Ontario Neurotrauma Foundation

Clinical Practice Guideline

For the rehabilitation of Adults with Moderate to Severe TBI

Ontario Neurotrauma Foundation INESSS
SECTION 2: Assessment and Rehabilitation of Brain Injury Sequelae > R. Neurobehaviour and Mental Health

R. Neurobehaviour and Mental Health

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Changes in behaviour are common after traumatic brain injury (TBI) due to the involvement of the frontal aspects of the brain. Early after brain injury, confusion, delirium and restlessness are common and improve as post traumatic amnesia state improves. These changes result in disrupted relationships, unemployment, decreased quality of life and increased caregiver burden. Behavioural rehabilitation is one of the highest priority topics that clinicians identified in surveys. Furthermore, it is believed that the brain injury causes changes in the neurotransmitters that predispose individuals for increased mental health issues such as anxiety, depression, mood disorders and possibly even psychosis. It is essential that clinicians be aware of the proper assessment of behaviour including understanding precipitating factors [antecedents] and the consequences of the behaviour that affect the chance of future problematic behaviour. Once a behavioural assessment has been completed, a detailed behavioural plan incorporating the goals and perspectives of the patient is necessary. A holistic approach is needed incorporating the behavioural assessment with both cognitive and behavioural as well pharmacological treatments, if required.

Note: Please refer to the Principles of Medication Management in section T.

Staff and clinicians should be trained in behavioural assessment and treatment techniques and understand the benefits and limitations. It is important that ethics of consent and capacity be respected and that the behavioural plan be explained to the individuals with brain injury, their family and caregivers. Specialized clinicians should be provided with specific training and should be accessible to brain injury rehabilitation teams on a timely basis to ensure patient and staff safety. In an emergency situation, staff should be trained in nonviolent crisis intervention and it may be necessary to use stronger sedative medications, however these should be limited. The use of screening tools for depression and anxiety may increase recognition of these important complications. There should be a robust program of patient and family education with regards to how to manage behavior.

 

Indicators exemples

  • Proportion of individuals with TBI who are screened for depression using a standardized tool monthly.

  • Proportion of individuals with TBI and depressive symptoms undergoing mindfulness-based cognitive therapy.

 

A detailed neurobehavioural assessment includes the understanding of the antecedents to the behaviour, collection of detailed behavioural data and understanding the consequence or function of the behaviour for that individual. Factors that should be considered in the assessment of neurobehavioral issues include a patient’s medical and metabolic status, patient’s level of self-awareness (Heinicke & Carr, 2014; Prigatano & Leathern, 1993; Spikman & van der Naalt, 2010; Ylvisaker, Turkstra, & Coelho, 2005), history of substance abuse or psychological issues (MacMillan et al., 2002; Taylor et al., 2003)and the presence of sleep disturbances (Bloomfield, Espie, & Evans, 2010), both prior to and after the TBI.

Bogner et al. (2015) studied 555 patients admitted for inpatient rehabilitation after index TBI between 2008 and 2011, who exhibited agitation during their stay to identify predictors of the severity of agitated behavior. Infection and lower FIM cognitive scores predicted more severe agitation. The medication classes associated with more severe agitation included sodium channel antagonist anticonvulsants, second-generation antipsychotics, and gamma-aminobutyric acid-A anxiolytics/hypnotics. Medication classes associated with less severe agitation included antiasthmatics, statins, and norepinephrine-dopamine-5 hydroxytryptamine (serotonin) agonist stimulants. It may be that the medications associated with severe agitation were being used for treatment and not causal of the agitation. They concluded that these associations support the importance of careful serial monitoring of both agitation and cognition to provide early indicators of possible beneficial or adverse effects of pharmacologic interventions used for any purpose. (Bhatnagar et al., 2016; Plantier & Luauté, 2016; Waldron-Perrine et al., 2008) provide overviews of current state of knowledge of medications used after brain injury. A detailed review can also be found in ERABI Neuropharmacology Chapter (Evidence-Based Review of Moderate To Severe Acquired Brain Injury (ERABI), 2016).

Aggression is the most dangerous neurobehavioural issue, as it can pose serious threats to the patient, caregivers and rehabilitation staff. For managing aggression, beta-blockers can be an effective medication. The results of RCTs have supported that pindolol (Greendyke & Kanter, 1986) and propranolol (Greendyke, Kanter, Schuster, Verstreate, & Wootton, 1986) treatment significantly reduced incidence of assaults by patients. Studies have found that carbamazepine, valproic acid and divalproex decrease irritability disinhibition and aggressiveness (Azouvi et al., 1999; Showalter & Kimmel, 2000; Wroblewski, Joseph, Kupfer, & Kalliel, 1997).

A recent RCT found that amantadine improves patients’ self-perception of their irritability compared to placebo treatments (Hammond et al., 2015). Similarly, methylphenidate can be a safe option to control agitation (Maryniak, Manchanda, & Velani, 2001). Antidepressants can also reduce irritability and aggression, as evidenced by a study on SSRIs (Kant et al., 1998) and TCA usage (Mysiw, Jackson, & Corrigan, 1988). Lastly antipsychotics may also be prescribed. A case series found quetiapine to reduce aggressive behaviour (E. Kim & Bijlani, 2006),  Ziprasidone in the PTA stage can control agitation (Noé, Ferri, Trénor, & Chirivella, 2007), and Lithium carbonate can decrease self-destructive behaviour but usage is prone to a high risk of neurotoxicity (Glenn et al., 1989). Depression screening is imperative as it is the most common diagnosed mood disorder following a TBI (Jorge & Starkstein, 2005; Seel, Macciocchi, & Kreutzer, 2010). When diagnosing depression, TBI specialists should be observant of symptoms of irritability, frustration, anger and aggression as these are more common than conventional apathy, sadness or tearfulness (Seel et al., 2010). In terms of treatment and management of depression, several non-pharmacological options are available. Exercise is a common intervention as it is both beneficial and cost-effective. Studies have found that exercise can increase mood (Blake & Batson, 2009; Driver & Ede, 2009; Gemmell & Leathem, 2006; Gordon et al., 1998), however these mood improvements are not always better than control treatments (Gemmell & Leathem, 2006).The amount of exercise can result in additional benefits to the individual. Music therapy is another positive mood regulator. Listening and playing music also improves mood (Guetin, Soua, Voiriot, Picot, & Herisson, 2009; Thaut et al., 2009).

The use of mindfulness based therapies in improving mood and stress reduction is another viable option for managing depression. Mindfulness training, which emphasizes new ways of positively thinking about life, was found to be effective in reducing stress and maintaining happiness (Bedard et al., 2003; Bedard et al., 2014; Behn et al., 2012). Coping skills should also be taught to patients (Anson & Ponsford, 2006a, 2006b). Although the improvement was not significantly greater than control treatments, two RCTs did not show improvements in mood with groups receiving cognitive behavioural therapy (D'Antonio, Tsaousides, Spielman, & Gordon, 2013; Ruff & Niemann, 1990).

Medications employed for depression treatment included selective serotonin reuptake inhibitors (SSRI), methyphendiate, and tricyclic antidepressants (TCAs), however their usefulness in a TBI population remains inconclusive. SSRIs including sertraline and citalopram have been studied. Two RCTs found that sertraline improved depressive symptoms but it was found to be no more effective than control treatments (Ashman et al., 2009; Lee et al., 2005). Similar results were found citalopram usage (Rapoport et al., 2008; Rapoport et al., 2010). Citalopram in combination with carbamazepine also can improve depressive symptoms (Perino, Rago, Cicolin, Torta, & Monaco, 2001). Desipramine, a TCA was found in a small RCT to be effective for treating long-standing depression (Wroblewski et al., 1996).

Anxiety is another common neurobehavioural problem following TBI that negatively affects a patient’s quality of life and their interactions with others. Cognitive behavioral therapy (CBT) is a promising option for treating anxiety after TBI. Three RCTs found that CBT improved social phobia, general anxiety, mood and community reintegration (Arundine et al., 2012a; Hodgson, McDonald, Tate, & Gertler, 2005; Hsieh, Ponsford, Wong, & McKay, 2012).

When dealing with hypersexual behaviours from individuals with TBI, the use of Depo-provera, an anti-androgen, may aid in minimizing inappropriate behaviour when taken continuously (Emory, Cole, & Meyer, 1995).

REFERENCES
Acquired Brain Injury Knowledge Uptake Strategy (ABIKUS). (2007). www.abiebr.com/pdf/abikus_aug_07.pdf.;

Anson, K., & Ponsford, J. (2006a). Evaluation of a coping skills group following traumatic brain injury. Brain Injury, 20(2), 167-178.

Anson, K., & Ponsford, J. (2006b). Who benefits? Outcome following a coping skills group intervention for traumatically brain injured individuals. Brain Injury, 20(1), 1-13.

Arundine, A., Bradbury, C. L., Dupuis, K., Dawson, D. R., Ruttan, L. A., & Green, R. E. (2012a). Cognitive behavior therapy after acquired brain injury: maintenance of therapeutic benefits at 6 months posttreatment. J Head Trauma Rehabil, 27(2), 104-112.

Ashman, T. A., Cantor, J. B., Gordon, W. A., Spielman, L., Flanagan, S., Ginsberg, A., . . . Greenwald, B. (2009). A randomized controlled trial of sertraline for the treatment of depression in persons with traumatic brain injury. Arch Phys Med Rehabil, 90(5), 733-740.

Azouvi, P., Jokic, C., Attal, N., Pierre, D., Sabria, M., & Bussel, B. (1999). Carbamazepine in agitation and aggressive behaviour following severe closed-head injury: results of an open trial. Brain Injury, 13(10), 797-804.

Bedard, M. Felteau, M., Mazmanian, D., Fedyk, K., Klein, R., Richardson, J., . . . Minthorn-Biggs, M.-B. (2003). Pilot evaluation of a mindfulness-based intervention to improve quality of life among individuals who sustained traumatic brain injuries. Disability & Rehabilitation, 25(13), 722-731.

Bedard, M., Felteau, M., Marshall, S., Cullen, N., Gibbons, C., Dubois, S., . . . Moustgaard, A. (2014). Mindfulness-based cognitive therapy reduces symptoms of depression in people with a traumatic brain injury: results from a randomized controlled trial. J Head Trauma Rehabil, 29(4), E13-22.

Behn, N., Togher, L., Power, E., & Heard, R. (2012). Evaluating communication training for paid carers of people with traumatic brain injury. Brain Inj, 26(13-14), 1702-1715.

Bhatnagar, S., Iaccarino, M. A., & Zafonte, R. (2016). Pharmacotherapy in Rehabilitation of Post-Acute Traumatic Brain Injury. Brain Research.

Blake, H., & Batson, M. (2009). Exercise intervention in brain injury: a pilot randomized study of Tai Chi Qigong. Clinical Rehabilitation.

Bloomfield, I. L., Espie, C. A., & Evans, J. J. (2010). Do sleep difficulties exacerbate deficits in sustained attention following traumatic brain injury? Journal of the International Neuropsychological Society, 16(01), 17-25.

Bogner, J., Barrett, R. S., Hammond, F. M., Horn, S. D., Corrigan, J. D., Rosenthal, J., . . . Reddin, C. J. (2015). Predictors of agitated behavior during inpatient rehabilitation for traumatic brain injury. Arch Phys Med Rehabil, 96(8), S274-S281. e274.

Bradbury, C. L., Wodchis, W. P., Mikulis, D. J., Pano, E. G., Hitzig, S. L., McGillivray, C. F., . . . Green, R. E. (2008). Traumatic brain injury in patients with traumatic spinal cord injury: clinical and economic consequences. Arch Phys Med Rehabil, 89(12 Suppl), S77-84.

Chew, E., & Zafonte, R. D. (2009). Pharmacological management of neurobehavioral disorders following traumatic brain injury--a state-of-the-art review. J Rehabil Res Dev, 46(6), 851-879.

D'Antonio, E., Tsaousides, T., Spielman, L., & Gordon, W. (2013). Depression and traumatic brain injury: Symptom profiles of patients treated with cognitive-behavioral therapy or supportive psychotherapy. Neuropsychiatry, 3(6), 601-609.

Driver, S., & Ede, A. (2009). Impact of physical activity on mood after TBI. Brain Injury, 23(3), 203-212.

Elovic, E. P., Jasey, N. N., Jr., & Eisenberg, M. E. (2008). The use of atypical antipsychotics after traumatic brain injury. J Head Trauma Rehabil, 23(2), 132-135.

Emory, L. E., Cole, C. M., & Meyer, W. J. (1995). Use of Depo-Provera to control sexual aggression in persons with traumatic brain injury. Journal of Head Trauma Rehabilitation, 10(3), 47-58.

Evidence-Based Review of Moderate To Severe Acquired Brain Injury (ERABI). (2016). www.abiebr.com/.;

Gemmell, C., & Leathem, J. M. (2006). A study investigating the effects of Tai Chi Chuan: Individuals with traumatic brain injury compared to controls. Brain Injury, 20(2), 151-156.

Glenn, M. B., Wroblewski, B., Parziale, J., Levine, L., Whyte, J., & Rosenthal, M. (1989). Lithium carbonate for aggressive behavior or affective instability in ten brain-injured patients. American Journal of Physical Medicine and Rehabilitation, 68(5), 221-226.

Gordon, W. A., Sliwinski, M., Echo, J., McLoughlin, M., Sheerer, M., & Meili, T. E. (1998). The benefits of exercise in individuals with traumatic brain injury: A retrospective study. Journal of Head Trauma Rehabilitation, 13(4), 58-67.

Greendyke, R. M., & Kanter, D. R. (1986). Therapeutic effects of pindolol on behavioral disturbances associated with organic brain disease: A double-blind study. Journal of Clinical Psychiatry, 47(8), 423-426.

Greendyke, R. M., Kanter, D. R., Schuster, D. B., Verstreate, S., & Wootton, J. (1986). Propranolol treatment of assaultive patients with organic brain disease. A double-blind crossover, placebo-controlled study. Journal of Nervous and Mental Disease, 174(5), 290-294.

Guetin, S., Soua, B., Voiriot, G., Picot, M.-C., & Herisson, C. (2009). The effect of music therapy on mood and anxiety–depression: An observational study in institutionalised patients with traumatic brain injury. Annals of Physical and Rehabilitation Medicine, 52(1), 30-40.

Hammond, F. M., Bickett, A. K., Norton, J. H., & Pershad, R. (2014). Effectiveness of amantadine hydrochloride in the reduction of chronic traumatic brain injury irritability and aggression. J Head Trauma Rehabil, 29(5), 391-399.

Hammond, F. M., Sherer, M., Malec, J. F., Zafonte, R. D., Whitney, M., Bell, K., . . . Pershad, R. (2015). Amantadine Effect on Perceptions of Irritability after Traumatic Brain Injury: Results of the Amantadine Irritability Multisite Study. J Neurotrauma, 32(16), 1230-1238.

Heinicke, M. R., & Carr, J. E. (2014). Applied Behavior Analysis in Acquired Brain Injury Rehabilitation: A Meta-Analysis of Single-Case Design in Intervention Research. Behavioral Interventions, 29(2), 77-105.

Hodgson, J., McDonald, S., Tate, R., & Gertler, P. (2005). A Randomised Controlled Trial of a Cognitive-Behavioural Therapy Program for Managing Social Anxiety After Acquired Brain Injury. Brain Impairment, 6(03), 169-180.

Hsieh, M. Y., Ponsford, J., Wong, D., & McKay, A. (2012). Exploring variables associated with change in cognitive behaviour therapy (CBT) for anxiety following traumatic brain injury. Disability and rehabilitation, 34(5), 408-415.

Jorge, R. E., & Starkstein, S. E. (2005). Pathophysiologic aspects of major depression following traumatic brain injury. J Head Trauma Rehabil, 20(6), 475-487.

Kant, R., Smith-Seemiller, L., & Zeiler, D. (1998). Treatment of aggression and irritability after head injury. Brain Inj, 12(8), 661-666.

Kim, E., & Bijlani, M. (2006). A pilot study of quetiapine treatment of aggression due to traumatic brain injury. Journal of Neuropsychiatry and Clinical Neurosciences, 18(4), 547-549.

Lee, H., Kim, S. W., Kim, J. M., Shin, I. S., Yang, S. J., & Yoon, J. S. (2005). Comparing effects of methylphenidate, sertraline and placebo on neuropsychiatric sequelae in patients with traumatic brain injury. Hum Psychopharmacol, 20(2), 97-104.

MacMillan, P. J., Hart, R. P., Martelli, M. F., & Zasler, N. D. (2002). Pre-injury status and adaptation following traumatic brain injury. Brain Injury, 16(1), 41-49.

Maryniak, O., Manchanda, R., & Velani, A. (2001). Methotrimeprazine in the treatment of agitation in acquired brain injury patients. Brain Injury, 15(2), 167-174.

Mysiw, W. J., Jackson, R. D., & Corrigan, J. D. (1988). Amitriptyline for post-traumatic agitation. American Journal of Physical Medicine and Rehabilitation, 67(1), 29-33.

Noé, E., Ferri, J., Trénor, C., & Chirivella, J. (2007). Efficacy of ziprasidone in controlling agitation during post-traumatic amnesia. Behavioural neurology, 18(1), 7-11.

Perino, C., Rago, R., Cicolin, A., Torta, R., & Monaco, F. (2001). Mood and behavioural disorders following traumatic brain injury: Clinical evaluation and pharmacological management. Brain Injury, 15(2), 139-148.

Plantier, D., & Luauté, J. (2016). Drugs for behavior disorders after traumatic brain injury: Systematic review and expert consensus leading to French recommendations for good practice. Annals of Physical and Rehabilitation Medicine.

Prigatano, G. P., & Leathern, J. M. (1993). Awareness of behavioral limitations after traumatic brain injury: A cross-cultural study of New Zealand Maoris and non-Maoris. The Clinical Neuropsychologist, 7(2), 123-135.

Rapoport, M. J., Chan, F., Lanctot, K., Herrmann, N., McCullagh, S., & Feinstein, A. (2008). An open-label study of citalopram for major depression following traumatic brain injury. J Psychopharmacol, 22(8), 860-864.

Rapoport, M. J., Mitchell, R. A., McCullagh, S., Herrmann, N., Chan, F., Kiss, A., . . . Lanctôt, K. L. (2010). A randomized controlled trial of antidepressant continuation for major depression following traumatic brain injury. Journal of Clinical Psychiatry, 71(9), 1125-1130.

Ruff, R. M., & Niemann, H. (1990). Cognitive rehabilitation versus day treatment in head-injured adults: Is there an impact on emotional and psychosocial adjustment? Brain Injury, 4(4), 339-347.

Seel, R. T., Macciocchi, S., & Kreutzer, J. S. (2010). Clinical considerations for the diagnosis of major depression after moderate to severe TBI. J Head Trauma Rehabil, 25(2), 99-112.

Showalter, P. E. C., & Kimmel, D. N. (2000). Agitated symptom response to divalproex following acute brain injury. The Journal of neuropsychiatry and clinical neurosciences.

Spikman, J. M., & van der Naalt, J. (2010). Indices of impaired self-awareness in traumatic brain injury patients with focal frontal lesions and executive deficits: implications for outcome measurement. J Neurotrauma, 27(7), 1195-1202.

Taylor, L. A., Kreutzer, J. S., Demm, S. R., & Meade, M. A. (2003). Traumatic brain injury and substance abuse: A review and analysis of the literature. Neuropsychol Rehabil, 13(1-2), 165-188.

Thaut, M. H., Gardiner, J. C., Holmberg, D., Horwitz, J., Kent, L., Andrews, G., . . . McIntosh, G. R. (2009). Neurologic music therapy improves executive function and emotional adjustment in traumatic brain injury rehabilitation (Vol. 1169, pp. 406-416).

Waldron-Perrine, B., Hanks, R. A., & Perrine, S. A. (2008). Pharmacotherapy for postacute traumatic brain injury: A literature review for guidance in psychological practice. Rehabilitation Psychology, 53(4), 426-444.

Warden, D. L., Gordon, B., McAllister, T. W., Silver, J. M., Barth, J. T., Bruns, J., . . . Zitnay, G. (2006). Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. J Neurotrauma, 23(10), 1468-1501.

Wroblewski, B. A., & Joseph, A. B. (1992). The use of intramuscular midazolam for acute seizure cessation or behavioral emergencies in patients with traumatic brain injury. Clin Neuropharmacol, 15(1), 44-49.

Wroblewski, B. A., Joseph, A. B., & Cornblatt, R. R. (1996). Antidepressant pharmacotherapy and the treatment of depression in patients with severe traumatic brain injury: a controlled, prospective study. J Clin Psychiatry, 57(12), 582-587.

Wroblewski, B. A., Joseph, A. B., Kupfer, J., & Kalliel, K. (1997). Effectiveness of valproic acid on destructive and aggressive behaviours in patients with acquired brain injury. Brain Injury, 11(1), 37-47.

Ylvisaker, M., Turkstra, L. S., & Coelho, C. (2005). Behavioral and social interventions for individuals with traumatic brain injury: a summary of the research with clinical implications. Semin Speech Lang, 26(4), 256-267.

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R1. Neurobehavioral Assessment

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 1.1 P C

During the subacute phase of traumatic brain injury, if the neurobehavioural status of the individual is deteriorating or not progressing as expected, an assessment by a licensed specialist should be made to differentiate neurobehavioural difficulties from symptoms of a comorbid illness or medication side effects.

(Adapted from INCOG 2014, Assess 7, p. 298)

Note: Comorbid illness may include seizures, mood and anxiety disorders, personality disorders, metabolic disorders, medication side effects, attention issues, hearing impairment, communication impairment and substance abuse.


Suggested tool: Health Canada Indications of Use

R 1.2 P C

In general, an assessment of neurobehavioural issues following traumatic brain injury must address pre-injury vulnerability factors, injury-related factors and postinjury factors.

(Adapted from INCOG 2014, Assess 6, p.297)

Note:
Pre-injury vulnerability factors include:
Prior medical/neurological conditions, mental health disorders, substance use disorders, temperamental/personality factors, cognitive/intellectual ability, academic/vocational function, psychosocial circumstances

Injury-related factors include:
Nature of injury (i.e., severity, focal vs. diffuse), cerebral involvement, anatomic injury location, extent of secondary injury, co-occurring extracranial injury

Post-injury factors include:
Psychological response / coping style, cognitive status, social/economic changes, new-onset mental health disorders, medical conditions (such as seizures, sensorimotor changes, endocrine dysfunction, pain, sleep/wake disturbance), medication effects

R 1.3 C

Clinicians should carefully define and characterize the presenting neurobehavioural issue through a combination of diagnostic interviews (including close relatives and the health care team) and direct observation of the person with traumatic brain injury.

(INESSS-ONF, 2015)

R 1.4 P B

Any behavioural management plan for individuals with traumatic brain injury must include a consideration of the precipitating factors or triggers possibly leading to the behaviour and reinforcing events.

(Adapted from ABIKUS 2007, G24, p. 20)

R 1.5 P C

Individuals who have sustained a traumatic brain injury after a known or suspected incident of self-harm or a suicide attempt should have a risk assessment performed and should be referred as appropriate.

(Adapted from NZGG 2006, 3.11, p. 66)

R2. Neurobehavioral Interventions

P Priority F Fundamental New Level of evidence A B C
R 2.1 C

At any point throughout the continuum of care, individuals with traumatic brain injury and significant behavioural problems that interfere with daily functions should be provided with access to specialized behavioural management services and interventions to assist in the management of their behavioural difficulties, including substance abuse.

(Adapted from ABIKUS 2007, G19, p. 19)

R 2.2 P C

In the case of individuals with significant behavioural problems following traumatic brain injury, especially those with a tendency to wander, the interdisciplinary team should develop an integrated approach to manage behaviour and refer to specialist behavioural management services when necessary and where available.

(Adapted NZGG 2006, 6.1.7, p. 103)

R3. Management of Sexual Behaviour

P Priority F Fundamental New Level of evidence A B C
R 3.1 C

Family, caregivers, and healthcare professionals should be provided with education and training on change management strategies regarding persistent inappropriate sexual behaviour following traumatic brain injury and how to avoid inadvertently reinforcing this behaviour.

(Adapted from NZGG 2006, 6.5, p. 113)

R4. Assessment of Mood and Depression

P Priority F Fundamental New Level of evidence A B C
R 4.1 P C

Individuals with traumatic brain injury (TBI) should be screened on a regular basis for depression using an appropriate screening tool. Depression screening tools should not be used as the sole indication for initiation of treatment. Diagnosis should always involve a full assessment as well as the clinical judgment of a specialist experienced in managing individuals with TBI.

(Adapted from ABIKUS 2007, G72, p. 27)

R5. Management of Mood and Depression

P Priority F Fundamental New Level of evidence A B C
R 5.1 P B

Individuals with traumatic brain injury who have been diagnosed with a depressive disorder should receive appropriate treatment, which can consist of non-pharmacological treatments including psychological intervention/counselling and exercise.

(Adapted from ABIKUS 2007, G70, p. 27)

R 5.2 P A

Mindfulness-based cognitive therapy, adapted for brain injury, should be considered for individuals with traumatic brain injury and depressive symptoms.

(INESSS-ONF, 2015)

REFERENCES:

- Bedard et al. (2014)
- ERABI Module 8-Mental Health Issues, p.18, 8.2.4

R 5.3 C

Teaching coping skills in groups to reduce depressive symptoms should be considered for individuals with traumatic brain injury who have good awareness of their difficulties.

(INESSS-ONF, 2015)

REFERENCE:

- ERABI Module 8-Mental Health Issues, p.18, 8.2.4

R 5.4 P B

Cognitive behaviour therapy (CBT) should be considered for individuals with depressive symptoms after traumatic brain injury, in individual, group, and modified telephone-based formats.

(INESSS-ONF, 2015)

REFERENCES:

- Arundine et al. (2012)
- Bradbury et al. (2008)

R6. Medication for Depression

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 6.1 P C

Given their favourable side-effect profile, selective serotonin reuptake inhibitors (SSRIs) are recommended as a first-line treatment for depression following traumatic brain injury (TBI). A limited body of evidence supports the efficacy of sertraline (starting at 25 mg; aiming for 50–200 mg/day) and citalopram (starting at 10 mg; aiming for 20–40 mg/day).

(INESSS-ONF, 2015)

Note: Depression after TBI is amenable to pharmacologic interventions and such treatment may alleviate not only the mood disturbance but also be of benefit for other symptoms.

If selective serotonin reuptake inhibitors (SSRIs) have been trialed and are not effective, or have produced unwanted side effects or drug interactions, the individual with TBI should be referred for review to a psychiatrist with expertise in treating individuals with TBI.


Suggested tool: Health Canada Indications of Use

REFERENCE:

- ERABI Module 8-Mental Health Issues, p.18, 8.2.3

R 6.2 P B

Stimulants such as methylphenidate may be considered for depression after traumatic brain injury over the shorter term; they may also be used to augment a partial response to selective serotonin reuptake inhibitors (SSRIs), especially in the setting of cognitive impairments, apathy, and/or fatigue.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use

REFERENCE:

- Lee et al. (2005)

R 6.3 C

Consider use of tricyclic antidepressants (TCAs) (desipramine) as a third-line option for depression following traumatic brain injury, although possible reduced efficacy and a higher risk of side effects (e.g., seizures) may limit their use.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use

REFERENCE:

- Wroblewski et al. (1996)

R7. Therapy for Anxiety

P Priority F Fundamental New Level of evidence A B C
R 7.1 P A

Cognitive behaviour therapy (CBT) is recommended to reduce anxiety post traumatic brain injury.

(INESSS-ONF, 2015)

REFERENCES:

- ERABI Module 8-Mental Health Issues, p.18, 8.2.3
- Arundine et al. (2012)
- Bradbury et al. (2008)

R8. Medication for Anxiety

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 8.1 P C

Given their favourable tolerability and broad utility, selective serotonin reuptake inhibitors (SSRIs) may be considered for anxiety treatment of individuals with traumatic brain injury (TBI).

(INESSS-ONF, 2015)

Note: There is a lack of research concerning medication treatment of anxiety disorders after TBI; however, much evidence exists supporting their treatment in the non-TBI population.


Suggested tool: Health Canada Indications of Use

R 8.2 P C

The use of benzodiazepines as first-line therapy for anxiety in individuals with traumatic brain injury (TBI) is NOT recommended due to potential effects on arousal, cognition, and motor coordination. The potential for abuse/dependency associated with these agents is also of concern, given the elevated rates of pre-injury substance use disorders observed among individuals with TBI. Nonetheless, short-term use of these agents may be helpful during periods of crisis or acute distress.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use

REFERENCE:

- Waldron-Perrine et al. (2008)

R9. Medication for Psychosis

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 9.1 C

The use of second generation neuroleptics is recommended for the treatment of psychosis as they are associated with fewer extrapyramidal symptoms (EPS) than first generation neuroleptics and exert their effects at sites other than the D2 receptor.

(Adapted from NGWG 2006, p. 1475)

Note: First generation neuroleptics have also been associated with greater impact on neuronal recovery. The ongoing need for antipsychotic medications should be periodically reassessed, and ongoing monitoring of weight, metabolic parameters, and late-emerging extrapyramidal symptoms is required. As all neuroleptics lower the seizure threshold to varying degrees, an initial trial with an anticonvulsant should be considered when heightened risk of seizures is of substantial concern.


Suggested tool: Health Canada Indications of Use

R10. Medication for Agitation/Aggression

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 10.1 C

For severe acute life threatening agitation and aggression that threatens staff or patient safety, the use of neuroleptic medications or intramuscular benzodiazepine can be considered.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCE:

- ERABI Module 12-Neuropharmacology, p. 25;36;38

R 10.2 C

For severe agitation and aggression that threatens staff or patient safety, consider the use of oral neuroleptic medications (while taking into consideration the onset of action). Second generation neuroleptic medications like quetiapine, ziprasidone, olanzapine and risperidone are preferred as older agents may have more side effects though methotrimeprazine have been used with limited side effects.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCES:

- Chew and Zafonte (2009)
- Bhatnagar et al. (2016)
- Elovic et al. (2008)

R 10.3 P A

Either propranolol or pindolol is recommended for the treatment of aggression after traumatic brain injury, particularly for individuals in post-traumatic amnesia (PTA). Studies have reported the efficacy of both propranolol (maximum dose 420–520 mg/day) and pindolol (maximum dose 40–100 mg/day) in the treatment of aggression in this population, if there are no medical contraindications.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCE:

- ERABI Module 8-Mental Health Issues, p.37-38

R 10.4 C

The use of valproate (750–2250 mg/day and/or carbamazepine (200–1200 mg/day) to reach therapeutic range should be considered as an option for the treatment of aggression in individuals with traumatic brain injury, particularly those who have a concomitant seizure disorder.

(Adapted from NGWG 2006, p.1492)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

R 10.5 P B

The use of amantadine 100 mg bid or methylphenidate can be considered for individuals with traumatic brain injury when impaired arousal and attention is suspected as a factor in agitation.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCES:

- Hammond et al. (2014)
- Hammond et al. (2015)

R 10.6 B

The use of sertraline may be considered as an option for the treatment of individuals with moderate agitation and irritability following traumatic brain injury. The use of other selective serotonin reuptake inhibitors (SSRIs) may be considered as an alternative if sertraline is not tolerated.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCES:

- ABIKUS (2007), G 29, p. 21
- Kant et al. (1998)

R 10.7 C

Tricyclic antidepressants may be considered as a third-line option for the treatment of aggression following traumatic brain injury, particularly for those who have an associated sleep-wake disorder. When used, nortriptyline or desipramine are preferable based upon their tolerability.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCE:

- Warden et al. (2006), p.1492

R 10.8 C

The use of first generation neuroleptics and benzodiazepines to treat agitation or aggression in individuals with traumatic brain injury should be minimized, as these medications may slow recovery after brain injury and may have a negative effect on cognition.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use
Suggested tool: Algorithm for Agitation and Aggression

REFERENCE:

- ABIKUS (2007), G 15, p. 19

R11. Medication for Bipolar Disorder / Mania

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 11.1 C

The use of commonly used medications such as lithium, anticonvulsants and neuroleptics in the management of symptoms resembling bipolar disorder (i.e., mania and depressed mood) should be considered, although insufficient evidence supports or refutes their use in individuals with traumatic brain injury. Lithium requires careful monitoring, as side effects may limit its use in this population.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use

REFERENCES:

- ERABI Module 12-Neuropharmacology, p. 25;36;38
- Chew and Zafonte (2009)

R12. Family Education in Neurobehavioral Issues

Medications should only be prescribed by qualified physicians, and guideline users should consult the section on "Principles of medication management" before prescribing.
P Priority F Fundamental New Level of evidence A B C
R 12.1 C

The family and key members of the network of the affected person should be provided with education about potential causes for behaviour and emotional disorders after traumatic brain injury, possible antecedents and triggers, appropriate management strategies, as well as possible side effects of medication. The family should receive timely information in writing on how to manage behaviour and emotions and should be invited to play a role in providing feedback and behavioural data.

(INESSS-ONF, 2015)


Suggested tool: Health Canada Indications of Use

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