admission and discharge are vastly different for forensic psychiatry inpatients. We propose that instead of focusing on recovery, forensic treatment planning should prioritize forensic outcomes, such as restoration of trial competence or mitigation of violence risk, as the first steps in a continuum of care that eventually leads to the patient’s ability to resolve forensic issues and return to the community for recovery-oriented care. Here we offer a model for treatment planning in the forensic setting.

Aggression and violence represent a significant public health concern and a clinical challenge for the mental healthcare provider. A great deal has been revealed regarding the neurobiology of violence and aggression, and an integration of this body of knowledge will ultimately serve to advance clinical diagnostics and therapeutic interventions. We will review here the latest findings regarding the neurobiology of aggression and violence. First, we will introduce the construct of aggression, with a focus on issues related to its heterogeneity, as well as the importance of refining the aggression phenotype in order to reduce pathophysiologic variability. Next we will examine the neuroanatomy of aggression and violence, focusing on regional volumes, functional studies, and interregional connectivity. Significant emphasis will be on the amygdala, as well as amygdala–frontal circuitry. Then we will turn our attention to the neurochemistry and molecular genetics of aggression and violence, examining the extensive findings on the serotonergic system, as well as the growing literature on the dopaminergic and vasopressinergic systems. We will also address the contribution of steroid hormones, namely, cortisol and testosterone. Finally, we will summarize these findings with a focus on reconciling inconsistencies and potential clinical implications; and, then we will suggest areas of focus for future directions in the field.