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. Author manuscript; available in PMC: 2018 Oct 4.
Published in final edited form as: Lancet Psychiatry. 2018 Feb 26;5(10):836–844. doi: 10.1016/S2215-0366(18)30062-2

Traumatic brain injury: a potential cause of violent crime?

W Huw Williams 1, Prathiba Chitsabesan 2, Seena Fazel 3, Tom McMillan 4, Nathan Hughes 5, Michael Parsonage 6, James Tonks 7
PMCID: PMC6171742  EMSID: EMS78825  PMID: 29496587

Abstract

Traumatic brain injury (TBI) is the biggest cause of death and disability in children and young people. TBI compromises important neurological functions for self-regulation and social behaviour and increases risk of behavioural disorder and psychiatric morbidity. Crime in young people is a major social issue. So-called early starters often continue for a lifetime. A substantial majority of young offenders are reconvicted soon after release. Multiple factors play a role in crime. We show how TBI is a risk factor for earlier, more violent, offending. TBI is linked to poor engagement in treatment, in-custody infractions, and reconviction. Schemes to assess and manage TBI are under development. These might improve engagement of offenders in forensic psychotherapeutic rehabilitation and reduce crime.

Introduction

Crime has substantial human and economic costs. Crime peaks in late adolescence and early adulthood.1 Prolific offenders are early starters and commit 77% of crime.2 The lifetime costs of crime by a single prolific offender are in the range £1·3–2·3 million.3 Within a year of release from prison, 47% of adults, and 73% of those under 18 years, are reconvicted.4 In England, reoffending by recent ex-prisoners is estimated to cost £10–13 billion a year.5 There have been repeated calls to improve management of mental and physical health of prisoners—which might reduce crime.6 Leading theories for antisocial behaviour hold that so-called difficult temperaments and neuropsychological deficits contribute to life problems linked to crime.79 Traumatic brain injury (TBI) is very common in young people. TBI often leads to cognitive and personality issues that might increase risk of crime. The links between TBI and crime are complex. Those who offend could be risk takers with a low threshold for harm avoidance.10 However, a range of potentially criminogenic pre-injury factors could also be risk factors for, and be exacerbated by, TBI. Socioeconomic deprivation, male sex, and risk taking are co-associated with TBI and incarceration—and might simply occur by coincidence.11 However, TBI in groups already at risk could amplify deficits and erode coping responses and social networks.12 A TBI could compromise educational and employment capacity.13 We aim to review the evidence for how TBI could be related to crime. We will first describe TBI and its neuropsychological and behavioural consequences and then examine the studies suggesting links between TBI and crime. We then look at how prevalent TBI is in offenders—in children and young people, and in adults. Finally, we provide a summary of what can be done to address TBI in relation to crime, and areas for future research.

TBI

Mechanism of injury

TBIs involve an insult to the brain from an external mechanical force (eg, a blow to the head in an assault, a fall, or car crash). These injuries can lead to lacerations and bruising of the brain structures, especially around bony protrusions on the basal surface of the skull.14 Internal bleeding and secondary hypoxia often occur.15 There could be focal injury—usually within frontal and temporal areas—and diffuse injury due to shearing of white matter tracts—particularly related to rotational injury at high speed.16 In milder injuries, there is potential for disruption to axonal connectivity.16

Severity of injury

A Glasgow Coma Scale of 13 or above (out of a maximum of 15) denotes mild; a score of 9–12 is moderate; 8 or below severe. Post-traumatic amnesia or loss of consciousness (LOC), or both, can be used to gauge severity of a historic TBI. Mild TBI is considered to involve 0–30 min of LOC, 30 min and over being moderate to severe.17 A very mild injury—typically referred to as a “concussion” (with some disorientation at the time but no, or brief, loss of consciousness) rarely leads to permanent brain changes. With increased severity there is a higher risk of chronic problems. With moderate to severe TBI there is, more likely than not, long-term neurocognitive, behavioural, and psychiatric disturbance (panel 1).

Panel 1.

Traumatic brain injury (TBI) and risk of psychiatric morbidity

Systematic reviews and large cohort studies have identified that psychiatric morbidity is high in individuals with TBI, with some finding that TBI increases risk.18 A 2009 review19 reported that depression was increased after a TBI, but that the information for other psychiatric disorders was limited. Another review20 has reported rates of post-traumatic stress disorder (PTSD) in 5–7% of individuals with mild TBIs.

Since these reviews, high-quality cohort studies have found increased risk of new psychiatric disorders, including PTSD, panic disorder, social phobia, and agoraphobia, with 22% of individuals having new diagnoses.21

Other relevant research has been done in the USA, where risk of incident psychiatric disorders was increased (relative risk [RR] 2·8, 95% CI 2·1–3·7),22 but this was not found for schizophrenia in Denmark.23 A recent large population-based cohort study24 using sibling controls reported new diagnoses of substance use and depression to be higher in those with TBIs than sibling controls, and higher risk of premature mortality (odds ratio 2·6, 95% CI 2·3–2·6) and suicide (2·3, 1·9–2·9) compared with siblings who did not have diagnoses of any head injury. A recent investigation of all individuals,25 identified using health-care registers, who sustained head injuries until the age of 25 years in Sweden found that risk of any inpatient psychiatric hospitalisation (RR 2·0, 95% CI 1·9–2·0) and any psychiatric episode (1·5, 1·5–1·6) was higher than in population controls. These risks were higher when head injury was sustained at older ages, and when it was more severe.25

Incidence, prevalence, and risk factors

TBI is the largest cause of mortality and morbidity in children and young people. It has been called a silent epidemic—as it is often not recognised by social and health-care professionals.26 There is an aggregate hospitalised (meaning those diagnosed at emergency department [ED] and not admitted as well as those admitted) plus fatal TBI incidence rate of about 235 per 100 000 people across European countries,27 with TBI severity ratio of hospitalised patients reported as 22:1·5:1 for mild versus moderate versus severe cases, respectively. In middle-income and low-income countries, three times as many people can suffer TBIs compared with high-income countries.28 TBI frequently occurs from falls, sporting injuries, fights, assaults, and road accidents. Rates of injury are high, and equal, for both sexes in the very young (under 5 years of age), while adolescents and young adult males are the group most at risk.29 In a general population, the lifetime prevalence of a TBI—with some LOC—has been estimated to be around 8%30 and 12%31—with men having twice the odds of having had a TBI compared with women.31 TBI has a strong socioeconomic gradient—disadvantage being a major risk factor.29

Neuropsychological functions and sociobehavioural problems

The neuropsychological effects of TBI tend to be amnestic and executive disorders (poor memory, attention, concentration, and planning). Deficits in emotional regulation—characterised by impulsiveness and poor social judgment—are common. Milder TBIs can lead to problems in attentional control and inhibitory functions.32 Injury to frontal systems can lead to increased risk of impulsive aggression, poor decision making, and lack of control of social behaviour.33,34 For example, veterans from the Vietnam War with injuries to the frontal ventromedial cortex (the part of the frontal cortex involved in fear and risk) were rated as more aggressive and violent compared with non-injured controls and patients with lesions in other brain areas.35

Self-regulation and the developing social brain

The early start of a large number of offenders could be due to immaturity or vulnerability of brain systems for social cognition, or both. The so-called social brain system is complex and distributed.36 It comprises systems for deducing emotions from facial expressions and vocal tone for reading others’ minds for intentions, and responding appropriately.37 These key abilities for socialisation have differential developmental trajectories.38 Reward systems become mature in the mid-teens with increased sensation-seeking behaviour. Meanwhile, areas for deliberate control of impulses and making judgments—the dorsolateral prefrontal cortex—reach maturity in the late teenage years.39 Adolescents and young adults are, consequently, poorer than adults at responding on problem-solving tasks under emotional demand, particularly in social contexts, which increases risk-taking behaviour.1,37,4043

TBI can disrupt development of these systems for social interaction and contribute to behavioural problems. Max and colleagues44 followed up 94 children aged 5–14 years post TBI. Personality change occurred in 59% of those with severe TBI (22/37) and 5% of those with mild/moderate TBI (3/57). Emotional lability, aggression, and disinhibition were most common. In a related study (n=177), children with such personality changes were found to have lesions of the dorsal prefrontal cortex.45 More recently, they found novel psychiatric disorders in 25 (36%) of 70 children after mild TBI;46 attention-deficit hyperactivity disorder (ADHD), personality change, and oppositional defiance being most common. Pre-existing conditions, such as ADHD, are risk factors for TBI.47 Interestingly, children with ADHD secondary to TBI tend to have worse dual attention and working memory compared with those with non-injury ADHD and children with TBI only.47

Changes in behaviour post-TBI could have detrimental effects on key social roles. In a study in children (n=850) at risk of high school dropout, it was found that head injury before young adulthood was associated with interpersonal violence (controlling for alcohol use, marijuana use, delinquency, and observing violence).48 Two linked cohort studies showed that adults who had had TBI as children were significantly poorer at emotion perception than controls and had externalising behaviour, poor pragmatic communication ability, and greater trouble with law enforcement.49,50

Injury in childhood and adolescence can, therefore, lead to impulsivity, poor sociocommunication skills, and concomitant externalising behaviours. Injury at this life stage could well disrupt the development of prosocial life roles. Such patterns of behaviour could underlie a drift from the classroom to the courtroom.

Epidemiological studies on TBI and crime

Birth cohort and data linkage studies in adolescents and adults indicate that TBI is associated with increased risk of perpetrating crime. However, although these studies implicate links between TBI and crime, there is a lack of clarity on actual causal mechanisms.

Birth cohort

In a study of around 12 000 males in Finland,51 TBI during childhood or adolescence was associated with a four times increased risk of mental disorder with coexisting offending in adulthood. TBI before 12 years of age was linked to earlier onset of criminality. There was no adjustment for familial and socioenvironmental confounds. Those injured younger might have had stronger risk factors for earlier TBI and criminality. In a study in New Zealand,52 in which 1265 children were followed up to age 25 years, a TBI group, relative to control, were more likely to be arrested. Although when alcohol and drug dependence were controlled for, TBI was no longer associated with crime in those who were injured between the ages of 0 and 5 years. Early substance use could be a mediating factor for crime in those injured at a very young age. In a birth cohort study in southwest England,53 a TBI group—categorised as mild (n=800)—was at increased risk of criminal behaviour by age 17 years compared with the non-TBI group (n=8307; unadjusted odds ratio [OR] 1·6, 95% CI 1·2–2·2). Associations were confounded by substance use. Furthermore, the TBI group were no different to an orthopaedic injury group (n=2305; adjusted OR 1·1, 95% CI 1·1–1·6). However, TBI was linked to hazardous alcohol use, externalising symptoms, conduct problems, and ADHD.

The evidence for TBI leading to crime from birth cohort studies is, therefore, mixed. There is a suggestion of a latent factor—linked to being injury prone—in orthopaedic and TBI groups, which might confer risk for crime. However, the measures used for TBI vary markedly across these studies. The Finnish study used data from health records—with high sensitivity and specificity—whereas the southwest England study relied on two self and carer reports of mild TBI. As such, the former included moderate to severe injury—which is more likely to be associated with problem behaviour in the long term—whereas the latter included only mild injury—with less substantial, life-changing, consequences.

Data linkage and population studies

Broadly consistent findings in four major data-linkage studies have indicated that TBI does increase criminality, although some preinjury characteristics remain important predictors of crime.54 In northern Finland, adolescents admitted to psychiatric care who had had a TBI were at increased risk of any criminality (by 6·8 times), conduct disorder (5·7 times), and concomitant criminality and conduct disorder (18·7 times) compared with those with no TBI.55 They had also committed significantly more violent (42·9% vs 9·1%) and non-violent crimes (29·4% vs 6·8%) crimes. However, reverse causality was possible. One of the most compelling studies indicating a risk of crime post-TBI is a 35-year, retrospective, total population study of Swedes.56 Fazel and colleagues56 found that 2·3% of population controls had committed violent crimes. By contrast, of TBI cases (a total of 22 914), 8·8% had committed violent crimes. This finding corresponded to a substantially increased risk of violent crime in the TBI population (adjusted OR 3·3, 95% CI 3·1–3·5). Risk was attenuated when cases were compared with unaffected siblings (adjusted OR 2·0, 1·8–2·3), who would have shared similar genetic, social, and economic backgrounds. Sibling controls were also examined in a retrospective cohort data linkage study in Western Australia.57 Hospital-recorded cases of TBI (n=7694) were compared to matched cohort (n=22 905) and full-sibling controls. TBI was associated with increased risk of all offending in males (hazard ratio [HR] 1·6, 95% CI 1·5–1·7) and females (1·5, 95% CI 1·3–1·8). When same-sex full-sibling controls were used in the adjusted analyses, increased risk of offending was evident only among males with TBI (HR 1·7, 95% CI 1·3–2·3). For violent convictions, relative to the general community, TBI was also associated with increased risk in men (HR 1·7, 95% CI 1·4–1·9) and women (1·7, 1·2–2·5). Analysis comparing full siblings with, and without, TBI showed that TBI was associated with violent offending only in men (HR 1·9, 95% CI 1·2–3·0). In these analyses, potential confounders (aboriginal background, substance abuse, social disadvantage, etc) were controlled for. A recent large-scale data-linkage cohort study58 of 1·4 million Ontarian adults also indicated that TBI is linked to more serious offending. Data on people aged 18–28 years who attended emergency departments were linked to records from correctional services. Incarceration was to a federal facility (most likely for more serious or repeated offending). Analyses showed that TBI—in men and women—was associated with a subsequent increased risk of incarceration (HR 2·5, 95% CI 2·2–2·8). Potential confounding factors were controlled for in models (eg, socioeconomic, substance misuse, psychiatric disorder). By contrast, a prospective cohort study54 with 6315 adult participants (which reduced to n=2690 at 5 years postinjury) from a US-based TBI Model System National Database found that premorbid variables, especially pre-TBI offending, were strongly linked to post-TBI arrests. However, higher numbers of post-TBI arrests were predicted by loss of consciousness (≥24 h) combined with retention of motor functions. Participants had moderate to severe TBI (greater than 30 min LOC) and were predominantly over 25 years of age (a stage of life less likely to be a risk period for crime). That the participants had been in a TBI model system might have had a protective effect on behaviour.

TBI might be, at the very least, a prominent marker for a range of issues that indicate a risk for crime. In addition, considering the range of evidence, across age groups, populations, and jurisdictions, these studies indicate that TBI is an independent risk factor for crime. In the very young, it could lead to later drug and alcohol misuse, which, in turn, increases likelihood of crime. In those injured after 5 years of age, including adults, TBI appears to be linked to increased likelihood of offending. However, established criminogenic risk factors are still important. TBI could add to greater risk of criminality by increasing likelihood of problem behaviour and eroding capacity for self-regulation and socialisation.

TBI prevalence studies in offender populations

In this section, we examine the prevalence, and associated features, of TBI in offenders. We consider how TBI could be linked to neuropsychological problems, mental health and drug and alcohol misuse issues, poor response to forensic rehabilitation, and recidivism.

Presence of neurological abnormalities

Two recent CT and MRI neuroimaging studies in adults in Germany have indicated higher levels of brain anomalies in offenders. Schiltz and colleagues,59 in a study of 287 male prison inmates, found that violent prisoners had significantly more morphological abnormalities than non-violent prisoners or controls (42% in violent prisoners vs 26% vs 8% respectively). They noted how the areas affected in the violent offenders were those typically associated with empathy. Witzel and colleagues60 found half of 148 patients in a secure mental health institution displayed signs of brain pathology compared with 8% in non-criminal controls. We note these studies were with highly selective samples, and causes of lesions were not known. We cannot know whether being violent led to injury or vice versa.

Youth populations

In incarcerated young people, TBI appears to be prevalent and linked to greater risk of violence. However, there are important comorbid and adversity-related factors that are criminogenic. Adversity could relate to trauma, severe economic disadvantage, parental loss, abuse, and neglect.61

In a meta-analysis11 of studies of TBI in juvenile offenders, nine studies were identified. The rate of TBI (with a history of LOC) across nine studies was approximately 30%. This is high relative to the general population. In the five studies that used a control group, a summary OR of 3·37 was calculated, which suggests that juvenile offenders are substantially more likely to have a TBI compared with controls.

There are few studies on severity of TBI, comorbid conditions, and patterns of crime. Williams and colleagues62 assessed 197 young incarcerated male offenders (average age 16 years)—60% reported a head injury. There was an LOC in 46% of the sample, and 16% reported moderate or severe TBI (defined as LOC for 10 min to 6 h, or 6 h or more).63 The main cause of injury was violence. Three or more TBIs were associated with greater violence. TBI was linked to mental health problems, misuse of cannabis, and more convictions. In a related study, Davies and colleagues63 found that complicated mild TBI (LOC of 10–30 min, or repeated injury) was associated with greater degree of ongoing postconcussion syndrome symptoms (forgetting, headaches, etc)—controlling for drug and alcohol misuse. LOC history was correlated with younger age of first conviction (12 vs 13 years). Similarly, in the USA, Perron and Howard64 found that 18% of 720 inmates (average age 15·5 years) had TBIs where they were unconscious for more than 20 min. Male sex, psychiatric diagnosis, and earlier onset of criminal behaviour and substance use were associated with brain injury.

Adversity and comorbid issues, when assessed, are very common in young offenders. Chitsabesan and colleagues65 reported a study with incarcerated adolescents in England (93 boys aged 15–18 years). 82% reported a TBI and 18% had moderate–severe current postconcussion symptoms. Those with moderate to severe TBI (msTBI) compared to no or mild TBI (NoM TBI) reported common comorbid problems: ADHD (29% of msTBI, 20% of NoM TBI); speech and language impairments (msTBI 36%, NoM TBI 41%); and alcohol (msTBI 71%, NoM TBI 58%) and cannabis misuse problems (msTBI 86%, NoM TBI 84%). The msTBI group were significantly more likely to have previously been in care (64% vs 34%), and to be at current risk of deliberate self-harm (57% vs 43%) and suicidality (50% vs 24%). A study by Vaughn and colleagues66 in the USA with adjudicated adolescents (n=1345, aged on average 16 years, mostly [86%] male), also found that those with TBI had higher scores for a range of comorbid problems—psychopathy, moral disengagement and impulsivity, bullying, peer delinquency, violent victimisation, and witnessing violence.

Adult populations

A meta-analysis of lifetime prevalence of TBI in incarcerated adults versus the general population indicates that it is significantly higher in the offenders.67 The unweighted pooled prevalence for TBI across 5049 participants in 24 studies was 51%. Both male and female groups were affected. There also appears to be a severity effect. In a study in the USA,68 for example, on the lifetime prevalence of TBI in prisoners, 65% of males and 72% of females reported one TBI with alteration of consciousness. Longer LOC was associated with more symptoms. In the UK, of 200 adult male prisoners, 60% reported a TBI of some form.69 Moderate to severe TBI (LOC of 10 min or more) was reported by 17%. Those with a self-reported history of TBI were, on average, 5 years younger at the age of first prison sentence than uninjured (age 16 compared to 21 years) and had higher rates of reconviction. Perkes and colleagues,70 who examined 200 men in custody (aged 30 years) and 200 non-offenders (aged 43 years) in the community—from a matched (by residence) background—found that TBI was more common among prisoners (82% vs 72%). There was a higher proportion of prisoners with histories of LOC (65% vs 35%). Prisoners had more multiple TBIs (42% vs 15%). Assault was the most common cause of injury in prisoners whereas sporting injury was in the community sample. The offender group also reported significantly greater ongoing psychological effects of injury, such as headaches, memory problems, and anger. This pattern suggests a history of TBI involving high speed mechanisms and actual brain changes in offenders.

This theme of consequential injury is consistent with a trend for prisoners with TBI to have been shown to have greater levels of neuropsychological deficits and treatment failure. Pitman and colleagues71 compared 139 male prisoners with 50 prison controls without TBI. They found no differences for premorbid intellectual functions. However, those with TBI were worse on current functions, particularly executive skills. Severity of TBI was associated with greater impairment. The TBI group had greater prevalence of violent crime (60% vs 38%). Fishbein and colleagues72,73 assessed executive functioning in 224 participants of a forensic rehabilitation programme. Of these, 28·3% (n=71) reported head injury (3 min of LOC). Those with TBI had more problems in executive control and made fewer gains in treatment. Dysexecutive disorders were linked to dropout from treatment and to less improvement on aggressive reactivity. Those with TBI were more likely to have a history of physical, emotional, and sexual abuse.

TBI also appears to be associated with infractions in prison and reconviction. Shiroma and colleagues,74 in a US state-wide study over 11 years using linked hospital and justice datasets of 17 569 inmates, found that males and females with TBI had significantly higher rates of violent infractions. Ray and Richardson75 did a longitudinal, prospective, follow-up study of 151 inmates released from incarceration during a period of 12–30 months. At 12 months postrelease, 63% of those without TBI had not recidivated, whereas 48% of TBI had not. The TBI group had a regression model hazard rate of 1·57 greater than non-TBI for recidivism.

TBI, as we have seen, occurs within a constellation of socioadversity factors. This is particularly evident in studies with girls and women. Of 113 female prisoners in the USA, Brewer-Smyth and colleagues76 found that 42% had TBI histories, and those who had committed violent offences had suffered an average of two TBIs. Domestic abuse, previous suicide attempts, and TBIs with LOC were all associated with current violent convictions. Similarly, Colantonio and colleagues77 found that females with TBI who offend had suffered more early physical and sexual abuse than those without TBI. Abuse, of various forms, could be associated with concussive blows or TBIs. Such injuries could complicate the experience of post-traumatic stress disorder (PTSD), with survivors having patchy recall of events.78

Economic costs

A UK charity, Centre for Mental Health, recently analysed the cost of TBI, including costs relating to crime.3 Calculations were based on cases of TBI with hospital admission (classified as mild or moderate). Modest likelihood risk ratios were used to predict the additional risk of offending post-TBI. On average, in a person representative of the general population aged 15 years, the lifetime costs of TBI would be around £155 000 per case, including £95 000 for non-crime costs (health care, lost earnings, etc) and £60 000 for the costs of additional offending. For a young person already in the criminal justice system, the lifetime costs increase to around £345 000 per case, reflecting the much higher costs in those already on a likely trajectory into persistent offending.

Opportunities for change

A range of measures could reduce the risk of crime following TBI. First, any form of neurorehabilitation could offset the risk of violent crime.79 Second, improved linkage between emergency departments, community mental health services, general practitioners, and school systems might lead to early identification and management of TBI in children and young people, particularly in lower socioeconomic areas. This approach could reduce the chances of school exclusion and social isolation. Third, on a person’s entry into the justice system (police, courts, or admission to probation or secure care), there is an opportunity to deliver routine screening for TBI and provision of treatment options. For young people in courts in the UK there is now recognition that TBI should be taken into account in sentencing.80 There are initiatives in England that allow screening for neurodisability in entrants into youth secure estate (secure children’s homes, secure training centres, and young offender institutions). There have also been pilot projects to assess for TBI and other neurodisabilities in young adult and adult prisons.71,81 Fourth, provision of brain injury link-workers within prisons to enable screening and support for those with TBI, and training and support for staff, has been shown possible and beneficial.65 Through such initiatives, forensic rehabilitation could be enhanced with interventions to manage the cognitive and behavioural issues stemming from TBI. One illustration of how this might work is in a non-TBI study in which medication for ADHD in offenders led to a 30% reduction in criminality on release—possibly owing to improved impulse control.82 In the UK, Parliamentary bodies have noted the need to take account of TBI in the criminal justice system (panels 2 and 3).83,84

Panel 2.

Justice Committee Report, UK Parliament82,83

The Justice Committee of the Parliament of the UK and Northern Ireland recently reported that: “We received compelling evidence that another important consideration for young adults in the criminal justice system is the potential presence of atypical brain development….those who persist in criminal behaviour into adulthood are more likely to have neuro-psychological deficits, including cognitive difficulties with thinking, acting, and solving problems, emotional literacy and regulation, learning difficulties and language problems associated with Attention Deficit Hyperactivity Disorder (ADHD), autism, learning and language disorders and head injuries…[furthermore] deficits, particularly ADHD and traumatic brain injury (TBI, an impairment to the brain from an external mechanical force) are associated with more violent offending” (p 9). The Committee also note that: “Navigating the [justice] system is particularly challenging for those with neuro-disabilities [which] impact on their experience of the system and their capacity to desist from crime” (p 56). They recommend a range of initiatives which include: screening, awareness raising of staff, specialist support, and data gathering for commissioning.

Panel 3.

Review of services for people with brain injury in the justice system, commissioned by the Justice Committee, Scottish Parliament83

  • A recent government report outlines a service pathway for people with brain injury in the criminal justice system in Scotland1

  • The pathway extends from police custody through to probation, utilising identification and screening to triage to appropriate services

  • Preliminary evidence obtained in the course of the report indicated a four-times greater risk of a history of admission to hospital with head injury than in matched general population controls

  • A need for specialised secure forensic provision for people with brain injury was identified

  • Linkage between brain injury services and the criminal justice service was found to be poor

  • A need for effective education and intervention packages was identified

Research directions

The causal mechanisms that link TBI and crime are unclear. It might be supposed that having a TBI would typically lead to—or exacerbate—problems in behavioural self-regulation and mood. For example, aggressive behaviour has been shown to be increased after TBI, but pre-TBI aggression is also a risk factor for post-TBI aggression.85 Higher quality research is needed to examine these links while accounting for the various factors that could confound this association.

It is clearly important to address some of the weaknesses in studies reviewed. Birth cohort, data-linkage, and prevalence studies lack agreed definitions or criteria for identifying TBI. In many studies there are binary yes or no classifications of presence or absence of TBI, and often there is no measure of injury severity. Furthermore, measures of crime are often limited (eg, only the type of sentence given). Studies also tend to be cross-sectional and lack verified medical records. They rarely have non-offending control groups. Although it is worth noting that one study with young offenders used self-reports and medical records and found that rates of injury were consistent.65 Similarly, one study with adults found 70% agreement between self-reported and medically recorded TBI.86 However, future research is needed with prospective, longitudinal designs, with well validated and agreed TBI criteria. They should also have appropriate control groups with measures of actual criminal behaviour, such as from police records.

It is particularly important that future studies are designed to characterise the nature and severity of neurotrauma in offenders versus controls. Ideally, there should be neuroimaging, such as diffusion tensor imaging, alongside measurement of chronic TBI biomarkers such as tau.87 Such analyses would allow a better understanding of the underlying pathology of TBI within offenders and offer windows for novel treatment options to be developed.88

Given the high levels of preinjury developmental adversity, comorbid neurodisability, and mental ill-health in the populations studied, it is vital to establish how much of current functioning and behaviour is determined by TBI or these other factors, or both.89 Of particular importance is a need to explain how TBI is situated within the criminogenic life histories of offenders. Crucially, offenders often report childhoods characterised by harsh or inconsistent parenting and abuse—with angry and coercive role models for emotional regulation.90,91 Such environments could underlie an adaptive behavioural response of hypervigilance for threat9294 and tendencies of being insensitive to others and impulsive.63 There is evidence that adversity is associated with neurological anomalies in exposed young people compared with controls.95 Furthermore, the lives of offenders, as illustrated by the levels of injuries sustained (eg, in fights and road accidents), would suggest a role for current PTSD in some form in this population.96 PTSD could contribute to problems with hypervigilance and impulsivity linked to criminality.97 A more detailed account of the legacy of such a trauma history, combined with TBI, would be important for determining how best to reduce the risk of crime.

Given the large populations of the criminal justice system, it is important to determine what forms of screening could be done quickly and reliably (at arrest, court, prison, release, and probation), and how those data could be used to guide interventions. This method could be tailored for particular regimens and within specific facilities (eg, segregation, close supervision, or health care). The use of sensitive screening tools could generate data for linkage (such as through criminal justice, health, and education) to identify trends in crime in relation to TBI. Furthermore, given that TBI appears to increase the chances of violent crime, it is important that it is considered as a factor for predicting future violence. Scalable tools such as OxRisk, enable stratification of prisoners into high, medium, and low risk groups.98 Adding TBI as a factor in the model could increase predictive accuracy and enable enhanced support plans to reduce crime risk. Pharmacoepidemiology offers one approach to identify treatment strategies in the absence of RCT evidence.99

Conclusions

TBI appears to be associated with earlier age of incarceration, increased risk of violence, and more convictions. Neurological abnormalities are common in offenders. Brain functions, in areas important for social functioning, such as impulse control and empathy, appear compromised. In those in custody, complicated mild TBI or moderate to severe head injury is prevalent in one to two in ten people, and another three or four in ten could have a milder form of TBI. Neuropsychological dysfunction is linked to violence, infractions in prison, poorer treatment gains, and reconviction. Life histories of abuse, neglect, and trauma appear particularly elevated in those with TBI versus those without TBI histories, as are ongoing mental health and drug and alcohol problems. Young offenders with TBI are particularly at risk of self-harm and suicidal behaviour. TBI could amplify any neurocognitive issues due to adverse life events. People with TBIs are incarcerated at high cost in facilities that might not be well placed to address their needs. There has been an assumption that TBI was just a coincidental occurrence in the lives of risk takers: people who were premorbidly set to be on a trajectory towards crime. But as we have shown in this review, the research evidence suggests otherwise. Addressing TBI offers a means not only to improve the lives of those who offend, but also, crucially, to reduce crime.

Search strategy and selection criteria.

We searched Ovid, MEDLINE, and Ovid-PsycINFO from April 15, 2007, to April 15, 2017, using the search terms: “TBI” or “Head Injury”, “Traumatic Brain Injury, Crime * [criminal], Offend, Prison, Juvenile + Delinquent”. English language only was used. We identified 806 articles, of which 102 were relevant to traumatic brain injury and crime.

Footnotes

Contributors

WHW conducted the literature search. SF produced panel 1. TM produced panel 3. WHW produced the search strategy and panel 2. All authors contributed to writing the manuscript.

Declaration of interests

TM holds grants from the Scottish Government; WHW from the Barrow Cadbury Trust. WHW is also a Vice Chair of the Criminal Justice and Acquired Brain Injury Group. SF is funded by the Wellcome Trust (202836/Z/16/Z). NH is funded by Barrow Cadbury Trust. All authors declare no competing interests. Since the original online publication, additional information has been provided regarding a perceived conflict of interest for MP in relation to personal circumstances. Following receipt of the complaint, the editors, authors, and MP’s employers have reviewed the circumstances and, while they do not believe that the information provided has any implications for the integrity of the background work or the published paper, they fully acknowledge and deeply regret the distress caused to the complainant. This statement has been included in the online and print versions of this paper.

Contributor Information

W Huw Williams, Department of Psychology, University of Exeter, Exeter, UK.

Prathiba Chitsabesan, Offender Health Research Network, University of Manchester, Manchester, UK.

Prof Seena Fazel, Department of Psychiatry, University of Oxford, Oxford, UK.

Prof Tom McMillan, Institute of Health and Wellbeing, University of Glasgow, Glasgow, UK.

Prof Nathan Hughes, Sociological Studies, University of Sheffield, Sheffield, UK.

Michael Parsonage, Centre for Mental Health, London, UK.

James Tonks, Medical School, University of Exeter, Exeter, UK.

References

  • 1.Shulman EP, Steinberg LD, Piquero AR. The age–crime curve in adolescence and early adulthood is not due to age differences in economic status. J Youth Adolesc. 2013;42:848–60. doi: 10.1007/s10964-013-9950-4. [DOI] [PubMed] [Google Scholar]
  • 2.Farrington DP, Cloid JW, Harnett L, Soteriou N, Turner R, West D. Criminal careers and life success: new findings from the Cambridge Study in Delinquent Development. London: Home Office; 2006. [accessed Feb 12, 2018]. http://www.crim.cam.ac.uk/people/academic_research/david_farrington/hofind281.pdf. [Google Scholar]
  • 3.Parsonage M. Traumatic brain injury and offending: an economic analysis. London: Centre for Mental Health; 2016. [Google Scholar]
  • 4.Ministry of Justice. Proven re-offending statistics quarterly bulletin—July 2010–June 2011. London: Ministry of Justice; 2013. [Google Scholar]
  • 5.The Rt Hon Chris Grayling SoSfJ. Crime in context speech. [accessed Feb 12, 2018];2013 https://www.gov.uk/government/speeches/crime-in-context-speech.
  • 6.The Lancet. Health care for prisoners and young offenders. Lancet. 2009;373:603. doi: 10.1016/S0140-6736(09)60374-3. [DOI] [PubMed] [Google Scholar]
  • 7.Moffitt TE, Caspi A, Harrington H, Milne BJ. Males on the life-course-persistent and adolescence-limited antisocial pathways: follow-up at age 26 years. Dev Psychopathol. 2002;14:179–207. doi: 10.1017/s0954579402001104. [DOI] [PubMed] [Google Scholar]
  • 8.Hirschi T, Gottfredson MR. In defense of self-control. Theor Criminol. 2000;4:55–69. [Google Scholar]
  • 9.Jolliffe D, Farrington DP. Empathy and offending: a systematic review and meta-analysis. Aggress Violent Behav. 2004;9:441–76. [Google Scholar]
  • 10.Beaver KM, Boutwell BB, Barnes JC, Vaughn MG, DeLisi M. The association between psychopathic personality traits and criminal justice outcomes: results from a nationally representative sample of males and females. Crime Delinquency. 2015;63:708–30. [Google Scholar]
  • 11.Farrer TJ, Frost RB, Hedges DW. Prevalence of traumatic brain injury in juvenile offenders: a meta-analysis. Child Neuropsychol. 2013;19:225–34. doi: 10.1080/09297049.2011.647901. [DOI] [PubMed] [Google Scholar]
  • 12.Williams WH, McAuliffe KA, Cohen MH, Parsonage M, Ramsbotham J, David GTL. Traumatic brain injury and juvenile offending: complex causal links offer multiple targets to reduce crime. J Head Trauma Rehabil. 2015;30:69–74. doi: 10.1097/HTR.0000000000000134. [DOI] [PubMed] [Google Scholar]
  • 13.Wehman PH, Targett PS, Avellone LE. Educational and vocational issues in traumatic brain injury. Phys Med Rehabil Clin N Am. 2017;28:351–62. doi: 10.1016/j.pmr.2016.12.010. [DOI] [PubMed] [Google Scholar]
  • 14.Bigler ED. Anterior and middle cranial fossa in traumatic brain injury: relevant neuroanatomy and neuropathology in the study of neuropsychological outcome. Neuropsychology. 2007;21:515–31. doi: 10.1037/0894-4105.21.5.515. [DOI] [PubMed] [Google Scholar]
  • 15.Hutchinson P, Kirkpatrick P. Acute head injury for the neurologist. J Neurol Neurosurg Psychiatry. 2002;73(suppl 1):i3–7. doi: 10.1136/jnnp.73.suppl_1.i3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Caeyenberghs K, Leemans A, Leunissen I, et al. Altered structural networks and executive deficits in traumatic brain injury patients. Brain Struct Funct. 2014;219:193–209. doi: 10.1007/s00429-012-0494-2. [DOI] [PubMed] [Google Scholar]
  • 17.Bruns J, Hauser WA. The epidemiology of traumatic brain injury: a review. Epilepsia. 2003;44:2–10. doi: 10.1046/j.1528-1157.44.s10.3.x. [DOI] [PubMed] [Google Scholar]
  • 18.Carroll LJ, Cassidy JD, Cancelliere C, et al. Systematic review of the prognosis after mild traumatic brain injury in adults: cognitive, psychiatric, and mortality outcomes: results of the International Collaboration on Mild Traumatic Brain Injury Prognosis. Arch Phys Med Rehabil. 2014;95:S152–73. doi: 10.1016/j.apmr.2013.08.300. [DOI] [PubMed] [Google Scholar]
  • 19.Hesdorffer DC, Rauch SL, Tamminga CA. Long-term psychiatric outcomes following traumatic brain injury: a review of the literature. J Head Trauma Rehabil. 2009;24:452–59. doi: 10.1097/HTR.0b013e3181c133fd. [DOI] [PubMed] [Google Scholar]
  • 20.Carlson KF, Kehle SM, Meis LA, et al. Prevalence, assessment, and treatment of mild traumatic brain injury and posttraumatic stress disorder: a systematic review of the evidence. J Head Trauma Rehabil. 2011;26:103–15. doi: 10.1097/HTR.0b013e3181e50ef1. [DOI] [PubMed] [Google Scholar]
  • 21.Bryant RA, O’Donnell ML, Creamer M, McFarlane AC, Clark CR, Silove D. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167:312–20. doi: 10.1176/appi.ajp.2009.09050617. [DOI] [PubMed] [Google Scholar]
  • 22.Fann JR, Burington B, Leonetti A, Jaffe K, Katon WJ, Thompson RS. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61:53–61. doi: 10.1001/archpsyc.61.1.53. [DOI] [PubMed] [Google Scholar]
  • 23.Nielsen AS, Mortensen PB, O’Callaghan E, Mors O, Ewald H. Is head injury a risk factor for schizophrenia? Schizophr Res. 2002;55:93–98. doi: 10.1016/s0920-9964(01)00205-5. [DOI] [PubMed] [Google Scholar]
  • 24.Fazel S, Wolf A, Pillas D, Lichtenstein P, Långström N. Suicide, fatal injuries, and other causes of premature mortality in patients with traumatic brain injury: a 41-year Swedish population study. JAMA Psychiatry. 2014;71:326–33. doi: 10.1001/jamapsychiatry.2013.3935. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Sariaslan A, Sharp DJ, D’Onofrio BM, Larsson H, Fazel S. Long-term outcomes associated with traumatic brain injury in childhood and adolescence: a nationwide Swedish cohort study of a wide range of medical and social outcomes. PLoS Med. 2016;13:e1002103. doi: 10.1371/journal.pmed.1002103. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26.Rusnak M. Traumatic brain injury: giving voice to a silent epidemic. Nat Rev Neurol. 2013;9:186–87. doi: 10.1038/nrneurol.2013.38. [DOI] [PubMed] [Google Scholar]
  • 27.Tagliaferri F, Compagnone C, Korsic M, Servadei F, Kraus J. A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien) 2006;148:255–68. doi: 10.1007/s00701-005-0651-y. [DOI] [PubMed] [Google Scholar]
  • 28.Roozenbeek B, Maas AIR, Menon DK. Changing patterns in the epidemiology of traumatic brain injury. Nat Rev Neurol. 2013;9:231–36. doi: 10.1038/nrneurol.2013.22. [DOI] [PubMed] [Google Scholar]
  • 29.Yates PJ, Williams WH, Harris A, Round A, Jenkins R. An epidemiological study of head injuries in a UK population attending an emergency department. J Neurol Neurosurg Psychiatry. 2006;77:699–701. doi: 10.1136/jnnp.2005.081901. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Silver JM, Kramer R, Greenwald S, Weissman M. The association between head injuries and psychiatric disorders: findings from the New Haven NIMH Epidemiologic Catchment Area Study. Brain Inj. 2001;15:935–45. doi: 10.1080/02699050110065295. [DOI] [PubMed] [Google Scholar]
  • 31.Frost RB, Farrer TJ, Primosch M, Hedges DW. Prevalence of traumatic brain injury in the general adult population: a meta-analysis. Neuroepidemiology. 2013;40:154–59. doi: 10.1159/000343275. [DOI] [PubMed] [Google Scholar]
  • 32.Wall SE, Williams WH, Cartwright-Hatton S, et al. Neuropsychological dysfunction following repeat concussions in jockeys. J Neurol Neurosurg Psychiatry. 2006;77:518–20. doi: 10.1136/jnnp.2004.061044. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Brower MC, Price BH. Neuropsychiatry of frontal lobe dysfunction in violent and criminal behaviour: a critical review. J Neurol Neurosurg Psychiatry. 2001;71:720–26. doi: 10.1136/jnnp.71.6.720. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Blake PY, Pincus JH, Buckner C. Neurologic abnormalities in murderers. Neurology. 1995;45:1641–47. doi: 10.1212/wnl.45.9.1641. [DOI] [PubMed] [Google Scholar]
  • 35.Grafman J, Schwab K, Warden D, Pridgen A, Brown HR, Salazar AM. Frontal lobe injuries, violence, and aggression: a report of the Vietnam Head Injury Study. Neurology. 1996;46:1231–38. doi: 10.1212/wnl.46.5.1231. [DOI] [PubMed] [Google Scholar]
  • 36.Ryan NP, Catroppa C, Godfrey C, et al. Social dysfunction after pediatric traumatic brain injury: a translational perspective. Neurosci Biobehav Rev. 2016;64:196–214. doi: 10.1016/j.neubiorev.2016.02.020. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37.Tonks J, Williams WH, Frampton I, Yates P, Slater A. The neurological bases of emotional dys-regulation arising from brain injury in childhood: a ‘when and where’ heuristic. Brain Impair. 2012;8:143–53. [Google Scholar]
  • 38.Anderson V, Catroppa C. Recovery of executive skills following paediatric traumatic brain injury (TBI): a 2 year follow-up. Brain Inj. 2005;19:459–70. doi: 10.1080/02699050400004823. [DOI] [PubMed] [Google Scholar]
  • 39.Lenroot RK, Giedd JN. Brain development in children and adolescents: insights from anatomical magnetic resonance imaging. Neurosci Biobehav Rev. 2006;30:718–29. doi: 10.1016/j.neubiorev.2006.06.001. [DOI] [PubMed] [Google Scholar]
  • 40.Steinberg L. A social neuroscience perspective on adolescent risk-taking. Dev Rev. 2008;28:78–106. doi: 10.1016/j.dr.2007.08.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Anderson SW, Damasio H, Tranel D, Damasio AR. Long-term sequelae of prefrontal cortex damage acquired in early childhood. Dev Neuropsychol. 2000;18:281–96. doi: 10.1207/S1532694202Anderson. [DOI] [PubMed] [Google Scholar]
  • 42.National Institute of Justice. Office of Justice Programs, USA. [accessed Feb 12, 2018];From juvenile delinquency to young adult offending. https://www.nij.gov/topics/crime/Pages/delinquency-to-adult-offending.aspx.
  • 43.Best JR, Miller PH. A developmental perspective on executive function. Child Dev. 2010;81:1641–60. doi: 10.1111/j.1467-8624.2010.01499.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Max JE, Robertson BAM, Lansing AE. The phenomenology of personality change due to traumatic brain injury in children and adolescents. J Neuropsychiatry Clin Neurosci. 2001;13:161–70. doi: 10.1176/jnp.13.2.161. [DOI] [PubMed] [Google Scholar]
  • 45.Max JE, Levin HS, Landis J, et al. Predictors of personality change due to traumatic brain injury in children and adolescents in the first six months after injury. J Am Acad Child Adolesc Psychiatry. 2005;44:434–42. doi: 10.1097/01.chi.0000156280.66240.61. [DOI] [PubMed] [Google Scholar]
  • 46.Max JE, Schachar RJ, Landis J, et al. Psychiatric disorders in children and adolescents in the first six months after mild traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2013;25:187–97. doi: 10.1176/appi.neuropsych.12010011. [DOI] [PubMed] [Google Scholar]
  • 47.Ornstein TJ, Sagar S, Schachar RJ, et al. Neuropsychological performance of youth with secondary attention-deficit/hyperactivity disorder 6- and 12-months after traumatic brain injury. J Int Neuropsychol Soc. 2014;20:971–81. doi: 10.1017/S1355617714000903. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.Stoddard SA, Zimmerman MA. Association of interpersonal violence with self-reported history of head injury. Pediatrics. 2011;127:1074. doi: 10.1542/peds.2010-2453. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Ryan NP, Anderson V, Godfrey C, et al. Predictors of very-long-term sociocognitive function after pediatric traumatic brain injury: evidence for the vulnerability of the immature “social brain”. J Neurotrauma. 2013;31:649–57. doi: 10.1089/neu.2013.3153. [DOI] [PubMed] [Google Scholar]
  • 50.Ryan NP, Anderson V, Godfrey C, et al. Social communication mediates the relationship between emotion perception and externalizing behaviors in young adult survivors of pediatric traumatic brain injury (TBI) Int J Dev Neurosci. 2013;31:811–19. doi: 10.1016/j.ijdevneu.2013.10.002. [DOI] [PubMed] [Google Scholar]
  • 51.Timonen M, Miettunen J, Hakko H, et al. The association of preceding traumatic brain injury with mental disorders, alcoholism and criminality: the Northern Finland 1966 Birth Cohort Study. Psychiatry Res. 2002;113:217–26. doi: 10.1016/s0165-1781(02)00269-x. [DOI] [PubMed] [Google Scholar]
  • 52.McKinlay A, Corrigan J, Horwood LJ, Fergusson DM. Substance abuse and criminal activities following traumatic brain injury in childhood, adolescence, and early adulthood. J Head Trauma Rehabil. 2014;29:498–506. doi: 10.1097/HTR.0000000000000001. [DOI] [PubMed] [Google Scholar]
  • 53.Kennedy E, Heron J, Munafo M. Substance use, criminal behaviour and psychiatric symptoms following childhood traumatic brain injury: findings from the ALSPAC cohort. Eur Child Adolesc Psychiatry. 2017;26:1197–206. doi: 10.1007/s00787-017-0975-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Elbogen EB, Wolfe JR, Cueva M, Sullivan C, Johnson J. Longitudinal predictors of criminal arrest after traumatic brain injury: results from the Traumatic Brain Injury Model System National Database. J Head Trauma Rehabil. 2015;30:E3–13. doi: 10.1097/HTR.0000000000000083. [DOI] [PubMed] [Google Scholar]
  • 55.Luukkainen S, Riala K, Laukkanen M, Hakko H, Rasanen P. Association of traumatic brain injury with criminality in adolescent psychiatric inpatients from Northern Finland. Psychiatry Res. 2012;200:767–72. doi: 10.1016/j.psychres.2012.04.018. [DOI] [PubMed] [Google Scholar]
  • 56.Fazel S, Lichtenstein P, Grann M, Langstrom N. Risk of violent crime in individuals with epilepsy and traumatic brain injury: a 35-year Swedish population study. PLoS Med. 2011;8:e1001150. doi: 10.1371/journal.pmed.1001150. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Schofield PW, Malacova E, Preen DB, et al. Does traumatic brain injury lead to criminality? A whole-population retrospective cohort study using linked data. PLoS One. 2015;10:e0132558. doi: 10.1371/journal.pone.0132558. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58.McIsaac KE, Moser A, Moineddin R, et al. Association between traumatic brain injury and incarceration: a population-based cohort study. CMAJ Open. 2016;4:E746–53. doi: 10.9778/cmajo.20160072. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 59.Schiltz K, Witzel JG, Bausch-Holterhoff J, Bogerts B. High prevalence of brain pathology in violent prisoners: a qualitative CT and MRI scan study. Eur Arch Psychiatry Clin Neurosci. 2013;263:607–16. doi: 10.1007/s00406-013-0403-6. [DOI] [PubMed] [Google Scholar]
  • 60.Witzel JG, Bogerts B, Schiltz K. Increased frequency of brain pathology in inmates of a high-security forensic institution: a qualitative CT and MRI scan study. Eur Arch Psychiatry Clin Neurosci. 2016;266:533–41. doi: 10.1007/s00406-015-0620-2. [DOI] [PubMed] [Google Scholar]
  • 61.Rutter ML. Psychosocial adversity and child psychopathology. Br J Psychiatry. 1999;174:480–93. doi: 10.1192/bjp.174.6.480. [DOI] [PubMed] [Google Scholar]
  • 62.Williams HW, Cordan G, Mewse AJ, Tonks J, Burgess CNW. Self-reported traumatic brain injury in male young offenders: a risk factor for re-offending, poor mental health and violence? Neuropsychol Rehabil. 2010;20:801–12. doi: 10.1080/09602011.2010.519613. [DOI] [PubMed] [Google Scholar]
  • 63.Davies RC, Williams WH, Hinder D, Burgess CNW, Mounce LTA. Self-reported traumatic brain injury and postconcussion symptoms in incarcerated youth. J Head Trauma Rehabil. 2012;27:E21–27. doi: 10.1097/HTR.0b013e31825360da. [DOI] [PubMed] [Google Scholar]
  • 64.Perron BE, Howard MO. Prevalence and correlates of traumatic brain injury among delinquent youths. Crim Behav Ment Health. 2008;18:243–55. doi: 10.1002/cbm.702. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65.Chitsabesan P, Lennox C, Williams H, Tariq O, Shaw J. Traumatic brain injury in juvenile offenders: findings from the comprehensive health assessment tool study and the development of a specialist linkworker service. J Head Trauma Rehabil. 2015;30:106–15. doi: 10.1097/HTR.0000000000000129. [DOI] [PubMed] [Google Scholar]
  • 66.Vaughn MG, Salas-Wright CP, DeLisi M, Perron B. Correlates of traumatic brain injury among juvenile offenders: a multi-site study. Crim Behav Ment Health. 2014;24:188–203. doi: 10.1002/cbm.1900. [DOI] [PubMed] [Google Scholar]
  • 67.Farrer TJ, Hedges DW. Prevalence of traumatic brain injury in incarcerated groups compared to the general population: a meta-analysis. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35:390–94. doi: 10.1016/j.pnpbp.2011.01.007. [DOI] [PubMed] [Google Scholar]
  • 68.Ferguson PL, Pickelsimer EE, Corrigan JD, Bogner JA, Wald M. Prevalence of traumatic brain injury among prisoners in South Carolina. J Head Trauma Rehabil. 2012;27:E11–20. doi: 10.1097/HTR.0b013e31824e5f47. [DOI] [PubMed] [Google Scholar]
  • 69.Williams WH, Mewse AJ, Tonks J, Mills S, Burgess CNW, Cordan G. Traumatic brain injury in a prison population: prevalence and risk for re-offending. Brain Inj. 2010;24:1184–88. doi: 10.3109/02699052.2010.495697. [DOI] [PubMed] [Google Scholar]
  • 70.Perkes I, Schofield PW, Butler T, Hollis SJ. Traumatic brain injury rates and sequelae: a comparison of prisoners with a matched community sample in Australia. Brain Inj. 2011;25:131–41. doi: 10.3109/02699052.2010.536193. [DOI] [PubMed] [Google Scholar]
  • 71.Pitman I, Haddlesey C, Ramos SDS, Oddy M, Fortescue D. The association between neuropsychological performance and self-reported traumatic brain injury in a sample of adult male prisoners in the UK. Neuropsychol Rehabil. 2015;25:763–79. doi: 10.1080/09602011.2014.973887. [DOI] [PubMed] [Google Scholar]
  • 72.Fishbein D, Sheppard M, Hyde C, et al. Deficits in behavioral inhibition predict treatment engagement in prison inmates. Law Hum Behav. 2009;33:419–35. doi: 10.1007/s10979-008-9163-7. [DOI] [PubMed] [Google Scholar]
  • 73.Fishbein D, Sheppard M. Assessing the role of neuropsychological funtioning in inmates’ treatment respnse. [accessed Feb 15, 2018]. Grant Award Report: 2002-MU-BX0013, document: 216303. https://www.ncjrs.gov/pdffiles1/nij/grants/216303.pdf. [Google Scholar]
  • 74.Shiroma EJ, Pickelsimer EE, Ferguson PL, et al. Association of medically attended traumatic brain injury and in-prison behavioral infractions: a statewide longitudinal study. J Correct Health Care. 2010;16:273–86. doi: 10.1177/1078345810378253. [DOI] [PubMed] [Google Scholar]
  • 75.Ray B, Richardson NJ. Traumatic brain injury and recidivism among returning inmates. Crim Justice Behav. 2017;44:472–86. [Google Scholar]
  • 76.Brewer-Smyth K, Burgess AW, Shults J. Physical and sexual abuse, salivary cortisol, and neurologic correlates of violent criminal behavior in female prison inmates. Biol Psychiatry. 2004;55:21–31. doi: 10.1016/s0006-3223(03)00705-4. [DOI] [PubMed] [Google Scholar]
  • 77.Colantonio A, Kim H, Allen S, Asbridge M, Petgrave J, Brochu S. Traumatic brain injury and early life experiences among men and women in a prison population. J Correct Health Care. 2014;20:271–79. doi: 10.1177/1078345814541529. [DOI] [PubMed] [Google Scholar]
  • 78.McMillan TM, Williams WH, Bryant R. Post-traumatic stress disorder and traumatic brain injury: a review of causal mechanisms, assessment, and treatment. Neuropsychol Rehabil. 2003;13:149–64. doi: 10.1080/09602010244000453. [DOI] [PubMed] [Google Scholar]
  • 79.León-Carrión J, Ramos FJC. Blows to the head during development can predispose to violent criminal behaviour: rehabilitation of consequences of head injury is a measure for crime prevention. Brain Inj. 2003;17:207–16. doi: 10.1080/0269905021000010249. [DOI] [PubMed] [Google Scholar]
  • 80.Sentencing Council. Sentencing children and young people overarching principles and offence specific guidelines for sexual offences and robbery. Definitive guideline. [accessed Feb 12, 2018];2017 https://www.sentencingcouncil.org.uk/mcsg-updates/item/definitive-guidelines-on-sentencing-children-and-young-people-and-reduction-in-sentence-for-a-guilty-plea-published/
  • 81.Williams WH, Chitsabesan P. Young people with traumatic brain injury in custody: an evaluation of a linkworker service for Barrow Cadbury Trust and The Disabilities Trust. 2016 [Google Scholar]
  • 82.Lichtenstein P, Halldner L, Zetterqvist J, et al. Medication for attention deficit–hyperactivity disorder and criminality. N Engl J Med. 2012;367:2006–14. doi: 10.1056/NEJMoa1203241. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 83.Justice Committee of the House of Commons. Neuro-disabilities and mental disorders. The treatment of young adults in the criminal justice system. [accessed Feb 12, 2018]; https://publications.parliament.uk/pa/cm201617/cmselect/cmjust/169/169.pdf.
  • 84.Scottish Prison Service/NHS Scotland. National Prisoner Healthcare Network: brain injury and offending. Edinburgh: 2016. [accessed Feb 13, 2018]. http://www.nphn.scot.nhs.uk/published-reports/ [Google Scholar]
  • 85.Cole WR, Gerring JP, Gray RM, et al. Prevalence of aggressive behaviour after severe paediatric traumatic brain injury. Brain Inj. 2008;22:932–39. doi: 10.1080/02699050802454808. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 86.Schofield P, Butler T, Hollis S, D’Este C. Are prisoners reliable survey respondents? A validation of self-reported traumatic brain injury (TBI) against hospital medical records. Brain Inj. 2011;25:74–82. doi: 10.3109/02699052.2010.531690. [DOI] [PubMed] [Google Scholar]
  • 87.Maas AIR, Menon DK, Adelson DP, et al. for the InTBIR Participants and Investigators Traumatic brain injury—integrated approaches to improve prevention, clinical care, and research. Lancet Neurol. 2017;16:987–1048. doi: 10.1016/S1474-4422(17)30371-X. [DOI] [PubMed] [Google Scholar]
  • 88.Bigler E. Traumatic brain injury, neuroimaging, and neurodegeneration. Front Hum Neurosci. 2013;7:395. doi: 10.3389/fnhum.2013.00395. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 89.Hughes N, Williams WH, Chitsabesan P, Walesby RC, Mounce LTA, Clasby B. The prevalence of traumatic brain injury among young offenders in custody: a systematic review. J Head Trauma Rehabil. 2015;30:94–105. doi: 10.1097/HTR.0000000000000124. [DOI] [PubMed] [Google Scholar]
  • 90.Patterson GR, DeBaryshe BD, Ramsey E. A developmental perspective on antisocial behavior. Am Psychol. 1989;44:329–35. doi: 10.1037//0003-066x.44.2.329. [DOI] [PubMed] [Google Scholar]
  • 91.Van Ryzin MJ, Dishion TJ. From antisocial behavior to violence: a model for the amplifying role of coercive joining in adolescent friendships. J Child Psychol Psychiatry Allied Discipl. 2013;54:661–66. doi: 10.1111/jcpp.12017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 92.Pollak SD. Multilevel developmental approaches to understanding the effects of child maltreatment: recent advances and future challenges. Dev Psychopathol. 2015;27:1387–97. doi: 10.1017/S0954579415000826. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 93.Barrasso-Catanzaro C, Eslinger PJ. Neurobiological bases of executive function and social-emotional development: typical and atypical brain changes. Family Relations. 2016;65:108–19. [Google Scholar]
  • 94.Teicher MH, Samson JA, Anderson CM, Ohashi K. The effects of childhood maltreatment on brain structure, function and connectivity. Nat Rev Neurosci. 2016;17:652–66. doi: 10.1038/nrn.2016.111. [DOI] [PubMed] [Google Scholar]
  • 95.McCrory E, De Brito SA, Viding E. The impact of childhood maltreatment: a review of neurobiological and genetic factors. Front Psychiatry. 2011;2:48. doi: 10.3389/fpsyt.2011.00048. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 96.Wolff N, Gregory Chugo M, Shi J, Huening J, Frueh BC. Screening for PTSD among incarcerated men: a comparative analysis of computer-administered and orally administered modalities. Crim Justice Behav. 2015;42:219–36. doi: 10.1177/0093854814551601. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 97.Elbogen EB, Johnson SC, Newton VM, et al. Criminal justice involvement, trauma, and negative affect in Iraq and Afghanistan war era veterans. J Consult Clin Psychol. 2012;80:1097–102. doi: 10.1037/a0029967. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 98.Fazel S, Chang Z, Fanshawe T, et al. Prediction of violent reoffending on release from prison: derivation and external validation of a scalable tool. Lancet Psychiatry. 2016;3:535–43. doi: 10.1016/S2215-0366(16)00103-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 99.Chang Z, Lichtenstein P, Långström N, Larsson H, Fazel S. Association between prescription of major psychotropic medications and violent reoffending after prison release. JAMA. 2016;316:1798–1807. doi: 10.1001/jama.2016.15380. [DOI] [PMC free article] [PubMed] [Google Scholar]

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