Substance use, criminal behaviour and psychiatric symptoms following childhood traumatic brain injury: findings from the ALSPAC cohort

Traumatic brain injury (TBI) is the leading cause of disability in young people [1]. A recent review of paediatric TBI estimated that each year TBI affects over 3 million children worldwide, and that over 80% of these are mild [2]. The definition of what constitutes a mild TBI varies between studies; however, the Centre for Disease Control suggests the following: “Mild TBI is an injury to the head (arising from blunt trauma or acceleration or deceleration forces) that results in one or more of the following: any period of confusion, disorientation, or impaired consciousness; any dysfunction of memory around the time of injury; loss of consciousness lasting less than 30 min; or the onset of observed signs or symptoms of neurological or neuropsychological dysfunction” [3]. Previous cross-sectional research has shown increased substance use [4], disruptive behaviour disorders [5], school violence [6] and conduct problems [7, 8] in participants with a history of mild TBI.

Evidence for a prospective association between mild TBI and negative behavioural outcomes comes from three cohort studies. In a sample of over one million Swedish people, having a TBI registered with hospital before age 25 years was associated with increased risk of adverse outcomes, including drawing a disability pension, psychiatric visit or hospitalisation, low educational attainment, and welfare recipiency. For those with a mild TBI, the risk ratios for these outcomes ranged from 1.18 to 1.52 [9]. Findings from the Northern Finland 1966 Birth Cohort Study indicate that a mild TBI before age 14 years was associated with drinking to intoxication at age 14 years [10]. In the same cohort, male participants with a TBI before age 15 years were at higher risk of committing a crime registered with the Ministry of Justice from ages 16 to 31 years, and those with a TBI had a twofold increased risk of developing a psychiatric disorder, which increased to fourfold for criminality combined with a psychiatric disorder [11]. In the Christchurch Health and Development Study (CHDS), participants who had experienced a mild TBI requiring an inpatient hospital stay between birth and age five years had higher self- and parent-ratings of conduct disorder/oppositional defiant disorder and substance abuse at age 14–16 years [12], and a higher likelihood of alcohol and drug dependence at age 16–25 years, which mediated a relationship between the same injury and an increased number of arrests, property offences and violent offences [13]. Any mild TBI at age 6–15 years was linked with increased arrests and property offences at age 16–25 years, hospitalisation for the injury was additionally associated with violent offences [13].

In this study, we investigated the association between mild TBI and risk behaviour in a United Kingdom birth cohort. TBI was based on incidences of skull fracture and loss of consciousness due to a head injury reported by parents and children at multiple time points up to age 16 years. Risk behaviour was defined as psychiatric symptoms, substance use, and criminal behaviours. To strengthen causal inference we incorporated a negative control exposure group, where confounding structures are likely to be similar but there is no pathway between the exposure and the outcome [14]. If the observed association is larger for exposure of interest than for the negative control exposure this increases confidence that the association may be causal [15]. Previously, in the Swedish population study, individuals who sustained non-TBI fall-related injuries were less likely to have poor adult outcomes than those with a TBI before age 25 years [9]. Additionally, Fazel and colleagues found that participants with a history of epilepsy were less likely to commit violent crime than those who sustained a TBI [16]. In our study, participants with a history of fracture or broken bone formed the negative control exposure group as this type of injury has a similar confounding structure to TBI but lacks the plausible biological mechanism (i.e., brain injury) for an association with risk behaviour. The effect of age at injury was investigated in secondary analyses separating the cohort into those with childhood injuries and those with adolescent injuries.

We used data from a longitudinal birth cohort to explore the association between sustaining a mild TBI before age 16 years and subsequent substance use, criminal behaviour and psychiatric symptoms. There are three main findings. First, relative to having no injury, sustaining a mild TBI between birth and age 16 was associated with problematic alcohol, tobacco and cannabis use, a higher likelihood of committing an offence and a higher likelihood of having conduct problems at age 17 years. Second, in negative control analyses, there was evidence that sustaining a mild TBI was associated with hazardous alcohol use relative to sustaining an OI–adding evidence for a possible causal association between TBI and later alcohol misuse—while both mild TBI and OI were associated with committing offences. Third, additional analyses suggest that age at injury may be important for certain outcomes; participants with a mild TBI between birth and age 11 years had higher odds of psychiatric symptoms at age 17 years, while participants who incurred a mild TBI between age 12 and 16 years had higher odds of problematic substance use and criminal behaviours at age 17 years.

The first main finding lends support to results from other birth cohort studies; although the strength of evidence for associations found in our study are somewhat weaker than those in other birth cohorts. This could reflect our use of self-report rather than medical records whereby non-TBI events may be recalled as TBI diluting the true exposure. We found that 7% of the cohort had experienced a TBI by age 16 years, this lies between the rate of 3.8% in the Northern Finland cohort and 31.6% in the CHDS [26]. Mild TBI was associated with 39–67% increased risk of six of the seven outcomes, which is comparable to the 18–52% increased risk of poor adult outcomes reported by Sariaslan and colleagues [9]. The increased odds of higher levels of alcohol consumption amongst the TBI group here is in keeping with the more frequent intoxication reported by 14 year olds with a TBI in The Northern Finland Birth Cohort [10]. In the CHDS, a TBI requiring hospitalisation was associated with increased odds of externalising disorders and substance abuse at age 14 to 16 years [12] and with increased odds of alcohol and drug dependence, and criminal behaviour at age 16 to 25 years [13]. In the current investigation, the association between TBI and criminal offences did not remain once substance use was added as a covariate. McKinlay and colleagues reported a similar association for those injured before age 5 years; however, for those injured from age 6 to 15 years, a strong association remained for arrests and property offences, but not violent offences. They concluded that a certain threshold of TBI may be required for these effects to be seen [13]. However, in our study it was not possible to index the severity of the TBI.

Second, we included a negative control exposure group to increase the confidence that the associations seen between TBI and risk behaviour may be causal, where several previous studies have only used an uninjured control group [27]. We found that participants who had sustained an OI were not at increased risk of problematic substance use or conduct problems compared to the no injury group, providing further support to previous literature. Interestingly, in a direct comparison between the two injury groups, the TBI group was only found to have a higher likelihood of hazardous alcohol use. This finding has implications for the treatment and management of youth post-TBI as alcohol use has previously been linked with recurrent TBI [28] and poorer recovery from TBI [29]. The lack of evidence for an association between TBI and the other risk outcomes when directly compared with OI highlights the importance of exercising caution when drawing conclusions about mild TBI from research that does not take other injuries into account. The association between OI and committing offences was an unexpected finding; one plausible explanation is that there may be common risk factors for both committing crimes and for being involved in accidents that result in physical injury. For example, sensation-seeking has previously been linked with both criminality and spinal cord injuries in a case–control study of 140 male spinal cord injury patients and 140 matched controls [30]. Although both TBI and OI were associated with committing offences, only those with a TBI were more likely to have been in trouble with the police. Previously it has been suggested that having a TBI may be a risk factor for criminal behaviour and it may place an individual at a disadvantage during legal proceedings [31]. Our finding raises the possibility that having a TBI may also be a factor in the initial transition into the legal system. Future studies in prison populations should measure the incidence rate of OI in addition to TBI in order to further explore this relationship.

Third, there were some differences in risk of outcomes for childhood and adolescent TBI. Childhood TBI (aged 0–11 years) was associated with conduct problems, while adolescent TBI (aged 12–16 years) was associated with increased likelihood of problematic alcohol and tobacco use, as well as criminality. Adolescent OI was associated with problematic tobacco use and committing offences, further highlighting a possible role for common risk factors mentioned above. TBI in both age groups showed weak association with cannabis use. Between these age ranges there was a change from parent-reported to self-reported TBI; however, we feel that this change is unlikely to have impacted the findings as it is more appropriate for the offspring to report their own injuries once they have entered secondary education. There may be some differences in severity of the injuries reported from childhood to adolescence—elsewhere the injuries occurring after 15 years were more severe [26]—it would be interesting to assess this possibility in future research.

The prospective birth cohort design is a major strength of this study. Each injury was reported in close proximity to the time it happened, minimising the issue of recall bias. The longitudinal nature of the study allows for causal inference based on the temporal relationship between exposure and outcome. Additionally, the lack of statistical support and weak associations between our negative control group and the main outcomes, with the exception of committing offences, adds to the strength of evidence for a causal association suggested by previous research. On the other hand, the findings from the direct comparison between TBI and OI showing that TBI was only associated with hazardous alcohol use highlights the importance of exercising caution when interpreting findings on mild TBI without inclusion of a negative control group. However, the study is not without limitations. In particular, we were unable to obtain any index of severity based on the TBI measure, meaning that some nuances in effects based on severity may have been missed. For example, increased alcohol use has previously been related to mild but not moderate-to-severe TBI [10]. Nonetheless the items used to identify TBI are similar to existing research, skull fractures based on ICD codes have been used to classify mild TBI elsewhere [10] and self-report questions asking about loss of consciousness have also been utilised [32‐34].

Evidence from cross-sectional work suggests that there is a relationship between mild TBI and risk behaviour in youth [4‐8]; however, there is a paucity of high quality longitudinal research investigating this association [27]. We have attempted to further explore a potential causal link by using data from a representative birth cohort and including a non-brain related injury group as a negative exposure control. Overall we found that participants who sustained a mild TBI before age 16 years were more likely than those with no injury or with a history of OI to use alcohol to problematic levels at age 17 years. Additionally, sustaining either a mild TBI or OI before age 16 years increased the likelihood of an individual committing offences at age 17 years. The study adds evidence for a possible causal association between mild TBI in youth and later hazardous alcohol use, and highlights the importance of including an extra injury group in mild TBI research.