Risk factors

Observation: Risk factors for irritable behaviour in TBI patients include loss of employment, social isolation, and depression, and males aged between 15 and 34 years are more at risk.

1.2.4. Abuse and excessive consumption: risky, excessive, addictive behaviour A variety of categories are currently accepted (cf. public hearing: abuse, addiction and multi-substance use: treatment strategies - HAS 2007): "Simple use: any conduct that is not an issue as long as consumption remains low. This notion varies from product to product and is often unclear, as the thresholds have only been defined for alcohol. In some cases, the risk is higher according to the products or the situation (pregnancy, driving, specific psychological factors...). Risky use:

consumption that is likely to induce additional medical, psychological or social damage in the short, medium or long term. Harmful use is characterised by the presence of medical, psychological or social damage induced by the consumption, whatever the frequency and level, and the absence of addiction. Addictive use is characterised by loss of control of consumption. Addiction is not defined in relation to levels or frequency of consumption, or in relation to the complications often associated.

Multi-substance use is defined simply by the consumption of at least 2 psycho-active substances."

In order to examine the links between TBI and addiction, it is important to identify the incidence of abuse or "misuse" of alcohol and drugs prior to the trauma, at the time of the trauma, and following the trauma, and to compare the data with those of the general population.

Alcohol and drugs before the trauma: History of alcohol abuse reported in 18 to 79% of TBI, and history of consumption of illicit drugs in 10 to 44% of TBI.

Alcohol at the time of the TBI: 31 to 51%

In the United States, alcohol is a major factor in TBI.

Studies show that alcohol and marijuana consumption are not predictive of TBI, and TBI is not predictive of post-traumatic substance use (level 2).

Alcohol consumption is associated with more severe lesions in Road Traffic Collisions (RTC) and a greater number of serious accidents.

Alcohol and drugs after TBI: between 1 and 5 years after the TBI, the prevalence of high alcohol consumption or addiction varies from 7 to 26% depending on the studies. Overall, the prevalence of alcohol abuse is lower following a TBI in comparison with before the TBI.

The consumption of illicit drugs after TBI varies from 2 to 20% depending on the studies.

Other substances: The literature review does not provide any information regarding the use and/or abuse of cocaine, stimulants and opioids in the TBI population. Eating disorders are often described after a traumatic brain injury, but the little information found in the literature was generally limited to case studies. These symptoms, and notably hyperphagia, can be integrated in other behavioural disturbances such as the Kluver-Bucy syndrome or endocrine disorders, which are also common after TBI.

Observation: Drug and alcohol consumption before a TBI is not significantly different from that of the general population.

Observation: Following a traumatic brain injury, alcohol abuse affects the severity of the brain damage, the depth of mental derangement, as well as the use of narcotic and psychotropic drugs.

Observation: Drug or alcohol consumption prior to a TBI increases the risk of subsequent behavioural disorders (EC).

Observation: The prevalence of alcohol or illicit substance abuse is minimal in the year following a TBI. However, even if the data from the literature are equivocal, the risk of harmful or addictive use seems to be greater after a TBI and in particular after returning home.

Observation: Additional studies (longitudinal studies) are necessary before any recommendations can be established.

Observation: The risk of addiction, depression or suicide is higher in TBI patients with a history of misuse and the probability of returning to work is lower.

Observation: In TBI patients, low level of education, and low social class, prior consumption, and depression are factors associated with harmful substance use or addiction. In addition, male TBI patients are more at risk.

1.2.5. Behaviour resulting in forensic consequences, misdemeanour, crime

The question regarding a link between TBI and behaviour resulting in forensic consequences is often raised. Several epidemiological studies have investigated the prevalence of prior TBI in prison populations.

Behavioural disorders secondary to a traumatic brain injury can be associated with criminal

behaviour, which in some cases leads to imprisonment. Therefore, a TBI in childhood or adolescence increases the risk of psychiatric disorders (OR=2.1), and in men, a TBI is significantly associated with subsequent psychiatric disorders linked to criminality (OR=4.1) (level 2).

The risk of violent crime is greater in TBI populations (level 2). The risk of committing violent acts depends on the age at the time of the TBI and co-morbidities (harmful use of drug or alcohol). The risk of committing a violent crime is higher in 5.8% of subjects with a TBI and is lower if the TBI occurred before the age of 16.

According to two meta-analyses, the prevalence of a prior TBI was significantly higher in prison populations compared with the general population (level 2). In the first meta-analysis, the prevalence of a prior TBI was globally 41.2%, ranging from 9.7% to 100% depending on the studies. In the second meta-analysis, the overall prevalence of prior TBI in the entire prison population was 60.3%.

A higher prevalence of prior TBI has been highlighted in a population of offenders (non-violent crime, misdemeanour) not imprisoned in comparison with non-offenders (level 3).

Insofar as these studies are based on questioning, the reliability of the answers could be called into question. However, a study on 200 Australian prisoners questioned regarding their history of traumatic brain injuries (TBI) shows that the answers correspond to reality.

Nevertheless, several important parameters were not always specified: characteristics of the control population, chronology of the TBI in relation to the imprisonment, severity of the TBI. It seems particularly fundamental, but also complex, to verify the pairing of the populations compared (sex, age, level of education, social background...).

For those entering prison, a prior TBI was often associated with contact sports, being expelled from school, use of drugs, a depressive syndrome, and psychosis (level 3).

In relation to prisoners with no history of TBI, prisoners who suffered a TBI were younger (16 years compared with 20 years), had longer prison sentences (7 months longer), had been imprisoned more times (level 3), were more prone to harmful substance use (level 3), and were at greater risk of anxiety-depressive disorders.

Prisoners with a prior TBI had more health problems, more memory problems, significantly higher levels of alcohol or marijuana consumption, more mental disorders, and problems socializing (level 3).

Infringement of prison rules was observed more often in prisoners with a prior TBI than those with no TBI (level 2). In addition, the risk of committing a violent offense was significantly higher in the female population with a prior TBI (RR = 2.44).

TBI, sexual delinquency and hormonal disorders

Hormonal disorders are common in TBI sufferers, and concern in particular the gonadal axis (Richard et al. 2001). The search for a connection between gonadal axis dysfunction and sexual behavioural disorders, especially when associated with a criminal offense, could be useful when looking for a causal link and could open up new therapeutic perspectives.

Observation: In studies investigating a link between the concomitance of TBI and criminal offenses, the characteristics of the control population, the chronology of the TBI in relation to the imprisonment, and the severity of the TBI must be specified. It is particularly fundamental to check the pairing of the populations compared (sex, age, level of education, social

background...).

Observation: A history of TBI in childhood or adolescence seems to be associated with an increased risk of psychiatric disorders and criminality.

Observation: The prevalence of a prior TBI in the prison population seems to be higher than that of the general population.

Observation: A prior traumatic brain injury could increase the risk of violent crime.

Observation: In relation to prisoners with no prior TBI, prisoners with a prior TBI are younger, have more health problems, more memory loss, are in prison for longer and more often, their substance use is harmful (alcohol or marijuana), and they have anxiety-depressive disorders more often.

1.3. Default behavioural disturbances

Essentially apathy is addressed in this chapter. Apragmatism, athymhormia, and aboulia are also part of this category of symptoms, but are not specific to traumatic brain injuries.

1.3.1. Apathy

1.3.1.1. Definition

There are currently numerous definitions of apathy in the literature. In the DSM-IV-R, apathetic symptoms are part of the diagnostic criteria of various disorders. Apathy is therefore considered as a symptom and not a syndrome.

Most definitions concur that apathy refers to various cognitive, behavioural and emotional symptoms.

A few rare studies have investigated the nature of the psychological mechanisms involved in the occurrence of apathetic behaviour in traumatic brain injury sufferers. In these studies, it was shown that apathy is associated with specific cognitive deficits linked to frontal lobe dysfunctions such as executive functions, speed of processing information or even learning new information.

In addition, it has been shown that apathy is associated with emotional and motivational dysfunction in TBI patients.

From an anatomical-functional perspective, apart from frontal lesions, apathy could be associated with lesions affecting the limbic circuit and the basal ganglia, and the nature of the brain damage could result in distinct apathetic symptoms. Damage to the prefrontal dorsolateral cortex could lead to a decrease in self-initiated behaviour due to an executive dysfunction. Damage to the orbitofrontal cortex could result in apathetic behaviour due to deficient emotional processes such a lower sensitivity to reward, and finally, damage to the anterior cingulate cortex could cause a decrease in motivated responses to external and internal stimuli thus resulting in apathetic symptoms.

The question concerning links between apathy and depression is frequently raised in the literature.

Double dissociations have been highlighted within the context of traumatic brain injuries (apathy without depression and depression without apathy). A few studies have shown that apathy can occur in the absence of depression, but most of the studies report that a significant number of patients have both apathetic and depressive symptoms. The common association of apathy and depression, as well as the similarity of the symptoms, raises the question of a joint patho-physiological and psychological process. From a clinical perspective, depressive mood can be distinguished from apathy by the wealth of affects mobilised. However, some very slow, anergic forms of depression bordering on depressive stupor can go hand in hand with a complete loss of emotional reactivity, thus resulting in a clinical picture of apathy. In addition, apathy differs from aboulia in the degree of

motivation deficiency, and is characterised by a lack of initiative, decreased activity, but

communication is generally intact, whereas a severe communication deficiency is often observed with aboulia.

The characteristics of apathy such as loss of motivation, anhedonia, social isolation, and poverty of speech are also described in schizophrenia. Schizophrenic patients have a much higher score than TBI sufferers (indicating a more severe deficiency) for "alogia, flattened affect, anhedonia", but not for attention (level 3). Symptoms of hebephrenic or catatonic forms of schizophrenia overlap with the notion of apathy in which negative "deficient" symptoms predominate. Avolition and emotional blunting, both aspects of apathy, are among the 5 "characteristic symptoms" of schizophrenia retained in the DSMIV (only two are required). Except in very rare cases, apathy is just a component of schizophrenia.

In traumatic brain injury sufferers, apathy can occur several years after the trauma. Apathy hinders rehabilitation, coping, professional future, autonomy at home, and increases the burden felt by the family.

Table 1: Main symptoms of apathy

Authors Definition

Marin (1991, 1996) Lack or loss of motivation, evidenced by diminished goal-directed overt behaviour, diminished goal-directed cognition and diminished emotional concomitants of goal- directed behaviour

Stuss, Van Reekum et Murphy (2000)

Lack of responsiveness to stimuli as demonstrated by a lack of self-initiated action (‘emotional–affective’, ‘behavioural’ or ‘cognitive’) Levy et Dubois (2006) Quantitative reduction of voluntary, goal-directed behaviours, three

subtypes of apathy: ‘emotional–affective’, ‘cognitive’ and ‘auto-activation’

Robert et al., (2009) ; Mulin et al.

(2011)

Loss of or diminished motivation, with presence of at least one symptom in at least two of the three following domains: loss of or diminished goal‐directed behaviour, loss of or diminished goal‐directed cognitive activity, loss of or diminished emotion

Levy, R., & Dubois, B. (2006). Apathy and the functional anatomy of the prefrontal cortex-basalganglia circuits. Cerebral Cortex, 16(7), 916-928.

Marin RS, Biedrzycki RC, Firinciogullari S. Reliability and validity of the Apathy Evaluation Scale. Psychiatry Res 1991; 38:143-62.

Marin RS. Apathy: Concept, syndrome, neural mechanisms, and treatment. Semin Clin Neuropsychiatry 1996; 1:304-314.

Mulin, E., Leone, E., Dujardin, K., Delliaux, M., Leentjens, A., Nobili, F., et al. (2011). Diagnostic criteria for apathy in clinical practice. International Journal of Geriatric Psychiatry, 26(2), 158-165.

Robert, P. H., Onyike, C. U., Leentjens, A. F., Dujardin, K., Aalten, P., Starkstein, S., et al. (2009). Proposed diagnostic criteria for apathy in Alzheimer's disease and other neuropsychiatric disorders. European Psychiatry, 24(2), 98-104.

Stuss, D. T., Van Reekum, R., & Murphy, K. J. (2000). Differentiation of states and causes of apathy. In J.

C. Borod (Ed.), The neuropsychology of emotion (pp. 340-363). New York: Oxford University Press .

R8: Apathy, apragmatism, athymhormia, aboulia are default behavioural disorders observed in TBI patients (EC).

R9: Apathy is characterised by a decrease in goal-directed behaviour and involves motivational, emotional and/or cognitive aspects (EC).

Observation: Apathy is commonly associated with depression (30 to 60% depending on the studies), but double dissociations have been observed suggesting that distinct processes are involved. Depressive mood can be differentiated from apathy by the wealth of affects

mobilised

Observation: Apathy can occur after the trauma. It hinders rehabilitation, affects autonomy at home, professional future, and the burden felt by families.

1.3.1.2. Incidence/prevalence

Prevalence: 20 to 71% of severe TBI depending on the studies (level 3-4).

Observation: The prevalence of apathy in severe TBI varies between 20 and 71% depending on the studies.

1.4. Emotional disorders, anxiety and psychosis 1.4.1. Post-traumatic depression

1.4.1.1. Definition

The different criteria used and the references can be found in the fourth revised edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) by the American Association of Psychiatry (AAP). There are no specificities regarding the diagnostic criteria applied to traumatic brain injuries, but anosognosia, often present in the initial stages, can affect the patient's mood.

Some neurological symptoms, in particular speech disorders and more generally communication, can make the diagnosis more complicated.

1.4.1.2. Incidence/prevalence

In the literature, the average prevalence of depression after moderate or severe cranio-encephalic traumas is 31%, with extremes ranging from 12 to 76% depending on the population characteristics and the evaluation method. No patterns in the natural progression or prevalence peaks were observed following repeated and prolonged evaluations. On average, 27% of criteria supported depression 3 to 6 months after the trauma, 32% between 6 and 12 months, and 33% after 12 months. Fatigue, low concentration, and sleep disorders are common in TBI patients in the absence of depression, which can lead to an overestimation of the diagnosis.

The prevalence of depression in the literature review was estimated at 7.5 times greater than in the general population.

Families of TBI sufferers also have a higher risk of depression.

1.4.1.3. Contributing or triggering factors

- The risk of suffering from major depression following a traumatic brain injury is reinforced by a prior psychiatric condition and a weak socio-economic status.

- Studies investigating links between depression and cerebral location are contradictory. According to several CT-based studies, the left anterior lesions involving the frontal dorsolateral cortex and/or the left basal ganglions are associated with an increased risk of depression when the location of the lesion is evaluated using a multivariate regression model (level 4). Lesions in the right hemisphere are associated with a decrease in the risk of acute depression due to frequently associated anosognosia.

- Awareness of the severity of the handicap when leaving hospital is strongly correlated with a depressive syndrome in the initial phase and later. On the contrary, anosognosia is associated with minimal expression of depressive symptoms (level 2).

- Age is an independent risk factor of depression and is inversely proportional: the risk decreases with age (level 2).

- Several studies have shown a higher risk in women.

- A low level of education and being underprivileged can contribute to the onset of depression.

- Substance or alcohol abuse increases the risk (level 3).

- Pain, involvement in the dispute relating to the accident, and the stress perceived, are risk factors identified in the cohorts followed in rehabilitation centres and prospective cohorts (level 4).

- "Psycho-social" stress is an independent risk factor

- Psychosocial helpers (caregivers, partners, family members), and the presence of a confidante reduce the risk of depression, whereas social isolation increases the risk. Family support also plays a major role in the long-term emotional well-being of TBI patients (level 2). The number of years of marriage is inversely linked to the risk, while the degree of cognitive and motor deficiency and social aggressiveness increase the risk.

- The concepts of resilience and personality traits have not been clearly studied, but an Israeli study showed that the Adult Hope Scale and the Life Orientation Test-Revised scores help predict depression and its severity.

- A history of depression, as well as depression at the time of the accident is a major risk (level 2).

- The loss or absence of employment increases the risk of depression, as well as dissatisfaction at

work or fear of being dismissed.

Observation: After moderate or severe TBI, the prevalence of depression varies from 12 to 76% according to the population characteristics and the evaluation method. Repeated and prolonged evaluations show that the average prevalence of depression varies little after the TBI. The estimated prevalence of depression was 7.5 times greater than in the general population. Families of TBI patients also have a higher risk of depression.

Observation: A prior psychiatric condition and a weak socio-economic status increase the risk of suffering from major depression.

Observation: Numerous factors are associated with depression: prior psychiatric condition, depression at the time of the accident, damage to the left hemisphere, high cognitive deficiency, social aggressiveness, loss, fear of losing or absence of employment, social isolation, weak socio-economic status, substance abuse, perceived stress, dispute, pain, and awareness of the severity of the handicap. Young women are more at risk.

Observation: The risk of depression is lower when the damage affects the right hemisphere and in particular the frontal dorsolateral cortex and/or the basal ganglions. Depressive symptoms are less common in anosognosic patients.

Observation: Family support, psychosocial helpers, as well as the presence of a confidante help protect against depression.

1.4.2. Anxiety

1.4.2.1. Definition

The DSM-IV defines 10 groups of anxiety disorders: agoraphobia, panic attack, specific phobia, social phobia, OCD, post-traumatic disorder, acute stress disorder, generalized anxiety disorder, anxiety disorders linked to a medical condition, and substance-induced anxiety disorders.

1.4.2.2. Incidence/prevalence

Panic disorders: 4 to 14% in TBI patients compared with 0.8 to 2% in the general population.

Generalized anxiety disorders: 2.5 to 24.5% in TBI patients compared with 3.1% in the general population.

Phobias: 0.8 to 10% compared with 1.1 to 13% in the general population.

1.4.2.3. Contributing or triggering factors

- Generalized anxiety disorder associated with weak functional status.

Observation: Generalized anxiety and panic disorders are more common in TBI than in the general population.

Observation: A weak functional status contributes to generalized anxiety disorders.

1.4.3. Post-traumatic stress disorder (PTSD) 1.4.3.1. Definition

Given the association of organic amnesia with severe TBI, the concomitance of post-traumatic stress

Given the association of organic amnesia with severe TBI, the concomitance of post-traumatic stress