Does traumatic brain injury cause violence?
Suppose you are called to testify in the trial of a suspect, abused as a child, who has been charged with aggravated assault. How would you respond to this question:
You would be fully justified to state that traumatic brain injury (TBI) can cause and worsen a wide range of psychiatric symptoms including psychosis, mood symptoms, anxiety, cognitive deficits, and impulsivity. Could you also present sufficient evidence of TBI as a cause of violence?
That could be more difficult. TBI-induced criminality remains a central and controversial area within forensic psychiatry. Behavior resulting from injury has been implicated in violence and crime, especially when coexisting with substance abuse, a violent environment during childhood including abuse, and pre-existing personality disorder. The literature is vast and covers a spectrum of opinions, allowing the forensic psychiatrist to find evidence that would support the prosecution or the defense. Judge for yourself.
For the prosecution: TBI is no defense
In his study, “Brain injury and criminality,” Virkkunen concluded that “sociopathy, alcoholism, and drug abuse are the types of psychiatric disorders associated with criminal behavior, not organic brain syndrome.”1
This statement was based upon a retrospective analysis of World War II veterans. A search was conducted through Finland’s Criminal Register to compare the frequencies of convictions for crimes punishable by imprisonment between a non-TBI control group and a TBI group. The overall crime rates between the two groups were not significantly different: 5.5% versus 4.2% for the control and TBI groups, respectively. Seventeen of 1,870 (0.9%) of the TBI patients committed violent crimes versus 3 of 500 (0.6%) of the control group. A closer examination revealed that most convictions were associated with alcohol in both groups.
Unlike Virkkunen, Kreutzer et al were unable to prove or disprove a cause and effect between TBI and violence. In their 1991 investigation based on 74 TBI patients, they found that 20% had been arrested pre-injury, and 10% had been arrested after the injury. 2 Most arrests occurred after use of alcohol or other drugs. The study concluded that criminal behavior might be a result of post-injury changes including poor judgment, apathy, and other new behaviors.
WHAT IS THE ETIOLOGY FOR IMPULSE DYSCONTROL IN TBI?
There are several coexisting theories. The vulnerable amygdala, located within the anterior temporal lobe, is often injured. The amygdala adjoins emotions to thoughts. Damage to the amygdala has led to poor impulse control and violent behavior. In addition, frontal lobe lesions frequently result from damage caused by bony upward projections from the skull. “Orbital frontal lesions resulting from contusions of neural tissue against the floor of the anterior cranial vault can occur when an individual falls backwards striking the occiput against a firm surface.”10 This damage impairs the TBI patient’s ability to regulate limbic input. Therefore, the disinhibited TBI patient with frontal lobe damage often reacts impulsively and even violently.
Damage to specific neurotransmitter systems also causes impulse dyscontrol in TBI patients. The locus ceruleus in the forebrain is often injured, leading to elevations in norepinephrine in post-TBI patients. Increased norepinephrine levels have been correlated with aggressiveness and impulsivity. In addition, studies by Porta et al12 and Hamill et al13 showed that dopamine was increased in post-TBI patients. Agitation and aggression have been proven to result from hyperdopaminergic states. In contrast to dopamine and norepinephrine, reduced serotonin levels (CSF 5-HIAA) lead to increased impulsivity and aggression. Although the results have varied, studies have shown changes in serotonin levels after TBI.10 Hence, much evidence supports the biological basis for impulsivity in TBI patients.
Substance abuse, traumatic brain injury, and crime were indeed interconnected, the researchers said, but they did not go so far as to conclude that TBI causes criminality and violence. Rather, they believed that substance abuse, which was most common among those younger than 35, led to legal difficulties and TBI.
In 1995, based on a larger sample of 327 patients, Kreutzer and associates found that the TBI criminal population has a relatively high incidence of alcohol abuse before and after head injury.3 Most crimes were associated with substance abuse, such as drug possession or driving under the influence of alcohol.
The study found that TBI patients with a history of arrest were more likely to have substance abuse problems after the injury. TBI patients with both a criminal and substance abuse history also were more likely to commit crimes after the head injury. Kreutzer concluded that TBI is not a risk factor for crime without such a history.
For the defense: TBI does lead to criminality
In one study by Brooks et al of 42 individuals with severe TBI, threats of violence increased from 15% 1 year after sustaining head injury to 54% 5 years after.4 What’s more, at the 5-year follow-up, 31% of these patients had legal problems and 20% of their relatives had been assaulted by them at least once.
A study by Sarpata et al also supports the argument that TBI leads to criminality.5 They argue that TBI patients should be expected to commit crimes because they have poor cognitive skills, impulsivity, and increased aggression, as well as low tolerance for frustration and poor judgment. In their study of 18 subjects in a community corrections day program in Vigo County, Indiana, they found that a large percentage of offenders (50%) reported head injury.5 In contrast, the prevalence of head injury in the general population is 2%to 5%.
By self-report, the TBI offenders at the day program had worse cognition, greater lability, and more aggressiveness than non-offenders and non-TBI offenders. They concluded, “it would appear that had most of these people not experienced a head injury, they may not have become offenders.”5 The Sarpata et al study did not involve an imprisoned population; therefore, these offenders did not become brain-injured while incarcerated. They argued that TBI patients may have more difficulty understanding the legal process, are less able to assist with their defense, and thus are more likely to be found guilty than are suspects without brain injury. The authors recommended cognitive rehabilitation as a way to reduce the propensity for crime.
In a report of the Vietnam Head Injury Study, Grafman et al concluded that ventromedial frontal lobe lesions could result in violent behavior because frontal lobe damage makes it more difficult for the brain to access social skills leading to disinhibition and aggression.6 In this study, 279 Vietnam veterans with a history of TBI were matched with 57 healthy people, based on age, education, and length of Vietnam experience. Each received comprehensive testing, including neuropsychological and personality testing. Family members completed questionnaires, which were rated on the Katz Adjustment Scale (KAS), including the Any Violence Scale and the Extreme Violence Scale, to assess aggressiveness.
Based on the observations of family members through the KAS, 14% of the group with frontal lobe injury exhibited physical violence compared with roughly 5% of the controls. These findings were independent of education, IQ scores, or Beck Depression Inventory scores. Patients with lesions in the mediofrontal and orbitofrontal regions had higher Any Violence Scale and Extreme Violence Scale scores than the control group, as reported by family members.
“Knowledge stored in the human prefrontal cortex plays a managerial role in the control of behavior and takes the form of mental models, thematic understanding, plans, and social rules,” the authors said.6 They theorized that a prefrontal cortex lesion would hinder the ability to manage one’s instincts, leading to impulsivity, aggression, and violence. However, all patients with ventromedial prefrontal cortex lesions did not display aggression or violent behavior. Further, patients with lesions elsewhere and some normal subjects displayed aggressive and violent behaviors.
Martell estimated the prevalence of organic brain dysfunction in maximum-security forensic psychiatric patients at the Kirby Forensic Psychiatric Center on Ward’s Island in New York City.7 Of the 50 randomly selected patients, 22% had a history of a head injury in which they lost consciousness. Whereas 84% had a history of some sort of brain impairment, only 16% were given an organic diagnosis.
“All of the subjects with a DSM-III-R diagnosis of organic brain disorder had been arrested and charged for violent crimes. Of these patients, 75% were charged with murder, manslaughter, or attempted murder. The remaining 25% were charged with violent sex offenses,” said Martell, arguing for a more careful evaluation of organic brain impairment in forensic evaluations.7
Lewis et al evaluated the neuropsychiatric status of 15 death-row inmates. 8 All had reached the final stage in the legal process prior to execution, and 4 had been executed by the time the study was published in 1986. All 15 had a history of TBI as evidenced by objective findings of scars, skull indents, neurologic findings, records, collateral from families, and neuroimaging. During childhood, for instance, one inmate had been beaten in the head by 2-by-4s and fell into a pit, with loss of consciousness for several hours. As an adult, he was in a motor vehicle accident, resulting in an injury to the right eye, and later fell from a roof after a blackout. Other inmates had seizures, abnormal CT scans, positive Babinski signs, ankle clonus, skull defects, and various other neurologic signs.
“When the Supreme Court reinstated the death penalty, it provided that there be a separate sentencing in which mitigating circumstances could be explored. Any evidence of mental disease or defect, including any evidence of central nervous system dysfunction, would be relevant to such hearings, since such disorders affect judgment, reality testing, and self-control,” the authors said.8
These 15 death-row inmates had numerous neuropsychiatric symptoms that were not addressed. It was thought that the attorneys and judges did not address the organic conditions because of their subtle nature. Objective evidence through collateral and testing ruled out malingering, as did the fact that these inmates were not searching for evaluations or exaggerating their symptoms. The authors concluded that neuropsychiatric status could be a potentially strong mitigating factor, but such evidence is often neglected.
TBI and the insanity defense
Criminal responsibility is dependent on actus reus, the harmful act, and mens rea, guilty or wrongful intent. The accountability and blameworthiness of the crime fall under mens rea. Do TBI patients have the mens rea for the crime? Can TBI be a basis for a plea of not guilty by reason of insanity (NGRI) or a diminished capacity defense? Can the worsening of TBI-related behaviors by substance abuse be the basis for an insanity defense or diminished capacity?
For an NGRI plea, a mental illness or defect must exist. TBI is an abnormal condition of the mind leading to a mental disease that can substantially affect control of emotions and behaviors. The NGRI plea historically had two prongs: cognitive and volitional impairment.9 The M’Naghten test, the cognitive prong, is based on whether the defendant knew the nature and quality of the criminal act or knew the act was wrong. Under the American Law Institute (ALI)test and American Bar Association standards, the defendant can meet the criteria for insanity by demonstrating a substantial lack of capacity to appreciate, rather than knowing, the criminality or wrongfulness of the act.
There is a substantial amount of evidence for cognitive impairment in TBI patients. The TBI patient may have several co-existing “neurolinguistic deficits associated with the pragmatics of language.”10 For example, a TBI patient with damage in the nondominant hemisphere may misinterpret the prosody of language, leading to an inappropriate response. Other neurolinguistic deficits in TBI patients include decreased intelligibility, a constricted operational vocabulary, perseveration, and limited listening.
TBI can also lead to short-term memory impairment due to injury to the vulnerable hippocampus within the anterior temporal lobe. When the hippocampus is damaged, the transformation of memories from long-term to active is impaired. Consequently, retrieval of learned information is more difficult for the TBI patient.10
Also, higher-order cognitive processes can be damaged after TBI. Executive functioning, through the frontal lobe, involves data collection, prioritizing, formulating a plan, and carrying out the plan. This process is almost always impaired in TBI patients, according to a study by Szekeres et al in 1987.14 Poor abstraction associated with frontal lobe damage can lead to difficulties of TBI patients in understanding or appreciating certain concepts related to the wrongfulness, nature, and quality of their acts.