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 improves fine motor function post ABI.
Virtual reality interventions may be an effective intervention for the recovery of upper extremity function post ABI.
Partial body weight supported gait training likely does not improve ambulation, mobility, or balance when compared to conventional gait training post ABI.
Robotic assisted treadmill training may be similar to manually assisted treadmill training at improving gait speed and mobility post ABI.
Electrical muscle stimulation with passive exercise may improve lower extremity muscle atrophy post ABI.
Sit-to-stand training and Intensive Mobility Training may improve lower extremity motor function post ABI.
Virtual reality can be used for the remediation of motor function in the lower extremities post-ABI.
Virtual reality training likely improves balance in individuals post ABI, however it may not be more effective than conventional physiotherapy programs.
Aerobic exercise programs, whether home-based or in the community, appear to improve motor function and balance post-ABI
Further research is needed in order to determine which components of exercise are the most effective for motor rehabilitation post-ABI.
Botulinum toxin type A injections, whether through a single point or multisite, likely reduce localized spasticity following ABI.
Phenol blocks of the musculocutaneous nerve may help decrease spasticity and improve range of motion temporarily up to five months post injection in individuals with ABI.
Electrical stimulation may acutely (24 hours) decrease spasticity in patients post ABI.
Oral baclofen appears to reduce lower extremity, but not upper extremity, spasticity in individuals with an ABI.
Bolus injections of intrathecal baclofen likely produce short-term reductions in upper and lower extremity spasticity and improvements in walking performance post ABI.
Prolonged intrathecal baclofen may reduce upper and lower extremity spasticity long-term post ABI.
Serial casting likely improves contractures and spasticity in individuals with an ABI compared to stretching; however, contracture improvement may not be maintained long-term.
Below-knee casting and stretching might increase passive ankle dorsiflexion in patients post ABI.
Serial below-knee casting may improve ankle range of motion and muscle extensibility in patients post TBI; however, this intervention may be associated with tissue breakdown.
Serial casting, whether for a short or long duration, might improve range of motion in individuals with an ABI. However, short duration casting may have a lower complication rate than long duration.
Hand splinting combined with stretching may be an effective treatment for spasticity and range of motion.
Botulinum toxin injections in combination with casting may be as effective as casting alone at reducing leg spasticity in patients post ABI.
Electrical stimulation in combination with tilt table standing and splinting may acutely improve spasticity (6 weeks) in patients post ABI.
Neural tension technique may be just as effective as random passive movement for improving lower extremity spasticity post ABI.
Computer based restitution training and rehabilitation programs directed at improving visual function likely improve the vision of those who sustain a TBI.
Base-in prisms and bi-nasal occluders may be effective in treating ambient vision disturbances.
Saccadic oculomotor rehabilitation may improve eye movements and reading in patients post ABI.
Combined aerobic dance and slide and step programs may improve balance and coordination post TBI.
A vestibular rehabilitation program may improve symptoms of vertigo in patients following TBI.
Cognitive behavioural therapy may be useful in managing post-traumatic headaches; however, may not be useful for headache-associated pain.
Cold therapy is likely not as effective as manual therapy at reducing post traumatic headache pain in patients post TBI.
Introduction
The primary cause of motor impairment and movement dysfunction post acquired brain injury(ABI) is upper motor neuron syndrome (UMNS), which can result in positive symptoms of enhanced stretch reflexes (spasticity) and released flexor reflexes in the lower limbs, such as the Babinski sign and mass synergy patterns, as well as negative symptoms including loss of dexterity and weakness (Mayer, 1997). These symptoms of UMNS have physiological implications for muscles that may subsequently develop stiffness and contractures, thereby further negatively affecting effective movement (Mayer, 1997).
For UMNS following brain injury, both the extent and timing of the individual’s symptoms should be considered when deciding on a course of action. Focal or diffuse spasticity may appear following an ABI and frequently follow common patterns in the upper and lower limbs (Mayer, 1997). Time post injury is another important consideration as spontaneous neurological recovery may continue for 9 to 15 months post injury. However, the potential for functional motor recovery beyond that point is possible through medical interventions, such as the correction of a deformity or the use of pharmacological agents that allow for improved motor control (Mayer et al., 1996). Motor impairment can also result from the independent effects of prolonged immobilization and bed rest during the acute period. Prolonged immobility affects multiple body systems, although it is the direct effect on the musculoskeletal and cardiovascular systems that impact motor function the most (Bushbacher & Porter, 2000).
Following diffuse central nervous system injury there are potential impairments involving the cognitive, behavioural, and physical domains. It is the physical domain that is emphasized early on within the rehabilitation process, as most acute in-patient rehabilitation programs focus on the improvement of activities of daily living (ADLs) a patient can perform— as assessed by outcome measures such as the Functional Independence Measure or the Barthel Index (Linacre et al., 1994; McDowell, 2006). The emphasis on physical impairments during rehabilitation is common because both the patient and family members are more likely to recognize and acknowledge physical impairments, in contrast to cognitive and behavioural impairments.
This module reviews the available evidence pertaining to interventions for motor and sensory rehabilitation following ABI.
4.2 Motor Impairment
Motor rehabilitation is a common focus of interventions provided to an individual post ABI. Motor rehabilitation is essential in helping the patient return to performing their ADLs, thus reestablishing independence post ABI. The following sections evaluate the interventions currently available for upper and lower extremity motor impairment, including spasticity.
4.2.1 Upper Extremity Interventions
Upper limb motor impairments are common in individuals with an ABI (Lannin et al. 2003). Interventions for the upper limb can focus broadly on arm mobility or on more specific outcomes such as finger dexterity. Despite the importance of upper extremity rehabilitation post ABI, there are limited studies evaluating available interventions.
4.2.1.1 Constraint Induced Movement Therapy
Key Points
Constraint induced movement therapy may improve function and use of the affected upper limb post ABI.
Constraint induced movement therapy (CIMT) is an intervention directed at improving the function of the more affected upper extremity following brain injury. The two primary components involve: 1) intensive motor training of the more affected upper extremity and 2) motor restriction of the less affected upper extremity (Dettmers et al., 2005). CIMT originated from research suggesting that the affected limb post brain injury is negatively impacted by “learned non-use” due to increased dependence on the intact limb (Grotta et al., 2004).
Although there is evidence in the stroke population to suggest that CIMT is clinically effective, many patients do not qualify for this type of therapy, which requires voluntary extension of the wrist and fingers, due to limited movement in the affected upper extremity. A further significant limitation of CIMT is the amount of resources required for its implementation (Grotta et al., 2004). Two studies evaluating the effect of CIMT post traumatic brain injury (TBI) were identified (Table 4.1).
Evidence Table(s)
Discussion
Conclusions
4.2.1.2 Hand Splinting and Stretching
Key Points
Soft hand splinting, but not manual therapy, may be beneficial for improving hand opening post ABI.
Evidence Table(s)
Discussion
Conclusions
There is level 4 evidence that soft hand splinting, but not manual therapy, may improve hand opening in individuals post ABI.
4.2.1.3 Interventions for Fine Motor Coordination
Key Points
Gesture recognition biofeedback and visual feedback-based training may improves fine motor function post ABI.
Evidence Table(s)
Discussion
The most recent fine motor coordination study compared the use of gesture recognition biofeedback to standard repetitive training without feedback (Yungher & Craelius, 2012). The results from the study showed a significant decrease in task completion time for those who received feedback, in comparison to those who did not. This intervention is both simple to execute (e.g., no precise placement of sensors, etc.) and the assessment is straightforward. The authors suggest that this intervention leads to improvements in fine motor function of the hand with minimal supervision (Yungher & Craelius, 2012). Despite these studies, there is limited evidence to guide clinical practice in this area.
Conclusions
There is level 4 evidence that visual feedback-based grip force training may improve tracking accuracy and transfer tasks in individuals post ABI.
There is level 2 evidence that gesture recognition biofeedback may improve fine motor function compared to standard repetitive training without feedback in individuals post ABI.
4.2.1.4 Virtual Reality for Upper Extremity Rehabilitation
Key Points
Evidence Table(s)
Discussion
Sietsema et al. (1993) reported that individuals who used a computer-controlled game aimed at improving reaching had better range of motion in the hip and wrist than individuals who completed rote exercise. Despite the study being performed in 1993, the game used by Sietsema et al. (1993) is still available for use.
Conclusions
4.2.2 Lower Extremity Interventions
4.2.2.1 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.
4.2.2.2 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.
4.2.2.3 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.
4.2.3 Combined Upper and Lower Extremity Interventions
4.2.3.1 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.
4.2.4 Exercise Programs
4.2.4.1 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 s participation in group exercise post ABI as it can foster feelings of well-being and self-esteem which could have a positive impact upon other rehabilitation strategies (Driver et al., 2006).
Bateman et al. (2001) compared cycling training (experimental group) to relaxation training (control group) and found that cycling training was associated with a significant improvement in exercise capacity; however, there was no significant difference between the groups in regards to balance, mobility, and functional independence (Bateman et al., 2001). This suggests that although exercise programs may improve physical fitness, gains in functional status often occur independently of aerobic exercise training (Bateman et al., 2001).
Hassett et al.(2012) examined the benefits of circuit training with encouragement from a physiotherapist and heart rate monitor feedback in individuals with severe TBI. More specifically, the intervention group had their heart rate monitor uncovered and it beeped when they did not reach their target heart rate, whereas the control group had their monitors covered and muted.
Results indicate there was no significant difference between the two groups in terms of the amount of time spent in the heart rate target zone. Earlier Hassett et al. (2009) found individuals assigned to exercise programs showed significant improvement in their cardiorespiratory levels regardless of where they worked out (in a gym or at home) or how often (2.4 sessions per week versus 0.5 sessions per week). However, adherence to the program was higher among those attending a fitness center. When compliance was explored further, those with greater adhered were found to be older, more severely injured and had exercised before the injury (Hassett et al., 2011).
Hoffman et al. (2010) compared individuals who exercised in a community-based program to individuals who did not participate in this program; however, the controls were able to exercise on their own. Although the intervention group was working out more days per week than controls, the total amount of time spent exercising per week was similar between groups, making comparisons challenging. When those who were active (more than 90 minutes of activity per week) were compared to those who were not as active, the authors found that mood was significantly higher in the participants who were exercising for more than 90 minutes each week, regardless of what treatment group they were originally placed in. Thus, any physical exercise is beneficial to patients post ABI. Furthermore, home-based exercise programs have shown to improve depressive symptoms, stability, and gait following intervention (Bellon et al., 2015). It is important to note that lower stability and dual-tasking scores were associated with poorer mental health outcomes (Damiano et al. 2016).
Conclusions
There is level 2 evidence that aerobic training compared to vocational rehabilitation may be more effective at improving co-ordination, strength, flexibility, and endurance in individuals post-ABI.
There is level 1b evidence that exercise programs may improve FIM scores, but not balance or mobility compared to relaxation training in individuals post-ABI.
There is level 4 evidence that multimodal exercise programs may improve gait and mobility in individuals post-ABI.
There is level 3 evidence that a home-based exercise program may improve stability to the level of healthy controls, but may not improve motor control, mobility, or dual-task performance in individuals post-ABI.
There is level 2 evidence that aerobic dance training compared to musculature training may improve sensory interaction and balance post-ABI.
4.2.5 Spasticity Interventions
Management of spasticity is not unique to brain injury survivors, since it is often associated with other conditions affecting the central nervous system such as spinal cord injury and multiple sclerosis. Spasticity may require intervention when it interferes with functional abilities such as mobility, positioning, hygiene, or when it is the cause of deformity or pain. Factors that must be taken into consideration when proposing treatment of spasticity include chronicity of the problem, the severity, the pattern of distribution (focal versus diffuse), the locus of injury, as well as comorbidities (Gormley et al., 1997). Some studies have found that spasticity of cerebral origin versus spinal cord injury respond differently to the same medications (Katz & Campagnolo, 1993). Typically, the clinical approach to spasticity is to first employ treatments that tend to be less interventional and costly; however, multiple strategies may need to be administered concurrently.
4.2.5.1 Botulinum Toxin Injections
Key Points
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.
4.2.5.2 Nerve Blocking Agents
Key Points
Discussion
Conclusions
4.2.5.3 Electrical Stimulation
Key Points
Discussion
Conclusions
4.2.5.4 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
4.2.5.5 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.
4.2.5.6 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.
Casting has been thought to reduce hypertonia and spasticity in individuals with an ABI. This is believed to be the result of reducing contractures by stretching the muscles of the immobilized limb (Pohl et al. 2002). Serial casting is a process in which the angle of the cast is changed periodically, with the objective of returning the joint to its original angle. However, despite the fact that serial casting has been utilized by physiotherapists for more than 40 years there is little empirical data to support its use in isolation. Conversely, evidence exists supporting the use of casting as a useful adjunct to other therapies for the management of spasticity and contracture in patients post TBI.
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. (2003) and Singer et al. (2003) also evaluated the efficacy of weekly casting and found casting to be effective in improving ankle movement. In addition, greater ankle mobility was shown to be associated with improved transfer independence (Singer et al., 2003). It should be noted, however, that casting can lead to tissue breakdown (Singer et al. 2003).
In a retrospective case comparison study, Pohl et al. (2002) compared short, one to four days casting to a longer duration, five to seven days casting, for both upper and lower extremity joints. Although improvements in range of motion were seen in each group immediately following the intervention and at a one-month follow-up, there was no significant difference found between groups. However, the discontinuation rate in the longer duration group due to complications was significantly higher than for the short casting interval group.
Conclusions
There is level 1b evidence that serial casting may be superior to passive stretching at improving spasticity of the elbow in individuals post ABI.
There is level 2 evidence that a below-knee casting and stretching protocol may increase passive ankle dorsiflexion in patients post ABI.
There is level 4 evidence that weekly below-knee casts may improve ankle range of motion, muscle extensibility, and passive torque in patients post ABI.
There is level 3 evidence that short duration (one to four days) and longer duration (five to seven days) serial casting may have similar effects on upper or lower extremity range of motion in individuals post ABI.
4.2.5.7 Adjustable Orthosis
4.2.5.8 Hand Splinting and Stretching
Key Points
Discussion
Conclusions
4.2.5.9 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.
4.3 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.
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). Recently, Conrad et al. (2016) studied a home-based computer vergence therapy program used to improve binocular visual dysfunction after ABI. Participants underwent home-based visual vergence therapy five days a week for 12 weeks. Negative vergence, positive vergence, near point convergence and vergence facility all showed significant improvements over the 12 week intervention period (Conrad et al., 2016).
When the reading dysfunction post ABI is a result of sensory-based hemifield deficits or neuromotor deficits, saccadic occulomotor rehabilitation can lead to improvements in eye movements which are required for accurate reading (Ciuffreda et al., 2006). Repetitive occulomotor conditioning reduces the cognitive and attentional load of reading and results in a structural and systematic approach to reading. The benefits of occulomotor rehabilitation were observed in other activities of daily living such as concentration and visual scanning. Most importantly, reducing visual deficits in patients post TBI may facilitate their involvement in other therapies and contribute to overall recovery (Ciuffreda et al., 2006).
Conclusions
There is level 2 evidence that saccade visual tracking compared to fixation and pursuit tracking may improve single-line and multi-line reading post ABI.
There is level 4 evidence showing that base-in prisms and bi-nasal occluders can be effective in treating ambient vision disturbances resulting from an ABI.
There is level 4 evidence that prismatic spectacle lenses may be effective in reducing symptom burden in patients with vertical heterophoria and post-concussive symptoms post injury.
There is level 4 evidence that rehabilitation programs directed at improving visual function can improve functional outcomes such as reading in patients post ABI.
4.4 Vestibular Dysfunction
Key Points
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). Current literature includes a variety of interventions for vestibular rehabilitation (Table 4.18).
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.
4.5 Pain Post TBI
Until very recently, there has been very little information in the literature regarding the prevalence, etiology, assessment, and treatment of pain post TBI (Zasler et al., 2011). This may be the result of pain syndromes being overlooked in patients with a TBI for a number of reasons (Gellman et al., 1996). Multiple etiologies including orthopedic injuries, burns, organ injuries, or central or peripheral nervous system injuries can result in acute or chronic pain in those recovering from a TBI (Ivanhoe & Hartman, 2004). A lack of recognition or diagnosis of pain can lead to an increase in aggression and agitation, or an inability to participate or benefit from rehabilitation (Ivanhoe & Hartman, 2004; Sherman et al., 2006). In individuals who have sustained a moderate or severe TBI, the diagnosis of pain is often made through the combination of symptoms described by the patient and information provided by family members. Pain post TBI can evolve from episodic pain to daily pain with an increasing negative impact over time; pain ultimately impacts participation in rehabilitation and thereby slows recovery (Branca & Lake, 2004).
Pain is believed to be more common immediately post injury (acute pain) and it is widely accepted that this pain will resolve as the damaged tissue recovers (Uomoto & Esselman, 1993). The focus is on management of symptoms over a relatively short defined period of time and on assisting the healing of damaged structures. Chronic pain by its very nature may not resolve, or is very slow to resolve, and often manifests itself as post traumatic headaches (PTH), neck and shoulder pain, back pain, peripheral nerve injury, heterotopic ossification, and pain related to spasticity (Hoffman et al., 2007; Lahz & Bryant, 1996; Ofek & Defrin, 2007). In a study conducted by Lahz and Bryant (1996), chronic pain was reported by 52% of those who were diagnosed with a moderate to severe TBI and 58% of those diagnosed with a mild TBI. Of those reporting pain, over 80% reported experiencing pain on a daily basis (Lahz & Bryant, 1996). Comparable rates were given by Hoffman et al. (2007) who examined a bodily pain scale one year post TBI. Of the 146 individuals who participated, 74% of participants reported experiencing pain and 55% of those reported that pain interfered with a variety of daily activities. Higher rates of pain were also related to gender, lower Functional Independence Measure scores, higher rates of depressive symptoms at baseline and again at one year post injury, and lower scores on the Community Integration Scale. Those who were injured in acts of violence reported experiencing greater pain (Hoffman et al., 2007). Pain is significantly associated with depression, with one study reporting rates of pain and depression as 70% and 31%, respectively and 34% and 22%, respectively at one year follow-up (Sullivan-Singh et al., 2014). Pain related to orthopedic injuries, spasticity, or heterotopic ossification will not be covered in this section. For a more detailed discussion on spasticity and treatments post ABI please see section 4.2.5 in this module and a detailed discussion on heterotopic ossification post ABI is available in Module 11. Due to the complexities of pain, we have decided to focus on pain post TBI specifically. The diagnosis of pain post TBI is an important part of an individual’s recovery.
Problems associated with pain include a delay in cognitive recovery, sleep disorders, fatigue, elevated levels of anxiety, depression, and post-traumatic stress disorder (Dobscha et al., 2009; Hoffman et al., 2007). Cognitive deficits associated with TBI may prevent individuals from using adaptive pain coping strategies that are critical to the management of chronic pain. When treating pain post TBI, it is important for clinicians to identify the causes of pain, not just the symptoms (Zasler et al., 2011). To reduce the impact on cognitive recovery, treatment plans should take into consideration the medications the patient is already receiving, as well as the location, type, and frequency of the pain. It should be acknowledged that in many cases the pain generator persists in which case pain can only be managed. Treatment for pain often involves an interdisciplinary approach (Branca & Lake, 2004). To increase the likelihood of compliance with treatments, a good working relationship between physicians and the patient is needed. Overall, more research is needed to assess the effectiveness and efficacy of these treatments in the TBI population. For a summary of these findings please see Figure 1.
4.5.1 Assessing Pain Post TBI
4.5.1.1 Visual Analog Scale
4.5.1.2 Numeric Rating Scale
4.5.1.3 McGill Pain Questionnaire
4.5.1.4 Headache Disability Inventory
4.5.1.5 Headache Diary
4.5.2 Pain Syndromes Post ABI
4.5.2.1 Neuropathic Pain
4.5.2.2 Central Pain Syndromes
4.5.2.3 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 4.5.3.1), Cognitive Behavioural Theory (section 4.5.3.2), Manual Therapy (section 4.5.3.4), and Cryotherapy and Thermotherapy (section 4.5.3.6).
4.5.3 Non-Pharmacological Interventions for Pain and Post Traumatic Headache
Non-pharmacological interventions for both chronic pain and PTH may include: biofeedback, cold and heat packs, massage therapy, acupuncture, and exercise (Medina, 1992). Biofeedback, relaxation, meditation, and CBT are considered the gold standard of behavioural treatments for pain (Branca & Lake, 2004). In a recent review of manual treatments for migraines, massage therapy, physiotherapy, relaxation, and chiropractic spinal manipulative therapy were found to be just as effective as propranolol and topiramate at reducing symptoms (Cassidy et al., 2014). Physiotherapy exercises have also been suggested to treat pain; however, unless the pain is controlled, caution is recommended when using these exercises to prevent aggravating the painful structures further (Medina, 1992). Lifestyle changes are also suggested to prevent the onset of PTH, such as getting enough sleep and daily exercise.
4.5.3.1 Biofeedback to Manage Post Traumatic Headache
In a study by Tatrow et al. (2003), PTHs were targeted for six weeks in 14 mild TBI individuals . The first four sessions consisted of progressive muscle relaxation, with biofeedback (thermal and EMG) being introduced in the fifth session. Participants learned to relax and control muscle tension, and relaxation ratings were on average 8.6 out of 10. Improvements in PTH were shown for most participants and the treatment also lowered post-concussion syndrome checklist scores significantly in the treatment group (Tatrow et al., 2003).
4.5.3.2 Cognitive Behavioural Therapy
Key Points
Evidence Table(s)
Discussion
Conclusions
4.5.3.3 Relaxation Training
4.5.3.4 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.
4.5.3.5 Acupuncture
4.5.3.6 Cryotherapy and Thermotherapy
Key Points
Evidence Table(s)
Discussion
Conclusions
4.5.4 Pharmacological Management of Pain and Post Traumatic Headache
4.5.4.1 Anticonvulsants
Evidence Table(s)
4.5.4.2 Antidepressants
Evidence Table(s)
4.5.4.3 Topical Analgesics
Evidence Table(s)
4.5.4.4 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.
4.5.4.5 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.
4.6 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 4 evidence that soft hand splinting, but not manual therapy, may improve hand opening in individuals post ABI.
There is level 2 evidence that functional retraining activities may be more effective than tabletop fine motor control retraining activities for improving fine motor function in the dominant hand in individuals post ABI.
There is level 4 evidence that visual feedback-based grip force training may improve tracking accuracy and transfer tasks in individuals post ABI.
There is level 2 evidence that gesture recognition biofeedback may improve fine motor function compared to standard repetitive training without feedback in individuals post ABI.
There is level 2 evidence that virtual reality training may improve neurobehavioral functioning as well as reaching accuracy and movements post-ABI.
There is level 2 evidence that body weight supported treadmill training may not improve ambulation or mobility compared to conventional gait training in individuals post ABI.
There is level 1b evidence that physical therapy with partial weight-bearing gait training may not improve ambulation, mobility, or balance compared to standard physical therapy in individuals post ABI.
There is level 2 evidence that robotic assisted body weight supported treadmill training may not improve ambulation or gait velocity compared to manually assisted treadmill training in individuals post ABI.
There is level 1b evidence that sit-to-stand training combined with usual rehabilitation may improve motor performance in sit-to-stand tasks compared to usual rehabilitation in individuals post ABI.
There is level 2 evidence that electrical muscle stimulation with passive exercise may reduce lower extremity muscle atrophy compared to passive exercise in individuals post ABI.
There is level 4 evidence that Intensive Mobility Training may improve ambulation and mobility in individuals post ABI.
There is level 1b evidence that virtual reality training compared to balance training may not be more effective for improving lower extremity function post-ABI. However, virtual reality training was shown to improve function independently.
There is level 4 evidence that visual feedback may reduce weight-bearing asymmetry in the lower extremities post-ABI.
There is level 1b evidence that virtual reality-based training may not improve balance and gait compared to standard physical therapy in individuals post ABI.
There is level 4 evidence that virtual reality therapy may improve balance, gait, and functional reaching in individuals post ABI.
There is level 1b evidence that participating in an exercise program at a fitness-center compared to home-based exercise program may lead to greater program adherence but not significantly different motor results in individuals post-ABI.
There is level 2 evidence that aerobic training compared to vocational rehabilitation may be more effective at improving co-ordination, strength, flexibility, and endurance in individuals post-ABI.
There is level 1b evidence that exercise programs may improve FIM scores, but not balance or mobility compared to relaxation training in individuals post-ABI.
There is level 4 evidence that multimodal exercise programs may improve gait and mobility in individuals post-ABI.
There is level 3 evidence that a home-based exercise program may improve stability to the level of healthy controls, but may not improve motor control, mobility, or dual-task performance in individuals post-ABI.
There is level 2 evidence that aerobic dance training compared to musculature training may improve sensory interaction and balance post-ABI.
There is level 4 evidence that botulinum toxin type A injections may be effective in the management of localized spasticity following ABI.
There is level 1b evidence that receiving botulinum toxin type A through a single motor point or multisite distributed injections are similar at reducing spasticity in individuals with an ABI.
There is level 4 evidence that phenol nerve blocks may reduce contractures and spasticity at the elbow, wrist, and finger flexors for up to five months post injection in individuals post ABI.
There is level 4 evidence that electrical stimulation may be effective for decreasing lower extremity spasticity for six or more hours, lasting up to 24 hours, in individuals post ABI.
There is level 4 evidence that oral baclofen may improve lower extremity spasticity, but not upper extremity spasticity, in individuals post ABI.
There is level 1b evidence that bolus intrathecal baclofen injections may produce short-term (up to six hours) reductions in upper and lower extremity spasticity compared to placebo following ABI.
There is level 4 evidence to suggest that prolonged intrathecal baclofen may result in longer-term (three months, and one year) reductions in spasticity in both the upper and lower extremities following an ABI.
There is conflicting level 4 evidence to suggest that intrathecal baclofen may result in short-term improvement of walking performance in ambulatory patients, particularly gait velocity, stride length, and step width, in individuals post ABI.
There is level 1b evidence that serial casting may improve contractures of the elbow initially, but not long-term, when compared to passive stretching in individuals with an ABI.
There is level 1b evidence that serial casting may be superior to passive stretching at improving spasticity of the elbow in individuals post ABI.
There is level 2 evidence that a below-knee casting and stretching protocol may increase passive ankle dorsiflexion in patients post ABI.
There is level 4 evidence that weekly below-knee casts may improve ankle range of motion, muscle extensibility, and passive torque in patients post ABI.
There is level 3 evidence that short duration (one to four days) and longer duration (five to seven days) serial casting may have similar effects on upper or lower extremity range of motion in individuals post ABI.
There is level 1b evidence that nocturnal hand splinting may not improve upper extremity range of motion or function compared to standard care in individuals post ABI.
There is level 1b evidence that electrical stimulation in combination with tilt table standing and splinting may decrease spasticity at 6 weeks post intervention compared to tilt table standing alone in patients with an ABI.
There is level 2 evidence that botulinum toxin combined with casting may not be more effective than botulinum toxin injections alone in improving leg spasticity in individuals with an ABI.
There is level 1b evidence that neural tension technique may not be more effective than random passive movement in improving lower extremity spasticity and range of motion in individuals with an ABI.
There is level 1b evidence that computer-based restitution training may be effective in improving the vision of those who sustain a TBI compared to visual fixation training.
There is level 2 evidence that saccade visual tracking compared to fixation and pursuit tracking may improve single-line and multi-line reading post ABI.
There is level 4 evidence showing that base-in prisms and bi-nasal occluders can be effective in treating ambient vision disturbances resulting from an ABI.
There is level 4 evidence that prismatic spectacle lenses may be effective in reducing symptom burden in patients with vertical heterophoria and post-concussive symptoms post injury.
There is level 4 evidence that rehabilitation programs directed at improving visual function can improve functional outcomes such as reading in patients post ABI.
There is level 4 evidence that vestibular rehabilitation programs, such as a behavioural exposure program, may improve symptoms of vertigo in patients after TBI.
There is level 2 evidence that vestibular rehabilitation programs, alone or in combination with betahistine dihydrochloride, can improve recovery time for balance disorders in individuals with an ABI compared to betahistine dihydrochloride alone.
There is level 2 evidence to that using a combined aerobic dancing and slide and step training program may reduce balance and coordination deficits post TBI.
There is level 4 evidence that cognitive behavioural therapy may improve post traumatic headache intensity and frequency but not pain, in those who have sustained a mild to severe TBI.
There is level 2 evidence that cold therapy may not be as effective as manual therapy for reducing post traumatic headache pain in individuals post ABI.
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