R. Neurobehaviour and Mental Health

Mental health and mental disorders post-TBI can represent a challenging area of rehabilitation. As many of the behaviours and disorders discussed above are internalizing, it is important to always screen for depression, anxiety, or other maladaptive behaviours after an TBI. Once a negative pattern or behaviour has been identified, a treatment plan can be developed in collaboration with the rest of the care team. With rates of suicidal ideation being high among the TBI population, it is critical to be aware and sensitive to the psychological needs of those with an TBI.

Many maladaptive behaviours discussed above have pharmacological and non-pharmacological interventions available to choose from, and each patient should be consulted on their preference when appropriate. Many pharmacological agents and non-pharmacological interventions have evidence supporting their efficacy and use and should be explored as options with the care team. It is also essential to keep in mind the stigma that exists around mental health and to approach the topic with compassion and understanding.

Mood is an internal subjective state, but it is often inferred from how we behave and express ourselves. Following TBI, individuals may suffer from mood disorders such as major depression and anxiety disorders. Challenging behaviours such as agitation and aggression, as well as addictive behaviours such as substance abuse, may also become a significant problem post-TBI. These mental health issues are associated with the worsening of other TBI sequela and poorer outcomes. Among 361 individuals with severe TBI, that the most prevalent issues were major substance abuse or dependence (34%) and depression (11.1%).

Staff and clinicians should be trained in behavioural assessment and treatment techniques and 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 is explained to the individuals with brain injury, their families, and caregivers. Specialized clinicians should be provided with specific training and access 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 patient and family education program regarding managing behaviour.

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.

The following are suggestions of tools and resources that can be used to support the implementation of the recommendations in this section. Healthcare professionals must respect the legal and normative regulations of the regulatory bodies, in particular with regards to scopes of practice and restricted/protected activities, as these may differ provincially

Depression and anxiety post-TBI are associated with an individual’s feeling tired, helpless, hopeless, socially withdrawn, and having difficulty concentrating. These disorders often arise once the implications of the injury become apparent, which may be a reaction to the injury or the result of the neurological changes that have taken place. For some, depression and anxiety will develop within months of the injury, but for others, it will be a few years before clinical symptoms are diagnosed (Deb et al., 1999). Pharmacotherapy, counselling, and exercise have demonstrated some efficacy in treating depression and anxiety post-TBI. Depression is the most common psychiatric condition following TBI, with incidence rates higher than the general population (Gould et al., 2011; Osborn et al., 2014; Osborn et al., 2018; Ouellet et al., 2018; Singh et al., 2018). Often, depression presents within the first year post-TBI (Alway et al., 2016; Scholten et al., 2016). In patients one-year post TBI reports of prevalence are variable, ranging from 13% to 61% (Alway et al., 2016; Fleminger et al., 2003; Gordon et al., 1998; Grauwmeijer et al., 2018; Osborn et al., 2014; Sigurdardottir et al., 2013). Accurate estimations of prevalence are challenging given mixed populations, risk factors that are not completely understood, and variable methods of diagnosis (Osborn et al., 2018). A meta-analysis conducted by Osborn et al. (2014) reported that 21% to 43% of individuals have depression within the first five years of TBI, which then stabilizes to approximately 22% after five years. A systematic review and meta-analysis by Scholten et al. (2016) reported pooled prevalence rates in TBI patients increased over time with long-term rates of depression estimated at 43%. Another meta-analysis by Osborn et al. (2018) estimated rates at 30%. However, these reviews, along with the majority of the literature, are specific to TBI, and reports rates of depression in populations of mixed injury severity. In two long-term prospective cohorts of patient with moderate to severe TBI, rates of depression were 4-6 times higher than the general population (Alway et al., 2016) and prevalence was 20% 10 years after TBI (Grauwmeijer et al., 2018). Overall, the risk for depression is high post TBI, and unlike many mood disorders, remains this way for years following injury (Alway et al., 2016; Grauwmeijer et al., 2018; Hoffman et al., 2010; Ponsford et al., 2018; Scholten et al., 2016). Moderate and high intensity aerobic exercise programs have been found to improve anxiety, tension, depression, anger, confusion, and psychological stress in individuals with TBI (Rzezak et al., 2015; Weinstein et al., 2017). Further, in a pre-post study by Damiano and colleagues (2016), participants completed a home-based, aerobic exercise program for 5 days/week over 8 weeks. Training included exercise of moderate intensity for 30 minutes on the elliptical machine. Measures were assessed at baseline, 8 weeks, and 16 weeks. Moderate intensity aerobic exercise program was noted to improve depression as a result of improved sleep quality in individuals with TBI.  

Following TBI, depression can be treated pharmacologically. Among these interventions are various antidepressants: selective serotonin reuptake inhibitors such as paroxetine, fluoxetine, sertraline, or citalopram; serotonin norepinephrine reuptake inhibitors such as duloxetine, milnacipran, and venlafaxine; and tricyclic antidepressants such as amitriptyline and nortriptyline (Waldron-Perrine et al., 2008). Anticonvulsants such as carbamazepine have also been used to treat depression post-TBI. A single, small crossover randomized control trial (RCT) found that desipramine, a tricyclic antidepressant, was effective in treating chronic depression (Wroblewski et al., 1996). One RCT randomized participants to a sertraline, methylphenidate, or placebo group (Lee et al., 2005). All participants improved on measures of depression; however, the study results indicated that those assigned to the sertraline and methylphenidate groups had significantly lower depression scores than the placebo group at the end of the study (Lee et al., 2005). As well, fewer adverse events were reported for individuals receiving methylphenidate than those receiving sertraline. Fann and colleagues (2017) randomized participants to receive sertraline (treatment group) starting at a dose of 25mg/d, increasing to a therapeutic dose (200mg/d) or placebo (control group) for 12 weeks. No significant differences on measures of depression were observed between groups (Hamilton Depression Rating Scale, Symptom Checklist-20). A pair-wise meta-analysis conducted by Cheng et al. (2021) demonstrated that only methylphenidate and sertraline showed treatment efficacies superior to those of placebo or control. Further, a systematic review of TBI RCTs for depression conducted by Beedham et al. (2020) found that methylphenidate resulted in a significant reduction in depression severity from pre to post-intervention. At post-intervention, depression severity was significantly lower following methylphenidate treatment compared to control. Fann et al., 2017 conducted a randomized controlled trial investigating sertraline (200mg/d for 12wk) vs. placebo. No significant differences on measures of depression were observed between groups (Hamilton Depression Rating Scale, Symptom Checklist-20). There is level 1b evidence that sertraline does not significantly improve depression in individuals with TBI.

Management of Mood and Depression. Aerobic exercise programs have been shown to improve anxiety, anger, confusion, psychological distress, mood, depression and sleep quality (Rzezak et al., 2015; Damiano et al., 2016; Weinstein et al., 2017). 

Rzezak et al. (2015) found that an aerobic exercise program (one session of moderate intensity, one session of high intensity exercise) may improve anxiety (State-Trait Anxiety Inventory), tension (Brunnel Mood Scale), depression (Brunnel Mood Scale), anger (Brunnel Mood Scale), confusion (Brunnel Mood Scale) and psychological distress (Subject Exercise Experience Scale). Weinstein and colleagues (2017) (Pre-Post, N=10, TPI=chronic) found an aerobic exercise program (high intensity exercise 3d/wk) significantly improved mood (Profile of Mood States). Further, Damiano et al. (2016) found that an aerobic exercise program (moderate intensity exercise on elliptical 5d/wk) improved sleep quality (Pittsburgh Sleep Quality Index) and was correlated with a decrease in depression.  

Cognitive Status & Cognitive Communication Challenges. Feiger et al. (2023) conducted a retrospective record review of 172 adults who received rehabilitation services for TBI to examine if the impact of performance across multiple cognitive domains would predict psychosocial adjustment difficulties at discharge. The mean length of the rehabilitation program was 88.76d. Outcomes were assessed at admission and discharge from the program. Psychosocial adjustment impairment significantly reduced from admission to discharge (p<.001).  Cognitive functioning at admission was associated with significantly greater impairment in psychosocial adjustment at discharge (p=.03). Togher et al. (2023) conducted a prospective longitudinal cohort study that examined predictive factors underlying communication and psychosocial outcomes at 3 months, 6 months and 2 years. Psychosocial outcomes at 2 years were significantly predicted by pre-injury/injury variables (p=.013), 3-mo variables (p=0.013), and 6-mo variables (p=0.006). Longer PTA duration was associated with reduced psychosocial outcome, as measured by Sydney Psychosocial Reintegration Scale-2 (SPRS-2) (p=0.005). The information processing speed/memory (p=0.000) and aphasia (p=0.013) were moderately correlated with psychosocial outcomes at 2 years. Aphasia was moderately correlated with psychosocial outcomes (p=0.001) at 6 months. 

Positive Behavior Support Intervention. In a randomized controlled trial conducted by Ponsford et al. (2022), participants were randomly allocated to either a 12-month Positive Behaviour Support (PBS) intervention or Waitlist treatment group. The intervention consisted of initial meeting, GAS/goal setting, PBS+PLUS sessions, and occasionally included other therapists, and focused on approaches to achieve goals. Participants had to receive at least 6 sessions over a 3-month period. Therapists included: 4 neuropsychologists, 2 occupational therapists, 2 speech pathologists, 2 dual-trained. On the Over Behavior Scale (OBS), the Intervention group showed a significant reduction in challenging behaviour (p<.05) over a 12-month intervention. The waitlist group showed a similar improvement on the OBS over the 12-month waitlist period. PBS+PLUS intervention resulted in significantly greater gains in close others' confidence in addressing challenging behaviors on the Challenging Behaviour Self-Efficacy Scale (CBSES), relative to those in the waitlist group who showed no gains (p=.000 to .03). Findings indicated that PBS+PLUS can result in significant and sustained reductions in challenging behaviour in individuals with severe ABI. 

Psychotherapy and Art Therapy. Di Vita (2022) investigated the efficacy of group Psychotherapy and Art Therapy in rebuilding self-identity after traumatic brain injury (TBI), assessing their effects on psychological aspects in twelve patients with severe TBI. Participants were allocated to either Psychotherapy or Art Therapy and were subsequently exposed to the alternate intervention. The intervention duration was 1.5hrx4mo. Subjective Well-Being subscale scores in the PsyArt (Psychotherapy then Art Therapy) group were significantly higher those in the ArtPsy (Art Therapy then Psychotherapy) group (p<.05). Significant difference recorded in Positive Refraining subscale score in Brief-COPE after the first treatment (p<.05). At the end of both treatments, patients showed a reduction in depressive symptoms and in the perception of physical problems. 

Exercise Intervention (Dance-based). Sarkamo et al. (2021) conducted a randomized controlled trial to assess the feasibility and preliminary effects of a novel dance-based intervention called Dual-Assisted Dance Rehabilitation (DARE). Participants were randomized to either the AB or BA group. The AB group received the dance intervention during the first 3-mo phase while the BA group received the intervention during the second 3-mo phase. The intervention duration was 60min a day, 2 sessions per week for 12 weeks. Scores on the depression measure (BDI-II) significantly improved as a result of the dance intervention (p=.002). There was a consistent, large effect size on the BDI-II (d=1.19-1.74) indicating overall improvement of mood. 

Cognitive Behavioural Therapy (CBT) is the primary psychotherapy for anxiety and depression in the general population (Butler et al., 2006). CBT focuses on teaching cognitive skills, such as challenging unhelpful thoughts, and behavioural skills, such as coping, relaxation, graded exposure, and activity scheduling. Two trials delivered CBT either in a group or by telephone (Bradbury et al., 2008; Fann et al., 2015), and one trial combined CBT with motivational interviewing or non-directive counselling (Ponsford et al., 2016). In the first trial, the authors reported significantly greater reductions in depression, anxiety, stress, and psychological impairment with CBT than control for up to six months after treatment (Arundine et al., 2012; Bradbury et al., 2008). As well, the authors found no significant differences between group CBT and telephone CBT in terms of efficacy. In the second trial, CBT did not demonstrate significant reductions in depression when compared to controls, whether in person, by phone, or combined (Fann et al., 2015). The telephone CBT significantly reduced psychological impairment relative to the control, but in-person CBT and combined CBT were not superior. Patients’ subjective response to telephone CBT and combined CBT were more favourable than the control, and all forms of CBT had greater levels of satisfaction with depression care than the control. In the third trial, CBT demonstrated significant reductions in depression compared to the control when combined with motivational interviewing, but not non-directive counselling; there were no significant differences between the CBT groups (Ponsford et al., 2016). The authors also noted that participants with greater baseline depression had a significantly greater response to CBT. Brenner et al., 2017 conducted a small-group CBT randomized controlled trial (2 hours/week for 10 weeks) focused on alleviating hopelessness versus waitlist control. CBT significantly improved hopelessness (Beck Hopelessness Scale) when compared to waitlist controls. Supportive psychotherapy was compared to CBT in one RCT and only included patients diagnosed with depression following ABI (Ashman et al., 2014). Overall depression scores decreased from baseline following treatment. However, there were no significant differences in effectiveness between the two treatments (Ashman et al., 2014). Further, in a systematic review conducted by Cheng and colleagues (2021), pair-wise meta-analysis showed that the efficacies of CBT, mindfulness-based CBT, telephone supportive psychotherapy and telephonic counselling were significantly better than usual care (SMD –0.45, 95% CI –0.85 to –0.06; SMD –0.52, 95% CI –0.98 to –0.06; SMD –0.73, 95% CI –1.11 to –0.35; and SMD –0.27, 95% CI –0.50 to –0.03, respectively). 

Mindfulness-based cognitive therapy is a program that incorporates mindful meditation, body awareness, and yoga to promote relaxation and stress management (Shapiro et al., 1998). It has been evaluated as a potential intervention for depression in individuals with ABI. Bedard (2014) investigated a Mindfulness-Based Stress Reduction (MBSR) program with aspects of cognitive behavioural therapy for patients with diagnosed depression, in comparison with usual care. The program consisted of 10 weeks of therapy designed to encourage new ways of thinking about life and disability. The authors found that the intervention group showed a significantly greater reduction on the Beck Depression Inventory, but not on the Patient Health Questionnaire, compared to the control group; these findings were maintained at follow-up. Combs et al. (2018) conducted a pre-post study examining the impact MBSR had on the beliefs of patients with a history of TBI. Patients were more likely to believe MBSR could benefit physical health, focus, self-awareness and overall health with the more sessions they attended. However, the only belief that was significantly changed pre to post-MBSR program was patient’s beliefs of the benefit of MBSR could have on sleep. 

Suicidal ideation and attempts are also more frequent among the TBI population. Suicidal ideations are the thoughts or considerations of suicide that when left unattended can lead to distress and attempted suicide. Risk factors for suicide overlap with characteristics present after a TBI which explains, in part, why there is an increased risk of suicide following a TBI (Ahmedani et al., 2017; Bahraini et al., 2013; Simpson & Tate, 2007). Unfortunately, the risk for suicidal ideation and attempt remains high even 20 years post-injury (Fisher et al., 2016). 

Rates of suicidal ideation (23-28%) (Mackelprang et al., 2014; Simpson & Tate, 2002; Tsaousides et al., 2011) and attempts (26%) (Simpson & Tate, 2005) are high post-TBI, but can be further augmented through the presence of emotional disturbance and substance abuse (Simpson & Tate, 2005). Males are more likely to have suicidal ideation compared to females (Wisco et al., 2014), while age at time of injury was not associated with suicidal ideation (Mackelprang et al., 2014; Simpson & Tate, 2002). 

Within other TBI populations, 23-28% of individuals report suicidal ideation post-injury (Mackelprang et al., 2014; Simpson & Tate, 2002; Tsaousides et al., 2011). The risk of suicidal ideation can be further augmented with a comorbid diagnosis of depression, anxiety, or PTSD (Tsaousides et al., 2011) and the number of sustained TBIs (Shura et al., 2018; Wisco et al., 2014). Furthermore, elevated suicidal ideation at one-year post-TBI is associated with continual elevation of ideation at five years (Fisher et al., 2016), demonstrating the necessity for therapies targeting such ideations. 

If suicide ideation is not minimized, the risk of suicide attempts is high (Simpson & Tate, 2007) and is further increased when emotional distress is present (Gutierrez et al., 2008; Simpson & Tate, 2002). Within their lifetime, 26% of individuals post-TBI attempt suicide, with half of these individuals making more than one attempt (Simpson & Tate, 2002, 2005). Moreover, emotional disturbance and substance abuse history increase the risk for attempted suicide by a factor of 21, compared to individuals with no history (Simpson & Tate, 2005). 

Counseling is a typical intervention for suicide prevention. The prevalence of suicide is much greater than the general population. A large retrospective cohort estimated an incidence rate ratio of 2.38 in patients with severe TBI compared to controls (Madsen et al., 2018). 

Behaviour can be defined as any interaction between an organism and their environment. Behavioural issues are often defined as antisocial, uncooperative, or negative interactions associated with interpersonal problems. Challenging behaviour following TBI occurs with a relatively high frequency (25-50%) (Baguley et al., 2006). Challenging behaviours include agitation, anger, aggression, non-compliance with treatment, and difficulties with emotional regulation. The emergence of these behaviours likely arises from injury to the frontal lobes, resulting in disinhibited behaviour and lack of recognition of the associated consequences. Individuals found to have poorer social functioning often engage in a variety of aggressive or agitated behaviours including refusing participation, hitting, kicking, throwing objects, verbal abuse, and self-harm (McNett et al., 2012; Rao et al., 2009). Behavioural management and pharmacological treatment are often used to address these challenges, each with varying levels of success.

Sleep Disturbances. Miles et al. (2021) conducted a prospective longitudinal cohort of TBI individuals enrolled in the VA TBI Model Systems (TBIMS) National Database. All participants received inpatient rehabilitation. This longitudinal study lasted 5yr and examined co-occurring sleep apnea and probable PTSD. Sleep apnea was a significant predictor (p<0.001) of PTSD severity. Other statistically significant predictors of PTSD severity include increasing number of TBIs, receiving mental health treatment in the past year, ever deploying to a combat zone, and years since TBI.  The 5-years post-TBI sensitivity sample had the largest percentage of the sample that met criteria for both sleep apnea and PTSD (42%).  

Addictive behaviours can be a serious problem for some individuals post TBI. In TBI populations, pre-injury substance use disorders are more common than the general population (Alway et al., 2016; Hibbard et al., 1998). Pre-injury substance use is a significant predictor of abuse after TBI (Alway et al., 2016). Alcohol abuse has also been linked to major depression both before (Dikmen et al., 2004; Seel et al., 2010) and after injury (Jorge, 2005), although it remains unclear as to which problem evolved first. Studies differ in the criteria used to determine if an individual has an issue with addiction, dependence, or abuse. Studies that only include subjects with a positive Blood Alcohol Concentration (BAC) at the time of admission will report an inflated incidence compared to patient-reported substance use disorders. Additionally, prevalence rates are variable between populations. Rates of pre-injury alcohol abuse in Australian and North American populations have been recorded at 20-40%, whereas rates in Finland are reported at 8%, which likely reflects cultural differences in alcohol consumption (Alway et al., 2016; Gould et al., 2011; Hibbard et al., 1998; Koponen et al., 2002).

Among those who sustain their injury in a motor vehicle collision, which is one of the leading causes of TBI, almost half were found to be intoxicated (DeLambo et al., 2008; Wehman et al., 2000; West et al., 2009). Studies suggest that alcohol and substance abuse decline within the first year of injury (Bombardier et al., 2003; Jorge, 2005; Kelly et al., 1997; Ponsford et al., 2007), but those who returned to drinking two years post injury are likely to consume more than before the injury (Bombardier et al., 2002; Ponsford et al., 2007). In fact, individuals who abused alcohol pre-injury were ten times more likely to demonstrate problematic alcohol use post injury (Bombardier et al., 2003). Individuals who drink excessively and have large negative consequences associated with their drinking are more likely to report alcohol as the cause of their TBI and are more likely to report pre-injury substance abuse (Turner et al., 2003). Moreover, the correlation between mood disorders and substance abuse has also been shown to be quite strong both before and after injury (Jorge, 2005). Recovery following TBI will likely be negatively impacted if individuals continue to abuse alcohol or other substances. Many of these individuals have been found to spend more time in rehabilitation programs due to accentuated deficits of sensory, motor, cognitive, and communication functions (Wehman et al., 2000). As well, continued abuse of alcohol and other substances increases the risk of developing medical complications (Salim et al., 2009a). Involvement in rehabilitation deters or prevents individuals from using various substances, as patients are monitored rather closely (Bjork & Grant, 2009). However, once patients are discharged from inpatient rehabilitation, no monitoring exists and patients may return to their previous behaviours as a coping strategy. Addictions to alcohol and other substance may lead to a failure to survive independently in the community (Burke et al., 1988). 

During acute recovery, high BAC was found to be predictive of poorer performance on a variety of neuropsychological measures, including orientation, concentration, reasoning, and memory (Bombardier & Thurber, 1998; Kelly et al., 1997; Tate et al., 1999; Wilde et al., 2004). Wilde and colleagues (2004) also noted that high BAC was associated with increased brain atrophy post injury. In terms of long-term recovery, the impact of BAC and substance abuse is unclear. One study reported that acute BAC was not associated with outcome on the Glasgow Outcome Scale up to one-year post injury (Alexander et al., 2004). Another study found that acute BAC was correlated with Functional Independence Measure (FIM) score upon admission to rehabilitation, but not with FIM at discharge or one year post injury (Schutte & Hanks, 2010). The authors also reported that acute BAC was not predictive of long-term cognitive outcomes as well (Schutte & Hanks, 2010). Comparatively, a smaller study found that many cognitive measures were negatively impacted by hazardous drinking both before and after injury (Ponsford et al., 2013). Vickery and colleagues (2008) demonstrated that acute BAC and a history of hazardous drinking were associated with outcome on the Disability Rating Scale (DRS) but not the FIM. Interestingly, while high acute BAC was associated with lower score on the DRS, a history of hazardous drinking was associated with a higher score (Vickery et al., 2008). 

Several programs have been proposed and developed in order to reduce substance abuse in the TBI population. In a systematic review, Corrigan and colleagues (2010) identified 28 studies of screening and/or interventions for substance abuse, but noted that most research specifically excluded participants with severe TBI. The authors suggested that researchers and clinicians should address barriers to routine use of screening and interventions, as well as develop systematic accommodations for individuals with neurobehavioural impairments post injury. 

Affective symptoms such as depression and anxiety along with aggression, agitation, and addictive behaviours appear to be important determinants of functional and quality of life outcomes. They frequently cause significant distress for individuals with TBI and their family members and may result in diminished access to services. This module will review the available evidence for both pharmacological and non-pharmacological treatments for each. Issues regarding the use of restraints will also be discussed.

Agitation and aggression occur in approximately 33% to 70% of patients with TBI (Janzen et al., 2014; Nott et al., 2006; Sabaz et al., 2014; Singh et al., 2014). Agitation is generally defined as restlessness, impulsiveness, edginess, distractibility, wandering, and/or non-compliance, while aggression is defined as physical or verbal violence that may put the individual and others at risk for injury (Eisenberg et al., 2009). These behaviours have been associated with several clinical factors in individuals with TBI, including younger age (Baguley et al., 2006; Jean-Bay, 2000; Wolffbrandt et al., 2013), frontal lobe lesions (Tateno et al., 2003; Warriner & Velikonja, 2006), premorbid major depression (Baguley et al., 2006; Bakchine et al., 1989; Jean-Bay, 2000; Kim & Humaran, 2002; Sabaz et al., 2014; Tateno et al., 2003), and premorbid substance abuse (Sabaz et al., 2014; Tateno et al., 2003). During rehabilitation, the severity and duration of these challenging behaviours can have a negative impact on functional outcomes (Jean-Bay, 2000; Singh et al., 2014). 

Agitation is often a recovery-limiting factor, as it creates both a disruptive and unsafe environment for rehabilitation (Rosati, 2002). An ideal medication should have “a rapid onset of action, achieve maximal effect with a single dose, cause minimal adverse effects, and allow the patient to resume normal daily activities as quickly as possible without causing protracted sedation or cognitive impairments” (Stanislav & Childs, 2000). 

Pharmacological interventions used to treat agitation include a variety of medications such as: antidepressants, stimulants, anticonvulsants, antipsychotics, and beta-blockers. Ideally, the safety and efficacy of pharmacological interventions for agitation and aggression would be studied using a RCT design (Levy et al., 2005; Williamson et al., 2018). Two RCTs compared the effects of amantadine and placebo on irritability and aggression post TBI. Hammond and colleagues (2014) found that the frequency and severity of irritability were reduced when individuals received amantadine for 28 days compared to placebo. However, amantadine only significantly reduced aggression in individuals who had moderate to severe aggression at baseline (Hammond et al., 2014). A subsequent trial by Hammond and colleagues (2015) found that amantadine produced a non-significant reduction in irritability compared to placebo at 28 and 60 days, according to the most problematic and aberrant items on the neuropsychiatric inventory (Hammond et al., 2015). Deb and colleagues (2020) found that use of risperidone (1mg 1x/d, increased as needed up to 4mg/d) decreased verbal and physical aggression at 12 weeks. 

A systematic review by Williamson et al. (2018) examined controlled trials of pharmacological interventions for agitated behaviours in patients with mixed severity of TBI. The authors concluded that propranolol, methylphenidate, valproic acid and olanzapine may offer some benefit, where as sertraline, lisdexamfetamine and dextroamphetamine were not supported. Additionally, antipsychotics could increase the length of post traumatic amnesia and decrease cognitive function. Another systematic review that included case-series and case-report studies also reported weak support for the use of propranolol and antiepileptics (Nash et al., 2018). The review by Nash et al. (2018) concluded amantadine was among the best supported medication in acute management of behavioral and emotional dysregulation. Williamson et al. (2018) reported mixed findings for the use of amantadine and cautioned that it may increase agitation in acutely ill patients. In a systematic review published by Rahmani and colleagues (2021) on agitation and aggression in TBI, the authors recommended benzodiazepines and typical antipsychotics (specifically haloperidol) should be avoided if possible, atypical antipsychotics (such as olanzapine) can be considered as practical alternatives, and amantadine (especially in the context of chronic TBI) and propranolol (particularly in the context of acute TBI) is recommended.

Use of Technologies to Delivery Rehabilitation. Borgen et al. (2023) evaluated the effect of a home-based, individualized, and goal-oriented rehabilitation intervention in the chronic phase of TBI. Participants were randomly allocated to either an individually tailored, goal-based, home rehabilitation intervention or a control group receiving usual care. This intervention used videoconference and phone calls to set SMART goals, lasting 8 sessions for 4 months. Psychoeducational topics were addressed, including cognitive impairment after TBI, stress management and mindfulness, and cognitive communication difficulties. There were no significant differences between groups for health-related quality of life or social participation. At 12 months, participants in the intervention group had significantly better scores for health related quality of life (p=.04), lower TBI symptoms (p=.04), and anxiety symptoms (p=.02). Findings from this study indicated that a home-based, individually tailored goal-oriented rehabilitation intervention improved individual’s quality of life, as well as TBI-related and anxiety-related symptoms.  

REFERENCES

Ahmedani, B. K., Peterson, E. L., Hu, Y., Rossom, R. C., Lynch, F., Lu, C. Y., Waitzfelder, B. E., Owen-Smith, A. A., Hubley, S., Prabhakar, D., Williams, L. K., Zeld, N., Mutter, E., Beck, A., Tolsma, D., & Simon, G. E. (2017). Major physical health conditions and risk of suicide. American Journal of Preventive Medicine, 53(3), 308-315. 

Alashram, A. R., Annino, G., Padua, E., Romagnoli, C., & Mercuri, N. B. (2019). Cognitive rehabilitation post traumatic brain injury: a systematic review for emerging use of virtual reality technology. Journal of Clinical Neuroscience, 66, 209-219. 

Alexander, S., Kerr, M. E., Yonas, H., & Marion, D. W. (2004). The effects of admission alcohol level on cerebral blood flow and outcomes after severe traumatic Brain Injury. Journal of Neurotrauma, 21(5), 575-583.  

Alway, Y., Gould, K. R., Johnston, L., McKenzie, D., & Ponsford, J. (2016). A prospective examination of Axis I psychiatric disorders in the first 5 years following moderate to severe traumatic Brain Injury. Psychol Med, 46(6), 1331-1341. 

Arundine, A., Bradbury, C. L., Dupuis, K., Dawson, D. R., Ruttan, L. A., & Green, R. E. A. (2012). Cognitive behavior therapy after acquired Brain Injury: Maintenance of therapeutic benefits at 6 months posttreatment. Journal of Head Trauma Rehabilitation, 27(2), 104-112.  

Ashman, T., Cantor, J. B., Tsaousides, T., Spielman, L., & Gordon, W. (2014). Comparison of cognitive behavioral therapy and supportive psychotherapy for the treatment of depression following traumatic Brain Injury: A randomized controlled trial. Journal of Head Trauma Rehabilitation, 29(6), 467-478.  

Baguley, I. J., Cooper, J., & Felmingham, K. (2006). Aggressive behavior following traumatic Brain Injury: How common is common? Journal of Head Trauma Rehabilitation, 21(1), 45-56.  

Bahraini, N. H., Simpson, G. K., Brenner, L. A., Hoffberg, A. S., & Schneider, A. L. (2013). Suicidal ideation and behaviours after traumatic Brain Injury: A systematic review. Brain Impairment, 14(1), 92- 112. 

Bedard, M., Felteau, M., Marshall, S., Cullen, N., Gibbons, C., Dubois, S., Maxwell, H., Mazmanian, D., Weaver, B., Rees, L., Gainer, R., Klein, R., & Moustgaard, A. (2014). Mindfulness-based cognitive therapy reduces symptoms of depression in people with a traumatic Brain Injury: Results from a randomized controlled trial. Journal of Head Trauma Rehabilitation, 29(4), E13-E22. 

Beedham, W., Belli, A., Ingaralingam, S., Haque, S., & Upthegrove, R. (2020). The management of depression following traumatic brain injury: A systematic review with meta-analysis. Brain injury, 34(10), 1287-1304.

Bhatnagar, S., Iaccarino, M. A., & Zafonte, R. (2016). Pharmacotherapy in rehabilitation of post-acute traumatic brain injury. Brain research, 1640, 164-179.

Bjork, J. M., & Grant, S. J. (2009). Does traumatic Brain Injury increase risk for substance abuse? Journal of Neurotrauma, 26(7), 1077-1082. 

Bombardier, C. H., & Thurber, C. A. (1998). Blood alcohol level and early cognitive status after traumatic Brain Injury. Brain Injury, 12(9), 725-734. 

Bombardier, C. H., Temkin, N. R., Machamer, J., & Dikmen, S. S. (2003). The natural history of drinking and alcohol-related problems after traumatic Brain Injury. Archives of Physical Medicine and Rehabilitation, 84(2), 185-191. 

Borgen, I. M., Løvstad, M., Hauger, S. L., Forslund, M. V., Kleffelgård, I., Andelic, N., ... & Røe, C. (2023). Effect of an Individually Tailored and Home-Based Intervention in the Chronic Phase of Traumatic Brain Injury: A Randomized Clinical Trial. JAMA Network Open, 6(5), e2310821-e2310821.

Bradbury, C. L., Christensen, B. K., Lau, M. A., Ruttan, L. A., Arundine, A. L., & Green, R. E. (2008). The efficacy of cognitive behavior therapy in the treatment of emotional distress after acquired Brain Injury. Archives of Physical Medicine and Rehabilitation, 89(12 Suppl), S61-68.  

Burke, W. H., Wesolowski, M. D., & Lane, I. (1988). A positive approach to the treatment of aggressive Brain Injuryured clients. International Journal of Rehabilitation Research, 11(3), 235-241. 

Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). The empirical status of cognitive- behavioral therapy: a review of meta-analyses. Clinical Psychology Review, 26(1), 17-31.  

Cheng, Y. S., Tseng, P. T., Wu, Y. C., Tu, Y. K., Wu, C. K., Hsu, C. W., ... & Sun, C. K. (2021). Therapeutic benefits of pharmacologic and nonpharmacologic treatments for depressive symptoms after traumatic brain injury: a systematic review and network meta-analysis. Journal of psychiatry and neuroscience, 46(1), E196-E207.

Chew, E., & Zafonte, R. D. (2009). Pharmacological management of neurobehavioral disorders following traumatic brain injury--a state-of-the-art review. Journal of rehabilitation research & development, 46(6). 

Combs, M. A., Critchfield, E. A., & Soble, J. R. (2018). Relax while you rehabilitate: A pilot study integrating a novel, yoga-based mindfulness group intervention into a residential military Brain Injury rehabilitation program. Rehabil Psychol, 63(2), 182-193.  

Corrigan, J. D., Bogner, J., Hungerford, D. W., & Schomer, K. (2010). Screening and brief intervention for substance misuse among patients with traumatic Brain Injury. J Trauma, 69(3), 722-726.  

Damiano, D. L., Zampieri, C., Ge, J., Acevedo, A., & Dsurney, J. (2016). Effects of a rapid-resisted elliptical training program on motor, cognitive and neurobehavioral functioning in adults with chronic traumatic brain injury. Experimental brain research, 234(8), 2245-2252.

Deb, S., Lyons, I., Koutzoukis, C., Ali, I., & McCarthy, G. (1999). Rate of psychiatric illness 1 year after traumatic Brain Injury. American Journal of Psychiatry, 156(3), 374-378.  

DeLambo, D. A., Chandras, K. V., Homa, D., & Chandras, S. V. (2008). Psychiatric disabilities and substance abuse: Applications for rehabilitation professionals. Compelling counseling intervention: Celebrating VISTAS'fifth anniversary, 149-159.

Di Vita, A., Procacci, M. A., Bellagamba, M., Jacomini, M., Massicci, R., & Ciurli, M. P. (2022). Psychotherapy and Art Therapy: A pilot study of group treatment for patients with traumatic brain injury. Journal of Health Psychology, 27(4), 836-846. 

Dikmen, S. S., Bombardier, C. H., MacHamer, J. E., Fann, J. R., & Temkin, N. R. (2004). Natural history of depression in traumatic Brain Injury. Archives of Physical Medicine and Rehabilitation, 85(9), 1457-1464. 

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

Fann, J. R., Bombardier, C. H., Temkin, N., Esselman, P., Warms, C., Barber, J., & Dikmen, S. (2017). Sertraline for major depression during the year following traumatic brain injury: a randomized controlled trial. The Journal of head trauma rehabilitation, 32(5), 332. 

Fann, J. R., Bombardier, C. H., Vannoy, S., Dyer, J., Ludman, E., Dikmen, S., Marshall, K., Barber, J., & Temkin, N. (2015). Telephone and in-person cognitive behavioral therapy for major depression after traumatic Brain Injury: A randomized controlled trial. Journal of Neurotrauma, 32(1), 45- 57. 

Feiger, J. A., Snell, J., & Chiou, K. S. (2023). Neuropsychological functioning predicts psychosocial adjustment after postacute rehabilitation for traumatic brain injury. Journal of the International Neuropsychological Society, 29(4), 410-414. 

Fisher, L. B., Pedrelli, P., Iverson, G. L., Bergquist, T. F., Bombardier, C. H., Hammond, F. M., Hart, T., Ketchum, J. M., Giacino, J., & Zafonte, R. (2016). Prevalence of suicidal behaviour following traumatic Brain Injury: Longitudinal follow-up data from the NIDRR Traumatic Brain Injury Model Systems. Brain Injury, 1-8.  

Fleminger, S., Oliver, D. L., Williams, W. H., & Evans, J. (2003). The neuropsychiatry of depression after Brain Injury. Neuropsychological Rehabilitation, 13(1-2), 65-87.  

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. 

Gould, K. R., Ponsford, J. L., Johnston, L., & Schonberger, M. (2011). The nature, frequency and course of psychiatric disorders in the first year after traumatic Brain Injury: a prospective study. Psychol Med, 41(10), 2099-2109.  

Grauwmeijer, E., Heijenbrok-Kal, M. H., Peppel, L. D., Hartjes, C. J., Haitsma, I. K., de Koning, I., & Ribbers, G. M. (2018). Cognition, health-related quality of life, and depression ten years after moderate to severe traumatic Brain Injury: A prospective cohort study. Journal of Neurotrauma, 35(13), 1543-1551.  

Gutierrez, P. M., Brenner, L. A., & Huggins, J. A. (2008). A preliminary investigation of suicidality in psychiatrically hospitalized veterans with traumatic Brain Injury. Archives of Suicide Research, 12(4), 336-343.  

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. Journal of Head Trauma Rehabilitation, 29(5), 391-399.  

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

Hibbard, M. R., Uysal, S., Kepler, K., Bogdany, J., & Silver, J. (1998). Axis I psychopathology in individuals with traumatic Brain Injury. Journal of Head Trauma Rehabilitation, 13(4), 24-39. 

Janzen, S., McIntyre, A., Meyer, M., Sequeira, K., & Teasell, R. (2014). The management of agitation among inpatients in a Brain Injury rehabilitation unit. Brain Injury, 28(3), 318-322. 

Jorge, R. E. (2005). Neuropsychiatric consequences of traumatic Brain Injury: A review of recent findings. Current Opinion in Psychiatry, 18(3), 289-299.

Kelly, M. P., Johnson, C. T., Knoller, N., Drubach, D. A., & Winslow, M. M. (1997). Substance abuse, traumatic Brain Injury and neuropsychological outcome. Brain Injury, 11(6), 391-402.

Koponen, S., Taiminen, T., Portin, R., Himanen, L., Isoniemi, H., Heinonen, H., Hinkka, S., & Tenovuo, O. (2002). Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study. American Journal of Psychiatry, 159(8), 1315-1321.

Lee, H., Kim, S. W., 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. Human Psychopharmacology, 20(2), 97-104.

Levy, M., Berson, A., Cook, T., Bollegala, N., Seto, E., Tursanski, S., Kim, J., Sockalingam, S., Rajput, A., Krishnadev, N., Feng, C., & Bhalerao, S. (2005). Treatment of agitation following traumatic Brain Injury: A review of the literature. NeuroRehabilitation, 20(4), 279-306.

Mackelprang, J. L., Bombardier, C. H., Fann, J. R., Temkin, N. R., Barber, J. K., & Dikmen, S. S. (2014). Rates and predictors of suicidal ideation during the first year after traumatic Brain Injury. American journal of public health, 104(7), e100-107.

Madsen, T., Erlangsen, A., Orlovska, S., Mofaddy, R., Nordentoft, M., & Benros, M. E. (2018). Association Between Traumatic Brain Injury and Risk of Suicide. Jama, 320(6), 580-588.

Manivannan, S., Al-Amri, M., Postans, M., Westacott, L. J., Gray, W., & Zaben, M. (2019). The effectiveness of virtual reality interventions for improvement of neurocognitive performance after traumatic brain injury: a systematic review. The Journal of head trauma rehabilitation, 34(2), E52-E65.

McNett, M., Sarver, W., & Wilczewski, P. (2012). The prevalence, treatment and outcomes of agitation among patients with Brain Injury admitted to acute care units. Brain Injury, 26(9), 1155-1162.

Miles, S. R., Silva, M. A., Lang, B., Hoffman, J. M., Venkatesan, U. M., Sevigny, M., & Nakase-Richardson, R. (2021). Sleep apnea and posttraumatic stress after traumatic brain injury (TBI): A Veterans Affairs TBI Model Systems study. Rehabilitation psychology, 66(4), 450.

Nash, R. P., Weinberg, M. S., Laughon, S. L., McCall, R. C., Bateman, J. R., & Rosenstein, D. L. (2018). Acute pharmacological management of behavioral and emotional dysregulation following a traumatic Brain Injury: A systematic review of the literature. Psychosomatics: Journal of Consultation and Liaison Psychiatry.

Nott, M. T., Chapparo, C., & Baguley, I. J. (2006). Agitation following traumatic Brain Injury: an Australian sample. Brain Injury, 20(11), 1175-1182.

Osborn, A. J., Mathias, J. L., & Fairweather-Schmidt, A. K. (2014). Depression following adult, non- penetrating traumatic Brain Injury: A meta-analysis examining methodological variables and sample characteristics. Neuroscience and Biobehavioral Reviews, 47, 1-15.

Osborn, A. J., Mathias, J. L., Fairweather-Schmidt, A. K., & Anstey, K. J. (2018). Traumatic Brain Injury and depression in a community-based sample: A cohort study across the adult life span. The Journal of Head Trauma Rehabilitation, 33(1), 62-72.

Ouellet, M.-C., Beaulieu-Bonneau, S., Sirois, M.-J., Savard, J., Turgeon, A. F., Moore, L., Swaine, B., Roy, J., Giguère, M., & Laviolette, V. (2018). Depression in the first year after traumatic Brain Injury. Journal of Neurotrauma, 35(14), 1620-1629.

Ownsworth, T., Arnautovska, U., Beadle, E., Shum, D. H., & Moyle, W. (2018). Efficacy of telerehabilitation for adults with traumatic brain injury: a systematic review. The Journal of head trauma rehabilitation, 33(4), E33-E46.

Ponsford, J. L., Hicks, A. J., Gould, K. R., Downing, M. G., Hopwood, M., & Feeney, T. J. (2022). Positive behaviour support for adults with acquired brain injury and challenging behaviour: A randomised controlled trial. Annals of physical and rehabilitation medicine, 65(2), 101604.

Ponsford, J., Lee, N. K., Wong, D., McKay, A., Haines, K., Alway, Y., Downing, M., Furtado, C., & O'Donnell, M. L. (2016). Efficacy of motivational interviewing and cognitive behavioral therapy for anxiety and depression symptoms following traumatic Brain Injury. Psychol Med, 46(5), 1079-1090. 

Ponsford, J., Tweedly, L., & Taffe, J. (2013). The relationship between alcohol and cognitive functioning following traumatic Brain Injury. J Clin Exp Neuropsychol, 35(1), 103-112.

Ponsford, J., Whelan-Goodinson, R., & Bahar-Fuchs, A. (2007). Alcohol and drug use following traumatic Brain Injury: A prospective study. Brain Injury, 21(13-14), 1385-1392.

Rahmani, E., Lemelle, T. M., Samarbafzadeh, E., & Kablinger, A. S. (2021). Pharmacological treatment of agitation and/or aggression in patients with traumatic brain injury: a systematic review of reviews. The Journal of Head Trauma Rehabilitation, 36(4), E262-E283.

Rao, V., Rosenberg, P., Bertrand, M., Salehinia, S., Spiro, J., Vaishnavi, S., Rastogi, P., Noll, K., Schretlen, D. J., Brandt, J., Cornwell, E., Makley, M., & Miles, Q. S. (2009). Aggression after traumatic Brain Injury: Prevalence and correlates. Journal of Neuropsychiatry and Clinical Neurosciences, 21(4), 420-429.

Rosati, D. L. (2002). Early polyneuropharmacologic intervention in Brain Injury agitation. American Journal of Physical Medicine and Rehabilitation, 81(2), 90-93.

Rzezak, P., Caxa, L., Santolia, P., Antunes, H. K., Suriano, I., Tufik, S., & de Mello, M. T. (2015). Affective responses after different intensities of exercise in patients with traumatic brain injury. Frontiers in psychology, 6, 839.

Sabaz, M., Simpson, G. K., Walker, A. J., Rogers, J. M., Gillis, I., & Strettles, B. (2014). Prevalence, comorbidities, and correlates of challenging behavior among community-dwelling adults with severe traumatic Brain Injury: A multicenter study. Journal of Head Trauma Rehabilitation, 29(2), E19-E30.  

Salim, A., Ley, E. J., Cryer, H. G., Margulies, D. R., Ramicone, E., & Tillou, A. (2009a). Positive serum ethanol level and mortality in moderate to severe traumatic Brain Injury. Archives of Surgery, 144(9), 865-871. 

Särkämö, T., Huttula, L., Leppelmeier, J., Molander, K., Forsbom, M. B., Säynevirta, K., ... & Koskinen, S. (2021). DARE to move: feasibility study of a novel dance-based rehabilitation method in severe traumatic brain injury. Brain Injury, 35(3), 335-344.

Scholten, A. C., Haagsma, J. A., Cnossen, M. C., Olff, M., van Beeck, E. F., & Polinder, S. (2016). Prevalence of and Risk Factors for Anxiety and Depressive Disorders after Traumatic Brain Injury: A Systematic Review. Journal of Neurotrauma, 33(22), 1969-1994.

Scholten, A. C., Haagsma, J. A., Cnossen, M. C., Olff, M., van Beeck, E. F., & Polinder, S. (2016). Prevalence of and Risk Factors for Anxiety and Depressive Disorders after Traumatic Brain Injury: A Systematic Review. Journal of Neurotrauma, 33(22), 1969-1994.

Schutte, C., & Hanks, R. (2010). Impact of the presence of alcohol at the time of injury on acute and one- year cognitive and functional recovery after traumatic Brain Injury. International Journal of Neuroscience, 120(8), 551-556.

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

Shapiro, S. L., Schwartz, G. E., & Bonner, G. (1998). Effects of mindfulness-based stress reduction on medical and premedical students. Journal of Behavioural Medicine, 21(6), 581-599.

Shura, R. D., Nazem, S., Miskey, H. M., Hostetter, T. A., Rowland, J. A., Brenner, L. A., Workgroup, V. A. M.-A. M., & Taber, K. H. (2018). Relationship between traumatic Brain Injury history and recent suicidal ideation in Iraq/Afghanistan-era veterans. Psychological Services. 

Sigurdardottir, S., Andelic, N., Røe, C., & Schanke, A. K. (2013). Depressive symptoms and psychological distress during the first five years after traumatic Brain Injury: Relationship with psychosocial stressors, fatigue and pain. Journal of Rehabilitation Medicine, 45(8), 808-814.  

Simpson, G., & Tate, R. (2002). Suicidality after traumatic Brain Injury: Demographic, injury and clinical correlates. Psychological Medicine, 32(4), 687-697. 

Simpson, G., & Tate, R. (2005). Clinical features of suicide attempts after traumatic Brain Injury. Journal of Nervous and Mental Disease, 193(10), 680-685.

Simpson, G. K., & Tate, R. L. (2007). Suicidality in people surviving a traumatic Brain Injury: Prevalence, risk factors and implications for clinical management. Brain Injury, 21(13-14), 1335-1351. 

Singh, R., Mason, S., Lecky, F., & Dawson, J. (2018). Prevalence of depression after TBI in a prospective cohort: The SHEFBIT study. Brain Injury, 32(1), 84-90. 

Singh, R., Venkateshwara, G., Nair, K. P. S., Khan, M., & Saad, R. (2014). Agitation after traumatic Brain Injury and predictors of outcome. Brain Injury, 28(3), 336-340. 

Stanislav, S. W., & Childs, A. (2000). Evaluating the usage of droperidol in acutely agitated persons with Brain Injury. Brain Injury, 14(3), 261-265.

Tate, P. S., Freed, D. M., Bombardier, C. H., Harter, S. L., & Brinkman, S. (1999). Traumatic Brain Injury: Influence of blood alcohol level on post-acute cognitive function. Brain Injury, 13(10), 767-784.

Togher, L., Elbourn, E., Kenny, B., Honan, C., Power, E., Tate, R., ... & MacWhinney, B. (2023). Communication and psychosocial outcomes 2-years after severe traumatic brain injury: Development of a prognostic model. Archives of physical medicine and rehabilitation, 104(11), 1840-1849.

Tsaousides, T., Cantor, J. B., & Gordon, W. A. (2011). Suicidal ideation following traumatic Brain Injury: prevalence rates and correlates in adults living in the community. Journal of Head Trauma Rehabilitation, 26(4), 265-275. 

Turner, A. P., Bombardier, C. H., & Rimmele, C. T. (2003). A Typology of Alcohol Use Patterns Among Persons With Recent Traumatic Brain Injury or Spinal Cord Injury: Implications for Treatment Matching. Archives of Physical Medicine and Rehabilitation, 84, 358-364.

Vickery, C. D., Sherer, M., Nick, T. G., Nakase-Richardson, R., Corrigan, J. D., Hammond, F., Macciocchi, S., Ripley, D. L., & Sander, A. (2008). Relationships Among Premorbid Alcohol Use, Acute Intoxication, and Early Functional Status After Traumatic Brain Injury. Archives of Physical Medicine and Rehabilitation, 89(1), 48-55.

Waldron-Perrine, B., Hanks, R. A., & Perrine, S. A. (2008). Pharmacotherapy for post-acute traumatic brain injury: A literature review for guidance in psychological practice. Rehabilitation Psychology, 53(4), 426–444. https://doi.org/10.1037/a0013530 

Warriner, E. M., & Velikonja, D. (2006). Psychiatric disturbances after traumatic Brain Injury: Neurobehavioral and personality changes. Current Psychiatry Reports, 8(1), 73-80.

Wehman, P., Targett, P., Yasuda, S., & Brown, T. (2000). Return to work for individuals with TBI and a history of substance abuse. NeuroRehabilitation, 15(1), 71-77.

Weinstein, A. A., Chin, L. M., Collins, J., Goel, D., Keyser, R. E., & Chan, L. (2017). Effect of aerobic exercise training on mood in people with traumatic brain injury: a pilot study. The Journal of head trauma rehabilitation, 32(3), E49. 

West, S. L., Graham, C. W., & Cifu, D. X. (2009). Rates of Alcohol/Other Drug Treatment Denials to Persons With Physical Disabilities: Accessibility Concerns. Alcoholism Treatment Quarterly, 27(3), 305-316.

Wilde, E. A., Bigler, E. D., Gandhi, P. V., Lowry, C. M., Blatter, D. D., Brooks, J., & Ryser, D. K. (2004). Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome. Journal of Neurotrauma, 21(2), 137-147.

Williamson, D., Frenette, A. J., Perreault, M., Burry, L., Charbonney, E., Lamontagne, F., Potvin, M. J., Giguere, J. F., Mehta, S., & Bernard, F. (2018). Pharmacological interventions for agitation in traumatic Brain Injury: A systematic review. Critical Care. Conference: 38th International Symposium on Intensive Care and Emergency Medicine, ISICEM, 22(Supplement 1). 

Wisco, B. E., Marx, B. P., Holowka, D. W., Vasterling, J. J., Han, S. C., Chen, M. S., Gradus, J. L., Nock, M. K., Rosen, R. C., & Keane, T. M. (2014). Traumatic Brain Injury, PTSD, and current suicidal ideation among Iraq and Afghanistan U.S. veterans. Journal of traumatic stress, 27(2), 244-248.  

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. Journal of Clinical Psychiatry, 57(12), 582-587.