Aggression and Violence

Overview

Aggression and violence are complex behaviors that occur both inside and outside of the medical setting. This chapter focuses on the differential diagnosis of aggressive acts as it pertains to the medical and psychiatric setting; an exhaustive review of aggression and violence within society and its larger economic and sociocultural impact is beyond the scope of this chapter. Although workplace violence has a significant impact on the medical and hospital environment, it is not discussed here. Instead, this chapter will focus on understanding the complex biopsychosocial context of each patient who displays aggressive behavior.

This chapter will discuss a systematic approach to the assessment and management of patients with aggressive and violent behaviors. Care of the violent or impulsive patient poses a serious challenge to the psychiatrist, who needs to evaluate rapidly and accurately the cause of aggression while initiating treatment. In the medical setting aggressive behavior can be associated with delirium, dementia, and other medical conditions; hence, ruling out medical causes must precede the conclusion that the behavior is the consequence of psychiatric pathology. The psychiatrist must have a frame of reference to adequately assess the risk of violence, as well as the skills to manage it.

Epidemiology and Risk Factors

There is debate as to whether individuals with mental illness are at greater risk for violence than are those in the general population. Current data suggest that people who suffer from mental illness commit violent acts more than twice as often as individuals without a psychiatric diagnosis. The Bureau of Justice Statistics has reported that over 1.2 million individuals with mental health problems were confined in US jails and prisons in 2005; roughly three-quarters of these individuals had co-occurring substance use disorders. In Sweden approximately 5.2% of the population's attributable risk for violent crime is due to individuals with severe mental illness, and similar rates have been found within the US. The elevated rates of violent behavior are of special concern to health care providers: patients with schizophrenia who are acutely agitated are thought to account for over 20% of psychiatric emergency department visits, and more than 70% of patients with dementia who live in nursing home facilities exhibit signs of agitation. Notably, however, the large majority of people with mental illness do not commit violent crimes. The MacArthur Study on violent behavior in the mentally ill population found that violence is more prevalent in this group than in the general population only if substances of abuse are involved or if the patients are not appropriately medicated, and other studies have also found substance use to be an independent risk factor for violence. Studies also show that up to 25% of people with mental illness report that violent acts have been committed against them; this is more than 11 times greater than it is in the general public, and it is itself a risk factor for the propagation of violent behavior. Therefore, while having a psychiatric diagnosis puts one at increased risk, other factors (including demographics, personal history, medical diagnoses, and psychosocial stressors) often act in an additive manner to determine an individual's likelihood of committing a violent act ( Figure 65-1 ).

Pathophysiology

Violent acts and aggression have biological, environmental, and psychological determinants. While an “aggression center” has never been identified in the brains of humans, animal studies have implicated several brain regions that may be involved in the hierarchical control of aggressive behaviors. Some of these areas are excitatory in nature; others are inhibitory. The anterior, lateral, ventromedial, and dorsomedial nuclei of the hypothalamus are often described as areas crucial to animal aggression and are considered to be involved in the control of aggression in humans. The limbic system (which includes the amygdala, hippocampus, septum, cingulate, and fornix) has regulatory control of aggressive behaviors in humans and animals. The prefrontal cortex modulates input from both the limbic system and the hypothalamus; it may have a role in the social context and judgmental aspects of aggression. Cortico-limbic circuits have been identified for psychiatric disorders associated with aggression including antisocial personality disorder and borderline personality disorder.

Neuroimaging studies have found abnormalities in the prefrontal areas of individuals who exhibit violent behavior. Using magnetic resonance imaging (MRI) techniques, violent individuals have been shown to have reductions in the volume of their prefrontal gray matter. The volume of the orbito-frontal cortex has been associated with aggression in psychiatric patients. Using single-photon emission computed tomography (SPECT) techniques, adolescent and adult psychiatric patients who had recently participated in an aggressive act had significantly depressed prefrontal activity when compared with control patients. Multiple positron emission tomography (PET) analyses have illustrated that violent patients have decreased prefrontal/frontal blood flow and metabolism. These findings are supported by clinical evidence showing that acquired lesions within, as well as injury to, the prefrontal cortex and frontal lobe put one at increased risk for impulsive behavior and lessen executive control of emotional reactivity. Multiple SPECT and PET analyses have also found abnormalities within the temporal lobe and the subcortical structures of the medial temporal lobe in violent patients.

Low central serotonin (5-HT) function has been correlated with impulsive aggression. Violent patients have been found to have a low turnover of 5-HT, as measured by its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in the cerebrospinal fluid (CSF). Acetylcholine in the limbic system stimulates aggression in animals; cholinergic pesticides have been cited as provoking violence in humans. Gamma-aminobutyric acid (GABA) is thought to have inhibitory effects on aggression in both humans and animals. Norepi­nephrine (noradrenaline) may enhance some types of aggression in animals and could play a role in impulsivity and episodic violence in humans. Dopamine increases aggressive behavior in animal models, but its effect in humans is less clear because of its psychotomimetic effects. Hormonal influences of androgens often are cited as a major factor in aggressive behavior. Some attribute a lower threshold for violence in women to lower levels of estrogen and progesterone during the menstrual cycle. Lower cholesterol levels in patients with personality disorders have been associated with aggressive and impulsive behavior ( Table 65-1 ).

In considering the genetics of aggressive behavior, no specific chromosomal abnormalities are yet associated with an increased risk for aggression; however, aggressive behavior has been shown to be highly heritable and can be unmasked by environmental stressors in those who are genetically prone. Using twin studies, a meta-analysis that examined the etiology of aggressive behavior showed that at least 50% of the pathology could be attributable to genetics. The relationship between the syndrome involving XYY and impulsivity is questionable, and the relationship remains inconclusive. Knock-out mice that lack the monoamine oxidase (MAO) _A gene (which encodes for the enzyme responsible for the catabolism of serotonin, dopamine, and norepinephrine, and subsequently leads to elevated serum levels of the three neurochemicals) were shown to exhibit increased aggression in genetic studies. Within a family in the Netherlands carrying an X-linked mutation in this gene, affected members showed increased levels of aggressive behavior. Human correlates also exist for the mouse knockout studies that examined catechol O -methyltransferase (COMT) (an enzyme also responsible for the catabolism of catecholamines) gene mutations leading to increased aggression. A study that examined the serotonin transporter gene (which regulates the duration of serotonin signaling) showed that a polymorphism in the promoter yielded low serotonin levels and increased aggressive behavior in children. Polymorphisms of tryptophan hydroxylase may also be correlated with impulsive aggression.

Clinical Features and Diagnosis

The etiologies of aggressive and violent behavior are vast; however, if they can be identified, it is critical to do so, because the management, in both the acute and long-term setting, relies on this information. It is critical for the evaluator to assess whether the pathology is a result of major mental illness, a result of a personality disorder, or a result of a medical condition because the level of acuity, the degree of violent behavior, and the treatment approach of each type of problem will vary. When beginning the assessment of a violent patient, it is useful to generate a working differential ( Table 65-2 ).