4. Motor and Sensory Impairment Rehabilitation Post Acquired Brain Injury
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 improve fine motor function post ABI.
Finger sequencing tasks may improve fine motor performance speeds, but not error rates.
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, balance, and cardiovascular parameters post ABI
Further research is needed in order to determine which components of exercise are the most effective for motor rehabilitation post ABI.
Physiotherapy likely improves ambulation and motor function following an ABI.
Botulinum toxin type A injections are effective in the management of localized spasticity following an 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 may 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.
Despite the positive results of the study investigating biofeedback and post traumatic headaches, further research needs to be completed using larger groups and only with those who have moderate and severe TBIs.
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.
Yoga and mindfulness may improve perceived pain and positively impact quality of life overall.
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.
4.1 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 interventions available for upper and lower extremity motor impairment, including spasticity.
4.1.1 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.
4.1.1.1 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) have been identified (Table 4.1).
Evidence Table(s)
Discussion
Conclusions
4.1.1.2 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.
Evidence Table(s)
Discussion
Conclusions
There is level 1b evidence that soft hand splinting, but not manual therapy, may improve hand opening in individuals post ABI.
4.1.1.3 Interventions for Fine Motor Coordination
Key Points
Gesture recognition biofeedback and visual feedback-based training may improve fine motor function post ABI.
Finger sequencing tasks may improve fine motor performance speeds, but not error rates.
Evidence Table(s)
Discussion
Another 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.
Korman et al. (2018) has found that finger-sequencing tasks may not be effective for improving fine motor compared to the effects of spontaneous recovery. Individuals were either trained or not trained on a finger sequencing task, ultimately there were no significant differences in error rates between groups, although the trained group did significantly improve their performance speed without increasing their error rate (Korman et al., 2018).
Conclusions
There is level 2 evidence that finger sequencing training may increase performance speed on this task, but not significantly improve error rates 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.
4.1.1.4 Virtual Reality for Upper Extremity Rehabilitation
Key Points
Evidence Table(s)
Discussion
Conclusions
4.1.2 Lower Extremity Interventions
4.1.2.1 Partial Body Weight Supported Gait Training
Key Points
Robotic assisted treadmill training may be similar to manually assisted treadmill training at improving gait speed and mobility post ABI.
Evidence Table(s)
Discussion
Conclusions
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.
4.1.2.2 Multimodal Interventions
Key Points
Sit-to-stand training and Intensive Mobility Training may improve lower extremity motor function post ABI.
Discussion
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 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.
4.1.2.3 Virtual Reality for Lower Extremity Rehabilitation
Key Points
Evidence Table(s)
Discussion
Conclusions
There is level 4 evidence that visual feedback may reduce weight-bearing asymmetry in the lower extremities post-ABI.
4.1.3 Combined Upper and Lower Extremity Interventions
4.1.3.1 Virtual Reality
Key Points
Evidence Table(s)
Discussion
Conclusions
There is level 4 evidence that virtual reality therapy may improve balance, gait, and functional reaching in individuals post ABI.
4.1.4 Exercise Programs
4.1.4.2 Physiotherapy
Key Points
Evidence Table(s)
Discussion
Conclusions
4.1.4.1 Aerobic Training
Key Points
Further research is needed in order to determine which components of exercise are the most effective for motor rehabilitation post-ABI.
Evidence Table(s)
Discussion
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 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). Corral et al. (2014) also concluded that cycling training resulted in increased oxygen uptake capacity.
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). Both groups, regardless of treatment condition significantly improved on the shuffle test. However, adherence to the program was higher among those attending a fitness center. When compliance was explored further, those with greater adherence 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. These individuals also reported a significantly higher quality of life. Furthermore, home-based exercise programs have shown to improve depressive symptoms, stability, motor control test scores, and gait following intervention as well (Bellon et al., 2015; Damiano et al., 2016). It is important to note that one study found that lower stability and dual-tasking scores were associated with poorer mental health outcomes (Damiano et al. 2016).
Two studies have examined the cardiovascular parameters of exercise programs as it relates to motor recovery (Bhambhani et al., 2005; Chin et al., 2015). The two studies examined the effects of supervised exercise training programs, one found that after completing the exercise program there was a significant increase in treadmill time (Chin et al., 2015), while the other found there was a significant increase in oxygen uptake and ventilation rate (Bhambhani et al., 2005). Overall, cardiovascular and respiratory parameters were seen to improve in both studies, but it should be noted that Chin et al. (2015) also observed a significant reduction in fatigue.
Conclusions
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 aerobic exercise programs may improve cardiovascular parameters following an ABI.
4.1.5 Spasticity Interventions
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. Although surgery is a viable intervention for the treatment of spasticity, no studies meeting our inclusion criteria have examined surgery as an intervention for the management of spasticity following an ABI (Duquette & Adkinson, 2018).
4.1.5.4 Oral Antispasticity Drugs
Key Points
Discussion
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
4.1.5.5 Intrathecal Baclofen
Key Points
Prolonged intrathecal baclofen may reduce upper and lower extremity spasticity long-term post ABI.
Evidence Table(s)
Discussion
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 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.
4.1.5.6 Casting
Key Points
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.
Evidence Table(s)
Discussion
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. (2003b) and Singer et al. (2003a) 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., 2003a). It should be noted, however, that casting can lead to tissue breakdown (Singer et al., 2003b).
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 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.
4.1.5.1 Botulinum Toxin Injections
Key Points
Botulinum toxin injections in combination with casting may be as effective as casting alone at reducing leg spasticity in patients post ABI.
Botulinum toxin type A injections, whether through a single point or multisite, likely reduce localized spasticity following ABI.
Evidence Table(s)
Discussion
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 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 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.
4.1.5.2 Nerve Blocking Agents
Key Points
Discussion
Conclusions
4.1.5.3 Electrical Stimulation
Key Points
Electrical stimulation in combination with tilt table standing and splinting may acutely improve spasticity (6 weeks) in patients post ABI.
Discussion
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.
4.1.5.7 Adjustable Orthosis
4.1.5.8 Hand Splinting and Stretching
Key Points
Discussion
Conclusions
4.1.5.8 Multimodal Interventions
Key Points
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.
Discussion
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 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.
4.2 Visual Dysfunction
Key Points
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.
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 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 4.19).
Discussion
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). 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 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.
4.3 Vestibular Dysfunction
Key Points
A vestibular rehabilitation program may improve symptoms of vertigo in patients following TBI.
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). The literature includes a variety of interventions for vestibular rehabilitation (Table 4.20).
Discussion
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 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.
4.4 Pain Post TBI
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, as 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.
4.4.1 Assessing Pain Post TBI
4.4.1.1 Visual Analog Scale
4.4.1.2 Numeric Rating Scale
4.4.1.3 McGill Pain Questionnaire
4.4.1.4 Headache Disability Inventory
4.4.1.5 Headache Diary
4.4.2 Pain Syndromes Post ABI
4.4.2.1 Neuropathic Pain
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 are discussed in sections 4.5.4.1 (anticonvulsants) and 4.5.4.5 (cannabinoids).
4.4.2.2 Central Pain Syndromes
4.4.2.3 Post Traumatic Headaches
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 4.4.3.1), Cognitive Behavioural Theory (section 4.4.3.2), Manual Therapy (section 4.4.3.4), and Cryotherapy and Thermotherapy (section 4.4.3.6).
4.4.3 Non-Pharmacological Interventions for Pain and Post Traumatic Headache
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 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.
4.4.3.7 Yoga and Mindfulness
Key Points
Discussion
Conclusions
4.4.3.1 Biofeedback to Manage Post Traumatic Headache
Key Points
Evidence Table(s)
Discussion
Conclusions
4.4.3.2 Cognitive Behavioural Therapy
Key Points
Evidence Table(s)
Discussion
Conclusions
4.4.3.3 Relaxation Training
4.4.3.4 Manual Therapy
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.
4.4.3.5 Acupuncture
4.4.3.6 Cryotherapy and Thermotherapy
Key Points
Evidence Table(s)
Discussion
Conclusions
4.4.4 Pharmacological Management of Pain and Post Traumatic Headache
4.4.4.1 Anticonvulsants
Valporic Acid and Divalproex Sodium
Valporic acid and divalproex sodium are antiepileptic medications that have been used to reduce pain, however, there are no clinical trials demonstrating its efficacy post moderate to severe TBI. A retrospective study was identified that investigated the effectiveness of divalproex sodium on PTH in a mild TBI population (Packard, 2000). The dosing was individualized, however the starting dose was 250 mg per day and was increased by 250 mg as needed. Results showed that 60% of those on divalproex found mild to moderate improvement in chronic daily PTH. Further, 19 of 28 participants who had chronic daily headaches reported mild to moderate improvement. Additionally, six participants were headache free after a single month of treatment. The authors suggest that divalproex is effective as it works by activating the inhibitory neurotransmitter γ aminobutryic acid (GABA). The authors noted that although PTHs that persist for more than one year are considered permanent, it is still possible to treat them effectively, allowing the patient to increase their activity level and perhaps reduce their dependence on other analgesics.
Pregabalin and Gabapentin
Pregabalin and gabapentin work by blocking neuronal calcium channels and have become widely used for the treatment of neuropathic pain, in particular, peripheral neuropathic pain. Gabapentin requires a longer time to reach a therapeutic dose compared to pregabalin, which can provide a faster response to pain as it has 90% bioavailability. Furthermore, pregabalin does not appear to have a negative effect on other medications that an individual may be taking (D’Arcy, 2011; Vranken et al., 2011). Gabapentin has been found to be very effective in the treatment of neuropathic pain in the elderly and is considered the first line of defense with this population (Guay, 2003). Again, despite these medications being administered to individuals post TBI, there is limited literature supporting their effectiveness in this population.
In a RCT by Vranken et al. (2008), the effects of pregabalin on pain in those with either an ABI or spinal cord injury were examined. The intervention group received a flexible dose of pregabalin, starting at 150 mg per day. If the pain relief was insufficient, the dose of pregabalin was increased to 300 mg, then 600 mg if needed. The control group received a placebo. Participants were administered the medication or placebo twice a day over the span of four weeks. Results indicate those in the pregabalin group reported a significant decrease in pain intensity, measured by a VAS, compared to the control group (p<0.010). When using the Pain Disability Index, no significant between-group differences were noted at the end of the intervention. Of note, those in the pregabalin group reported few side effects, indicating that the medication was well tolerated (Vranken et al., 2008).
Carbamazepine and Oxcarbazepine
Carbamazepine was once considered the drug of first choice for treating neuropathic pain (Gould, 2007). Despite its success, there has been considerable concern regarding the adverse effects that many individuals experience while on the medication. If administering carbamazepine, the monitoring of such adverse events is strongly recommended (Backonja, 2003). Oxcarbazepine has been found to be effective in the treatment of neuropathic pain and has also been reported to have an improved side effect profile compared to carbamazepine (Nasreddine & Beydoun, 2007). In patients experiencing painful diabetic neuropathy, oxcarbazepine resulted in decreased VAS pain scores; however, changes were not always statistically significant. When administered to patients with the pain of trigeminal neuralgia, oxcarbazepine was found to be effective in reducing pain (Nasreddine & Beydoun, 2007).
Lamotrigine
Lamotrigine, a newer anticonvulsant medication, has also been found to aid in the treatment of neuropathic pain often associated with diabetic neuropathy, spinal cord injury pain, phantom limb pain, postoperative and traumatic neuropathic pain, and cancer related neuropathy (Ettinger & Argoff, 2007; Wiffen et al., 2011).
Topiramate
Topiramate has been found to be successful in treating migraine and cluster headaches
(Ettinger & Argoff, 2007). Although topiramate is believed to be effective in treating pain, it has been noted that any preexisting cognitive impairments (language, attentions, cognitive functioning, or memory) due to the brain injury itself may be exacerbated by topiramate (Tang et al., 2007).
Evidence Table(s)
4.4.4.2 Antidepressants
Amitriptyline
Amitriptyline is often used to treat headaches in those who suffer from migraines and has been found to be very effective in reducing symptoms (Pringsheim et al., 2012). Along with treating migraines, amitriptyline has been used to treat pain in patients since 1964 when its efficacy was first demonstrated (Adelman et al., 2000). In addition, amitriptyline is used to treat pain in those who have suffered a stroke or spinal cord injury, and in those who have been diagnosed with dementia, multiple sclerosis, fibromyalgia, or chronic diabetic peripheral neuropathic pain. The effectiveness of amitriptyline in the treatment of pain post TBI is not well studied.
Venlafaxine
Venlafaxine, a serotonin and norepinephrine reuptake inhibitor, has been shown to be a safe and effective medication in the treatment of depression and anxiety, as well as various pain syndromes including: neuropathic pain, headaches, fibromyalgia, painful peripheral diabetic neuropathy, and post-mastectomy pain (Dharmshaktu et al., 2012). Venlafaxine, amitriptyline, and propranolol are the most prescribed medications in the treatment of migraine-related pain, and chronic tension type headaches (Adelman et al., 2000).
Evidence Table(s)
4.4.4.3 Topical Analgesics
Evidence Table(s)
4.4.4.4 Opioids
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.
4.4.4.5 Cannabinoids
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.
4.5 Conclusions
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 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 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 2 evidence that finger sequencing training may increase performance speed on this task, but not significantly improve error rates 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 dexterity 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 alone 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 2 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 aerobic exercise programs may improve cardiovascular parameters following an ABI.
There is level 4 evidence that physiotherapy may improve motor outcomes such as ambulation, spasticity and gross motor function following an 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 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 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 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 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 2 evidence from a single, small sampled cohort study suggesting that biofeedback is effective in the treatment of post-traumatic headaches; although, the severity of the participants was not clearly stated.
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.
There is level 4 evidence that the number of mindfulness and yoga sessions attended is positively correlated with a perceived reduction in pain and an increase in overall health.
References
Aggarwal, S. K. (2013). Cannabinergic pain medicine: a concise clinical primer and survey of randomized-controlled trial results. Clinical Journal of Pain, 29(2), 162-171.
Arnstein, P. (2004). Chronic neuropathic pain: issues in patient education. Pain Managment Nursing, 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.
Baagoe, S. K., Kofoed-Hansen, M., & Poulsen, I. (2018). Occurrence of dystonia, spasticity and contractures in patients with severe acquired brain injury a prospective cohort study. Neurorehabilitation and Neural Repair, 32 (4-5), 430-431.
Backonja, M. (2003). Anticonvulsants for the treatment of neuropathic pain syndromes. Current Pain and Headache Report, 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. Archives of Physical Medicine and Rehabilitation, 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 Injury, 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. American Journal of Occupational Therapy, 70(3), 7003180010p7003180011-7003180017.
Bhambhani, Y., Rowland, G., & Farag, M. (2005). Effects of circuit training on body composition and peak cardiorespiratory responses in patients with moderate to severe traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 86(2), 268-276.
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. Journal of Head Trauma Rehabilitation, 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. Journal of Head Trauma Rehabilitation, 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. Clinical Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 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 Injury, 1-7.
Chin, L. M., Chan, L., Woolstenhulme, J. G., Christensen, E. J., Shenouda, C. N., & Keyser, R. E. (2015). Improved Cardiorespiratory Fitness With Aerobic Exercise Training in Individuals With Traumatic Brain Injury. Journal of Head Trauma Rehabilitation, 30(6), 382-390.
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. Neurorehabilitation and 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. Archives of Physical Medicine and Rehabilitation, 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.
Combs, M. A., Critchfield, E. A., & Soble, J. R. (2018). Relax while you rehabilitate: A pilot study integrating a novel, yoga-based mindfulness group intervention into a residential military brain injury rehabilitation program. Rehabilitation Psychologyl, 63(2), 182-193.
Conrad, J. S., Mitchell, G. L., & Kulp, M. T. (2016). Vision Therapy for Binocular Dysfunction Post Brain Injury. Optometry and Vision Science.
Corral, L., Javierre, C., Blasi, J., Viscor, G., Ricart, A., & Ventura, J. L. (2014). Combined intermittent hypobaric hypoxia and muscle electro-stimulation: a method to increase circulating progenitor cell concentration? Journal of Translational Medicine, 12(1), 174.
Costigan, M., Scholz, J., & Woolf, C. J. (2009). Neuropathic pain: a maladaptive response of the nervous system to damage. Annual Review of Neuroscience, 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 Neurologica Scandinivica, 105(2), 83-87. 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. Archives of Physical Medicine and Rehabilitation, 86(2), 204-209.
Dharmshaktu, P., Tayal, V., & Kalra, B. S. (2012). Efficacy of antidepressants as analgesics: a review. Journal of Clinical Pharmacology, 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. The 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. Physical Medicine and Rehabilitation, 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 Medicine, 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 Injury, 20(2), 133-141.
Duquette, S. P., & Adkinson, J. M. (2018). Surgical Management of Spasticity of the Forearm and Wrist. Hand Clinics, 34(4), 487-502.
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. Archives of Neurology, 60(11), 1524-1534.
Elkind, A. H. (1989). Headache and head trauma. Clin Journal of Pain, 5(1), 77-87.
Ersek, M., Cherrier, M. M., Overman, S. S., & Irving, G. A. (2004). The cognitive effects of opioids. Pain Managment Nursing, 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. Physical Medicine and Rehabilitation, 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. European Review of Medical Pharmacological Science, 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 Injury, 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. Journal of 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. Journal of the American Medical Directors Association, 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. Archives of Physical Medicine and Rehabilitation, 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. Rehabilitation Psychology, 54(3), 247-258.
Godbout, A. (1997). Structured habituation training for movement provoked vertigo after severe traumatic brain injury: a single-case experiment. Brain Injury, 11(9), 629-641.
Gordon, D. B., & Love, G. (2004). Pharmacologic management of neuropathic pain. Pain Managment Nursing, 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. Journal of Head Trauma Rehabilitation, 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 Supply, 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 Supply, 6, S92-120.
Greenwell, G. T. (2012). Medical marijuana use for chronic pain: risks and benefits. Journal of Pain and Palliative Care Pharmacotherapy, 26(1), 68-69.
Gregory, C. M., & Bickel, C. S. (2005). Recruitment patterns in human skeletal muscle during electrical stimulation. Physical Therapy, 85(4), 358-364.
Grissom, S. P., & Blanton, S. (2001). Treatment of upper motoneuron plantarflexion contractures by using an adjustable ankle-foot orthosis. Archives of Physical Medicine and Rehabilitation, 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. American Journal of Geriatric Pharmacotherapy, 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 Injury, 19(7), 481-491.
Gurr, B., & Moffat, N. (2001). Psychological consequences of vertigo and the effectiveness of vestibular rehabilitation for brain injury patients. Brain Injury, 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 Clinic Proceedings, 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 Regulation, 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. Journal of Rehabilitation Medicine, 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. Journal of Physiotherapy, 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 Injury, 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 Research (Hoboken), 63(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 Injury, 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. Physical Medicine and Rehabilitation, 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. Journal of 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 Journal of Physical Medicine and Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 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. Journal of Head Trauma Rehabilitation, 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. New England Journal of Medicine, 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. Journal of Cognitive Neuroscience, 12(6), 1001-1012.
Kasten, E., Wust, S., Behrens-Baumann, W., & Sabel, B. A. (1998). Computer-based training for the treatment of partial blindness. Natural Medicine, 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. Journal of Hand Surgery of America, 15(2), 340-346.
Khan, M. I., Walsh, D., & Brito-Dellan, N. (2011). Opioid and adjuvant analgesics: compared and contrasted. American Journal of Hospice and Palliative Care, 28(5), 378-383.
Korman, M., Shaklai, S., Cisamariu, K., Gal, C., Maaravi-Hesseg, R., Levy, I., Keren, O., Karni, A., & Sacher, Y. (2018). Atypical within-session motor procedural learning after traumatic brain injury but well-preserved between-session procedural memory consolidation. Frontiers in Human Neuroscience, 12, 14.
Kriz, G., Hermsdorfer, J., Marquardt, C., & Mai, N. (1995). Feedback-based training of grip force control in patients with brain damage. Archives of Physical Medicine and Rehabilitation, 76(7), 653-659.
Lahz, S., & Bryant, R. A. (1996). Incidence of chronic pain following traumatic brain injury. Archives of Phys Medicine and Rehabilitation, 77(9), 889-891.
Lainez, M. J., & Pesquera, B. L. (2011). Headache after trauma: physiological considerations. Current Pain Headache Report, 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. Archives of Physical Medicine and Rehabilitation, 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. Journal of Physiotherapy, 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. American Journal of Physical Medicine and Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 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. Disability and Rehabilitation, 34(23), 1978-1985.
Lucas, S. (2011). Headache management in concussion and mild traumatic brain injury. Physical Medicine and Rehablitation, 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 Supply, 6, S1-13.
Mayer, Esquenazi, A., & Childers, M. K. (1997). Common patterns of clinical motor dysfunction. Muscle Nerve Supply, 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. Archives of Physical Medicine and Rehabilitation, 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. (1999a). Continuously infused intrathecal baclofen for spastic/dystonic hemiplegia: a preliminary report. American Journal of Physical Medicine and Rehabilitation, 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. Journal of Head Trauma Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 77(5), 461-466.
Meythaler, J. M., Guin-Renfroe, S., Grabb, P., & Hadley, M. N. (1999b). Long-term continuously infused intrathecal baclofen for spastic-dystonic hypertonia in traumatic brain injury: 1-year experience. Archives of Physical Medicine and Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 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. Journal of Neurosurgery, 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. Physical Therapy, 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. Physical Therapy, 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. Clinical Rehabilitation, 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). Australian Journal of Physiotherapy, 48(1), 43-49.
Mossberg, K. A., Kuna, S., & Masel, B. (2002). Ambulatory efficiency in persons with acquired brain injury after a rehabilitation intervention. Brain Injury, 16(9), 789-797.
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 Injury, 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 Opinion Investiating 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. American Journal of Occupational Therapy, 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 Injury, 8(2), 125-
133.
Page, S., & Levine, P. (2003). Forced use after TBI: promoting plasticity and function through practice. Brain Injury, 17(8), 675-684.
Pangarkar, S., & Lee, P. C. (2011). Conservative treatment for neck pain: medications, physical therapy, and exercise. Physical Medicine Rehabilitation Clinics North America, 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. Archives of Physical Medicine Rehabilitation, 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. Archives of Physical Medicine Rehabilitation, 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 Injury, 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. Canadian Journal of Neurological Science, 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. American Journal of Physical Medicine Rehabilitation, 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. Physical Therapy, 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. Archives of Physical Medicine and Rehabilitation, 75(7), 746-750.
Seif-Naraghi, A. H., & Herman, R. M. (1999). A novel method for locomotion training. Journal of Head Trauma Rehabilitation, 14(2), 146-162.
Seifert, T. D., & Evans, R. W. (2010). Posttraumatic headache: a review. Current Pain Headache Report, 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. Journal Rehabilitation Research Development, 42(6), 769-778.
Shepard, N. T., & Telian, S. A. (1995). Programmatic vestibular rehabilitation. Otolaryntology: Head Neck Surgery, 112(1), 173-182.
Sherman, K. B., Goldberg, M., & Bell, K. R. (2006). Traumatic brain injury and pain. Physical Medicine Rehabilitation Clinics North America, 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. American Journal of Occupational Therapy, 47(1), 19-24.
Singer, Jegasothy, G. M., Singer, K. P., & Allison, G. T. (2003a). Evaluation of serial casting to correct equinovarus deformity of the ankle after acquired brain injury in adults. Archives of Physical Medicine and Rehabilitation, 84(4), 483-491.
Singer, B. J., Singer, K. P., & Allison, G. T. (2003b). Evaluation of extensibility, passive torque and stretch reflex responses in triceps surae muscles following serial casting to correct spastic equinovarus deformity. Brain Injury, 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. Archives of Physical Medicine and Rehabilitation, 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. Archives of Physical Medicine and Rehabilitation, 95(6), 1100-1105.
Tang, V., Warden, J., Cullen, N., & Rutledge, E. (2007). Topiramate in traumatic brain injury: adverse effects on cognitive function. Journal of Head Trauma Rehabilitation, 22(6), 409-410.
Tatrow, K., Blanchard, E. B., & Silverman, D. J. (2003). Posttraumatic headache: an exploratory treatment study. Applied Psychophysiological 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. Current Treatment Options Neurology, 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 Injury, 29(7-8), 830-836.
Thibaut, A., Wannez, S., Deltombe, T., Martens, G., Laureys, S., & Chatelle, C. (2018). Physical therapy in patients with disorders of consciousness: Impact on spasticity and muscle contracture. NeuroRehabilitation, 42(2), 199-205.
Uomoto, J. M., & Esselman, P. C. (1993). Traumatic brain injury and chronic pain: differential types and rates by head injury severity. Archives of Physical Medicine and Rehabilitation, 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. Physiotherapy Theory Practice, 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. Clinical Rehabilitation, 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 Medical Journal, 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. Canadian Medical Association Journal, 182(14), E694-701.
Waszkielewicz, A. M., Gunia, A., Sloczynska, K., & Marona, H. (2011). Evaluation of anticonvulsants for possible use in neuropathic pain. Current Medicinal Chemistry, 18(28), 4344-4358.
Watanabe, T. K., Bell, K. R., Walker, W. C., & Schomer, K. (2012). Systematic review of interventions for post-traumatic headache. Physical Medicine and Rehabilitation, 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 Systematic Review (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. American Journal of Physical Medicine and Rehabilitation, 85(1), 68-74.
Wong, V., Cheuk, D. K., Lee, S., & Chu, V. (2012). Accupouncture for acute management and rehabilitation of traumatic brain injury. European Journal of Physical Rehabilitation Medicine, 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. Clinical Orthopedics and Related Research (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.