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4. Motor and Sensory Impairment Rehabilitation Post Acquired Brain Injury

by | Oct 17, 2018

4. Motor and Sensory Impairment Rehabilitation Post Acquired Brain Injury

Shawn Marshall MD FRCPC, Shannon Janzen MSc, Tristan Duffy MD(c), Pavlina Faltynek MSc, Magdalena Mirkowski MSc MScOT OT Reg. (Ont.), Scott Janssen MSc, Robert Teasell MD FRCPC

Abbreviations

ABI Acquired Brain Injury

BPPV Benign Paroxysmal Positional Vertigo

BTX-A Botulinum Toxin Type A

CBT Cognitive Behavioural Therapy

CIMT Constraint Induced Movement Therapy

NRS Numeric Rating Scale

PTH Post Traumatic Headaches

RCT Randomized Controlled Trial

TBI Traumatic Brain Injury

UMNS Upper Motor Neuron Syndrome

VAS Visual Analog Scale

Key Points


Constraint induced movement therapy may improve function and use of the affected upper limb post ABI.
Overnight hand splinting may not improve upper limb function post ABI.

Soft hand splinting, but not manual therapy, may be beneficial for improving hand opening post ABI.

Functional dexterity tasks may be superior to tabletop fine motor control activities for improving fine motor coordination post ABI.

Gesture recognition biofeedback and visual feedback-based training may improves fine motor function post ABI.

Virtual reality interventions may be an effective intervention for the recovery of upper extremity function post ABI.

Partial body weight supported gait training likely does not improve ambulation, mobility, or balance when compared to conventional gait training post ABI.

Robotic assisted treadmill training may be similar to manually assisted treadmill training at improving gait speed and mobility post ABI.

Electrical muscle stimulation with passive exercise may improve lower extremity muscle atrophy post ABI.

Sit-to-stand training and Intensive Mobility Training may improve lower extremity motor function post ABI.

Virtual reality can be used for the remediation of motor function in the lower extremities post-ABI.

Virtual reality training likely improves balance in individuals post ABI, however it may not be more effective than conventional physiotherapy programs.

Aerobic exercise programs, whether home-based or in the community, appear to improve motor function and balance post-ABI

Further research is needed in order to determine which components of exercise are the most effective for motor rehabilitation post-ABI.

Botulinum toxin type A injections, whether through a single point or multisite, likely reduce localized spasticity following ABI.

Phenol blocks of the musculocutaneous nerve may help decrease spasticity and improve range of motion temporarily up to five months post injection in individuals with ABI.

Electrical stimulation may acutely (24 hours) decrease spasticity in patients post ABI.

Oral baclofen appears to reduce lower extremity, but not upper extremity, spasticity in individuals with an ABI.

Bolus injections of intrathecal baclofen likely produce short-term reductions in upper and lower extremity spasticity and improvements in walking performance post ABI.

Prolonged intrathecal baclofen may reduce upper and lower extremity spasticity long-term post ABI.

Serial casting likely improves contractures and spasticity in individuals with an ABI compared to stretching; however, contracture improvement may not be maintained long-term.

Below-knee casting and stretching might increase passive ankle dorsiflexion in patients post ABI.

Serial below-knee casting may improve ankle range of motion and muscle extensibility in patients post TBI; however, this intervention may be associated with tissue breakdown.

Serial casting, whether for a short or long duration, might improve range of motion in individuals with an ABI. However, short duration casting may have a lower complication rate than long duration.

Hand splinting combined with stretching may be an effective treatment for spasticity and range of motion.

Botulinum toxin injections in combination with casting may be as effective as casting alone at reducing leg spasticity in patients post ABI.

Electrical stimulation in combination with tilt table standing and splinting may acutely improve spasticity (6 weeks) in patients post ABI.

Neural tension technique may be just as effective as random passive movement for improving lower extremity spasticity post ABI.

Computer based restitution training and rehabilitation programs directed at improving visual function likely improve the vision of those who sustain a TBI.

Base-in prisms and bi-nasal occluders may be effective in treating ambient vision disturbances.

Saccadic oculomotor rehabilitation may improve eye movements and reading in patients post ABI.

Combined aerobic dance and slide and step programs may improve balance and coordination post TBI.

A vestibular rehabilitation program may improve symptoms of vertigo in patients following TBI.

Cognitive behavioural therapy may be useful in managing post-traumatic headaches; however, may not be useful for headache-associated pain.

Cold therapy is likely not as effective as manual therapy at reducing post traumatic headache pain in patients post TBI.

Introduction

The primary cause of motor impairment and movement dysfunction post acquired brain injury(ABI) is upper motor neuron syndrome (UMNS), which can result in positive symptoms of enhanced stretch reflexes (spasticity) and released flexor reflexes in the lower limbs, such as the Babinski sign and mass synergy patterns, as well as negative symptoms including loss of dexterity and weakness (Mayer, 1997). These symptoms of UMNS have physiological implications for muscles that may subsequently develop stiffness and contractures, thereby further negatively affecting effective movement (Mayer, 1997).

For UMNS following brain injury, both the extent and timing of the individual’s symptoms should be considered when deciding on a course of action. Focal or diffuse spasticity may appear following an ABI and frequently follow common patterns in the upper and lower limbs (Mayer, 1997). Time post injury is another important consideration as spontaneous neurological recovery may continue for 9 to 15 months post injury. However, the potential for functional motor recovery beyond that point is possible through medical interventions, such as the correction of a deformity or the use of pharmacological agents that allow for improved motor control (Mayer et al., 1996). Motor impairment can also result from the independent effects of prolonged immobilization and bed rest during the acute period. Prolonged immobility affects multiple body systems, although it is the direct effect on the musculoskeletal and cardiovascular systems that impact motor function the most (Bushbacher & Porter, 2000).

Following diffuse central nervous system injury there are potential impairments involving the cognitive, behavioural, and physical domains. It is the physical domain that is emphasized early on within the rehabilitation process, as most acute in-patient rehabilitation programs focus on the improvement of activities of daily living (ADLs) a patient can perform— as assessed by outcome measures such as the Functional Independence Measure or the Barthel Index (Linacre et al., 1994; McDowell, 2006). The emphasis on physical impairments during rehabilitation is common because both the patient and family members are more likely to recognize and acknowledge physical impairments, in contrast to cognitive and behavioural impairments.

This module reviews the available evidence pertaining to interventions for motor and sensory rehabilitation following ABI.

4.2 Motor Impairment

Motor rehabilitation is a common focus of interventions provided to an individual post ABI. Motor rehabilitation is essential in helping the patient return to performing their ADLs, thus reestablishing independence post ABI. The following sections evaluate the interventions currently available for upper and lower extremity motor impairment, including spasticity.

4.2.1 Upper Extremity Interventions

Upper limb motor impairments are common in individuals with an ABI (Lannin et al. 2003). Interventions for the upper limb can focus broadly on arm mobility or on more specific outcomes such as finger dexterity. Despite the importance of upper extremity rehabilitation post ABI, there are limited studies evaluating available interventions.

4.2.1.1 Constraint Induced Movement Therapy

Key Points

Constraint induced movement therapy may improve function and use of the affected upper limb post ABI.

Constraint induced movement therapy (CIMT) is an intervention directed at improving the function of the more affected upper extremity following brain injury. The two primary components involve: 1) intensive motor training of the more affected upper extremity and 2) motor restriction of the less affected upper extremity (Dettmers et al., 2005). CIMT originated from research suggesting that the affected limb post brain injury is negatively impacted by “learned non-use” due to increased dependence on the intact limb (Grotta et al., 2004).

Although there is evidence in the stroke population to suggest that CIMT is clinically effective, many patients do not qualify for this type of therapy, which requires voluntary extension of the wrist and fingers, due to limited movement in the affected upper extremity. A further significant limitation of CIMT is the amount of resources required for its implementation (Grotta et al., 2004). Two studies evaluating the effect of CIMT post traumatic brain injury (TBI) were identified (Table 4.1).

Discussion

The effectiveness of modified CIMT was studied by Page and Levine (2003), with participants showing improvements in both the amount and quality of use of the more affected limb. CIMT was also studied by Shaw et al. (2005) and showed similar results. Significant improvements were seen in both laboratory and real world spontaneous use of the more affected upper limb following two weeks of CIMT (Shaw et al. 2015). Although all participants benefited from the intervention, the gains made by those placed in the “less adherent” group were strongly correlated with the participant’s degree of adherence (Shaw et al., 2005). This correlation was not evident in the “more adherent” group; with the authors suggesting that adherence beyond a certain level does not contribute to additional benefits (Shaw et al., 2005). The gains were maintained at one month, however use of the affected limb decreased by 21% at two years post treatment. Given these two studies, CIMT for the upper extremity appears to have a positive impact on upper limb motor recovery post ABI.

Conclusions

There is level 4 evidence that constraint induced movement therapy (CIMT) or modified CIMT may improve upper extremity function in individuals post ABI.

4.2.1.2 Hand Splinting and Stretching

Key Points

Overnight hand splinting may not improve upper limb function post ABI.

Soft hand splinting, but not manual therapy, may be beneficial for improving hand opening post ABI.

The purpose of hand splinting following an ABI is to prevent contractures and deformities, and to reduce spasticity. There are biomechanical and neurophysiologic rationales for splinting the spastic hand (Lannin et al., 2003); the biomechanical approach attempts to prevent contractures by physically preventing shortening of muscle and connective tissues. Conversely, the neurophysiologic approach is based on the concept that the splint can inhibit reflexive contraction of the muscle. Ultimately, the aim is to reduce deformity and contractures in the hand (Table 4.2).

Discussion

One study evaluated the effect of night time hand splinting in conjunction with conventional therapy compared to therapy alone (Lannin et al., 2003). Overall, the results did not demonstrate significant benefits of nocturnal hand splinting. A second randomized controlled trial (RCT) compared manual stretching, soft hand splinting, and manual stretching plus soft hand splinting to determine the optimal intervention (Thibaut et al., 2015). Results suggested that soft hand splinting for 30 minutes resulted in improved hand opening and reduced spasticity of the flexor finger muscles, however improvements in hand opening were not maintained after the break period. The hand splint was said to be feasible to use in daily care, as the splint was comfortable and easy to apply. There is a need to further research the effect of splinting in individuals with ABI as this practice is used in both acute and rehabilitation settings.

Conclusions

There is level 1b evidence that nocturnal hand splinting may not improve upper extremity range of motion or function compared to standard care in individuals post ABI.

There is level 4 evidence that soft hand splinting, but not manual therapy, may improve hand opening in individuals post ABI.

4.2.1.3 Interventions for Fine Motor Coordination

Key Points

Functional dexterity tasks may be superior to tabletop fine motor control activities for improving fine motor coordination post ABI.

Gesture recognition biofeedback and visual feedback-based training may improves fine motor function post ABI.

As discussed previously, the negative symptoms of UMNS, independent of spasticity, include: weakness, slowness of movement, and loss of finger dexterity (Mayer, 1997). Although gross motor function may return early in the recovery period following an ABI, fine motor deficits may persist and present a considerable challenge for both the individual and the clinicians treating them. The following studies highlight some of the treatment modalities that are being utilized to improve fine motor ability post ABI (Table 4.3).

Discussion

Neistadt (1994) examined fine motor coordination in a group of adult men with TBIs after two types of coordination retraining activities: tabletop activities (i.e., peg board activities, puzzles etc.) and functional activities (i.e., meal preparation). The study results suggested that functional activities may be more effective than table top activities in promoting fine motor coordination in persons with brain injury, as indicated by the improvement in “picking up small objects with the dominant hand” that the meal preparation group experienced (Neistadt 1994). Another study found that visual feedback-based training of grip force is beneficial for individuals post brain injury (Kriz et al., 1995). More specifically, a light weight force transducer was held between the pulp of index finger and thumb of the impaired hand. In response to visual cues delivered via computer monitor, all tasks involved the gradual increase and decrease of grip force in training and transfer protocols. Regardless of the individual pattern of impairments, all but one patient succeeded in improving their tracking performance and transferring regained capabilities to other tasks (Kriz et al. 1995).

The most recent fine motor coordination study compared the use of gesture recognition biofeedback to standard repetitive training without feedback (Yungher & Craelius, 2012). The results from the study showed a significant decrease in task completion time for those who received feedback, in comparison to those who did not. This intervention is both simple to execute (e.g., no precise placement of sensors, etc.) and the assessment is straightforward. The authors suggest that this intervention leads to improvements in fine motor function of the hand with minimal supervision (Yungher & Craelius, 2012). Despite these studies, there is limited evidence to guide clinical practice in this area.

Conclusions

There is level 2 evidence that functional retraining activities may be more effective than tabletop fine motor control retraining activities for improving fine motor function in the dominant hand in individuals post ABI.

There is level 4 evidence that visual feedback-based grip force training may improve tracking accuracy and transfer tasks in individuals post ABI.

There is level 2 evidence that gesture recognition biofeedback may improve fine motor function compared to standard repetitive training without feedback in individuals post ABI.

4.2.1.4 Virtual Reality for Upper Extremity Rehabilitation

Key Points

Virtual reality interventions may be an effective intervention for the recovery of upper extremity function post ABI.

With the advancement of technology, virtual reality is now a viable motor rehabilitation intervention for individuals following an ABI.

Discussion

Mumford et al. (2012) used virtual reality therapy with an interactive LCD surface and tracking cameras over 12 1-hour sessions. The authors found that accuracy and dexterity improved significantly in both upper extremities, but speed and efficiency only improved significantly for the right arms of patients.
Sietsema et al. (1993) reported that individuals who used a computer-controlled game aimed at improving reaching had better range of motion in the hip and wrist than individuals who completed rote exercise. Despite the study being performed in 1993, the game used by Sietsema et al. (1993) is still available for use.

Conclusions

There is level 2 evidence that virtual reality training may improve neurobehavioral functioning as well as reaching accuracy and movements post-ABI.

4.2.2 Lower Extremity Interventions

Outcomes targeted by lower extremity interventions following ABI tend to be gait and balance related. Gait improvement can be beneficial for re-establishing independence post ABI. Current methods being used for lower extremity rehabilitation include — but are not limited to — casting, orthosis, and partial body weight supported gait training.

4.2.2.1 Partial Body Weight Supported Gait Training

Key Points

Partial body weight supported gait training likely does not improve ambulation, mobility, or balance when compared to conventional gait training post ABI.

Robotic assisted treadmill training may be similar to manually assisted treadmill training at improving gait speed and mobility post ABI.

Movement disorders post ABI decrease the independence of a person due to loss of ambulation. The inability to maintain an erect posture, due to a lack of sufficient strength and balance, may prevent the training necessary for the restoration of self-ambulation following brain injury. Partial body weight supported gait training is postulated to result in earlier gait rehabilitation and earlier weight-bearing to increase strength and reduce spasticity. Additionally, this gait intervention allows for the simulation of task-specific walking movements and enables rehabilitation therapists to assist patients in the components of gait, rather than focusing on bearing the patient’s body weight. This type of gait training physically supports patients in a way that does not generate compensatory ambulation strategies that may develop while using a cane or a walker (Seif-Naraghi & Herman, 1999). In addition, partial body weight support reduces the demands on muscles while the patient works on improving the coordination of the movement. Body weight support can be gradually adjusted, as the patient improves, to encourage postural control and balance (Table 4.4).

Discussion

Brown et al. (2005) conducted an RCT in which 20 ABI patients were randomized to either body weight supported treadmill training or conventional over-ground gait training. The authors reported that body weight supported treadmill training provided no additional benefit over conventional gait training in measures of ambulation following three months of training. However, it was noted that conventional gait training improved Step Length Differential significantly more than the body weight supported treadmill training. Similarly, in another RCT, Wilson et al. (2006) randomized 40 ABI patients to either standard physical therapy or physical therapy supplemented with partial body weight-bearing gait training. The authors also reported that although each group made functional improvements, there were no significant between-group differences on measures of balance, ambulation, and mobility at the end of the eight-week training period (Wilson et al., 2006). Once again, Esquenazi et al. (2013) compared robotic assisted treadmill training to manually assisted treadmill training for individuals with TBI. The researchers noted that while both interventions resulted in significant improvement in gait parameters, there were no differences between the two interventions for gait velocity, endurance, or mobility.. From these studies, it appears that body weight supported gait training is not superior to more conventional methods.

Conclusions

There is level 2 evidence that body weight supported treadmill training may not improve ambulation or mobility compared to conventional gait training in individuals post ABI.

There is level 1b evidence that physical therapy with partial weight-bearing gait training may not improve ambulation, mobility, or balance compared to standard physical therapy in individuals post ABI.

There is level 2 evidence that robotic assisted body weight supported treadmill training may not improve ambulation or gait velocity compared to manually assisted treadmill training in individuals post ABI.

4.2.2.2 Multimodal Interventions

Key Points

Electrical muscle stimulation with passive exercise may improve lower extremity muscle atrophy post ABI.

Sit-to-stand training and Intensive Mobility Training may improve lower extremity motor function post ABI.

Multimodal interventions provide an opportunity to compare or combine interventions to better evaluate rehabilitation options. Combining interventions allows multiple physical impairments to be targeted in a single program, while comparing them assists in determining the relative effect of each therapy for motor rehabilitation (Table 4.5).

Discussion

Canning et al. (2003) in a single blinded RCT compared the addition of an intensive sit-to-stand training program to a traditional rehabilitation program. The experimental group demonstrated an increased ability to repeat sit-to-stand within a defined time frame in comparison to the traditional rehabilitation group, however there were no differences between groups in the increase of exercise capacity or efficiency. Hirose et al. (2013) used passive exercise as a control, and compared it with electrical muscle stimulation (EMS) to determine the effects of EMS on muscle atrophy in the lower limbs. The use of EMS resulted in significantly reduced amounts of atrophy when compared to passive exercise.

Clark et al. (2012) demonstrated that using body-weight-support treadmill training with handrail support reduces the amount of center of mass displacement and movement instability. However, they also noted that support alters timing and variability components of gait patterns. Although the study explored seven gait training methods, Clark et al. (2012) concluded that no one method provides the optimal stimulus and that combining various methods may be the most beneficial. Peters et al. (2014) identified that with intensive therapy using body-weight-support treadmill training, balance activities, strength coordination, and range of motion activities, individuals can significantly improve their walking speed and Timed Up and Go test scores. The benefits lasted up to three months post intervention.

Conclusions

There is level 1b evidence that sit-to-stand training combined with usual rehabilitation may improve motor performance in sit-to-stand tasks compared to usual rehabilitation in individuals post ABI.

There is level 2 evidence that electrical muscle stimulation with passive exercise may reduce lower extremity muscle atrophy compared to passive exercise in individuals post ABI.

There is level 4 evidence that Intensive Mobility Training may improve ambulation and mobility in individuals post ABI.

4.2.2.3 Virtual Reality for Lower Extremity Rehabilitation

Key Points

Virtual reality can be used for the remediation of motor function in the lower extremities post-ABI.

In addition to providing support for the rehabilitation of upper extremity function, virtual reality interventions have also been used to examine their efficacy on lower extremity remediation.

Discussion

Cuthbert et al. (2014) also demonstrated a significant within-group improvement on balance using virtual reality-based therapy; however, the gains made using this intervention were not significantly different compared to participants receiving standard physical therapy. Finally, during static balance tasks, visual feedback provided using a Wii Balance board helped reduce weight-bearing asymmetry (Foo et al., 2013).

Conclusions

There is level 1b evidence that virtual reality training compared to balance training may not be more effective for improving lower extremity function post-ABI. However, virtual reality training was shown to improve function independently.

There is level 4 evidence that visual feedback may reduce weight-bearing asymmetry in the lower extremities post-ABI.

4.2.3 Combined Upper and Lower Extremity Interventions

Unlike the studies referenced above, some programs combine interventions that treat both the upper and lower extremities. One of the challenges with combined rehabilitation is the choice of testing method. With a larger range of potential outcomes, it can be difficult to choose the proper test to evaluate the effect of the intervention.

4.2.3.1 Virtual Reality

Key Points

Virtual reality training likely improves balance in individuals post ABI, however it may not be more effective than conventional physiotherapy programs.

Virtual reality training has been gaining popularity in recent years. The advancement of virtual reality treatments has partly been influenced by commercial availability of programs, such as the Wii Fit Balance Board, that provide reliable testing and virtual reality games (Foo et al. 2013). Despite the increasing availability of virtual reality programs, there are a limited number of studies evaluating their efficacy (Table 4.8).

Discussion

Virtual reality interventions have been shown to be beneficial for improving balance post ABI. Ustinova et al. (2014) had participants complete 15 sessions of virtual reality therapy targeting the recovery of postural and coordination abnormalities, and demonstrated significant improvements for balance and dynamic stability following treatment. Schafer and Ustinova (2013) compared reaches in the physical environment after having participants with TBI and controls practice reaches in a virtual environment. Reaching distances in the physical environment increased for both groups, but a greater effect was noted among those with TBI.

Conclusions

There is level 1b evidence that virtual reality-based training may not improve balance and gait compared to standard physical therapy in individuals post ABI.

There is level 4 evidence that virtual reality therapy may improve balance, gait, and functional reaching in individuals post ABI.

4.2.4 Exercise Programs

Following an ABI, motor impairments in combination with cognitive impairment can have a significant impact on functional abilities (Boake et al., 2000). Unlike the more uniform focal deficits seen following stroke, the motor deficits following ABI tend to be diverse. These deficits include: impairment of force, endurance, coordination, and balance (Boake et al., 2000). Frequently, rehabilitation efforts are directed at specific motor impairments with the aim of improving overall functional ability.

4.2.4.1 Aerobic Training

Key Points

Aerobic exercise programs, whether home-based or in the community, appear to improve motor function and balance post-ABI

Further research is needed in order to determine which components of exercise are the most effective for motor rehabilitation post-ABI.

Many ABI patients have gone through a period of prolonged bed rest as a result of comorbid injuries or a prolonged loss of consciousness; consequently, cardiovascular changes, muscular atrophy, and loss of lean body mass commonly occur (Boake et al., 2000). General fitness training following ABI has the potential to influence multiple outcomes beyond the mere direct physical benefits such as improved aerobic capacity (Bushbacher & Porter, 2000). When comparing individuals with TBI that exercise to those that do not, the exercisers were less depressed, had less symptoms and better self-reported health status than non-exercising brain injury survivors (Gordon et al., 1998). The following studies examined the effectiveness of aerobic training on motor outcomes in individuals with an ABI (Table 4.9).

Discussion

It appears that the introduction of an aerobic training program can have a positive influence on individuals post ABI. Furthermore, general aerobic programs have been found to improve balance (Dault and Dugas, 2002; Ustinova et al., 2015). It is important to note that despite improvements in balance, Ustinova and colleagues (2015) did not find improvements in functional independence after the intervention. This suggests that although exercise programs may improve physical fitness, gains in functional status often occur independently of aerobic exercise training. Charrette et al. (2016) conducted a study of intensive exercise programs, consisting of endurance and full body strength training, for adults with chronic severe ABI. Results suggest that intensive combination of interventions improves gait distance and velocity, as well as mobility (Charrette et al., 2016).

Aquatic exercise was found to improve almost all subscales on the Health Promoting Lifestyle Profile, including interpersonal relationships, and also self-esteem— as measured by the Physical Self-Description Questionnaire (Driver et al., 2006). This study encourages s participation in group exercise post ABI as it can foster feelings of well-being and self-esteem which could have a positive impact upon other rehabilitation strategies (Driver et al., 2006).

Bateman et al. (2001) compared cycling training (experimental group) to relaxation training (control group) and found that cycling training was associated with a significant improvement in exercise capacity; however, there was no significant difference between the groups in regards to balance, mobility, and functional independence (Bateman et al., 2001). This suggests that although exercise programs may improve physical fitness, gains in functional status often occur independently of aerobic exercise training (Bateman et al., 2001).

Hassett et al.(2012) examined the benefits of circuit training with encouragement from a physiotherapist and heart rate monitor feedback in individuals with severe TBI. More specifically, the intervention group had their heart rate monitor uncovered and it beeped when they did not reach their target heart rate, whereas the control group had their monitors covered and muted.
Results indicate there was no significant difference between the two groups in terms of the amount of time spent in the heart rate target zone. Earlier Hassett et al. (2009) found individuals assigned to exercise programs showed significant improvement in their cardiorespiratory levels regardless of where they worked out (in a gym or at home) or how often (2.4 sessions per week versus 0.5 sessions per week). However, adherence to the program was higher among those attending a fitness center. When compliance was explored further, those with greater adhered were found to be older, more severely injured and had exercised before the injury (Hassett et al., 2011).

Hoffman et al. (2010) compared individuals who exercised in a community-based program to individuals who did not participate in this program; however, the controls were able to exercise on their own. Although the intervention group was working out more days per week than controls, the total amount of time spent exercising per week was similar between groups, making comparisons challenging. When those who were active (more than 90 minutes of activity per week) were compared to those who were not as active, the authors found that mood was significantly higher in the participants who were exercising for more than 90 minutes each week, regardless of what treatment group they were originally placed in. Thus, any physical exercise is beneficial to patients post ABI. Furthermore, home-based exercise programs have shown to improve depressive symptoms, stability, and gait following intervention (Bellon et al., 2015). It is important to note that lower stability and dual-tasking scores were associated with poorer mental health outcomes (Damiano et al. 2016).

Conclusions

There is level 1b evidence that participating in an exercise program at a fitness-center compared to home-based exercise program may lead to greater program adherence but not significantly different motor results in individuals post-ABI.

There is level 2 evidence that aerobic training compared to vocational rehabilitation may be more effective at improving co-ordination, strength, flexibility, and endurance in individuals post-ABI.

There is level 1b evidence that exercise programs may improve FIM scores, but not balance or mobility compared to relaxation training in individuals post-ABI.

There is level 4 evidence that multimodal exercise programs may improve gait and mobility in individuals post-ABI.

There is level 3 evidence that a home-based exercise program may improve stability to the level of healthy controls, but may not improve motor control, mobility, or dual-task performance in individuals post-ABI.

There is level 2 evidence that aerobic dance training compared to musculature training may improve sensory interaction and balance post-ABI.

4.2.5 Spasticity Interventions

Spasticity is a common symptom encountered post ABI and is an element of UMNS. Spasticity has been formally defined as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon reflexes, resulting from excitability of the stretch reflex” (Lance, 1980). Common features of spasticity include increased muscle tone, exaggerated tendon jerks, and clonus.

Management of spasticity is not unique to brain injury survivors, since it is often associated with other conditions affecting the central nervous system such as spinal cord injury and multiple sclerosis. Spasticity may require intervention when it interferes with functional abilities such as mobility, positioning, hygiene, or when it is the cause of deformity or pain. Factors that must be taken into consideration when proposing treatment of spasticity include chronicity of the problem, the severity, the pattern of distribution (focal versus diffuse), the locus of injury, as well as comorbidities (Gormley et al., 1997). Some studies have found that spasticity of cerebral origin versus spinal cord injury respond differently to the same medications (Katz & Campagnolo, 1993). Typically, the clinical approach to spasticity is to first employ treatments that tend to be less interventional and costly; however, multiple strategies may need to be administered concurrently.

4.2.5.1 Botulinum Toxin Injections

Key Points

Botulinum toxin type A injections, whether through a single point or multisite, likely reduce localized spasticity following ABI.

Botulinum toxin type A (BTX-A) acts at the pre-synaptic terminal to block acetylcholine release into the neuromuscular junction. When selectively injected into a specific muscle BTX-A is thought to cause local muscle paralysis, thereby alleviating hypertonia caused by excessive neural activity (Jankovic & Brin, 1991). It has been suggested that BTX-A may be useful in the treatment of localized spasticity if oral interventions such as benzodiazepines, baclofen, dantrolene sodium, or tizanidine cause significant adverse effects (Gracies et al., 1997b). Currently, limited numbers of RCTs exist evaluating botulinum toxin for spasticity in individuals with an ABI (Table 4.10).

Discussion

Five studies examining the effects of BTX-A on spasticity following ABI were identified. Intiso et al. (2014) showed a reduction in spasticity for the upper extremity (elbow, wrist, and hand), as well as ankle joints at one and four months post intervention. Although pain was also significantly reduced, no significant improvements in function were shown— as measured by the Glasgow Outcome Scale and the Frenchay Arm Test (Intiso et al., 2014). These findings were similar to those found by Yablon et al. (1996) who reported that BTX-A injections into the upper extremities improved range of motion and spasticity in 21 patients with ABI. These improvements were shown for patients who received the injections within one year of injury and also for those who received the injection more than one year post injury (Yablon et al., 1996). The time between injury and injection was also studied by Clemenzi et al. (2012). The results were similar to the previous study for pain and spasticity; however, the time between onset and injection did have an effect on functional outcomes. Patients with a shorter period of time between their injury and first injection had greater improvements on the Barthel Index (Clemenzi et al., 2012).

In terms of the administration of BTX-A, Mayer et al. (2008) found that a single motor point injection and multisite distributed injection resulted in similar outcomes, with both groups showing a clinical effect at three weeks post intervention.

Conclusions

There is level 4 evidence that botulinum toxin type A injections may be effective in the management of localized spasticity following ABI.

There is level 1b evidence that receiving botulinum toxin type A through a single motor point or multisite distributed injections are similar at reducing spasticity in individuals with an ABI.

4.2.5.2 Nerve Blocking Agents

Key Points

Phenol blocks of the musculocutaneous nerve may help decrease spasticity and improve range of motion temporarily up to five months post injection in individuals with ABI.

Local nerve blocks are a potential management solution in circumstances where there is muscle spasticity affecting only a few muscle groups in a focal pattern. Essentially, a nerve block involves the application of a chemical agent to impair nerve functioning. The effect of the chemical agent may be temporary or permanent (Katz et al., 2000). Temporary acting compounds include local anesthetic agents that block sodium ion channels, typically lasting only a few hours. Local anesthetic agents are used for diagnostic procedures or for assistance with activities such as casting (Gracies et al., 1997a). Agents used for permanent nerve blocks to treat spasticity last between 2 and 36 months, and include ethyl alcohol (>10%) and phenol (>3%). Complications of this type of block have included chronic dysesthesia, pain and permanent peripheral nerve palsies (Gracies et al., 1997a). Studies of nerve blocking agents to improve spasticity in individuals with an ABI are limited (Table 4.11).

Discussion

We identified two studies which evaluated the efficacy of nerve blocks as a treatment for spasticity. Keenan et al. (1990) evaluated the effect of percutaneous phenol block of the musculocutaneous nerve to decrease elbow flexor spasticity. The results indicated that there was improved range of motion of the elbow lasting a mean of five months. In the second study, 11 closed head injury patients with spastic paralysis of the upper extremity were treated with percutaneous phenol injections into the spastic wrist and finger flexors (Garland et al., 1984). The authors reported that relaxation of muscle tone persisted for up to two months following the injections. Furthermore, there was a mean increase in resting wrist angle, active wrist extension, and passive wrist extension with fingers flexed of 25, 30, and 5, respectively (Garland et al., 1984). Evidently, these studies found that percutaneous phenol blocks are effective in temporarily controlling spasticity in patients post TBI, however due to the retrospective nature of the studies and lack of controls there is insufficient evidence to make definitive conclusions on the efficacy of phenol injections.

Conclusions

There is level 4 evidence that phenol nerve blocks may reduce contractures and spasticity at the elbow, wrist, and finger flexors for up to five months post injection in individuals post ABI.

4.2.5.3 Electrical Stimulation

Key Points

Electrical stimulation may acutely (24 hours) decrease spasticity in patients post ABI.

Electrical stimulation uses an electrical current to elicit a muscle contraction either directly by stimulating the skeletal muscle (Gregory & Bickel, 2005), or indirectly by stimulating the nerve supplying that muscle. Electrical stimulation has seen some applications with regards to assisting paraplegic patients with standing and walking (Katz et al., 2000). Reports from spinal cord injury populations suggest that electrical stimulation is associated with significant reductions in spasticity for up to 24 hours post stimulation (Halstead et al., 1993) (Table 4.10).

Discussion

One study by Seib et al. (1994) was identified which examined the effects of electrical stimulation applied to the lower extremity in participants with either a TBI or spinal cord injury. Electrical stimulation significantly decreased spasticity in the stimulated extremity, whereas the tone in the non-stimulated extremity did not change. Furthermore, the effect of one stimulation session was noted to last up to 24 hours post intervention.

Conclusions

There is level 4 evidence that electrical stimulation may be effective for decreasing lower extremity spasticity for six or more hours, lasting up to 24 hours, in individuals post ABI.

4.2.5.4 Oral Antispasticity Drugs

Key Points

Oral baclofen appears to reduce lower extremity, but not upper extremity, spasticity in individuals with an ABI.

Oral agents are often used to manage spasticity particularly when a systemic agent to treat upper and lower extremity spasticity is required (Gracies et al., 1997b). Although antispasticity agents may be used for other medical conditions such as spinal cord injury or multiple sclerosis (Gracies et al., 1997b), the effectiveness of these agents should not be presumed to be similar for brain injury survivors. Multiple medications have been evaluated to treat spasticity of both cerebral and spinal cord origin. The more common medications include GABA agonists, that affect ion flux such as baclofen, benzodiazepines, dantrolene sodium, as well as agents that affect alpha-2 adrenergic receptors such as tizanidine and clonidine. The use of any of these drugs must be weighed against potential side effects, such as sedation, which are complicated by the cognitive and behavioural changes associated with brain injury (Table 4.11).

Discussion

Meythaler et al. (2004) completed a retrospective study evaluating the use of oral baclofen to manage spasticity in a mixed brain injury and stroke population. Pre and post testing revealed that oral baclofen improved spasticity in the lower extremity assessed using the Ashworth Rigidity Scale and Spasm Frequency Scale; however, no changes for tone, spasm frequency, or reflexes were found for the upper extremity (Meythaler et al., 2004). The authors suggest that the lack of effect may be due in part to receptor specificity issues. Of note, a common adverse effect of the oral baclofen was the onset of considerable sleepiness in 17% of patients (Meythaler et al., 2004).

Of note, Meythaler et al. (2001) completed a randomized, double blinded placebo controlled cross over trial examining tizanidine for the management of spasticity. This study evaluated both stroke (53%) and TBI (47%) survivors. For both lower and upper extremity, there was a significant decrease in the Ashworth scores on the affected side with the active drug compared to placebo. However, significant differences between interventions were not found for upper and lower extremity spasm and reflex scores. Overall the authors felt that tizanidine was effective in decreasing the spastic hypertonia associated with ABI; however, a common side effect was increased somnolence (41%) (Meythaler et al., 2001). Despite the study showing effectiveness, no level of evidence will be assigned for this drug due to more than 50% of the population being stroke.

Conclusions

There is level 4 evidence that oral baclofen may improve lower extremity spasticity, but not upper extremity spasticity, in individuals post ABI.

4.2.5.5 Intrathecal Baclofen

Key Points

Bolus injections of intrathecal baclofen likely produce short-term reductions in upper and lower extremity spasticity and improvements in walking performance post ABI.

Prolonged intrathecal baclofen may reduce upper and lower extremity spasticity long-term post ABI.

A limitation of oral baclofen is the inability to achieve sufficiently high concentrations in the cerebrospinal fluid (CSF) in order to modify spasticity without first causing significant sedation (Gracies et al., 1997b). Intrathecal baclofen refers to direct administration of baclofen into the intrathecal space and CSF at the lumbar level. For therapeutic treatment, a subcutaneous pump is required to provide continuous administration of the medication into the intrathecal space. This treatment procedure, however, is invasive and associated with complications including infection, pump failure, and tube complications such as kinking or disconnection (Gracies et al., 1997b) (Table 4.12).

Discussion

Meythaler et al. (1996) confirmed the effectiveness of intrathecal baclofen in decreasing upper and lower extremity spasticity in a randomized, double blinded, placebo controlled cross-over trial. In subsequent studies, the same investigators went on to demonstrate the effectiveness of intrathecal baclofen for decreasing spasticity for up to three months (Meythaler et al., 1997) and 1 year (J. M. Meythaler et al., 1999). Investigations carried out by other research groups have reported similar findings regarding the efficacy of intrathecal baclofen for the management of spasticity post ABI (Becker et al., 1997; Chow et al., 2015; Dario et al., 2002; Francisco et al., 2005; Hoarau et al., 2012b; Margetis et al., 2014; Posteraro et al., 2013; Stokic et al., 2005; Wang et al., 2016). However, a common limitation of these studies is the lack of a control group. Regardless, it appears that intrathecal baclofen is an effective treatment for spasticity. It should be noted, however, that some adverse effects, such as urinary hesitancy, were reported. Hoarau et al. (2012a) conducted a 10-year follow up of individuals with dysautonomia and hypertonia treated with intrathecal baclofen therapy. The study found that 62.8% of participants had some type of complication, with infections at the operative site being the most common (20.9%), followed by overdosed with profound flaccidity, sedation, and vomiting (16.3%) (Hoarau et al., 2012a).

Studies have also evaluated the functional consequences by assessing walking performance, gait speed, and range of motion following a bolus injection of intrathecal baclofen (Chow et al., 2015; Horn et al., 2010; Horn et al., 2005). Horn et al. (2005) found that although the injections produced changes in joint range of motion during gait, only ankles showed a significant result. Chow et al. (2015) similarly found an increase in ankle range of motion but found no significant differences in terms of gait speed, stride length, cadence, or stance. Future studies should be conducted using a prospective controlled trial or RCT study design that includes control groups to further establish the efficacy of intrathecal baclofen for the management of spasticity post ABI.

Conclusions

There is level 1b evidence that bolus intrathecal baclofen injections may produce short-term (up to six hours) reductions in upper and lower extremity spasticity compared to placebo following ABI.

There is level 4 evidence to suggest that prolonged intrathecal baclofen may result in longer-term (three months, and one year) reductions in spasticity in both the upper and lower extremities following an ABI.

There is conflicting level 4 evidence to suggest that intrathecal baclofen may result in short-term improvement of walking performance in ambulatory patients, particularly gait velocity, stride length, and step width, in individuals post ABI.

4.2.5.6 Casting

Key Points

Serial casting likely improves contractures and spasticity in individuals with an ABI compared to stretching; however, contracture improvement may not be maintained long-term.

Below-knee casting and stretching might increase passive ankle dorsiflexion in patients post ABI.

Serial below-knee casting may improve ankle range of motion and muscle extensibility in patients post TBI; however, this intervention may be associated with tissue breakdown.

Serial casting, whether for a short or long duration, might improve range of motion in individuals with an ABI. However, short duration casting may have a lower complication rate than long duration.

Spasticity frequently results in musculoskeletal contractures (Mayer et al., 1997) and has been estimated in one study to have an incidence as high as 84% in TBI patients (Yarkony & Sahgal, 1987). As with hand splinting, the theoretical premise for the effect of casting on hypertonia and joint mobility is based on different neurophysiological and biomechanical principles (Mortenson & Eng, 2003). Spasticity may be reduced by the effect of prolonged stretch, or possibly the effects of neutral warmth or prolonged pressure which may in turn reduce the cutaneous sensory input to the spinal cord. From a biomechanical perspective, muscle and connective tissues are likely elongated when immobilized in a stretched position, thus reducing the incidence on contractures (Mortenson & Eng, 2003) (Table 4.14).

Casting has been thought to reduce hypertonia and spasticity in individuals with an ABI. This is believed to be the result of reducing contractures by stretching the muscles of the immobilized limb (Pohl et al. 2002). Serial casting is a process in which the angle of the cast is changed periodically, with the objective of returning the joint to its original angle. However, despite the fact that serial casting has been utilized by physiotherapists for more than 40 years there is little empirical data to support its use in isolation. Conversely, evidence exists supporting the use of casting as a useful adjunct to other therapies for the management of spasticity and contracture in patients post TBI.

Discussion

In comparison to passive stretching, serial casting was beneficial in improving contracture of the elbow (Moseley et al. 2008). The improvement in contracture, however, was no longer significant after 4 weeks. In addition, the researchers noted a greater improvement in spasticity in the casting group when compared to the stretching group. The results from this study suggest that while serial casting may be effective initially, it does not appear to have long-term effects on contractures.

In order to evaluate the efficacy of lower extremity casting post ABI, Moseley (1997) used a randomized open cross-over design to compare one week of casting combined with stretching to a week of no therapy (control) for ankle plantar flexion contractures. The experimental group had a significantly improved range of passive ankle dorsiflexion whereas the control group tended to have overall deterioration of ankle range of motion (Moseley, 1997). In two separate studies, Singer et al. (2003) and Singer et al. (2003) also evaluated the efficacy of weekly casting and found casting to be effective in improving ankle movement. In addition, greater ankle mobility was shown to be associated with improved transfer independence (Singer et al., 2003). It should be noted, however, that casting can lead to tissue breakdown (Singer et al. 2003).

In a retrospective case comparison study, Pohl et al. (2002) compared short, one to four days casting to a longer duration, five to seven days casting, for both upper and lower extremity joints. Although improvements in range of motion were seen in each group immediately following the intervention and at a one-month follow-up, there was no significant difference found between groups. However, the discontinuation rate in the longer duration group due to complications was significantly higher than for the short casting interval group.

Conclusions

There is level 1b evidence that serial casting may improve contractures of the elbow initially, but not long-term, when compared to passive stretching in individuals with an ABI.

There is level 1b evidence that serial casting may be superior to passive stretching at improving spasticity of the elbow in individuals post ABI.

There is level 2 evidence that a below-knee casting and stretching protocol may increase passive ankle dorsiflexion in patients post ABI.

There is level 4 evidence that weekly below-knee casts may improve ankle range of motion, muscle extensibility, and passive torque in patients post ABI.

There is level 3 evidence that short duration (one to four days) and longer duration (five to seven days) serial casting may have similar effects on upper or lower extremity range of motion in individuals post ABI.

4.2.5.7 Adjustable Orthosis

Similar to casting, an adjustable pre-fabricated orthosis could potentially provide prolonged stretching of an ankle plantar flexion contracture. Advantages of the orthosis over a rigid cast include the ease of adjustability and the ability to remove it daily for short periods of time. A pre-post study by Grissom and Blanton (2001) examined six participants with mixed etiologies who received a 2% lidocaine block of the posterior tibial nerve and then wore an adjustable ankle-foot orthosis on the affected ankle for 23 hours per day for two weeks for plantarflexion contractures. Adjustments were attempted every two to three days to increase passive dorsiflexion range of motion. The group reported a significant mean gain in ankle dorsiflexion of 20.1° (p=0.0078). Of concern, there was a relatively high complication rate of skin breakdown and pain that occurred with splinting (44%). Further, the only individual with a TBI dropped out as the orthosis was thought to agitate the individual (Grissom & Blanton, 2001). As a result, more research is needed with an ABI population before conclusions on adjustable orthoses can be made.

4.2.5.8 Hand Splinting and Stretching

Key Points

Hand splinting combined with stretching may be an effective treatment for spasticity and range of motion.

Hand splinting and stretching is another way that patients may experience relief from spasticity and contracture post-ABI. The study below examines the effectiveness of combination splinting and stretching for spasticity relief (Table 14.16).

Discussion

A randomized controlled trial (RCT) compared manual stretching, soft hand splinting, and manual stretching plus soft hand splinting to determine the optimal intervention (Thibaut et al., 2015). Results suggested that soft hand splinting for 30 minutes resulted in improved hand opening and reduced spasticity of the flexor finger muscles, however improvements in hand opening were not maintained after the break period. The hand splint was said to be feasible to use in daily care, as the splint was comfortable and easy to apply. There is a need to further research the effect of splinting in individuals with ABI as this practice is used in both acute and rehabilitation settings.

Conclusions

There is level 1b evidence that nocturnal hand splinting may not improve upper extremity range of motion or function compared to standard care in individuals post ABI.

4.2.5.9 Multimodal Interventions

Key Points

Botulinum toxin injections in combination with casting may be as effective as casting alone at reducing leg spasticity in patients post ABI.

Electrical stimulation in combination with tilt table standing and splinting may acutely improve spasticity (6 weeks) in patients post ABI.

Neural tension technique may be just as effective as random passive movement for improving lower extremity spasticity post ABI.

Multimodal interventions can consist of combining two or more interventions or comparing different interventions to each other. The following studies use a multimodal approach to determining effective interventions for the treatment of spasticity post ABI.

Discussion

For the lower extremity, Verplancke et al. (2005) found that active prophylaxis of leg spasticity using casting is beneficial; however, there was no difference in outcomes between those casted with or without Botulinum toxin. This indicates that BTX may not be beneficial when paired with casting (Verplancke et al., 2005). Future studies, with a larger sample size, are needed to examine this further.

Electrical stimulation was then studied as a multimodal intervention, combined with standing on a tilt table, and splinting for ankle contractures (Leung et al., 2014). This RCT found improvements in passive ankle dorsiflexion that favoured the control group; however, neither group reached values of clinical significance. Leung et al. (2014) did find a significant reduction in spasticity favouring the intervention group at week 6 but it no longer existed by week 10. Of note, 10 participants had issues with adhering to the tilt table procedure due to fainting, fatigue, or behavioural issues. In addition, due to the fact that the experimental group received a combination of 3 treatments (tilt table, electrical stimulation, and casting) while the control group only underwent tilt table treatment, it is unclear which intervention was responsible for the short-term reduction in spasticity in the experimental group.

In a RCT by Lorentzen et al. (2012), participants received either neural tension technique (NTT) treatment or random passive movement (RPM) therapy on knee joints. No significant changes in spasticity were observed between groups in the knee flexor or extensor muscles. Furthermore, range of motion may be improved to the same effect by NTT and RPM therapies Hirose et al. (2013).

Conclusions

There is level 1b evidence that electrical stimulation in combination with tilt table standing and splinting may decrease spasticity at 6 weeks post intervention compared to tilt table standing alone in patients with an ABI.

There is level 2 evidence that botulinum toxin combined with casting may not be more effective than botulinum toxin injections alone in improving leg spasticity in individuals with an ABI.

There is level 1b evidence that neural tension technique may not be more effective than random passive movement in improving lower extremity spasticity and range of motion in individuals with an ABI.

4.3 Visual Dysfunction

Key Points

Computer based restitution training and rehabilitation programs directed at improving visual function likely improve the vision of those who sustain a TBI.

Base-in prisms and bi-nasal occluders may be effective in treating ambient vision disturbances.

Saccadic oculomotor rehabilitation may improve eye movements and reading in patients post ABI.

Dysfunctions of the visual system are quite common following TBI (Morton, 2004). The overall incidence of cranial nerve injury in individuals hospitalized following TBI has been reported to be 19% (Bontke et al., 1993). It is a relatively new concept that the visual system can respond to treatments directed towards visual-perceptual and/or visual motor skills in individuals with acquired neurological damage. The visual system is highly integrated with many functions other than sight, as it also acts as a primary sensory receptor for motor, social, cognitive, communicative, and emotive tasks. Improvements in visual-perceptual and visual-motor disorders can increase function in all the aforementioned areas and can enhance maximal functional recovery. Consequently, it is necessary to direct a fair amount of attention to visual system disorders in individuals with TBI and this aspect should be considered an essential part of any rehabilitation program (Morton, 2004). In a review conducted by Riggs et al. (2007), the authors noted that visual rehabilitation studies have primarily involved stroke patients and have largely neglected the TBI population. Their review indicates that visual neglect disorders resulting from a stroke and brain injury show improvement after treatment with prisms, visuomotor feedback training, and patching interventions. Moreover, a recent review by Berger et al. (2016) examined specific interventions for improving occupational performance in adults with visual impairments as a result of TBI. Results indicate that there is limited evidence on the effectiveness of vision therapy for oculomotor dysfunction, however there is sufficient evidence to support vision therapy as a method to improve visual field deficits in patients with TBI (Berger et al., 2016) (Table 4.17).

Discussion

A small pre-post study reported that visual dysfunction post ABI can be corrected with base-in prisms, as they affect the ambient visual process by increasing the effectiveness of binocular cortical cells (Padula et al., 1994). Base-in prisms and bi-nasal occluders incorporated within the lenses of both eyes increase the amplitude of visual-evoked potentials (Padula et al., 1994). A different group suggested that prismatic spectacle lenses are also effective in reducing symptoms related to vertical heterophoria and concussion, as they reduce the faulty vertical alignment signal generated by the brain injury (Doble et al., 2010).

Kasten et al. (1998) found that individuals with optic nerve or post-chiasmic injury associated with ABI who complete computer-based Visual restitution training (VRT) experience visual field enlargement and increased light detection. Furthermore, detection training has shown improvements in visual detection, as well as improvements in other visual functions such as shape and color recognition (Kasten et al., 2000). Recently, Conrad et al. (2016) studied a home-based computer vergence therapy program used to improve binocular visual dysfunction after ABI. Participants underwent home-based visual vergence therapy five days a week for 12 weeks. Negative vergence, positive vergence, near point convergence and vergence facility all showed significant improvements over the 12 week intervention period (Conrad et al., 2016).

When the reading dysfunction post ABI is a result of sensory-based hemifield deficits or neuromotor deficits, saccadic occulomotor rehabilitation can lead to improvements in eye movements which are required for accurate reading (Ciuffreda et al., 2006). Repetitive occulomotor conditioning reduces the cognitive and attentional load of reading and results in a structural and systematic approach to reading. The benefits of occulomotor rehabilitation were observed in other activities of daily living such as concentration and visual scanning. Most importantly, reducing visual deficits in patients post TBI may facilitate their involvement in other therapies and contribute to overall recovery (Ciuffreda et al., 2006).

Conclusions

There is level 1b evidence that computer-based restitution training may be effective in improving the vision of those who sustain a TBI compared to visual fixation training.

There is level 2 evidence that saccade visual tracking compared to fixation and pursuit tracking may improve single-line and multi-line reading post ABI.

There is level 4 evidence showing that base-in prisms and bi-nasal occluders can be effective in treating ambient vision disturbances resulting from an ABI.

There is level 4 evidence that prismatic spectacle lenses may be effective in reducing symptom burden in patients with vertical heterophoria and post-concussive symptoms post injury.

There is level 4 evidence that rehabilitation programs directed at improving visual function can improve functional outcomes such as reading in patients post ABI.

4.4 Vestibular Dysfunction

Key Points

Combined aerobic dance and slide and step programs may improve balance and coordination post TBI.

A vestibular rehabilitation program may improve symptoms of vertigo in patients following TBI.

Vestibular dysfunction is commonly overlooked when diagnosing an individual with TBI. Vertigo, balance problems, visual complaints (double vision, blurriness), and nausea are possible symptoms of vestibular injury. The most common persisting vestibular symptom after TBI is positional vertigo, or vertigo caused by head movement. Vertigo is caused by dysfunction of the vestibular nerve or the labyrinth (Shepard & Telian, 1995) and the inability of the central nervous system to effectively compensate for the dysfunction (Gurr & Moffat, 2001). Provoked vertigo manifests as either unilateral peripheral hypofunction, bilateral peripheral hypofunction, or benign paroxysmal positional vertigo (BPPV) (Godbout, 1997).

Although it is common for spontaneous resolution of vertigo to occur within 6 months of onset, recovery in the TBI population is constricted due to the frequent combination of central and peripheral vestibular structure injury. Vestibular rehabilitation following TBI is therefore needed to promote vestibular adaptation and recovery. Techniques which are typically used in vestibular rehabilitation are gaze stability exercises, vestibulo-ocular reflex gain adaptation, substitution exercises, habituation techniques, and static and dynamic balance and gait exercises (Scherer & Schubert, 2009). The optimal recovery of vestibular dysfunction is thought to be based on selecting the appropriate vestibular exercises for a specific individual and progressing gradually through the assigned exercises while increasing difficulty and intensity (Wee, 2002). Current literature includes a variety of interventions for vestibular rehabilitation (Table 4.18).

Discussion

Patients with TBI suffering from BPPV should be specifically treated with repositioning maneuvers until complete resolution (Motin et al., 2005). Vestibular rehabilitation, alone or in combination with pharmacological treatment (i.e., betahistine dihydrochloride), as a treatment for balance disorders post TBI has been shown to significantly reduce recovery time when compared to pharmacological management alone (Naguib & Madian, 2014).

In a small sample of adults, aerobic dancing and slide-and-step training improved balance and coordination in patients many years following TBI, suggesting that long-term improvement of vestibular dysfunction is possible with the appropriate program (Dault & Dugas, 2002). Further, Gurr and Moffat (2001) added a cognitive aspect to vestibular rehabilitation. The authors attempted to restructure the maladaptive thoughts and belief patterns associated with the symptoms of provoked vertigo. This multidimensional psychological approach was effective in improving vertigo symptoms, independence, emotional distress, physical flexibility and postural stability (Gurr & Moffat, 2001).

In terms of more familiar therapy interventions for balance, one study compared standard physiotherapy and standard therapy in addition to a home-based rehabilitation program (Peirone et al., 2014). Both groups showed significant improvements on the Goal Attainment Scaling and the Balance Evaluation System Test. However, when comparing these interventions, those receiving home-based rehabilitation made significantly greater improvements on the Balance Evaluation System Test (Peirone et al., 2014). Despite these findings, this study was underpowered and further investigation is needed before definitive conclusions are made.

Conclusions

There is level 4 evidence that vestibular rehabilitation programs, such as a behavioural exposure program, may improve symptoms of vertigo in patients after TBI.

There is level 2 evidence that vestibular rehabilitation programs, alone or in combination with betahistine dihydrochloride, can improve recovery time for balance disorders in individuals with an ABI compared to betahistine dihydrochloride alone.

There is level 2 evidence to that using a combined aerobic dancing and slide and step training program may reduce balance and coordination deficits post TBI.

4.5 Pain Post TBI

Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage…” (p.210) (International Association for the Study of Pain, 1994); the relationship between pain and tissue damage is not constant nor uniform. Pain following an injury or surgery can be either acute or chronic, and often lasts for months or years post injury. Acute pain is usually associated with defined tissue damage or a pathological process, and although it usually occurs at the time of injury as a one-time event, it may reoccur as a series of time limited events (Gould, 2007). Chronic pain is usually defined as pain that continues for more than three to six months and is often not as well associated with tissue damage or a pathological process. Using a sepate classification, pain can also be defined as subacute (pain between the end of the first month post injury and six months post injury) and recurrent acute (pain that persists over an extended period of time but recurs as isolated pain episodes).

Until very recently, there has been very little information in the literature regarding the prevalence, etiology, assessment, and treatment of pain post TBI (Zasler et al., 2011). This may be the result of pain syndromes being overlooked in patients with a TBI for a number of reasons (Gellman et al., 1996). Multiple etiologies including orthopedic injuries, burns, organ injuries, or central or peripheral nervous system injuries can result in acute or chronic pain in those recovering from a TBI (Ivanhoe & Hartman, 2004). A lack of recognition or diagnosis of pain can lead to an increase in aggression and agitation, or an inability to participate or benefit from rehabilitation (Ivanhoe & Hartman, 2004; Sherman et al., 2006). In individuals who have sustained a moderate or severe TBI, the diagnosis of pain is often made through the combination of symptoms described by the patient and information provided by family members. Pain post TBI can evolve from episodic pain to daily pain with an increasing negative impact over time; pain ultimately impacts participation in rehabilitation and thereby slows recovery (Branca & Lake, 2004).

Pain is believed to be more common immediately post injury (acute pain) and it is widely accepted that this pain will resolve as the damaged tissue recovers (Uomoto & Esselman, 1993). The focus is on management of symptoms over a relatively short defined period of time and on assisting the healing of damaged structures. Chronic pain by its very nature may not resolve, or is very slow to resolve, and often manifests itself as post traumatic headaches (PTH), neck and shoulder pain, back pain, peripheral nerve injury, heterotopic ossification, and pain related to spasticity (Hoffman et al., 2007; Lahz & Bryant, 1996; Ofek & Defrin, 2007). In a study conducted by Lahz and Bryant (1996), chronic pain was reported by 52% of those who were diagnosed with a moderate to severe TBI and 58% of those diagnosed with a mild TBI. Of those reporting pain, over 80% reported experiencing pain on a daily basis (Lahz & Bryant, 1996). Comparable rates were given by Hoffman et al. (2007) who examined a bodily pain scale one year post TBI. Of the 146 individuals who participated, 74% of participants reported experiencing pain and 55% of those reported that pain interfered with a variety of daily activities. Higher rates of pain were also related to gender, lower Functional Independence Measure scores, higher rates of depressive symptoms at baseline and again at one year post injury, and lower scores on the Community Integration Scale. Those who were injured in acts of violence reported experiencing greater pain (Hoffman et al., 2007). Pain is significantly associated with depression, with one study reporting rates of pain and depression as 70% and 31%, respectively and 34% and 22%, respectively at one year follow-up (Sullivan-Singh et al., 2014). Pain related to orthopedic injuries, spasticity, or heterotopic ossification will not be covered in this section. For a more detailed discussion on spasticity and treatments post ABI please see section 4.2.5 in this module and a detailed discussion on heterotopic ossification post ABI is available in Module 11. Due to the complexities of pain, we have decided to focus on pain post TBI specifically. The diagnosis of pain post TBI is an important part of an individual’s recovery.

Problems associated with pain include a delay in cognitive recovery, sleep disorders, fatigue, elevated levels of anxiety, depression, and post-traumatic stress disorder (Dobscha et al., 2009; Hoffman et al., 2007). Cognitive deficits associated with TBI may prevent individuals from using adaptive pain coping strategies that are critical to the management of chronic pain. When treating pain post TBI, it is important for clinicians to identify the causes of pain, not just the symptoms (Zasler et al., 2011). To reduce the impact on cognitive recovery, treatment plans should take into consideration the medications the patient is already receiving, as well as the location, type, and frequency of the pain. It should be acknowledged that in many cases the pain generator persists in which case pain can only be managed. Treatment for pain often involves an interdisciplinary approach (Branca & Lake, 2004). To increase the likelihood of compliance with treatments, a good working relationship between physicians and the patient is needed. Overall, more research is needed to assess the effectiveness and efficacy of these treatments in the TBI population. For a summary of these findings please see Figure 1.

4.5.1 Assessing Pain Post TBI

Pain itself is both complex and subjective; thus, self-reports are vital to any treatment plan. Descriptive details related to the intensity, the length of time the pain is felt, the location, and what exacerbates or relieves the pain are vital in developing an individualized treatment strategy (Zasler et al., 2011). Currently there are a number of tools and assessments used by physicians and therapists to assist in diagnosing and measuring pain. Amongst these is the numeric rating scale (NRS), the visual analogue scale (VAS), the Headache Diary, the Headache Disability Inventory, and the McGill Pain Questionnaire.

4.5.1.1 Visual Analog Scale

The Visual Analog Scale (VAS) is available at no cost and has been used with many adult populations to assess pain intensity. The scale is a horizontal or vertical line, usually 10 centimeters in length and is completed by the respondent. Two verbal descriptors, no pain and the worst pain imaginable, anchor the scale (Zasler et al., 2011). Generally, those completing the scale are asked to describe the pain within the past 24 hours. A ruler is used to the distance between the no pain anchor and the line that the respondent has drawn. Higher scores indicate greater pain (Hawker et al., 2011).

4.5.1.2 Numeric Rating Scale

The Numeric Rating Scale (NRS) is also commonly used to assess pain. Here the patient rates the pain they are experiencing on a scale of 0 to 10. The NRS, like the VAS, is anchored with no pain and the worst pain imaginable. Individuals are generally asked to report on pain intensity within the past 24 hours. This scale can be administered verbally or graphically. A higher score indicates higher levels of pain (Hawker et al., 2011). A 30% reduction on the NRS is clinically important and has been found to be equivalent to ratings of moderate relief or much improved (Farrar et al., 2001).

4.5.1.3 McGill Pain Questionnaire

The McGill pain questionnaire, designed for adults with chronic pain, measures the sensory, affective, and evaluative aspects of pain and pain intensity (Hawker et al., 2011). This paper and pencil questionnaire is administered by an interviewer with the respondent present. The respondent is asked questions and must select one word from a list presented to them which best describes their present pain. If the pain an individual is feeling cannot be described by the words presented to them, then no word is selected. Scores are based on the number of words selected with higher scores indicating greater levels of pain.

4.5.1.4 Headache Disability Inventory

The headache disability inventory was designed to measure the impact of headaches on activities of daily living (Jacobson et al., 1994). This self-report scale consists of 25 items designed to probe the functional and emotional impact of headaches in a patient’s life. The scale has been found to be easy to complete – items are measured as either a yes or a no – and simple to score and interpret (Jacobson et al., 1994).

4.5.1.5 Headache Diary

Those who are asked to maintain a headache diary are required to log their headaches on a daily basis. Recorded in the diary is the time of day the headache begins, the intensity of the pain, any medication being taken, and any triggers for the headache. Additionally, individuals are asked to record alcohol consumed, periods of fasting, foods eaten, sleep patterns, weather, stress levels, emotional ups and downs, and for women, date of their menstrual cycle (Arnstein, 2004). A variety of headache diaries or headache calendars are currently available. These diaries potentially allow the patient to gain better control over their pain by identifying its potential causes, and provide feedback regarding treatment efficacy (Branca & Lake, 2004).

4.5.2 Pain Syndromes Post ABI

While the pain an individual with an ABI experiences can vary, there are several defined pain syndromes that are common post ABI. Defining the pain someone experiences as a specific pain syndrome can be valuable in determining the ideal treatment method.

4.5.2.1 Neuropathic Pain

Neuropathic pain is initiated or caused by a primary lesion or by dysfunction of the nervous system (International Association for the Study of Pain, 1994). Peripheral nervous system pain can result from mechanical trauma, metabolic disease, neurotoxic chemicals, infection, or tumor (Costigan et al., 2009; O’Connor & Dworkin, 2009). On the other hand, central nervous system pain may be associated with spinal cord injury, stroke, TBI or multiple sclerosis (Costigan et al., 2009). Neuropathic pain can result from compression of peripheral nerves when patients are immobilized for long periods of time and diagnosis is often based on careful medical evaluation (careful history, physical and neurological exams, MRI findings, blood and serologic tests) (Dworkin et al., 2003). Despite clear diagnostic guidelines, treatment remains a challenge, as even effective treatments offer only partial pain relief (Finnerup et al., 2005). Common interventions for the treatment of neuropathic pain include pharmacological agents, such as: amitriptyline, pregabalin, gabapentin, duloxetine, carbamazepine, lidocaine, and opioids (Waszkielewicz et al., 2011). When considering treatments, it is important to keep in mind the safety and efficacy of these drugs; particularly how they interact with other medications and how they will impact neurological recovery post TBI. More specific information on interventions for neuropathic pain is discussed in sections 4.5.4.1 (anticonvulsants) and 4.5.4.5 (cannabinoids).

4.5.2.2 Central Pain Syndromes

Zaslar et al. (2012) have defined central pain as “pain associated with lesions of the central nervous system” (p 967). Treatments are limited in number and efficacy (Nicholson, 2004); however, the goal is often a reduction in pain and not complete relief. For example, studies have examined the effects of lidocaine and IV morphine in alleviating central pain syndromes, but the results have been mixed (Attal et al., 2000; Attal et al., 2002).

4.5.2.3 Post Traumatic Headaches

Damage to the skull, brain tissue, or cervical spine can result in PTHs that can be serious and incapacitating (Watanabe et al., 2012). According to Elkind (1989), a headache is a common and dominant symptom of TBI, with approximately 44% of those who sustain a closed head injury developing PTHs. Head, neck, and shoulder pain usually begins within the first 24 to 48 hours post injury, however PTH may appear immediately after the injury and subside, or occur days, weeks or months following the injury (Young, 2001). Factors that may lead to PTHs include chronic muscle contraction, chronic and diffuse muscle strain, and anxiety (Hillier et al., 1997). Visual or vestibular system complications may also result in headache syndromes. Studies have found that a PTH often resolves itself within the first 6 to 12 months of injury; however, in 18-33% of the TBI population headaches persist longer than one year (Lew et al., 2006; Seifert & Evans, 2010). Estimating the number of individuals who develop PTH is difficult as there is lack of consistency in how PTH is defined which may reflect limited understanding of its pathophysiology.

Previously, studies looking at the incidence of PTH reported that those who sustained a mild TBI were more likely to report problems with headaches than those who sustained moderate to severe TBIs (Couch & Bearss, 2001; Gurr & Coetzer, 2005; Uomoto & Esselman, 1993). However, more recent studies have found that individuals with moderate or severe TBIs report experiencing headaches even at one year post TBI (Hoffman et al., 2011; Hoffman et al., 2007; Lainez & Pesquera, 2011). In a survey of 485 individuals, Hoffman and colleagues (2011) found the prevalence of headaches during the first year of recovery post TBI was 40%, regardless of the severity of injury. Lucas (2011) found that almost 60% of respondents who reported experiencing headaches, also reported experiencing migraines or probable migraines. Other headaches reported were tension type headaches, cervicogenic headaches, or unclassifiable headaches. Despite what is known about PTH, there remains a need for further epidemiological, clinical, and pathophysiological studies (Lainez & Pesquera, 2011). Studies evaluating interventions for post traumatic headache can be found in the following sections: Biofeedback to Manage Post Traumatic Headache (section 4.5.3.1), Cognitive Behavioural Theory (section 4.5.3.2), Manual Therapy (section 4.5.3.4), and Cryotherapy and Thermotherapy (section 4.5.3.6).

4.5.3 Non-Pharmacological Interventions for Pain and Post Traumatic Headache

Early detection and treatment of pain is regarded as crucial to reduce its impact and help individuals develop appropriate approaches to dealing with their pain (Ivanhoe & Parrilla, 2002). As mentioned previously, deciding on a treatment for both general pain and PTHs may be challenging due to the many underlying factors of TBI and the fact that some pain conditions are only partially responsive to treatment. Given that pharmacological interventions may worsen cognitive deficits post TBI, non-pharmacological interventions should be incorporated into the treatment plan.

Non-pharmacological interventions for both chronic pain and PTH may include: biofeedback, cold and heat packs, massage therapy, acupuncture, and exercise (Medina, 1992). Biofeedback, relaxation, meditation, and CBT are considered the gold standard of behavioural treatments for pain (Branca & Lake, 2004). In a recent review of manual treatments for migraines, massage therapy, physiotherapy, relaxation, and chiropractic spinal manipulative therapy were found to be just as effective as propranolol and topiramate at reducing symptoms (Cassidy et al., 2014). Physiotherapy exercises have also been suggested to treat pain; however, unless the pain is controlled, caution is recommended when using these exercises to prevent aggravating the painful structures further (Medina, 1992). Lifestyle changes are also suggested to prevent the onset of PTH, such as getting enough sleep and daily exercise.

4.5.3.1 Biofeedback to Manage Post Traumatic Headache

According to a study by Mullally et al. (2009), biofeedback therapy was not found to significantly reduce the number and severity of headaches in individuals who were diagnosed with migraines or tension type headaches. However, several earlier studies found more positive results. A study by Ham and Packard (1996) studied 40 individuals who sustained a mild TBI and were experiencing post traumatic headaches. Subjects participated in biofeedback sessions and were placed on anti-depressants and anti-inflammatory or non-narcotic analgesics. Participants began treatment on average 12.7 months post injury, although in half of the participants PTHs occurred immediately post injury. Biofeedback was reported to help 93% of participants to some degree with those who waited longer to begin biofeedback therapy found it less successful. Individuals who had more sessions and began treatment sooner found the sessions to be very beneficial. Unfortunately, the research on this topic for the moderate to severe TBI population is limited.

In a study by Tatrow et al. (2003), PTHs were targeted for six weeks in 14 mild TBI individuals . The first four sessions consisted of progressive muscle relaxation, with biofeedback (thermal and EMG) being introduced in the fifth session. Participants learned to relax and control muscle tension, and relaxation ratings were on average 8.6 out of 10. Improvements in PTH were shown for most participants and the treatment also lowered post-concussion syndrome checklist scores significantly in the treatment group (Tatrow et al., 2003).

4.5.3.2 Cognitive Behavioural Therapy

Key Points

Cognitive behavioural therapy may be useful in managing post-traumatic headaches; however, may not be useful for headache-associated pain.

Cognitive behavioural therapy (CBT) has been used to assist individuals in managing their pain. It is considered a diverse set of problem-specific interventions and incorporates physical, psychological, and behavioural approaches to managing pain (Roth & Pilling, 2008). With CBT the individual is taught to use self-regulation and self-control, and to take responsibility for one’s lifestyle (Martelli, 2012). This therapy has been used to help patients cope with the pain, depression, and anxiety associated with chronic headaches (Gurr & Coetzer, 2005; Wetherell et al., 2011). Despite the extensive use of CBT, there are not many studies evaluating its efficacy in treating pain post ABI (Table 4.20).

Discussion

Gurr and Coetzer (2005) studied twenty participants who had sustained a mild to severe TBI and who had completed a CBT program for PTH. The CBT program consisted of progressive muscle relations, psycho-education, cognitive behavioral strategies, lifestyle management and maintenance, and relapse prevention. After the intervention, headache intensity and frequency, and disability significantly decreased, while emotional wellbeing increased. Results from the Nottingham Health Profile pain scale found no significant differences in pain pre and post intervention.

Conclusions

There is level 4 evidence that cognitive behavioural therapy may improve post traumatic headache intensity and frequency but not pain, in those who have sustained a mild to severe TBI.

4.5.3.3 Relaxation Training

Relaxation training, or progressive muscle relaxation, is a possible treatment for chronic pain and PTHs. Individuals are taught how to breathe from the diaphragm and how to tense and relax various muscles. Through such techniques, the muscle tension triggers associated with headaches can be better controlled (Arnstein, 2004). Over time, patients may be able to reduce the number of headaches or prevent the pain from worsening.

4.5.3.4 Manual Therapy

Manual therapy refers to more hands-on types of therapy such as massage therapy, traction, mobilization, and physical therapy. The purpose of these therapies is to reduce muscle tension, increase muscle length, enhance circulation, and increase mobility in the joints (Gould, 2007). The results from an earlier study indicated that manual therapy was more effective than cold packs in reducing pain associated with PTHs (Jensen et al., 1990).

Massage therapy involves either deep tissue massage or a lighter massage technique. Massage therapy has been shown to increase oxygenation and blood flow to the muscles being treated as well as to reduce pain (D’Arcy, 2011). Physical therapy involves the patients and a physical therapist working together to identify the areas where pain is being experienced. Therapy may involve stretching and or strengthening exercises, ultrasound to the affected areas, or the application of hot and cold packs. Physical therapy for both pain and chronic daily headaches focuses on the upper body, including the upper back, neck, and face (Sherman et al., 2006).

In an earlier study, Medina (1992) investigated the treatment of PTHs in 20 patients post TBI or spinal cord injury through individualized therapeutic sessions each lasting 30 minutes. Patients received educational sessions, biofeedback training, electromyographic biofeedback, or physical therapy sessions, and were placed on appropriate medication to treat the pain. The combination therapies were effective as 17 patients were able to return to work and 19 patients reported a decrease in PTH intensity.

4.5.3.5 Acupuncture

Acupuncture, one of the oldest forms of physical therapies, is a non-medicinal intervention involving a certified acupuncturist selecting specific points on the body to insert acupuncture needles. The points of insertion differ in every individual. Although research indicates that there is some benefit to acupuncture therapy, there is a lack of strong evidence supporting its effectiveness with the TBI population (Gould, 2007; Wong et al., 2012).

4.5.3.6 Cryotherapy and Thermotherapy

Key Points

Cold therapy is likely not as effective as manual therapy at reducing post traumatic headache pain in patients post TBI.

Heating and cooling therapy can provide relief to TBI patients who suffer chronic headaches and neck pain. Specifically, cryotherapy involves the application of cold to relieve pain while thermotherapy involves the application of heat to relieve pain (Pangarkar & Lee, 2011). Both therapies are typically used in conjunction with other treatments.

Discussion

Jensen et al. (1990) compared manual therapy to cold pack therapy for the treatment of PTH pain in 19 participants with head injury. Those in the manual therapy group reported a significantly greater reduction in pain following the intervention when compared to the cold pack group. The pain index for all participants was also correlated with the frequency of associated symptoms (dizziness, visual disturbances, and ear symptoms) and the use of analgesics.

Conclusions

There is level 2 evidence that cold therapy may not be as effective as manual therapy for reducing post traumatic headache pain in individuals post ABI.

4.5.4 Pharmacological Management of Pain and Post Traumatic Headache

There are a variety of medications used in the treatment of chronic pain post ABI and PTH. Aspirin or aspirin compounds, acetaminophen, and ibuprofen are often the first lines of treatment prescribed for chronic pain; however, adjuvant medications such as anticonvulsants, antidepressants, benzodiazepines, bisphosphonates, local anesthetics, antispasmodic agents, and topical agents may also be prescribed (Gould, 2007; Khan et al., 2011). In some cases, the prescription of opioids may be considered.

4.5.4.1 Anticonvulsants

The administration of anticonvulsants to treat pain post brain injury has been a common practice since the 1960’s. It is thought that epilepsy and pain share a common pathogenesis, thus allowing anticonvulsant medications to be used in pain management, particularly neuropathic pain that is either peripheral or central in origin (Dickinson et al., 2000; Zasler et al., 2011). It has also been noted that the use of anticonvulsant medication seems to produce fewer adverse events (Gould, 2007). Anticonvulsants currently used to treat pain include carbamazepine, oxcarbamazepine, lamotrigine, gabapentin, pregabalin, and topiramate; however, there are limited studies investigating their effectiveness either in isolation or in combination with other medications. Table 4.22 summarizes several antiepileptic medications that are used to treat pain post ABI.

4.5.4.2 Antidepressants

Among the antidepressant medications available, tricyclic antidepressants are the most commonly used for the treatment of pain; in particular neuropathic pain (Gironda et al., 2009; Gordon & Love, 2004; Guindon et al., 2007). Medications such as fluoxetine, sertraline, paroxetine, or citalopram work best at controlling pain when there is an underlying primary problem such as depression. Tricyclic antidepressants used to treat pain include amitriptyline, nortriptyline, desipramine, doxepin, and imipramine (Gould, 2007); however, the mechanism of action for these medications in the treatment of pain is not yet fully understood. Currently, there is no evidence to support the administration of antidepressants to treat pain or PTH; Table 4.23 summarizes several antidepressants that are used to treat pain post ABI.

4.5.4.3 Topical Analgesics

Pain that is described as localized and superficial has been treated effectively with topical treatments. Topical analgesics include menthol/methylsalicylates, capsaicin, and anesthetics; however, as with the previously discussed medications, there is no clinical evidence to support the use of topical analgesics. Menthol has been shown to be somewhat effective as it releases a cooling sensation over the painful area (Pangarkar & Lee, 2011). Capsaicin cream has been found to cause a burning sensation, so it is strongly recommended to apply the cream only to where the pain is located. Despite this, capsaicin cream has been found to decrease neck pain (Pangarkar & Lee, 2011). The lidocaine patch is applied to the painful area and worn for typically 12 hours. The patch tends to be well tolerated by most (D’Arcy, 2011). More studies are required to determine the efficacy of topical treatments; Table 4.24 summarizes several topical anesthetics that are used to treat pain post ABI.

4.5.4.4 Opioids

The use of opioids to manage non-cancer pain has been on the rise for the past several decades (Martelli, 2012). It is believed that neuropathic pain can be relieved by the administration of opioids, provided a balance exists between the optimal dose and any unmanageable side-effects (Dellemijn, 1999). A decrease in libido, sedation, mental dullness, difficulties concentrating, and a higher risk for developing osteoporosis have been reported when taking opioids (Ersek et al., 2004; Haanpaa et al., 2010). The risk of exacerbating cognitive impairments of patients with TBI is one of the reasons for clinicians’ hesitancy to administer opioids for pain management. Although opioid use within a TBI population has been discussed in the literature, few studies investigate its efficacy for reducing pain within this population. When opioids are administered it has been suggested to start with a low dose and titrate up (Gallagher et al., 2006). Unfortunately with narcotics there is no recommended therapeutic dose (Khan et al., 2011); although with musculoskeletal complaints it is recommended that the dose not exceed 120-200 mg/day morphine equivalent dose (Haanpaa et al., 2010). Moreover, with opioids, because the risk of physical dependency and addiction is problematic, patients should be screened for addiction and dependency risk factors. Psychological problems and a history of substance abuse are considered the two most common risk factors for opioid misuse and addiction.

Franceschi et al. (2008) administered oxycodone to a group of polytrauma patients, five of which had mild head injury, admitted to an emergency department suffering from acute pain. Main pain sites for the group were the chest, neck, lower back, leg, heel, pelvis, upper arm, and shoulder. Oxycodone (10 mg twice per day for three days given orally) was found to significantly reduce pain for 14 of the 15 patients. One patient required an increase in medication (20 mg twice per day) to achieve pain relief. Overall the medication was well tolerated by patients with some reporting mild side effects (light headaches, constipation and nausea) (Franceschi et al., 2008). Oxycodone has been found to be successful in reducing pain; however, it remains unclear as to whether this medication would be effective and well tolerated in those who sustain a moderate or severe ABI.

4.5.4.5 Cannabinoids

Cannabis sativa has been used to treat pain for centuries. However the use of cannabis and its derivatives to treat pain had fallen out of favour in the mid 1940’s to the mid 1990’s, possibly due to the suspected risk of addiction, abuse, dependence, cognitive effects, and other adverse medical and psychiatric effects (Aggarwal, 2013; Greenwell, 2012). The utility of the medication is gaining increasing recognition as physicians and other health care professionals increase their knowledge regarding the efficacy and safety of cannabinoid based medications (Aggarwal, 2013). Cannabis is generally administered through either inhalation, ingestion, or topically, with the method of delivery determining the rate at which the drug begins to take effect. According to Aggarwal (2013), the use of cannabinoids can result in muscle relaxation, anti-inflammatory effects, and neuroprotection in ischemia and hypoxia. Currently, cannabinoids are used to treat cancer pain, pain associated with multiple sclerosis, human immunodeficiency virus, fibromyalgia, and rheumatoid arthritis. Although many studies have looked at the benefits of using cannabinoids to treat chronic pain, the results of many of these studies were inconclusive (Greenwell, 2012).

A study by Ware et al. (2010) examined the effects of cannabis at different potencies (0%, 2.5%, 6% and 9.4%) in individuals with post-traumatic or postsurgical neuropathic pain. Pain intensity was found to be significantly lower on 9.4% tetrahydrocannabinol cannabis than on 0% tetrahydrocannabinol (p=0.023). Further, when 9.4% tetrahydrocannabinol cannabis was compared to taking a placebo, patients experienced more drowsiness and fewer periods of wakefulness. Results from Ware et al. (2010) suggest cannabis is effective in the treatment of neuropathic pain. Due to the addictive properties of this group, cannabinoids should only be administered if there is no history of alcohol or drug addiction. Once on these medications, monitoring of patients is paramount.

4.6 Conclusions

Overall, a wide variety of interventions exist for sensory and motor rehabilitation post ABI. For motor impairment specifically a variety of interventions such as splinting, constraint induced movement therapy, and exercise programs have been shown to be effective for the remediation of motor deficits post ABI.

More pharmacological based interventions exist for the treatment of spasticity in general, compared to other areas of motor rehabilitation. The spasticity studies presented here present multiple therapeutic options as well as compare their efficacy in ABI specific populations. It is important to keep in mind that some of the pharmacological interventions discussed have a longer history of investigation than others, such as botulinum toxin injections, while newer pharmacological interventions may want to be interpreted with more care.

Ultimately the appropriate interventions should be agreed upon by the care-team with what is in the best interest of the patient, as well as discussing realistic expectations for recovery.

Summary


There is level 4 evidence that constraint induced movement therapy (CIMT) or modified CIMT may improve upper extremity function in individuals post ABI.

There is level 1b evidence that nocturnal hand splinting may not improve upper extremity range of motion or function compared to standard care in individuals post ABI.

There is level 4 evidence that soft hand splinting, but not manual therapy, may improve hand opening in individuals post ABI.

There is level 2 evidence that functional retraining activities may be more effective than tabletop fine motor control retraining activities for improving fine motor function in the dominant hand in individuals post ABI.

There is level 4 evidence that visual feedback-based grip force training may improve tracking accuracy and transfer tasks in individuals post ABI.

There is level 2 evidence that gesture recognition biofeedback may improve fine motor function compared to standard repetitive training without feedback in individuals post ABI.

There is level 2 evidence that virtual reality training may improve neurobehavioral functioning as well as reaching accuracy and movements post-ABI.

There is level 2 evidence that body weight supported treadmill training may not improve ambulation or mobility compared to conventional gait training in individuals post ABI.

There is level 1b evidence that physical therapy with partial weight-bearing gait training may not improve ambulation, mobility, or balance compared to standard physical therapy in individuals post ABI.

There is level 2 evidence that robotic assisted body weight supported treadmill training may not improve ambulation or gait velocity compared to manually assisted treadmill training in individuals post ABI.

There is level 1b evidence that sit-to-stand training combined with usual rehabilitation may improve motor performance in sit-to-stand tasks compared to usual rehabilitation in individuals post ABI.

There is level 2 evidence that electrical muscle stimulation with passive exercise may reduce lower extremity muscle atrophy compared to passive exercise in individuals post ABI.

There is level 4 evidence that Intensive Mobility Training may improve ambulation and mobility in individuals post ABI.

There is level 1b evidence that virtual reality training compared to balance training may not be more effective for improving lower extremity function post-ABI. However, virtual reality training was shown to improve function independently.

There is level 4 evidence that visual feedback may reduce weight-bearing asymmetry in the lower extremities post-ABI.

There is level 1b evidence that virtual reality-based training may not improve balance and gait compared to standard physical therapy in individuals post ABI.

There is level 4 evidence that virtual reality therapy may improve balance, gait, and functional reaching in individuals post ABI.

There is level 1b evidence that participating in an exercise program at a fitness-center compared to home-based exercise program may lead to greater program adherence but not significantly different motor results in individuals post-ABI.

There is level 2 evidence that aerobic training compared to vocational rehabilitation may be more effective at improving co-ordination, strength, flexibility, and endurance in individuals post-ABI.

There is level 1b evidence that exercise programs may improve FIM scores, but not balance or mobility compared to relaxation training in individuals post-ABI.

There is level 4 evidence that multimodal exercise programs may improve gait and mobility in individuals post-ABI.

There is level 3 evidence that a home-based exercise program may improve stability to the level of healthy controls, but may not improve motor control, mobility, or dual-task performance in individuals post-ABI.

There is level 2 evidence that aerobic dance training compared to musculature training may improve sensory interaction and balance post-ABI.

There is level 4 evidence that botulinum toxin type A injections may be effective in the management of localized spasticity following ABI.

There is level 1b evidence that receiving botulinum toxin type A through a single motor point or multisite distributed injections are similar at reducing spasticity in individuals with an ABI.

There is level 4 evidence that phenol nerve blocks may reduce contractures and spasticity at the elbow, wrist, and finger flexors for up to five months post injection in individuals post ABI.

There is level 4 evidence that electrical stimulation may be effective for decreasing lower extremity spasticity for six or more hours, lasting up to 24 hours, in individuals post ABI.

There is level 4 evidence that oral baclofen may improve lower extremity spasticity, but not upper extremity spasticity, in individuals post ABI.

There is level 1b evidence that bolus intrathecal baclofen injections may produce short-term (up to six hours) reductions in upper and lower extremity spasticity compared to placebo following ABI.

There is level 4 evidence to suggest that prolonged intrathecal baclofen may result in longer-term (three months, and one year) reductions in spasticity in both the upper and lower extremities following an ABI.

There is conflicting level 4 evidence to suggest that intrathecal baclofen may result in short-term improvement of walking performance in ambulatory patients, particularly gait velocity, stride length, and step width, in individuals post ABI.

There is level 1b evidence that serial casting may improve contractures of the elbow initially, but not long-term, when compared to passive stretching in individuals with an ABI.

There is level 1b evidence that serial casting may be superior to passive stretching at improving spasticity of the elbow in individuals post ABI.

There is level 2 evidence that a below-knee casting and stretching protocol may increase passive ankle dorsiflexion in patients post ABI.

There is level 4 evidence that weekly below-knee casts may improve ankle range of motion, muscle extensibility, and passive torque in patients post ABI.

There is level 3 evidence that short duration (one to four days) and longer duration (five to seven days) serial casting may have similar effects on upper or lower extremity range of motion in individuals post ABI.

There is level 1b evidence that nocturnal hand splinting may not improve upper extremity range of motion or function compared to standard care in individuals post ABI.

There is level 1b evidence that electrical stimulation in combination with tilt table standing and splinting may decrease spasticity at 6 weeks post intervention compared to tilt table standing alone in patients with an ABI.

There is level 2 evidence that botulinum toxin combined with casting may not be more effective than botulinum toxin injections alone in improving leg spasticity in individuals with an ABI.

There is level 1b evidence that neural tension technique may not be more effective than random passive movement in improving lower extremity spasticity and range of motion in individuals with an ABI.

There is level 1b evidence that computer-based restitution training may be effective in improving the vision of those who sustain a TBI compared to visual fixation training.

There is level 2 evidence that saccade visual tracking compared to fixation and pursuit tracking may improve single-line and multi-line reading post ABI.

There is level 4 evidence showing that base-in prisms and bi-nasal occluders can be effective in treating ambient vision disturbances resulting from an ABI.

There is level 4 evidence that prismatic spectacle lenses may be effective in reducing symptom burden in patients with vertical heterophoria and post-concussive symptoms post injury.

There is level 4 evidence that rehabilitation programs directed at improving visual function can improve functional outcomes such as reading in patients post ABI.

There is level 4 evidence that vestibular rehabilitation programs, such as a behavioural exposure program, may improve symptoms of vertigo in patients after TBI.

There is level 2 evidence that vestibular rehabilitation programs, alone or in combination with betahistine dihydrochloride, can improve recovery time for balance disorders in individuals with an ABI compared to betahistine dihydrochloride alone.

There is level 2 evidence to that using a combined aerobic dancing and slide and step training program may reduce balance and coordination deficits post TBI.

There is level 4 evidence that cognitive behavioural therapy may improve post traumatic headache intensity and frequency but not pain, in those who have sustained a mild to severe TBI.

There is level 2 evidence that cold therapy may not be as effective as manual therapy for reducing post traumatic headache pain in individuals post ABI.

References

Adelman, L. C., Adelman, J. U., Von Seggern, R., & Mannix, L. K. (2000). Venlafaxine extended release (XR) for the prophylaxis of migraine and tension-type headache: A retrospective study in a clinical setting. Headache, 40(7), 572-580.
Aggarwal, S. K. (2013). Cannabinergic pain medicine: a concise clinical primer and survey of randomized-controlled trial results. Clin J Pain, 29(2), 162-171.
Arnstein, P. (2004). Chronic neuropathic pain: issues in patient education. Pain Manag Nurs, 5(4 Suppl 1), 34-41.
Attal, N., Gaude, V., Brasseur, L., Dupuy, M., Guirimand, F., Parker, F., & Bouhassira, D. (2000). Intravenous lidocaine in central pain: a double-blind, placebo-controlled, psychophysical study. Neurology, 54(3), 564-574.
Attal, N., Guirimand, F., Brasseur, L., Gaude, V., Chauvin, M., & Bouhassira, D. (2002). Effects of IV morphine in central pain: a randomized placebo-controlled study. Neurology, 58(4), 554-563.
Backonja, M. (2003). Anticonvulsants for the treatment of neuropathic pain syndromes. Curr Pain Headache Rep, 7(1), 39-42.
Bateman, A., Culpan, F. J., Pickering, A. D., Powell, J. H., Scott, O. M., & Greenwood, R. J. (2001). The effect of aerobic training on rehabilitation outcomes after recent severe brain injury: a randomized controlled evaluation. Arch Phys Med Rehabil, 82(2), 174-182.
Becker, R., Alberti, O., & Bauer, B. L. (1997). Continuous intrathecal baclofen infusion in severe spasticity after traumatic or hypoxic brain injury. Journal of Neurology, 244(3), 160-166.
Bellon, K., Kolakowsky-Hayner, S., Wright, J., Huie, H., Toda, K., Bushnik, T., & Englander, J. (2015). A home-based walking study to ameliorate perceived stress and depressive symptoms in people with a traumatic brain injury. Brain Inj, 29(3), 313-319.
Berger, S., Kaldenberg, J., Selmane, R., & Carlo, S. (2016). Effectiveness of Interventions to Address Visual and Visual-Perceptual Impairments to Improve Occupational Performance in Adults With Traumatic Brain Injury: A Systematic Review. Am J Occup Ther, 70(3), 7003180010p7003180011-7003180017.
Boake, C., Francisco, G. E., Ivanhoe, C. B., & Kothari, S. (2000). Brain injury rehabilitation. In B. RL (Ed.), Physical medicine and rehabilitation (pp. 1073-1116). Toronto: Saunders Company.
Bontke, C. F., Lehmkuhl, D. I., Englander, J., Mann, N., Ragnarsson, K. T., Zasler, N. D., Graves, D. E., Thoi, L. I., & Jung, C. (1993). Medical complications and associated injuries of persons treated in the traumatic brain injury model systems programs. The Journal of Head Trauma Rehabilitation, 8(2), 34-46.
Branca, B., & Lake, A. E. (2004). Psychological and neuropsychological integration in multidisciplinary pain management after TBI. J Head Trauma Rehabil, 19(1), 40-57.
Brown, T. H., Mount, J., Rouland, B. L., Kautz, K. A., Barnes, R. M., & Kim, J. (2005). Body weight-supported treadmill training versus conventional gait training for people with chronic traumatic brain injury. J Head Trauma Rehabil, 20(5), 402-415.
Bushbacher, R. M., & Porter, C. D. (2000). Deconditioning, conditioning, and the benefits of exercise. In Braddom RL (Ed.), Physical Medicine and Rehabilitation (pp. 702-726). Toronto: Saunders Company.
Canning, C. G., Shepherd, R. B., Carr, J. H., Alison, J. A., Wade, L., & White, A. (2003). A randomized controlled trial of the effects of intensive sit-to-stand training after recent traumatic brain injury on sit-to-stand performance. Clin Rehabil, 17(4), 355-362.
Cassidy, J. D., Boyle, E., & Carroll, L. J. (2014). Population-based, inception cohort study of the incidence, course, and prognosis of mild traumatic brain injury after motor vehicle collisions. Arch Phys Med Rehabil, 95(3 SUPPL), S278-S285.
Charrette, A. L., Lorenz, L. S., Fong, J., O’Neil-Pirozzi, T. M., Lamson, K., Demore-Taber, M., & Lilley, R. (2016). Pilot study of intensive exercise on endurance, advanced mobility and gait speed in adults with chronic severe acquired brain injury. Brain Inj, 1-7.
Chow, J. W., Yablon, S. A., & Stokic, D. S. (2015). Effect of intrathecal baclofen bolus injection on ankle muscle activation during gait in patients with acquired brain injury. Neurorehabil Neural Repair, 29(2), 163-173.
Ciuffreda, K. J., Han, Y., Kapoor, N., & Ficarra, A. P. (2006). Oculomotor rehabilitation for reading in acquired brain injury. NeuroRehabilitation, 21(1), 9-21.
Clark, R. A., Williams, G., Fini, N., Moore, L., & Bryant, A. L. (2012). Coordination of dynamic balance during gait training in people with acquired brain injury. Arch Phys Med Rehabil, 93(4), 636-640.
Clemenzi, A., Formisano, R., Matteis, M., Gallinacci, L., Cochi, G., Savina, P., & Cicinelli, P. (2012). Care management of spasticity with botulinum toxin-A in patients with severe acquired brain injury: A 1-year follow-up prospective study. Brain Injury, 26(7-8), 979-983.
Conrad, J. S., Mitchell, G. L., & Kulp, M. T. (2016). Vision Therapy for Binocular Dysfunction Post Brain Injury. Optom Vis Sci.
Costigan, M., Scholz, J., & Woolf, C. J. (2009). Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci, 32, 1-32.
Couch, J. R., & Bearss, C. (2001). Chronic daily headache in the posttrauma syndrome: relation to extent of head injury. Headache, 41(6), 559-564.
Cuthbert, J. P., Staniszewski, K., Hays, K., Gerber, D., Natale, A., & O’Dell, D. (2014). Virtual reality-based therapy for the treatment of balance deficits in patients receiving inpatient rehabilitation for traumatic brain injury. Brain Injury, 28(2), 181-188.
D’Arcy, Y. (2011). Compact Clinical Guide to Chronic Pain Management: An Evidence-Based Approach for Nurses: Spencer Publishing Company.
Damiano, D., 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.
Dario, A., Di Stefano, M. G., Grossi, A., Casagrande, F., & Bono, G. (2002). Long-term intrathecal Baclofen infusion in supraspinal spasticity of adulthood. Acta Neurol Scand, 105(2), 83-87.
Dault, M. C., & Dugas, C. (2002). Evaluation of a specific balance and coordination programme for individuals with a traumatic brain injury. Brain Inj, 16(3), 231-244.
Dellemijn, P. (1999). Are opioids effective in relieving neuropathic pain? Pain, 80(3), 453-462.
Dettmers, C., Teske, U., Hamzei, F., Uswatte, G., Taub, E., & Weiller, C. (2005). Distributed form of constraint-induced movement therapy improves functional outcome and quality of life after stroke. Arch Phys Med Rehabil, 86(2), 204-209.
Dharmshaktu, P., Tayal, V., & Kalra, B. S. (2012). Efficacy of antidepressants as analgesics: a review. J Clin Pharmacol, 52(1), 6-17.
Dickinson, K., Bunn, F., Wentz, R., Edwards, P., & Roberts, I. (2000). Size and quality of randomised controlled trials in head injury: review of published studies. Bmj, 320(7245), 1308-1311.
Doble, J. E., Feinberg, D. L., Rosner, M. S., & Rosner, A. J. (2010). Identification of binocular vision dysfunction (vertical heterophoria) in traumatic brain injury patients and effects of individualized prismatic spectacle lenses in the treatment of postconcussive symptoms: a retrospective analysis. Pm r, 2(4), 244-253.
Dobscha, S. K., Clark, M. E., Morasco, B. J., Freeman, M., Campbell, R., & Helfand, M. (2009). Systematic review of the literature on pain in patients with polytrauma including traumatic brain injury. Pain Med, 10(7), 1200-1217.
Driver, S., Rees, K., O’Connor, J., & Lox, C. (2006). Aquatics, health-promoting self-care behaviours and adults with brain injuries. Brain Inj, 20(2), 133-141.
Dworkin, R. H., Backonja, M., Rowbotham, M. C., Allen, R. R., Argoff, C. R., Bennett, G. J., Bushnell, M. C., Farrar, J. T., Galer, B. S., Haythornthwaite, J. A., Hewitt, D. J., Loeser, J. D., Max, M. B., Saltarelli, M., Schmader, K. E., Stein, C., Thompson, D., Turk, D. C., Wallace, M. S., Watkins, L. R., & Weinstein, S. M. (2003). Advances in neuropathic pain: diagnosis, mechanisms, and treatment recommendations. Arch Neurol, 60(11), 1524-1534.
Elkind, A. H. (1989). Headache and head trauma. Clin J Pain, 5(1), 77-87.
Ersek, M., Cherrier, M. M., Overman, S. S., & Irving, G. A. (2004). The cognitive effects of opioids. Pain Manag Nurs, 5(2), 75-93.
Esquenazi, A., Lee, S., Packel, A. T., & Braitman, L. (2013). A Randomized Comparative Study of Manually Assisted Versus Robotic-Assisted Body Weight Supported Treadmill Training in Persons With a Traumatic Brain Injury. PM and R, 5(4), 280-290.
Ettinger, A. B., & Argoff, C. E. (2007). Use of antiepileptic drugs for nonepileptic conditions: psychiatric disorders and chronic pain. Neurotherapeutics, 4(1), 75-83.
Farrar, J. T., Young, J. P., Jr., LaMoreaux, L., Werth, J. L., & Poole, R. M. (2001). Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain, 94(2), 149-158.
Finnerup, N. B., Otto, M., McQuay, H. J., Jensen, T. S., & Sindrup, S. H. (2005). Algorithm for neuropathic pain treatment: an evidence based proposal. Pain, 118(3), 289-305.
Foo, J., Paterson, K., Williams, G., & Clark, R. (2013). Low-cost evaluation and real-time feedback of static and dynamic weight bearing asymmetry in patients undergoing in-patient physiotherapy rehabilitation for neurological conditions. Journal of NeuroEngineering and Rehabilitation, 10(1).
Franceschi, F., Marini, M., Ursella, S., Carbone, L., Candelli, M., Pignataro, G., Gabrielli, M., Santarelli, L., Ojetti, V., Giupponi, B., Fiore, V., Barbaro, F., De Marco, G., Buccelletti, F., Mancini, F., Roccarina, D., Gigante, G., Gasbarrini, A., Gasbarrini, G., & Silveri, N. G. (2008). Use of oxycodone in polytrauma patients: the “Gemelli” experience. Eur Rev Med Pharmacol Sci, 12(2), 123-126.
Francisco, G. E., Hu, M. M., Boake, C., & Ivanhoe, C. B. (2005). Efficacy of early use of intrathecal baclofen therapy for treating spastic hypertonia due to acquired brain injury. Brain Inj, 19(5), 359-364.
Francois, B., Vacher, P., Roustan, J., Salle, J. Y., Vidal, J., Moreau, J. J., & Vignon, P. (2001). Intrathecal baclofen after traumatic brain injury: early treatment using a new technique to prevent spasticity. J Trauma, 50(1), 158-161.
Gallagher, R., Drance, E., & Higginbotham, S. (2006). Finding the person behind the pain: chronic pain management in a patient with traumatic brain injury. J Am Med Dir Assoc, 7(7), 432-434.
Garland, D. E., Lilling, M., & Keenan, M. A. (1984). Percutaneous phenol blocks to motor points of spastic forearm muscles in head-injured adults. Arch Phys Med Rehabil, 65(5), 243-245.
Gellman, H., Keenan, M. A. E., & Botte, M. J. (1996). Recognition and Management of Upper Extremity Pain Syndromes in the Patient with Brain Injury. The Journal of Head Trauma Rehabilitation, 11(4), 23-30.
Gironda, R. J., Clark, M. E., Ruff, R. L., Chait, S., Craine, M., Walker, R., & Scholten, J. (2009). Traumatic brain injury, polytrauma, and pain: challenges and treatment strategies for the polytrauma rehabilitation. Rehabil Psychol, 54(3), 247-258.
Godbout, A. (1997). Structured habituation training for movement provoked vertigo after severe traumatic brain injury: a single-case experiment. Brain Inj, 11(9), 629-641.
Gordon, D. B., & Love, G. (2004). Pharmacologic management of neuropathic pain. Pain Manag Nurs, 5(4 Suppl 1), 19-33.
Gordon, W. A., Sliwinski, M., Echo, J., McLoughlin, M., Sheerer, M. S., & Meili, T. E. (1998). The benefits of exercise in individuals with traumatic brain injury: a retrospective study. J Head Trauma Rehabil, 13(4), 58-67.
Gormley, M. E., Jr., O’Brien, C. F., & Yablon, S. A. (1997). A clinical overview of treatment decisions in the management of spasticity. Muscle Nerve Suppl, 6, S14-20.
Gould, H. J. I. (2007). Pain Defined Understanding Pain: What it is, Why it happens and How it’s managed. In S. LM (Ed.), American Academy of Neurology (1 ed., pp. 1-8).
Gracies, Elovic, E., McGuire, J., & Simpson, D. M. (1997a). Traditional pharmacological treatments for spasticity. Part I: Local treatments. Muscle Nerve Suppl, 6, S61-91.
Gracies, Nance, P., Elovic, E., McGuire, J., & Simpson, D. M. (1997b). Traditional pharmacological treatments for spasticity. Part II: General and regional treatments. Muscle Nerve Suppl, 6, S92-120.
Greenwell, G. T. (2012). Medical marijuana use for chronic pain: risks and benefits. J Pain Palliat Care Pharmacother, 26(1), 68-69.
Gregory, C. M., & Bickel, C. S. (2005). Recruitment patterns in human skeletal muscle during electrical stimulation. Phys Ther, 85(4), 358-364.
Grissom, S. P., & Blanton, S. (2001). Treatment of upper motoneuron plantarflexion contractures by using an adjustable ankle-foot orthosis. Arch Phys Med Rehabil, 82(2), 270-273.
Grotta, J. C., Noser, E. A., Ro, T., Boake, C., Levin, H., Aronowski, J., & Schallert, T. (2004). Constraint-induced movement therapy. Stroke, 35(11 Suppl 1), 2699-2701.
Guay, D. R. (2003). Oxcarbazepine, topiramate, zonisamide, and levetiracetam: potential use in neuropathic pain. Am J Geriatr Pharmacother, 1(1), 18-37.
Guindon, J., Walczak, J. S., & Beaulieu, P. (2007). Recent advances in the pharmacological management of pain. Drugs, 67(15), 2121-2133.
Gurr, B., & Coetzer, B. R. (2005). The effectiveness of cognitive-behavioural therapy for post-traumatic headaches. Brain Inj, 19(7), 481-491.
Gurr, B., & Moffat, N. (2001). Psychological consequences of vertigo and the effectiveness of vestibular rehabilitation for brain injury patients. Brain Inj, 15(5), 387-400.
Haanpaa, M. L., Gourlay, G. K., Kent, J. L., Miaskowski, C., Raja, S. N., Schmader, K. E., & Wells, C. D. (2010). Treatment considerations for patients with neuropathic pain and other medical comorbidities. Mayo Clin Proc, 85(3 Suppl), S15-25.
Halstead, L. S., Seager, S. W., Houston, J. M., Whitesell, K., Dennis, M., & Nance, P. W. (1993). Relief of spasticity in SCI men and women using rectal probe electrostimulation. Paraplegia, 31(11), 715-721.
Ham, L. P., & Packard, R. C. (1996). A retrospective, follow-up study of biofeedback-assisted relaxation therapy in patients with posttraumatic headache. Biofeedback Self Regul, 21(2), 93-104.
Hassett, L. M., Moseley, A. M., Tate, R. L., Harmer, A. R., Fairbairn, T. J., & Leung, J. (2009). Efficacy of a fitness centre-based exercise programme compared with a home-based exercise programme in traumatic brain injury: a randomized controlled trial. J Rehabil Med, 41(4), 247-255.
Hassett, L. M., Moseley, A. M., Whiteside, B., Barry, S., & Jones, T. (2012). Circuit class therapy can provide a fitness training stimulus for adults with severe traumatic brain injury: a randomised trial within an observational study. J Physiother, 58(2), 105-112.
Hassett, L. M., Tate, R. L., Moseley, A. M., & Gillett, L. E. (2011). Injury severity, age and pre-injury exercise history predict adherence to a home-based exercise programme in adults with traumatic brain injury. Brain Inj, 25(7-8), 698-706.
Hawker, G. A., Mian, S., Kendzerska, T., & French, M. (2011). Measures of adult pain: Visual Analog Scale for Pain (VAS Pain), Numeric Rating Scale for Pain (NRS Pain), McGill Pain Questionnaire (MPQ), Short-Form McGill Pain Questionnaire (SF-MPQ), Chronic Pain Grade Scale (CPGS), Short Form-36 Bodily Pain Scale (SF-36 BPS), and Measure of Intermittent and Constant Osteoarthritis Pain (ICOAP). Arthritis Care Res (Hoboken), 63 Suppl 11, S240-252.
Hillier, S. L., Sharpe, M. H., & Metzer, J. (1997). Outcomes 5 years post-traumatic brain injury (with further reference to neurophysical impairment and disability). Brain Inj, 11(9), 661-675.
Hirose, T., Shiozaki, T., Shimizu, K., Mouri, T., Noguchi, K., Ohnishi, M., & Shimazu, T. (2013). The effect of electrical muscle stimulation on the prevention of disuse muscle atrophy in patients with consciousness disturbance in the intensive care unit. Journal of Critical Care, 28(4), 536.e531-537.
Hoarau, X., Richer, E., Dehail, P., & Cuny, E. (2012a). A 10-year follow-up study of patients with severe traumatic brain injury and dysautonomia treated with intrathecal baclofen therapy. Brain Injury, 26(7-8), 927-940.
Hoarau, X., Richer, E., Dehail, P., & Cuny, E. (2012b). Comparison of long-term outcomes of patients with severe traumatic or hypoxic brain injuries treated with intrathecal baclofen therapy for dysautonomia. Brain Injury, 26(12), 1451-1463.
Hoffman, J. M., Bell, K. R., Powell, J. M., Behr, J., Dunn, E. C., Dikmen, S., & Bombardier, C. H. (2010). A randomized controlled trial of exercise to improve mood after traumatic brain injury. Pm r, 2(10), 911-919.
Hoffman, J. M., Lucas, S., Dikmen, S., Braden, C. A., Brown, A. W., Brunner, R., Diaz-Arrastia, R., Walker, W. C., Watanabe, T. K., & Bell, K. R. (2011). Natural history of headache after traumatic brain injury. J Neurotrauma, 28(9), 1719-1725.
Hoffman, J. M., Pagulayan, K. F., Zawaideh, N., Dikmen, S., Temkin, N., & Bell, K. R. (2007). Understanding pain after traumatic brain injury: impact on community participation. Am J Phys Med Rehabil, 86(12), 962-969.
Horn, T. S., Yablon, S. A., Chow, J. W., Lee, J. E., & Stokic, D. S. (2010). Effect of intrathecal baclofen bolus injection on lower extremity joint range of motion during gait in patients with acquired brain injury. Arch Phys Med Rehabil, 91(1), 30-34.
Horn, T. S., Yablon, S. A., & Stokic, D. S. (2005). Effect of intrathecal baclofen bolus injection on temporospatial gait characteristics in patients with acquired brain injury. Arch Phys Med Rehabil, 86(6), 1127-1133.
International Association for the Study of Pain. (1994). Part III Pain Terms: A Current List with Definitions and Notes on Usage. In H. Merskey & N. Bogduk (Eds.), Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms (2 ed.). Seattle: IASP Press.
Intiso, D., Simone, V., Di Rienzo, F., Iarossi, A., Pazienza, L., Santamato, A., Maruzzi, G., & Basciani, M. (2014). High doses of a new botulinum toxin type A (NT-201) in adult patients with severe spasticity following brain injury and cerebral palsy. NeuroRehabilitation, 34(3), 515-522.
Ivanhoe, C. B., & Hartman, E. T. (2004). Clinical caveats on medical assessment and treatment of pain after TBI. J Head Trauma Rehabil, 19(1), 29-39.
Ivanhoe, C. B., & Parrilla, Z. M. (2002). Pain Management in Traumatic Brain Injury. In G. M. Monga TN (Ed.), Pain Management in Rehabilitation (pp. 101-125). New York, NY: Demos Medical Publishing.
Jacobson, G. P., Ramadan, N. M., Aggarwal, S. K., & Newman, C. W. (1994). The Henry Ford Hospital Headache Disability Inventory (HDI). Neurology, 44(5), 837-842.
Jankovic, J., & Brin, M. F. (1991). Therapeutic uses of botulinum toxin. N Engl J Med, 324(17), 1186-1194.
Jensen, O. K., Nielsen, F. F., & Vosmar, L. (1990). An open study comparing manual therapy with the use of cold packs in the treatment of post-traumatic headache. Cephalalgia, 10(5), 241-250.
Kasten, E., Poggel, D. A., & Sabel, B. A. (2000). Computer-based training of stimulus detection improves color and simple pattern recognition in the defective field of hemianopic subjects. J Cogn Neurosci, 12(6), 1001-1012.
Kasten, E., Wust, S., Behrens-Baumann, W., & Sabel, B. A. (1998). Computer-based training for the treatment of partial blindness. Nat Med, 4(9), 1083-1087.
Katz, & Campagnolo, D. I. (1993). Pharmacological management of spasticity. In K. RT (Ed.), Spasticity: State of the Art Reviews; Physical Medicine and Rehabilitation (Vol. 8, pp. 473-480). Philadelphia: Hanley and Belfus;.
Katz, Dewald, J. P., & Schmit, B. D. (2000). Spasticity. In B. RL (Ed.), Physical medicine and rehabilitation. (pp. 592-615). Toronto: Saunders Company.
Keenan, M. A., Tomas, E. S., Stone, L., & Gersten, L. M. (1990). Percutaneous phenol block of the musculocutaneous nerve to control elbow flexor spasticity. J Hand Surg Am, 15(2), 340-346.
Khan, M. I., Walsh, D., & Brito-Dellan, N. (2011). Opioid and adjuvant analgesics: compared and contrasted. Am J Hosp Palliat Care, 28(5), 378-383.
Kriz, G., Hermsdorfer, J., Marquardt, C., & Mai, N. (1995). Feedback-based training of grip force control in patients with brain damage. Arch Phys Med Rehabil, 76(7), 653-659.
Lahz, S., & Bryant, R. A. (1996). Incidence of chronic pain following traumatic brain injury. Arch Phys Med Rehabil, 77(9), 889-891.
Lainez, M. J., & Pesquera, B. L. (2011). Headache after trauma: physiological considerations. Curr Pain Headache Rep, 15(6), 467-473.
Lance, J. W. (1980). The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology, 30(12), 1303-1313.
Lannin, N. A., Horsley, S. A., Herbert, R., McCluskey, A., & Cusick, A. (2003). Splinting the hand in the functional position after brain impairment: a randomized, controlled trial. Arch Phys Med Rehabil, 84(2), 297-302.
Leung, J., Harvey, L. A., Moseley, A. M., Whiteside, B., Simpson, M., & Stroud, K. (2014). Standing with electrical stimulation and splinting is no better than standing alone for management of ankle plantarflexion contractures in people with traumatic brain injury: a randomised trial. J Physiother, 60(4), 201-208.
Lew, H. L., Lin, P. H., Fuh, J. L., Wang, S. J., Clark, D. J., & Walker, W. C. (2006). Characteristics and treatment of headache after traumatic brain injury: a focused review. Am J Phys Med Rehabil, 85(7), 619-627.
Linacre, J. M., Heinemann, A. W., Wright, B. D., Granger, C. V., & Hamilton, B. B. (1994). The structure and stability of the Functional Independence Measure. Arch Phys Med Rehabil, 75(2), 127-132.
Lorentzen, J., Nielsen, D., Holm, K., Baagøe, S., Grey, M. J., & Nielsen, J. B. (2012). Neural tension technique is no different from random passive movements in reducing spasticity in patients with traumatic brain injury. Disabil Rehabil, 34(23), 1978-1985.
Lucas, S. (2011). Headache management in concussion and mild traumatic brain injury. Pm r, 3(10 Suppl 2), S406-412.
Margetis, K., Korfias, S. I., Gatzonis, S., Boutos, N., Stranjalis, G., Boviatsis, E., & Sakas, D. E. (2014). Intrathecal baclofen associated with improvement of consciousness disorders in spasticity patients. Neuromodulation, 17(7), 699-704: discussion 704.
Martelli, M. F., Nicholson, K., & Zasler N.D. (2012). Psychological Assessment and Management of Port Traumatic Pain. In N. D. Zasler, Katz, D.I. & Zafonte, R.D (Ed.), Brain Injury Medicine: Principles and Practice (2 ed., pp. 974-987).
Mayer. (1997). Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion. Muscle Nerve Suppl, 6, S1-13.
Mayer, Esquenazi, A., & Childers, M. K. (1997). Common patterns of clinical motor dysfunction. Muscle Nerve Suppl, 6, S21-35.
Mayer, Esquenazi, A., & Keenan, M. A. (1996). Analysis and management of spasticity, contracture and impaired motor control. In Z. N. Horn LJ (Ed.), Medical rehabilitation of traumatic brain injury (pp. 411-458). Toronto: Mosby.
Mayer, N. H., Whyte, J., Wannstedt, G., & Ellis, C. A. (2008). Comparative impact of 2 botulinum toxin injection techniques for elbow flexor hypertonia. Arch Phys Med Rehabil, 89(5), 982-987.
McDowell, I. (2006). Measuring Health. A Guide to Rating Scales and Questionnaires. New York: Oxford University Press.
Medina, J. L. (1992). Efficacy of an individualized outpatient program in the treatment of chronic post-traumatic headache. Headache, 32(4), 180-183.
Meythaler, Guin-Renfroe, S., & Hadley, M. N. (1999). Continuously infused intrathecal baclofen for spastic/dystonic hemiplegia: a preliminary report. Am J Phys Med Rehabil, 78(3), 247-254.
Meythaler, J. M., Clayton, W., Davis, L. K., Guin-Renfroe, S., & Brunner, R. C. (2004). Orally delivered baclofen to control spastic hypertonia in acquired brain injury. J Head Trauma Rehabil, 19(2), 101-108.
Meythaler, J. M., DeVivo, M. J., & Hadley, M. (1996). Prospective study on the use of bolus intrathecal baclofen for spastic hypertonia due to acquired brain injury. Arch Phys Med Rehabil, 77(5), 461-466.
Meythaler, J. M., Guin-Renfroe, S., Grabb, P., & Hadley, M. N. (1999). Long-term continuously infused intrathecal baclofen for spastic-dystonic hypertonia in traumatic brain injury: 1-year experience. Arch Phys Med Rehabil, 80(1), 13-19.
Meythaler, J. M., Guin-Renfroe, S., Johnson, A., & Brunner, R. M. (2001). Prospective assessment of tizanidine for spasticity due to acquired brain injury. Arch Phys Med Rehabil, 82(9), 1155-1163.
Meythaler, J. M., McCary, A., & Hadley, M. N. (1997). Prospective assessment of continuous intrathecal infusion of baclofen for spasticity caused by acquired brain injury: a preliminary report. J Neurosurg, 87(3), 415-419.
Mortenson, P. A., & Eng, J. J. (2003). The use of casts in the management of joint mobility and hypertonia following brain injury in adults: a systematic review. Phys Ther, 83(7), 648-658.
Morton, R. (2004). Visual Dysfunction Following Traumatic Brain Injury. In A. MJ (Ed.), Traumatic Brain Injury – Rehabilitative Treatment and Case Management. (pp. 183-207). Boca Raton, Florida: CRC Press;.
Moseley, A. M. (1997). The effect of casting combined with stretching on passive ankle dorsiflexion in adults with traumatic head injuries. Phys Ther, 77(3), 240-247; discussion 248-259.
Moseley, A. M., Hassett, L. M., Leung, J., Clare, J. S., Herbert, R. D., & Harvey, L. A. (2008). Serial casting versus positioning for the treatment of elbow contractures in adults with traumatic brain injury: a randomized controlled trial. Clin Rehabil, 22(5), 406-417.
Moseley, A. M., Herbert, R. D., Sherrington, C., & Maher, C. G. (2002). Evidence for physiotherapy practice: a survey of the Physiotherapy Evidence Database (PEDro). Aust J Physiother, 48(1), 43-49.
Motin, M., Keren, O., Groswasser, Z., & Gordon, C. R. (2005). Benign paroxysmal positional vertigo as the cause of dizziness in patients after severe traumatic brain injury: diagnosis and treatment. Brain Inj, 19(9), 693-697.
Mullally, W. J., Hall, K., & Goldstein, R. (2009). Efficacy of biofeedback in the treatment of migraine and tension type headaches. Pain Physician, 12(6), 1005-1011.
Mumford, N., Duckworth, J., Thomas, P. R., Shum, D., Williams, G., & Wilson, P. H. (2012). Upper-limb virtual rehabilitation for traumatic brain injury: a preliminary within-group evaluation of the elements system. Brain Injury, 26(2), 166-176.
Naguib, M. B., & Madian, Y. T. (2014). Betahistine Dihydrochloride With and Without Early Vestibular Rehabilitation for the Management of Patients With Balance Disorders Following Head Trauma: A Preliminary Randomized Clinical Trial. Journal of Chiropractic Medicine, 13(1), 14-20.
Nasreddine, W., & Beydoun, A. (2007). Oxcarbazepine in neuropathic pain. Expert Opin Investig Drugs, 16(10), 1615-1625.
Neistadt, M. E. (1994). The effects of different treatment activities on functional fine motor coordination in adults with brain injury. Am J Occup Ther, 48(10), 877-882.
Nicholson, B. D. (2004). Evaluation and treatment of central pain syndromes. Neurology, 62(5 Suppl 2), S30-36.
O’Connor, A. B., & Dworkin, R. H. (2009). Treatment of neuropathic pain: an overview of recent guidelines. Am J Med, 122(10 Suppl), S22-32.
Ofek, H., & Defrin, R. (2007). The characteristics of chronic central pain after traumatic brain injury. Pain, 131(3), 330-340.
Packard, R. C. (2000). Treatment of chronic daily posttraumatic headache with divalproex sodium. Headache, 40(9), 736-739.
Padula, W. V., Argyris, S., & Ray, J. (1994). Visual evoked potentials (VEP) evaluating treatment for post-trauma vision syndrome (PTVS) in patients with traumatic brain injuries (TBI). Brain Inj, 8(2), 125-133.
Page, S., & Levine, P. (2003). Forced use after TBI: promoting plasticity and function through practice. Brain Inj, 17(8), 675-684.
Pangarkar, S., & Lee, P. C. (2011). Conservative treatment for neck pain: medications, physical therapy, and exercise. Phys Med Rehabil Clin N Am, 22(3), 503-520, ix.
Peirone, E., Goria, P. F., & Anselmino, A. (2014). A dual-task home-based rehabilitation programme for improving balance control in patients with acquired brain injury: a single-blind, randomized controlled pilot study. Clinical Rehabilitation, 28(4), 329-338.
Peters, D. M., Jain, S., Liuzzo, D. M., Middleton, A., Greene, J., Blanck, E., Sun, S., Raman, R., & Fritz, S. L. (2014). Individuals with chronic traumatic brain injury improve walking speed and mobility with intensive mobility training. Arch Phys Med Rehabil, 95(8), 1454-1460.
Pohl, M., Ruckriem, S., Mehrholz, J., Ritschel, C., Strik, H., & Pause, M. R. (2002). Effectiveness of serial casting in patients with severe cerebral spasticity: a comparison study. Arch Phys Med Rehabil, 83(6), 784-790.
Posteraro, F., Calandriello, B., Galli, R., Logi, F., Iardella, L., & Bordi, L. (2013). Timing of intrathecal baclofen therapy in persons with acquired brain injury: influence on outcome. Brain Inj, 27(13-14), 1671-1675.
Pringsheim, T., Davenport, W., Mackie, G., Worthington, I., Aube, M., Christie, S. N., Gladstone, J., & Becker, W. J. (2012). Canadian Headache Society guideline for migraine prophylaxis. Can J Neurol Sci, 39(2 Suppl 2), S1-59.
Riggs, R. V., Andrews, K., Roberts, P., & Gilewski, M. (2007). Visual deficit interventions in adult stroke and brain injury: a systematic review. Am J Phys Med Rehabil, 86(10), 853-860.
Roth, A. D., & Pilling, S. (2008). Using an Evidence-Based Methodology to Identify the Competences Required to Deliver Effective Cognitive and Behavioural Therapy for Depression and Anxiety Disorders. Behavioural and Cognitive Psychotherapy, 36(2), 129-147.
Schafer, A. Y., & Ustinova, K. I. (2013). Does use of a virtual environment change reaching while standing in patients with traumatic brain injury? Journal of NeuroEngineering and Rehabilitation, 10(1).
Scherer, M. R., & Schubert, M. C. (2009). Traumatic brain injury and vestibular pathology as a comorbidity after blast exposure. Phys Ther, 89(9), 980-992.
Seib, T. P., Price, R., Reyes, M. R., & Lehmann, J. F. (1994). The quantitative measurement of spasticity: effect of cutaneous electrical stimulation. Arch Phys Med Rehabil, 75(7), 746-750.
Seif-Naraghi, A. H., & Herman, R. M. (1999). A novel method for locomotion training. J Head Trauma Rehabil, 14(2), 146-162.
Seifert, T. D., & Evans, R. W. (2010). Posttraumatic headache: a review. Curr Pain Headache Rep, 14(4), 292-298.
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., Meythaler, J. M., & Taub, E. (2005). Constraint-induced movement therapy for recovery of upper-limb function following traumatic brain injury. J Rehabil Res Dev, 42(6), 769-778.
Shepard, N. T., & Telian, S. A. (1995). Programmatic vestibular rehabilitation. Otolaryngol Head Neck Surg, 112(1), 173-182.
Sherman, K. B., Goldberg, M., & Bell, K. R. (2006). Traumatic brain injury and pain. Phys Med Rehabil Clin N Am, 17(2), 473-490, viii.
Sietsema, J. M., Nelson, D. L., Mulder, R. M., Mervau-Scheidel, D., & White, B. E. (1993). The use of a game to promote arm reach in persons with traumatic brain injury. Am J Occup Ther, 47(1), 19-24.
Singer, Jegasothy, G. M., Singer, K. P., & Allison, G. T. (2003). Evaluation of serial casting to correct equinovarus deformity of the ankle after acquired brain injury in adults. Arch Phys Med Rehabil, 84(4), 483-491.
Singer, B. J., Singer, K. P., & Allison, G. T. (2003). Evaluation of extensibility, passive torque and stretch reflex responses in triceps surae muscles following serial casting to correct spastic equinovarus deformity. Brain Inj, 17(4), 309-324.
Stokic, D. S., Yablon, S. A., & Hayes, A. (2005). Comparison of clinical and neurophysiologic responses to intrathecal baclofen bolus administration in moderate-to-severe spasticity after acquired brain injury. Arch Phys Med Rehabil, 86(9), 1801-1806.
Sullivan-Singh, S. J., Sawyer, K., Ehde, D. M., Bell, K. R., Temkin, N., Dikmen, S., Williams, R. M., & Hoffman, J. M. (2014). Comorbidity of pain and depression among persons with traumatic brain injury. Arch Phys Med Rehabil, 95(6), 1100-1105.
Tang, V., Warden, J., Cullen, N., & Rutledge, E. (2007). Topiramate in traumatic brain injury: adverse effects on cognitive function. J Head Trauma Rehabil, 22(6), 409-410.
Tatrow, K., Blanchard, E. B., & Silverman, D. J. (2003). Posttraumatic headache: an exploratory treatment study. Appl Psychophysiol Biofeedback, 28(4), 267-278.
Theeler, B. J., & Erickson, J. C. (2012). Posttraumatic headache in military personnel and veterans of the iraq and afghanistan conflicts. Curr Treat Options Neurol, 14(1), 36-49.
Thibaut, A., Deltombe, T., Wannez, S., Gosseries, O., Ziegler, E., Dieni, C., Deroy, M., & Laureys, S. (2015). Impact of soft splints on upper limb spasticity in chronic patients with disorders of consciousness: A randomized, single-blind, controlled trial. Brain Inj, 29(7-8), 830-836.
Uomoto, J. M., & Esselman, P. C. (1993). Traumatic brain injury and chronic pain: differential types and rates by head injury severity. Arch Phys Med Rehabil, 74(1), 61-64.
Ustinova, K. I., Chernikova, L. A., Dull, A., & Perkins, J. (2015). Physical therapy for correcting postural and coordination deficits in patients with mild-to-moderate traumatic brain injury. Physiother Theory Pract, 31(1), 1-7.
Ustinova, K. I., Perkins, J., Leonard, W. A., & Hausbeck, C. J. (2014). Virtual reality game-based therapy for treatment of postural and co-ordination abnormalities secondary to TBI: A pilot study. Brain Injury, 28(4), 486-495.
Verplancke, D., Snape, S., Salisbury, C. F., Jones, P. W., & Ward, A. B. (2005). A randomized controlled trial of botulinum toxin on lower limb spasticity following acute acquired severe brain injury. Clin Rehabil, 19(2), 117-125.
Vranken, J. H., Dijkgraaf, M. G., Kruis, M. R., van der Vegt, M. H., Hollmann, M. W., & Heesen, M. (2008). Pregabalin in patients with central neuropathic pain: a randomized, double-blind, placebo-controlled trial of a flexible-dose regimen. Pain, 136(1-2), 150-157.
Vranken, J. H., Hollmann, M. W., van der Vegt, M. H., Kruis, M. R., Heesen, M., Vos, K., Pijl, A. J., & Dijkgraaf, M. G. (2011). Duloxetine in patients with central neuropathic pain caused by spinal cord injury or stroke: a randomized, double-blind, placebo-controlled trial. Pain, 152(2), 267-273.
Wang, Z. M., Law, J. H., King, N. K., Rajeswaran, D. K., Soh, S., Rao, J. P., Ng, W. H., & Chua, K. S. (2016). Treatment of severe, disabling spasticity with continuous intrathecal baclofen therapy following acquired brain injury: the experience of a tertiary institution in Singapore. Singapore Med J, 57(1), 8-12.
Ware, M. A., Wang, T., Shapiro, S., Robinson, A., Ducruet, T., Huynh, T., Gamsa, A., Bennett, G. J., & Collet, J. P. (2010). Smoked cannabis for chronic neuropathic pain: a randomized controlled trial. CMAJ, 182(14), E694-701.
Waszkielewicz, A. M., Gunia, A., Sloczynska, K., & Marona, H. (2011). Evaluation of anticonvulsants for possible use in neuropathic pain. Curr Med Chem, 18(28), 4344-4358.
Watanabe, T. K., Bell, K. R., Walker, W. C., & Schomer, K. (2012). Systematic review of interventions for post-traumatic headache. Pm r, 4(2), 129-140.
Wee, S. K. (2002). Vestibular rehabilitation for a patient with severe traumatic brain injury: a case study. Physiotherapy Singapore, 5, 59-65.
Wetherell, J. L., Afari, N., Rutledge, T., Sorrell, J. T., Stoddard, J. A., Petkus, A. J., Solomon, B. C., Lehman, D. H., Liu, L., Lang, A. J., & Atkinson, J. H. (2011). A randomized, controlled trial of acceptance and commitment therapy and cognitive-behavioral therapy for chronic pain. Pain, 152(9), 2098-2107.
Wiffen, P. J., Derry, S., & Moore, R. A. (2011). Lamotrigine for acute and chronic pain. Cochrane Database Syst Rev(2), Cd006044.
Wilson, D. J., Powell, M., Gorham, J. L., & Childers, M. K. (2006). Ambulation training with and without partial weightbearing after traumatic brain injury: results of a randomized, controlled trial. Am J Phys Med Rehabil, 85(1), 68-74.
Wong, V., Cheuk, D. K., Lee, S., & Chu, V. (2012). Accupouncture for acute management and rehabilitation of traumatic brain injury. Eur J Phys Rehabil Med, 48(1), 71-86.
Yablon, S. A., Agana, B. T., Ivanhoe, C. B., & Boake, C. (1996). Botulinum toxin in severe upper extremity spasticity among patients with traumatic brain injury: an open-labeled trial. Neurology, 47(4), 939-944.
Yarkony, G. M., & Sahgal, V. (1987). Contractures. A major complication of craniocerebral trauma. Clin Orthop Relat Res(219), 93-96.
Young, W. B., Packard, R.C. & Ramadan. (2001). Headaches associated with head trauma. In S. D. Silverstein, Lipton, R.B. & Dalessio, D.J. (Ed.), Wolfe’s Headache and other Head Pain (7 ed., pp. 325-348).
Yungher, D., & Craelius, W. (2012). Improving fine motor function after brain injury using gesture recognition biofeedback. Disability and Rehabilitation: Assistive Technology, 7(6), 464-468.
Zasler, N. D., Martelli, M. F., & Nicholson, K. (2011). Chronic Pain. In M. T. Silver JM, Yudofsky SC (Ed.), Textbook of Traumatic Brain Injury (pp. 375-396). Washington, DC: American Psychiatric Publishing, Inc.

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