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Good Practice Guidelines Behavioural disorders in traumatic brain injury patients:

Therapeutic options.

Recommendations

These good practice guidelines have been granted the HAS label. This label means that these good practice guidelines have been developed according to the methodological rules and procedures recommended by the HAS (French Supreme Authority for Health). Any dispute regarding the merits must

be addressed directly to the promoter.

This work was supported by the French Traumatic Brain Injury Society (Association France Traumatisme Crânien)

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Contents

Glossary...5

Abbreviations ...5

Introduction ...6

1. Context ...6

2. Theme ...6

3. Objective...6

4. Patients concerned...6

5. Professionals concerned ...7

Working Method...7

1. Recommendations in clinical practice ...7

2. Conflicts of interest ...7

3. Documentation research ...7

4. Participants...7

4.1. HAS Project Leaders ...7

4.2. Steering Committee ...7

4.3. Work group ...8

4.4. Reading group ...8

5. Grading of recommendations ...9

Recommendations ...9

1. Question 1: What are the different types of disruptive symptoms that can be treated...10

1.1. General information………10

1.2. Excessive behavioural disturbances ...10

1.2.1. Agitation ...11

1.2.1.1. Definition ...11

1.2.1.2. Incidence/prevalence ...11

1.2.1.3. Contributing or triggering factors...12

1.2.2. Aggressiveness ...12

1.2.3. Irritability ...13

1.2.3.3. Risk factors ...13

1.2.4. Abuse and excessive consumption: high-risk, excessive, addictive behaviour... 13

1.2.5. Behaviour resulting in forensic consequences, misdemeanour, crime...14

1.3. Default behavioural disturbances ...15

1.3.1. Apathy ...15

1.4. Emotional disorders, anxiety and psychosis...17

1.4.1. Post-traumatic depression...17

1.4.2. Anxiety...18

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1.4.3. Post-traumatic stress disorder (PTSD)...18

1.4.4. Obsessive-compulsive disorders...19

1.4.4.1 Incidence/prevalence ...19

1.4.4.2 Contributing or triggering factors...19

1.4.5. Post-traumatic psychosis...19

1.5. Attempted suicide and suicide ...20

2. Question 2: Assessment...21

3. Question 3: Treatment techniques and non-medical interventions...23

3.1. General recommendations... ...23

3.2. Specific approaches and treatments:...23

3.2.1 Holistic and institutional approaches ...23

3.2.2. Behavioural therapy (BT) and Cognitive behavioural therapy (CBT)...24

3.2.3. Systemic family approaches...24

3.2.4. Psychoanalytic and psychodynamic psychotherapy ...25

3.2.5. Physical activity treatment techniques...25

3.3 Relational treatment techniques and approaches...26

4. Question 4: Use of drugs...26

4.1. Beta-blockers...27

4.2. Neuroleptic and antipsychotic drugs...27

4.3. Anticonvulsant mood stabilizers and other anticonvulsants...27

4.4. Antidepressants ...28

4.5. Benzodiazepines ...29

4.6. Amantadine...29

4.7. Other molecules...29

4.7.1. Buspirone (Buspar®)...29

4.7.2. Hydroxyzine (Atarax®) ...30

4.7.3 Use of hormonal agents ...30

5. Question 5: Treatment strategies ...30

5.1 Episode of agitation in ICU ...30

5.2 Therapeutic strategy for excessive behavioural disorders... 31

5.3. Episode in a medico-social setting...33

5.4 Restraint and surveillance...34

5.5 Episodes at home ...34

5.6 Therapeutic strategy for default behavioural disorders...35

5.7. Psychiatric care...35

5.8. Suicidal crisis ...36

5.9. Forensic incidence ... ...36

5.9.1 Behaviour resulting in forensic consequences, misdemeanour, crime ...36

5.9.2 Distribution of physical injury and legal distribution...36

6. Question 6: Monitoring and prevention of behavioural disorders ...37

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6.1 Return to the community, GP, outpatient monitoring, support for families. Social and

paramedical interventions (rehabilitation, information and training for the patient, family, relatives, and helpers, support, etc.) ...37

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Glossary

Akathisia: associates stereotypic movements with a sensory component (pain, restlessness...).

These movements primarily affect the lower limbs and seem to be worse at night. It is the inability to remain sitting, at rest.

Dysexecutive Syndrome: consists of various symptoms involving the executive functions. It concerns in particular elaborate cognitive control functions involved in situations requiring the coordination of thoughts or actions to reach an ultimate goal, and affects predominantly the frontal lobe. Traditionally, there are two categories: behavioural and cognitive dysexecutive syndromes.

Klüver-Bucy syndrome: initially described in monkeys following damage to the temporal lobe and in particular the amygdale, this syndrome is more particularly characterised by sexual behavioural disorders (hypersexuality) and eating disorders (bulimia; compulsion to place objects in the mouth). It can also be associated with a blunted affect, memory problems, and gnostic disorders.

Coping: the term coping concerns all processes that an individual interposes between themselves and a distressing event in order to control or decrease the impact on their physical and mental well- being.

Abbreviations

To make the document easier to read, the abbreviations and acronyms used are explained below.

ABS: Agitated Behaviour Scale;

AES: Apathy Evaluation Scale;

MA: Marketing Authorisation;

PTA: Post-traumatic amnesia;

RTC: Road Traffic Collision;

DA: Daily Activities;

BZD: Benzodiazepines;

CBZ: Carbamazepine;

DSM: Diagnostic and Statistical Manual of Mental Disorders;

EHIEC: European Head Injury Evaluation Chart;

EMDR: Eye Movement Desensitisation Reprocessing;

FrSBE: Frontal System Behaviour Scale;

MHG: Mutual Help Groups;

GCS: Glasgow Coma Scale;

IRSPC: Iowa Rating Scale of Personality Change;

SSRI: Selective Serotonin Reuptake Inhibitors;

SNRI: Selective Noradrenaline Reuptake Inhibitors;

BDSI: Behavioural Dysexecutive Syndrome Inventory;

PSSM: Personalised Social Support Measures;

LSM: Legal Support Measures;

MDPH: County Centre for the Disabled [Maison départementale des personnes handicapées];

FIM: Functional Independence Measure;

MINI: Mini International Neuropsychiatric Interview;

MPAI-4: Mayo-Portland Adaptability Inventory;

NFI: Neurobehavioural Functioning Inventory;

NL: Neuroleptic drugs;

NRS-R: Neurobehavioural Rating Scale-Revised;

OAS: Overt Aggression Scale;

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OAS-MNR-E: Overt Aggression Scale Modified for Neurorehabilitation-Extended;

PTSD: Post-traumatic Stress Disorder;

QOLIBRI: Quality of Life after Brain Injury;

SAMSAH: Medico-Social Support Service for Disabled Adults [Service d’Accompagnement Médico- Social pour Adultes Handicapés];

SAVS: Social Support Services [Services d’Accompagnement à la vie Sociale]

SRPR: Post-Intensive Care Rehabilitation Service [Service de Rééducation Post Réanimation];

STAXI-2: State-Trait Anger Expression Inventory;

TBI: Traumatic Brain Injury;

CBT: Cognitive Behavioural Therapy;

Mild TBI: Mild Traumatic Brain Injury;

MTBI: Moderate TBI;

STBI Severe TBI;

OCD: Obsessive-compulsive disorders

UEROS: Evaluation, Retraining and Socio-Professional Orientation Units [Unités d’évaluation, de Réentraînement et d’Orientation Socioprofessionnelle];

UPPS: Impulsive Behaviour Scale;

VPA: Valproate.

Introduction 1. Context

Behavioural disorders are a major after-effect for traumatic brain injury sufferers and are a considerable constraint for families and society.

The diversity and low efficacy of conventional therapies hinder the long-term treatment, and some treatment protocols are still poorly understood. Hospital teams, the National Union of Families of Traumatic Brain Injury Sufferers (UNAFTC), and the French Paralysis Society (APF) have requested a study to be conducted regarding the best choice of drugs and the management of their harmful effects, particularly neuroleptic drugs.

The detrimental effects of behavioural disorders on families, carers, and many other professionals (magistrates, solicitors, insurers, etc.) are numerous. In February 2010, the French Prime Minister announced the development of a specific action plan in favour of traumatic brain injury sufferers and patients with medullar injuries, and requested the exploration of ways to improve more particularly the continuity of treatment of patients in the health, medico-social, and social sectors. The French Society of Physical Medicine and Rehabilitation (SOFMER) decided to draft these good practice guidelines in response to the guidelines published on 19 April 2010 by the Minister of Health and Sports, the Minister of Labour, Social Welfare and the Civil Service, and the Secretary of State in charge of Family and Social welfare.

2. Theme

These good practice guidelines concern the treatment of behavioural disorders in traumatic brain injury sufferers, of which the symptoms, frequency, and triggering factors are defined in chapter 2.

3. Objective

• Organise the healthcare procedure, ensuring that parties involved intermittently are informed better.

• Provide a practical treatment guide for the practitioner.

• Improve the efficiency of the different treatment protocols: medicinal and non-medicinal treatments, therapeutic strategy, hospitalisation, outpatient follow-up, professional insertion,

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including in an appropriate environment.

4. Patients concerned

Adults who suffered a traumatic brain injury in childhood and who have a behavioural disorder.

· Traumatic brain injury patients during acute post-traumatic phase: several hundred each year in France in the various neurotraumatology, post-intensive care, and neurological PMR units

· Sufferers at home: several thousand

· Sufferers in institutions: ESAT, EA, FAM or MAS.

5. Professionals concerned

· Hospital anaesthetists, neuro-traumatologists, PMR physicians, psychiatrists, GPs, expert physicians

· Healthcare staff in departments that receive and treat these injured patients, psychologists

· Staff in medico-social institutions who provide long-term care for these patients.

All these people are confronted at one time or another with behavioural problems, their consequences and treatment. Specialist care networks and/or follow-up consultations exist, but are dispersed unevenly throughout the country and are often little known by practitioners and families.

Working Method

1. Recommendations in clinical practice

In the healthcare sector, Good Practice Guidelines (GPG) are proposals developed methodologically to help practitioners and patients find the most appropriate treatment for a given clinical situation.

GPG provide a rigorous overview of the state of the art and the scientific data at a given time according to the scientific rationale. However, healthcare professionals must still exercise good judgement and propose the treatment they consider the most appropriate according to their own observations.

These good practice guidelines have been developed in accordance with the method summarized in the scientific rationale and described in the HAS methodological guide available on its website:

Drafting good practice guidelines - "Recommendations in clinical practice" - www.has-sante.fr.

2. Conflicts of interest

The declarations of interest of all participants in the various meetings have been given to the HAS, analysed according to the evaluation grid in the "Guide for declarations of interest and managing conflicts of interest", and taken into account to avoid any conflicts of interest. The conflicts of interest management committee has affirmed that the declarations of the work group members are

compatible with their participation in this group.

The guide and the declarations of interest of the experts who participated in one or several work group meetings can be consulted on the HAS website: www.has-sante.fr.

3. Documentary research

The HAS documentation department conducted the documentary research using predominantly the Medline database for the period from 1990 to 2012. The research equations are detailed in the scientific rationale, which can be consulted on the HAS website: www.has-sante.fr.

4. Participants

4.1. HAS Project Leaders Dr Muriel DHENAIN, HAS, project leader.

Dr Philippe BLANCHARD, HAS, project leader.

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Mrs Emmanuelle BLONDET, HAS, documentalist.

4.2. Steering committee

Pr Jean-François MATHÉ, PMR physician, Nantes - steering committee chair.

Dr Jean-Jacques DUMOND, psychiatrist, Limoges.

Maître Emeric GUILLERMOU, solicitor, family representative, chair of the UNAFTC.

Pr Jean-Michel MAZAUX, PMR physician, Bordeaux.

Mr Michel ONILLON, establishment manager.

Pr Pascale PRADAT-DIEHL, PMR physician, Paris.

4.3. Work group

Pr Jacques LUAUTÉ, PMR physician, Lyon - work group chair.

Dr Angélique STÉFAN, PMR physician, Nantes, project leader.

Dr David PLANTIER, PMR physician, Giens, project leader.

Dr Laurent WIART, PMR physician, Bordeaux, project leader.

Dr Julia HAMONET, PMR physician, Limoges, project leader.

Mrs Annabelle ARNOULD, psychologist, Garches.

Mrs Suzanne AUBERT, family representative, UNAFTC.

Dr Jean-Marie BEIS, PMR physician, Nancy.

Mr Laurent BLAIS, Director, Maison Douglas, Mercœur.

Mrs Marie-Christine CAZALS, UNAFTC.

Dr Jean-Marc DESTAILLATS, psychiatrist, Bordeaux.

Dr Eric DURAND, PMR physician, Saint Maurice Hospital, Paris.

Dr Patrick FAYOL, psychiatrist, Limoges.

Dr Christine FIEYRE, MDPH physician, Paris.

Mr Luc JAGOT, psychologist, Nantes.

Dr Christophe LERMUZEAUX, psychiatrist, Institut Marcel Riviere, La Verrière.

Mr Jean-Michel LUCAS, PE teacher, Maison Douglas, Mercoeur.

Dr Dominique MALAUZAT, psychiatrist, pharmacologist, Limoges.

Mrs Nelly MONTROBERT, social worker, Aveize.

Maître Jacques Antoine PREZIOSI, solicitor, Marseille Mrs Antoinette PROUTEAU, psychologist, Bordeaux.

Pr Isabelle RICHARD, PMR physician, Angers.

Dr Laurence TELL, PMR physician, Lyon.

4.4. Reading group

Pr Philippe ALLAIN, Psychologist, Angers Dr Laurent ATLANI, PMR physician, Marseille Pr Philippe AZOUVI, PMR physician, Garches Dr Eleonore BAYEN, PMR physician, Paris Mr Christian BELIO, ergotherapist, Bordeaux Maître Richard BOMETON, magistrate, Limoges Mrs Céline BONNYAUD, physiotherapist, Garches Maître Marc CECCALDI, solicitor, Marseille

Mrs Renée CHAIGNON, social worker, Nantes Dr Emmanuel CHEVRILLON, PMR physician, Paris

Mr Dominique CHOPINAUD, healthcare executive, Limoges Mrs Christine CROISIAUX, psychologist, EBIS chair, Brussels Dr Xavier DEBELLEIX, PMR physician, Bordeaux

Mrs Brigitte DHERBEY, patient's family, UNAFTC

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Mr Philippe HINGRAY, MAAF insurance, Niort Dr Corinne JOCKIC, PMR physician, Caen

Mrs Françoise JOYEUX, psychologist, Aunay sur Odon Dr Françoise LALOUA, PMR physician, Grenoble Pr Didier LE GALL, psychology, Angers

Mrs Jacqueline MADINIER, patient's family, UNAFTC Mrs Anne-Cécile MARQUET, IDE executive, Nancy Pr Michèle MONTREUIL, psychologist, Paris

Dr Hélène OPPENHEIM-GLUCKMAN, psychiatrist and psychoanalyst, Paris and Institut Marcel Rivière (La Verrière) Mrs Annie PERUSSEL, establishment manager, Nantes

Dr Bruno POLLEZ, PMR physician, Lille

Mr Stéphane RAFFARD, psychologist, Montpellier Dr André-Jean REMY, hepatologist – prison, Perpignan Dr Marc ROUSSEAU, PMR physician, Lille

Mrs Véronique ROUSSENAC, Psychologist, Kerpape Dr Virginie SAOUT, PMR physician, Angers

Pr Jean-Luc TRUELLE, neurologist, Garches Pr Yves ZERBIB, GP, Lyon

We would also like to thank Mrs Jacqueline MADINIER for proofreading the final version of the document.

5. Grading of recommendations

Each article selected was analysed according to the principles of critical literature reading using reading grids, thus providing a level of scientific proof for each one. According to the level of proof of the studies on which the recommendations are based, the grade varies from A to C in accordance with the HAS scale ("Literature analysis guide and grading of recommendations" January 2000, downloadable from the HAS website: www.has-sante.fr).

When no studies are available, recommendations are based on the agreement of the work group experts, after consulting the reading group. The absence of grading does not mean that the

recommendations are not pertinent and useful, but must encourage the implementation of additional studies.

Level of scientific proof in the literature

(therapeutic studies) Grade of Recommendation Level 1

High-power randomized comparative studies Meta-analysis of randomized comparative studies Decision analysis based on well-conducted studies

Established scientific proof A

Level 2

Low-power randomized comparative studies Well-conducted non-randomized comparative studies

Cohort studies

B

Scientific presumption Level 3

Case-control studies Level 4

Comparative studies with significant bias Retrospective studies

Case series

C

Low level of proof

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Recommendations

1. Question 1: What are the different types of disruptive symptoms that can be treated 1.1. General information:

In the absence of consensus in the literature, we propose to divide behavioural disorders into 4 symptom sub-groups: (i) excessive behavioural disturbances; (ii) default behavioural disturbances;

(iii) behavioural disorders secondary to depression, anxiety and psychosis; (iv) attempted suicide and suicide.

Cognitive disorders and anosognosia are very common impairments that have a major impact on the long-term handicap of TBI sufferers. They are not specifically addressed, but are regularly mentioned due to the overlap with cognitive disorders, anosognosia, and behavioural disorders. Likewise, behavioural disorders secondary to sleep disorders and pain are voluntarily not addressed.

One objective is to provide a common nomenclature for professionals, patients and families based on well-accepted definitions. Another is to specify, according to the data in the literature, the incidence and factors for predicting these disruptions.

R1: All those involved must share the same definitions and nomenclature with regard to behavioural disorders (EC).

R2: Behavioural disorders can be classified as excessive behavioural disturbances, default behavioural disturbances, behavioural disorders secondary to depression, anxiety and psychosis, or attempted suicide and suicide (EC).

Observation: Behavioural disorders are twice as common following a traumatic brain injury compared with an orthopaedic trauma without TBI.

Observation: Behavioural disorders after TBI persist over time.

1.2. Excessive behavioural disturbances

This chapter groups several types of symptoms such as agitation, conflict, inappropriate wandering behaviour, disinhibition, irritability, impulsiveness, screaming, risk taking, bulimia, addiction, hypersexuality, exhibitionism, Klüver-Bucy* syndrome, hostility, aggressiveness, and verbal and physical violence. Each term satisfies more or less well-defined criteria.

Several of these symptoms are also observed in Alzheimer's and have the same characteristics (cf.

good practice guidelines: Alzheimer's and related diseases: treatment of disruptive behavioural disorders - HAS 2009). The generic term “agitated behaviour” can therefore include conflict,

aggressiveness, circadian rhythm disorders, wandering or inappropriate motor behaviour, screaming, and motor disinhibition.

Conflict corresponds to the patient's refusal to be treated, eat, wash, respect social rules, cooperate...

Anger can be defined as an emotional state consisting of feelings of varying intensity, from moderate irritation or annoyance to intense fury and rage. It emerges in response to provocative, abusive or frustrating situations. More generally, anger includes emotional, cognitive, behavioural, and

physiological reactions to certain situations. Three modes of expressing anger have been described:

anger-in, anger-out, and anger-control. Anger-in corresponds to anger expressed inwardly, anger-out corresponds to anger expressed outwardly aimed at people or surrounding objects, and anger control is an individual's capacity to control their anger.

In the Anglo-Saxon literature, anger is often grouped with hostility and aggression within the context

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of the Anger-Hostility-Aggression (AHA) syndrome.

Inappropriate wandering behaviour is sometimes likened to agitation. It can involve verification, incessant pursuit, repetitive or excessive activity, wandering aimlessly or with an inappropriate goal, nocturnal wandering, roaming, with the need to be taken home...

Disinhibition corresponds to impulsive and inappropriate behaviour in relation to social or domestic standards at the time this behaviour is observed. Symptoms include absent-mindedness, emotional instability, inappropriate or overt behaviour: roaming, incongruous sexual attitude, indecent or invasive behaviour, self-aggression or aggression towards others. Abnormal sexual behaviour and hypersexuality can have a major impact on the family and society (cf. chapter on behaviour and forensic consequences). Disinhibition is characterised by poor control of impulsions (DSM*-IV-TR), and is a symptom of the frontal lobe syndrome. This behavioural disorder is more specifically linked to orbitofrontal cortex damage, which could modulate limbic system activity according to the

environmental context.

Some disruptions correspond to the alteration of normal functions. Therefore, impulsiveness could result in the alteration of one or several psychological factors such as imperiousness, premeditation, perseverance, and "sensation seeking". These disruptions can generally be addressed within the framework of dysexecutive syndrome behavioural disorders*.

The analysis of the literature highlights five sub-chapters: (i) agitation; (ii) aggressiveness; (iii) irritability; (iv) abuse and excessive consumption: high-risk, excessive, addictive behaviour; (v) behaviour resulting in forensic consequences, misdemeanour, crime.

R3: Agitation, conflict, inappropriate wandering behaviour, disinhibition, irritability, impulsiveness, screaming, risk taking, bulimia, addiction, hypersexuality, exhibitionism, Klüver-Bucy* syndrome, hostility, aggressiveness, verbal and physical violence... are excessive behavioural disorders (EC).

1.2.1. Agitation

1.2.1.1. Definition

Most authors consider that agitation occurs during a period of alteration of the state of awareness, which, in the case of a traumatic head injury, concerns in particular coming out of a coma. For some, it is an essential progressive stage following a traumatic brain injury. Indeed, observations have shown that cognitive improvement precedes a decrease in agitation, while interventions that decrease waking increase agitation.

Agitation is defined as excessive behaviour occurring during the alteration of the state of consciousness. This definition highlights the importance of "excessiveness" which is characterised by the degree above which the behaviour interferes with functional activities. No specific type of behaviour defines agitation, even if some behaviour such as psychomotor agitation may predominate.

* The DSM V is now available

According to some authors, post-traumatic agitation corresponds to a delirious state during a period of post-traumatic amnesia (PTA) characterised by excessive behaviour combining aggressiveness, akathisia, disinhibition, and/or emotional lability.

R4: Agitation following severe or moderate TBI occurs while awake (EC), and particularly during the period of PTA. Agitation includes one or more of the following signs:

impulsiveness, disrupted thought, disrupted perception, increased psychomotor activity, physical or verbal aggression, explosive anger, increased difficulty sustaining or adapting attention (EC).

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R5: Factors contributing to post-traumatic agitation must be identified: pain, effect of psycho- stimulants (alcohol, drugs), benzodiazepine withdrawal, epilepsy, endocrine disorders, sleep disorders... (EC).

1.2.1.2. Incidence/prevalence

The average incidence of agitation in the population of traumatic brain injury sufferers is estimated at 46.3% (ranging from 35% to 70%). Post-traumatic agitation is generally brief (1 to 14 days), but can sometimes continue for longer or emerge later.

Observation: The average incidence of agitation in the population of traumatic brain injury sufferers is estimated at 46.3% (ranging from 35% to 70% depending on the studies).

1.2.1.3. Contributing or triggering factors

Observation: Environmental causes, sleep disorders, and pain have been as identified as factors that contribute to agitation.

Observation: Agitation is inversely proportional to participation in the rehabilitation programme.

1.2.2. Aggressiveness 1.2.2.1. Definition

The DSM-IV classification proposes the diagnosis of a personality change linked to a medical cause, with different sub-types according to the type of hostile behaviour (Theme III). The aggressive type is characterised by predominant aggressive behaviour directed at inanimate objects, self or others. The disinhibited type is characterised by disinhibition and sexual indiscretions; the patient can become aggressive if they are redirected or frustrated.

Aggressiveness also includes severe irritability, hostile, violent behaviour, assaults, and loss of self- control ("dyscontrol"). A distinction is often made between goal-directed aggressiveness and hostile or explosive aggressiveness. The latter is observed more often after a traumatic brain injury.

Emotional lability can lead to verbal outbursts in reaction to minimal provocation, but with no substantial threat or violent behaviour.

In the Anglo-Saxon literature, several terms are used interchangeably: aggression, assaults, violence.

Other authors define aggressiveness as complex behaviour which includes one of the following components: (i) behaviour resulting in injury to an individual or damage to property; (ii) attitude, mood, gestures that people find threatening or intimidating; (iii) persistent behaviour which disrupts the rehabilitation activities and social reintegration.

R6: Aggressiveness includes verbal and physical aggressiveness against self, objects, and others, as well as severe irritability, violent, hostile behaviour, assaults, and loss of self- control (EC).

Observation: The incidence of aggressiveness in the population of traumatic brain injury sufferers reported in the different studies varies from 25 to 39%.

The initial severity of the traumatic brain injury is correlated with a higher probability of hyperactivity, disinhibition and unhelpful thoughts (level 4). Prefrontal lesions, and in particular orbitofrontal lesions, are more common in aggressive patients. Increased anger and confusion are correlated with

executive control disorders (level 3).

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Older age, a noisy environment, occurrence of epileptic fits in the previous 24 hours, and speech disorders (level 4) are also correlated with aggressive behaviour. Men are also more at risk.

Finally, serious depression and anxiety are the most common co-morbidities in aggressive TBI patients. The results of these studies are however influenced by the difficulty in interpreting whether the patient’s aggressive behaviour is recent or not, as the patient’s behaviour before the traumatic brain injury is rarely specified and difficult to assess.

Observation: Anger and confusion are more common in traumatic brain injury sufferers in the case of executive control disorders following prefrontal, and in particular orbitofrontal

damage.

Observation: Aggressive behaviour is more common in older men, in the case of speech disorders, in a noisy environment, or within 24 hours following an epileptic fit.

1.2.3. Irritability

1.2.3.1. Definition

Irritability can be defined as an excessive reaction with unjustified outbursts of anger. This term is used in numerous categories of the DSM with no specific definition. Irritable mood is defined in the DSM-IV as "easily vexed and angered", and is for example a characteristic of major depressive episodes. Symptoms include persistent anger, a tendency to react to events with outbursts of anger, accusing others, or feelings of extreme frustration for trivial reasons. Irritability is the main component of hostility.

R7: Irritability can be defined as a disproportionate reaction with unjustified outbursts of anger (EC).

Observation: The incidence of irritability in patients with severe TBI varies between 29 and 71% depending on the studies.

1.2.3.3. 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.

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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.

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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.

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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.

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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.

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

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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.

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.

- 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

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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.

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.

- 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 and severe TBI was for a long time considered as improbable, even impossible. However,

conceptions have changed; recent studies show that organic amnesia (PTA, retrograde amnesia) only actually provides very limited protection against PTSD.

Various phenomena are likely to result in the concomitance of TBI / PTSD:

- Presence of "mnestic clusters" during PTA, the subject remembers fragments of the traumatic event.

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- Absence of conscious recollection of the event, but the trauma is re-experienced through a subconscious response mechanism ("fear response").

- No mnestic trace of the event, but the presence of imaginary or reconstructed traces ("pseudo- memory" generated from what the patient thinks happened, or what they have been told; such pseudo-memories are likely to form the main trait of a PTSD).

In addition, traumatic experiences linked to the event but experienced afterwards (painful medical treatments, stressful perceptions in the PTA exit phase...) can also result in the onset of PTSD.

PTSD can be difficult to diagnose due to the degree of overlap between PTSD symptoms and other common symptoms of severe TBI (sleep disorders, irritability, memory and concentration problems, decrease in speed of processing information, fatigue, depression, cephalalgia, etc.).

The figures vary considerably between the studies, probably due to the different methodologies used (choice of indicators, self vs. hetero-assessment of symptoms, etc.). However, some studies report substantial percentages: between 11 and 18% of cases, or even higher.

Observation: The concomitance of post-traumatic stress and severe TBI was for a long time considered as improbable due to post-traumatic amnesia (PTA). Cases are in fact not uncommon, with a frequency of between 11 and 18%, and can be explained by the existence of "mnestic clusters" during PTA, unconscious mnestic traces of the trauma, reconstructed memories (pseudo-memory), and/or traumatic experiences associated with the event but experienced afterwards (painful medical treatments, stressful perception in the PTA exit phase...).

1.4.4. Obsessive-compulsive disorders 1.4.4.1. Incidence/prevalence

- Incidence of 1.2 to 30% of TBI in comparison with 1.2 to 3% in the general population. According to some authors, the incidence is 2.6 times higher than in the general population.

Symptoms can appear soon after the lesion (a few hours to a week).

OCD can occur preferentially following a lesion of the orbitofrontal cortex, the cingulate cortex, or the caudate nucleus.

Observation: The incidence of obsessive-compulsive disorders (OCD) is higher than in the general population (estimated relative risk of 2.6).

Observation: OCD are stimulated by damage to the orbitofrontal cortex, the cingulate cortex, and the caudate nucleus.

1.4.5. Post-traumatic psychosis

Even if the CIM-10 includes the diagnosis "post-traumatic delirious (schizophrenic-like) disorder"

(F06.2), the notion of psychosis and above all post-traumatic schizophrenia is discussed. Insofar as the age of onset of schizophrenia (between 15 and 25 years) corresponds to a frequency peak of traumatic brain injury, it is often difficult to rule out the development of psychosis independently of the traumatic brain injury. Moreover, it is difficult to establish a cause from the epidemiological data as self-assessments are used to evaluate prior traumatic brain injuries, the period and the severity of the trauma are reported in different ways, and the diagnostic criteria of psychosis often vary from one study to another. Nevertheless, several studies have shown a statistical relationship between the occurrence of a traumatic brain injury and the onset of a psychotic disorder. These data suggest that

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a traumatic brain injury is a risk factor in the onset of a psychotic disorder.

In a case-control study, the main symptoms of patients who developed psychosis following a TBI were paranoid illusions (55% of cases, relating mainly to persecution), and delusions of grandeur (20%). Hallucinations were also common, most often aural, and negative symptoms such as catatonia and thought disorders were not very common (level 3).

1.4.5.1. Incidence/prevalence Incidence: 0.1-9.8% / Prevalence: 0.7%.

The risk of developing post-traumatic psychosis is greater if there is a family history of psychosis, when the TBI occurs before adolescence, and when the lesion affects the temporal lobe. The period between the TBI and the onset of the psychotic disorders, as well as the nature of the psychotic disorders vary from study to study.

Observation: Proof of psychosis associated with severe or moderate TBI is limited.

Observation: The main symptoms of patients who developed psychosis following a TBI were paranoid illusions (55% of cases, relating mainly to persecution), and delusions of grandeur (20%). Hallucinations were also common, most often aural. Aggressiveness was observed in 40% of cases, and negative symptoms such as catatonia and thought disorders were not very common.

Observation: The risk of developing post-traumatic psychosis is greater if there is a family history of psychosis, when the TBI occurs before adolescence, and when the lesion affects the temporal lobe.

1.5. Attempted suicide and suicide 1.5.1.1. Incidence/prevalence

A literature review shows a high rate of suicide, attempted suicide and suicidal thoughts in the TBI population in comparison with the general population, even after controlling psychiatric disorders. The relative risk of suicide in cases of severe TBI is estimated at 3-4 times that of the general population (level 4) with a cumulative suicide rate of 1% in the 15 years post-TBI. Suicidal thoughts are

observed in 21-22% of TBI sufferers (level 4). Attempted suicide is however hard to assess but can reach 18% (level 4).

Another literature review regarding the long-term psychiatric outcome of TBI patients concludes that there is suggestive but limited proof of a connection between TBI and suicide, as well as inadequate proof of a connection between TBI and attempted suicide. Attempted suicide and suicide are the most serious consequences of mood disorders. An increased risk of suicide was observed in 2 out of 3 studies examining the link between TBI and suicide (level 4).

Two studies report a higher risk of suicide in the case of a severe traumatic brain injury in relation to concussion (hazard ratio 1.4, 95% CI 1.15-1.75) and a higher risk of attempted suicide in the event of suicidal thoughts (OR 4.9, 95% CI 1.79-13.17) or psychiatric/emotional disorder (OR 7.8 95% 2.11- 29.04). Suicidal thoughts could be a risk factor in suicide and are more common in the case of depression, anxiety, and post-traumatic stress (level 2). Aggressiveness (premorbid and post-TBI) and substance abuse must be considered as suicide risk factors in depressed mild TBI patients (level 4).

Observation: The relative risk of suicide in cases of severe TBI is estimated at 3-4 times that

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of the general population with a cumulative suicide rate of 1% in the 15 years post-TBI.

Suicidal thoughts are observed in 21-22% of TBI sufferers.

Observation: There is suggestive but limited proof of a causal link between TBI and suicide.

Observation: Suicidal thoughts could be a suicide risk factor and are more common in the case of depression, anxiety, and post-traumatic stress.

2. Question 2: Assessment

The assessment process of behavioural disorders in traumatic brain injury patients is based on expert consensus (EC). The role of scales in clinical practice or the development of research protocols is addressed from the data in the literature regarding their specificity, validation and translation.

R10: Professionals involved should learn about and gain experience in the treatment of TBI, and in particular cognitive disorders resulting from a traumatic brain injury due to their very close relationship with behavioural disorders (EC).

R11: An initial assessment of behavioural disorders through direct observation of the patient is essential (by the physician, carer, psychologist...) (EC).

R12: If self-assessment is necessary (evaluation of the patient by themselves), hetero- assessment (evaluation by another source) is also crucial as the patient is not always aware of their symptoms (anosognosia) (EC).

R13: The source can be a caregiver or family helper, close friend or professional (carer, care assistant, social worker, etc.). Identifying a close friend or relation who knew the patient before the accident is useful to assess changes in behaviour (EC).

R14: Assessment by a helper or close friend should be carried out when possible with the patient’s consent. Multi-disciplinary assessments, which include the viewpoint of the different carers involved in the patient’s treatment, are strongly recommended (EC).

R15: Ideally, the assessment of behavioural disorders should be cross-disciplinary grouping the information gathered from different sources (multisource evaluation) and providing new, supplementary information. The subjective information declared can then be crosschecked (EC).

R16: The overlap between behavioural disorders and cognitive and psychological disorders justifies why a psychologist trained to deal with cognitive disorders in traumatic brain injuries must assess them (EC).

R17: The symptoms to be analysed need to be clearly distinguished and their interactions identified, as psychiatric-like, behavioural, psychosocial, and environmental disorders all overlap (EC).

R18: The existence of behavioural symptoms needs to be explored, from the least apparent to the most obvious (EC).

R19: Behavioural disorders must be accurately characterised, in particular in relation to the medical history, according to their duration, frequency, severity and impact on daily life and relatives. Their nature, mechanisms, and context of onset must be identified. Finally, it is important to look for factors contributing to their emergence and persistence (predisposition, trigger, notably addictions), as well as the most suitable attitude to be adopted by helpers and professionals to reduce them and the consequences (EC).

R20: The degree of urgency and gravity must be evaluated. The risk of suicide (Beck's suicide intent scale can be used for help) and violence should be addressed. In this respect, public hearing recommendation 39 can be given as an example. "Psychiatric gravity: study and

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assessment of risk factors of hetero-aggressive violence in people with schizophrenic disorders and mood disorders" - HAS 2011: first ask the person if they have ever been a victim of violent acts, it is then easier to ask questions such as "Have you ever lost your temper?”, “under what circumstances?”, “with whom?”, “did you then regret it?" It is also possible to use the "violence screening list" (EC).

R21: Ideally, tools should be used to assess behavioural disorders (cf. table 2). However, a tool is not an end in itself, but provides a reliable, rigorous, methodological assessment framework. Consequently, the tools used must be validated. Finally, using a tool is desirable, but not enough, and must be supplemented with observations and interviews (EC).

R22: The high frequency of post-traumatic behavioural disorders requires these routine symptoms to be investigated throughout the treatment (see question 6) (EC).

R23: The natural progression of the disorders and the response to different therapies introduced must result in repeated assessments (EC).

R24: The assessment must be carried out at different levels: emotional, cognitive (combining a neuropsychological evaluation and an ecological assessment), relational, and

environmental. Only an accurate identification of all the processes involved can lead to the appropriate treatment (EC).

R25: The impact on helpers (particularly psychological consequences) must be regularly assessed (EC).

Data collection:

R26: In the health sector, the assessment data are used within the framework of the

healthcare procedure, and can be exchanged among professionals in charge of the patient to define and adapt the treatment strategy in compliance with the rules regarding patient

confidentiality and information (EC).

R27: The assessment data must be in a file to facilitate use / traceability / transmission (with an adequate level of confidentiality) (EC).

R28: In a healthcare facility, the coordinating physician (when there is one) and a referring health care professional play a key role in centralizing and distributing the data. This concerns in particular elements regarding the biography, care pathway, type of disorders encountered (frequency, severity, and progression) and their treatment; triggering, aggravating or improving factors; and the consequences (other residents, professionals, helpers) (EC).

R29: There must be links between all those involved so they can access the medical and health care information (for example via a follow-up book) (EC).

Assessment tools: role of scales:

R30: Scales make it possible to standardise the assessment data, obtain quantitative

measurements of the symptoms, follow the progression over time, and measure the effect of a treatment. These scales are useful in clinical practice, but also within the framework of a clinical research approach (EC).

R31: The scales comply with "metrological" requirements: Validity, Reliability, Sensitivity, and Specificity. The adaptation of these English scales sets the problem of their translation into French and their validation. Specific training is often required. Some characterise the intensity or the severity of the symptoms (EC).

R32: The use of tools requires a sound understanding of the underlying models and the methodology that led to their development, notably regarding their significance, indications,

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and limits, and to avoid misinterpretation. The tools must be used by professionals or helpers with enough training (either initial training, or through additional specific training) (EC).

R33: An ecological assessment in real life conditions in addition to neuropsychological assessments is highly recommended (EC).

3. Question 3: Treatment techniques and non-medical interventions 3.1. General recommendations:

R34: Non-medical interventions are recommended for the first line treatment of behavioural disorders in traumatic brain injury patients as well as the distress experienced by families throughout the progression. This treatment must be conducted by therapists specialising in neuropsychological disorders of TBI, in consultation and in collaboration with the

professional teams and relatives (EC).

R35: The non-medical treatment of behavioural disorders involves various approaches:

holistic (programmed paths, social, professional, occupational activities...), cognitive- behavioural, family systemic, psychoanalytical, as well as adaptation of the behaviour of the patient's relatives, and healthcare and follow-up teams (EC).

R36: Different approaches can be combined according to the predominance of some symptoms or co-morbidities, and can be associated if necessary with specific treatments (post-traumatic syndrome, drug addiction...) (EC).

R37: Studies conducted using a scientifically validated methodology will be required to determine the most efficient non-medical approach for treating behavioural disorders in TBI patients: holistic, cognitive-behavioural, systemic, psychoanalytical (EC).

R38: Rehabilitation activities such as neuropsychology, speech therapy, physiotherapy, and ergotherapy help improve behavioural disorders. However, they must be personalised and specific, particularly with regard to neuropsychological rehabilitation (targeting dysfunctional processes), and are recommended within the framework of TBI patient care pathways (EC).

R39: A programme of occupational activities (sports, artistic, cultural...), or a socio-

professional project when possible, involving medico-social organisations such as SAMSAH, SAVS, GEM, UEROS in collaboration with the MDPH, are recommended due to their personal structuring, socialising and enhancing role. These programmes must an integral part of the patient’s overall treatment (EC).

R40: Additional studies are necessary to evaluate the adequacy and efficacy of the measures or the social or professional reinsertion programmes (EC).

3.2. Specific approaches and treatments 3.2.1. Holistic and institutional approaches

The holistic approach derived from holism in the 1920s considers that humans function as a complex whole within the framework of a model defined recently in the medical and biopsychosocial domain.

Contrary to the three previous approaches, holistic psychotherapy was not derived from an existing technique, but was specially designed for TBI patients. The principle is to address generally, progressively and in a coordinated manner the question of awareness of the handicap and its acceptance, through individual and group psychotherapy sessions, as well as cognitive rehabilitation in order to improve social and professional insertion. The patient progresses in successive stages according to the following conventional scheme: commitment, awareness, malleability, control of compensation processes, acceptance, identity, social reintegration.

In the United States, these programmes are extremely intensive, with up to 20 hours a week for 4 to