Statement of the Rehabilitation Medicine Society of Australia and New Zealand for the therapeutic use of botulinum toxin A in spasticity management.

The Rehabilitation Medicine Society of Australia and New Zealand advocates the safe, effective and evidence-based use of botulinum toxin type A for spasticity management. The process requires appropriate training, alongside considerable knowledge and skills, to maximise efficacy. The processes before and after injection contribute to effectiveness. The gold standard of managing spasticity is for assessment by a multidisciplinary specialist team, deriving patient-centric goals, and designing an injection protocol to match these goals. The patient and/or carers are considered part of the decision-making team. Postinjection therapy and measurement of goal achievement are highly recommended as part of the wider holistic approach to management. The Society believes treatment failures can be minimised by following clear clinical guidelines.

Investigating Inducible Muscle Overactivity in Acquired Brain Injury and the Impact of Botulinum Toxin A.

OBJECTIVE: To investigate the pattern of change in muscle overactivity during repetitive grasp/release using dynamic computerized dynamometry (DCD; objective 1) and the effect of botulinum toxin A (BTX-A; objective 2). DESIGN: Secondary analysis of an observational cohort study. SETTING: Hospital outpatient spasticity management service. PARTICIPANTS: A convenience sample (N=65), comprising adults with upper motor neuron syndrome affecting the arm after acquired brain injury (ABI; n=38) and participants without ABI (n=27). INTERVENTIONS: After clinical assessment, a subgroup of participants with ABI (n=28) underwent BTX-A injections as part of their spasticity management. MAIN OUTCOME MEASURES: Post hoc DCD data processing extracted the values of minimum force generation between 10 sequential contractions. The pattern of change was analyzed. RESULTS: The ABI injected group exerted greater force at baseline than both other groups (ABI injected=1.04 kg, ABI noninjected=0.74 kg, participants without ABI=0.53 kg; P=.011). After the first contraction, minimum force values increased for all groups and were greatest in the ABI injected group. With subsequent cycles, the group without ABI showed a linear pattern of decreasing force generation, whereas both ABI groups showed a quadratic increasing pattern, which was of greater magnitude in the ABI injected group. After injection, values for the ABI injected group showed a 51% reduction in inducible muscle overactivity (P=.003) to magnitudes similar to those of the ABI noninjected group. CONCLUSIONS: This study showed that hand relaxation deteriorated during repetitive movements in people with spasticity, a feature hypothesized to adversely influence everyday hand function. After BTX-A injection, the magnitude but not the pattern of this inducible muscle overactivity improved.

Altered sexual function after central neurological system trauma is reflective of region of injury; brain vs spinal cord.

OBJECTIVE: To compare and contrast the contributory effects of traumatic brain injury (TBI) and spinal cord injury (SCI) on sexual function and social relationship opportunities, hypothesizing that patterns of change in sexual function would follow etiology. DESIGN: Cross-sectional, case-matched survey of community living individuals with TBI, SCI or both (termed dual diagnosis). PARTICIPANTS: Consecutive sample of participants with TBI (n = 25), SCI (n = 24) and dual diagnosis (n = 28), an average 3.6 years post-rehabilitation discharge. METHODS: Participants were interviewed using a modified version of the 'Sexuality after Spinal Injury Questionnaire.' RESULTS: Almost all respondents (97%) perceived adverse post-injury change in their experience of neurosexual function and/or social relationships. Physiological aspects of sexual function (e.g., erection, orgasm) were most affected by SCI whereas social relationships appeared more affected by TBI. People with dual diagnoses exhibited a combination of features. Participants with SCI (with or without TBI) were significantly more likely to have their concerns about sexual function discussed during rehabilitation than the TBI group. CONCLUSION: TBI and SCI produce predictable impacts upon sexual function following injury, the impact of which were less frequently addressed during inpatient rehabilitation for those with TBI.

External causes of death after severe traumatic brain injury in a multicentre inception cohort: clinical description and risk factors.

Objective: To characterize the clinical profile of patients dying from external causes (EC) following severe traumatic brain injury (TBI). Design and Methods: Data from 2545 patients forming the NSW-BIRP inception cohort discharged from post-acute inpatient rehabilitation between 1 July 1990 and 1 October 2007 were retrospectively reviewed. Standardized mortality ratios (SMRs) were calculated for EC sub-categories. Demographic, clinical and rehabilitation service factors were compared between deaths from EC, deaths from other causes (OC), and non-deceased. Clinical profiles of EC sub-categories were analysed descriptively. Results: Overall, patients with TBI were 5.2x more likely to die from EC relative to the general population. Risk of death was elevated in all EC sub-categories examined, with the largest risks relating to other accidental threats to breathing (SMR = 33.0; 95%CI = 13.79-60.45) and falls (SMR = 14.3; 95%CI = 5.01-28.39). The EC group were younger, more likely to have pre-injury psychiatric histories, less severe injuries, greater functional independence, and die earlier than the OC group. There was considerable heterogeneity in the clinical profiles of patients dying from different EC sub-categories. Conclusions: EC constitutes one of the largest causes of mortality following TBI in patients surviving beyond the post-acute phase. Potential implications for risk modification and prevention of premature and avoidable deaths are discussed.

Cost Effectiveness of Long-Term Incobotulinumtoxin-A Treatment in the Management of Post-stroke Spasticity of the Upper Limb from the Australian Payer Perspective.

BACKGROUND: In Australia, the reimbursement of botulinum neurotoxin-A (BoNT-A) on the Pharmaceutical Benefits Scheme for the treatment of moderate to severe spasticity of the upper limb following a stroke (PSS-UL) is restricted to four treatment cycles per upper limb per lifetime. This analysis examined the cost effectiveness of extending the treatment beyond four treatments among patients with an adequate response to previous treatment cycles. METHODS: A Markov state transition model was developed to perform a cost-utility analysis of extending the use of incobotulinumtoxin-A beyond the current restriction of four treatment cycles among patients who have shown a successful response in previous treatment cycles ('known responders'). The Markov model followed patients in 12-weekly cycles for 5 years, estimating the proportion of patients with or without response over this period in each of the modelled treatment arms. Post hoc analysis of an open-label extension phase study informed the Markov model. The perspective of the analysis was the Australian healthcare system, meaning only direct healthcare costs were included. Utility values by response status were derived from EQ-5D data from a published double-blind, placebo-controlled study. The primary outcome measure was the incremental cost per quality-adjusted life-year (QALY). Univariate and probabilistic sensitivity analyses were conducted. RESULTS: The open-label extension study data demonstrated the probability of treatment response after four injections was greater among 'known responders' than those without prior response. The incremental cost per QALY gained of continued use of incobotulinumtoxin-A beyond the current restriction of four treatments was A$59,911. CONCLUSION: Limiting BoNT-A treatment to four cycles per patient per lifetime is likely to be suboptimal in many patients with PSS-UL. Treatment response beyond four cycles is highest among known responders, and allowing such patients to continue treatment beyond four cycles appears cost effective.

Incidence of paroxysmal sympathetic hyperactivity following traumatic brain injury using assessment tools.

INTRODUCTION: A consensus statement proposed a diagnostic framework to systematise the identification of paroxysmal sympathetic hyperactivity (PSH) using the PSH-Assessment Measure (PSH-AM). METHODS: This retrospective study identified adult patients with a primary diagnosis of traumatic brain injury and a hospital length of stay >14 days. Based on PSH-AM scores, patients were grouped into 'unlikely', 'possible', or 'probable' PSH. For this study, 'possible' and 'probable' PSH patients were collapsed into a single group (PSH+), and resultant data were compared with 'unlikely' diagnoses (PSH-). PSH-AM data were assessed against clinical diagnoses to establish sensitivity and specificity data. RESULTS: Sixty five patients met inclusion criteria, with 45/65 (69%) categorised as either 'possible' or 'probable' PSH on the PSH-AM. Only 16 of these patients were diagnosed by clinicians. The most common symptoms triggering clinical diagnosis were tachycardia, fever and posturing. Increased respiratory rate, blood pressure or the presence of diaphoresis were not used in diagnosing PSH if the PSH-AM was not utilised. Assuming clinical assessment as the current gold standard, the PSH-AM yielded a sensitivity of 94% and a specificity of 35% when used retrospectively. Patients clinically diagnosed with PSH were discharged 5 days earlier compared to those identified by the PSH-AM. CONCLUSIONS: The recently proposed diagnostic framework may reduce misdiagnosis, length of stay and hospitalisation costs.

Functional neurological symptom disorder (conversion disorder): A role for microglial-based plasticity mechanisms?

Functional Neurological Symptom Disorder (FND) is a relatively common neurological condition, accounting for approximately 3-6% of neurologist referrals. FND is considered a transient disorder of neuronal function, sometimes linked to physical trauma and psychological stress. Despite this, chronic disability is common, for example, around 40% of adults with motor FND have permanent disability. Building on current theoretical models, this paper proposes that microglial dysfunction could perpetuate functional changes within acute motor FND, thus providing a pathophysiological mechanism underlying the chronic stage of the motor FND phenotypes seen clinically. Core to our argument is microglia's dual role in modulating neuroimmunity and their control of synaptic plasticity, which places them at a pathophysiological nexus wherein coincident physical trauma and psychological stress could cause long-term change in neuronal networks without producing macroscopic structural abnormality. This model proposes a range of hypotheses that are testable with current technologies.

Understanding the pathophysiology of depression: From monoamines to the neurogenesis hypothesis model - are we there yet?

A number of factors (biogenic amine deficiency, genetic, environmental, immunologic, endocrine factors and neurogenesis) have been identified as mechanisms which provide unitary explanations for the pathophysiology of depression. Rather than a unitary construct, the combination and linkage of these factors have been implicated in the pathogenesis of depression. That is, environmental stressors and heritable genetic factors acting through immunologic and endocrine responses initiate structural and functional changes in many brain regions, resulting in dysfunctional neurogenesis and neurotransmission which then manifest as a constellation of symptoms which present as depression.

A comprehensive person-centered approach to adult spastic paresis: a consensus-based framework.

Spastic paresis is a common feature of an upper motor neuron impairment caused by stroke, brain injury, multiple sclerosis and other central nervous system (CNS) disorders. Existing national and international guidelines for the treatment of adult spastic paresis tend to focus on the treatment of muscle overactivity rather than the comprehensive approach to care, which may require life-long management. Person-centered care is increasingly adopted by healthcare systems in a shift of focus from "disease-oriented" towards "person-centered" medicine. The challenge is to apply this principle to the complex management of spastic paresis and to include an educative process that engages care providers and patients and encourages them to participate actively in the long-term management of their own disease. To address this issue, a group of 13 international clinicians and researchers used a pragmatic top-down methodology to evaluate the evidence and to formulate and grade the strength of recommendations for applying the principles of person-centered care to the management of spastic paresis. There is a distinct lack of clinical trial evidence regarding the application of person-centered medicine to the rehabilitation setting. However, the current evidence base supports the need to ensure that treatment interventions for spastic paresis should be centered on as far as reasonable on the patient's own priorities for treatment. Goal setting, negotiation and formal recording of agreed SMART goals should be an integral part of all spasticity management programs, and goal attainment scaling should be recorded alongside other standardized measures in the evaluation of outcome. When planning interventions for spastic paresis, the team should consider the patient and their family's capacity for self-rehabilitation, as well as ways to enhance this approach. Finally, the proposed intervention and treatment goals should consider the impact of any neuropsychological, cognitive and behavioral deficits on rehabilitation. These recommendations support a person-centric focus in the management of spastic paresis.

Paroxysmal sympathetic hyperactivity: the storm after acute brain injury.

A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome-paroxysmal sympathetic hyperactivity (PSH)-and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials.

The impact of compensation on late mortality after traumatic brain injury: A multi-centre study.

OBJECTIVES: To determine the impact of financial compensation on long-term mortality in adults with severe traumatic brain injury (TBI). DESIGN, SETTING AND PARTICIPANTS: An inception cohort of 2545 adults consecutively discharged from three metropolitan, post-acute inpatient rehabilitation services of the NSW Brain Injury Rehabilitation Programme from 1 July 1990 to 1 October 2007. MAIN OUTCOME MEASURE: Survival status at 1 October 2009. RESULTS: Compensation data were available for 1851 (73%) participants, with 826 (45%) receiving financial compensation. Yearly standardized mortality ratios remained elevated above general population norms for six to ten years for both groups. Compensation had a protective effect on mortality risk as a univariate predictor. However, when considered in multivariate Cox regression analysis, compensation had minimal effect on mortality risk when modelled with non-modifiable demographic factors and pre-existing medical history. Conversely, compensation trended towards a protective effect when modelled with post-injury variables. CONCLUSIONS: Financial compensation had a protective effect against late mortality following rehabilitation for severe TBI through complex interactions with rehabilitation service variables but not with injury-related variables. This finding suggests that wider access to compensation (and hence rehabilitation) through recently implemented schemes (e.g., NSW Lifetime Care and Support) may further improve life expectancy for this clinical population.

Early Fever As a Predictor of Paroxysmal Sympathetic Hyperactivity in Traumatic Brain Injury.

OBJECTIVE: Paroxysmal sympathetic hyperactivity (PSH) is characterized by episodic, hyperadrenergic alterations in vital signs after traumatic brain injury (TBI). We sought to apply an objective scale to the vital sign alterations of PSH in order to determine whether 1 element might be predictive of developing PSH. SETTING/PARTICIPANTS/DESIGN: We conducted an observational study of consecutive TBI patients (Glasgow Coma Scale score ≤12) and monitored the cohort for clinical evidence of PSH. PSH was defined as a paroxysm of 3 or more of the following characteristics: (1) tachycardia, (2) tachypnea, (3) hypertension, (4) fever, (5) dystonia (rigidity or decerebrate posturing), and (6) diaphoresis, with no other obvious causation (ie, alcohol withdrawal, sepsis). MAIN MEASURES: The Modified Clinical Feature Severity Scale (mCFSS) was applied to each participant once daily for the first 5 days of hospitalization. RESULTS: Nineteen (11%) of the 167 patients met criteria for PSH. Patients with PSH had a higher 5-day cumulative mCFSS score than those without PSH (median [interquartile range] = 36 [29-42] vs 29 [22-35], P = .01). Of the 4 components of the mCFSS, elevated temperature appeared to be most predictive of the development of PSH, especially during the first 24 hours (odds ratio = 1.95; 95% confidence interval, 1.12-3.40). CONCLUSION: Early fever after TBI may signal impending autonomic dysfunction.

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury.

Paroxysmal sympathetic hyperactivity (PSH) affects a significant minority of people in the intensive care unit after severe traumatic brain injury. Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences in the condition. Data were prospectively collected on 80 consecutive patients, 18 of whom developed clinical signs of PSH (22.5%). Catecholamine and hormonal data were collected sequentially at 4-h intervals or during and between episodes of PSH. Evaluated variables showed 200-300% increases in catecholamines and, to a lesser extent, adrenocortical hormones during paroxysms. The majority of PSH episodes (72%) were noted to be in response to an observable triggering event. These changes were not observed in subjects without PSH. These data go some way to explain why PSH produces adverse consequences in survivors of TBI with the condition.

Quantifying patterns of upper limb motor change following BTX-A injection in adult spasticity management.

OBJECTIVE: To evaluate the capacity of the Upper Limb Performance Analysis: Comparative Analysis of Performance-Motor (CAP-M) to quantify change in adults with focal spasticity following injection of Botulinum Toxin-A (BTX-A) as a focal treatment for positive Upper Motor Neuron (UMN) features. METHODS: Twenty-three adults with moderate-to-severe spasticity were assessed pre- and post-BTX-A injection using CAP-M. Post-hoc video analysis of three sub-tests from the Action Research Arm Test were analysed against expected movements for each task. RESULTS: Post-injection, spasticity as measured by Modified Ashworth and Tardieu Composite scores decreased significantly (p < 0.001). Grouped CAP-M data showed a significant reduction (z = 2.1-2.7, ES = 0.51-0.56) in positive UMN features, with 145 fewer Excessive movements recorded. In addition, 31 more Expected movements were demonstrated (z = 2.9, ES = 0.60), consistent with 'unmasking' of movements. CONCLUSION: CAP-M analysis revealed that BTX-A injection decreased unwanted movement almost 5-times more frequently than 'unmasking' hidden voluntary muscle activity during active simulated tasks. In this way, CAP-M was able to simultaneously assess positive and negative UMN features. This quantitative framework may have greater functional relevance than traditional uni-dimensional, passive spasticity measures such as MAS and Tardieu Scale.

Measuring task performance after acquired brain injury: Construct and concurrent validity of 'Upper Limb Performance Analysis'.

OBJECTIVE: This preliminary investigation studies selected aspects of validity of the Upper Limb Performance Analysis (ULPA), an occupation-based functional upper limb (UL) measure. METHODS: The study investigated the ULPA-Task Performance Mastery (ULPA-TPM) in 35 community dwelling adults with upper motor neuron syndrome following acquired brain injury and 26 healthy controls. Construct and concurrent validity of the ULPA were determined via group discrimination between adults with and without ABI; and ABI participants who were and were not referred for UL spasticity management with botulinum toxin-A injections (injected and non-injected group). Concurrent validity was examined by investigating the relationships between the ULPA and an existing functional UL measure, the Action Research Arm Test, using Spearman's rank-order correlation. RESULTS: Significant differences in UL performance were demonstrated between the ABI and the Control group on all ULPA sub-scales (including: Omission (z = -2.6 to -3.6, rspb = 0.37-0.48), Accuracy (z = -5.8 to -6.0, rspb = 0.78-0.82), Repetition (z = -5.1 to -5.4, rspb = 0.63-0.73) and Timing errors (z = -5.9 to -6.2, rspb = 0.77-0.88). Those in the Injected group demonstrated more task performance errors than the Non-injected group, with significant differences in Accuracy (z = -2.1 to -2.4, rspb = 0.37-0.45), Repetition (z = -2.5 to -2.1, rspb = 0.43) and Timing (z = -2.0, rspb = 0.37). CONCLUSIONS: This study demonstrated good construct and concurrent validity of the ULPA-TPM.

Autonomic dysfunction syndromes after acute brain injury.

The central autonomic nervous system (CAN) is a multifaceted, richly connected neural network incorporating the hypothalamus, its descending tracts through the brainstem, the insular cortex and down into the spinal cord. All levels of the CAN are susceptible to injury following traumatic brain injury (TBI), whether from focal or diffuse injury. Focal injuries would be expected to produce localized damage to CAN control centers, whereas the effects of diffuse injuries are presumed to be more diverse and/or widely distributed. As the combination of focal and diffuse injury following TBI can vary widely from one individual to the next, the impact of focal injuries is best understood with reference to the focal ischemic stroke literature. Subarachnoid hemorrhage (SAH), a common complication following TBI, also has predictable effects on autonomic control that can be understood with reference to spontaneous SAH literature. Finally, paroxysmal sympathetic hyperactivity (PSH), a syndrome incorporating episodes of heightened sympathetic drive and motor overactivity following minor stimulation, is discussed as an example of what happens when central inhibitory control of spinal cord autonomics is impaired.

Age-related trends in late mortality following traumatic brain injury: A multicentre inception cohort study.

AIM: To investigate age-related mortality risk following traumatic brain injury (TBI). METHODS: Review of 2545 consecutive discharges from three metropolitan rehabilitation centres in New South Wales, between 1 January 1990 and 1 October 2007. Survival status was censored on 1 October 2009. Between-group differences were assessed for older/younger patients. Multivariate Cox hazard regression was used to evaluate age-related mortality risk. Crude mortality rates, standardised mortality ratios and cause of death data were derived for each age decade. RESULTS: After controlling for known mortality risk factors, older patients were three times more likely to die than younger patients. Crude mortality rates increased exponentially with advancing age. However, when compared to normative population data, younger adults with TBI (<50 years) had the highest risk of death relative to their non-injured peers. CONCLUSIONS: Crude mortality rates, which do not account for the naturally increasing rate of death associated with ageing, artificially inflate estimates of age-related mortality risk following TBI.

Effects of concomitant spinal cord injury and brain injury on medical and functional outcomes and community participation.

BACKGROUND: There are limited data on the interactions between concomitant spinal cord injury (SCI) and traumatic brain injury (TBI) in terms of medical, psychological, functional, and community outcomes. OBJECTIVE: To investigate the hypothesis that in addition to SCI-associated sensory-motor impairments, people with dual diagnosis would experience additional TBI-associated cognitive impairments that would have a negative impact on community reintegration. METHODS: Cross-sectional, case-matched study comparing a consecutive sample of participants with dual diagnosis (n = 30) to an SCI group (n = 30) and TBI group (n = 30). Participants who were on average 3.6 years postrehabilitation discharge were interviewed using a battery of standardized outcome measures. RESULTS: Length of rehabilitation stay was significantly longer in SCI and dual diagnosis participants. Fatigue, pain, sexual dysfunction, depression, and sleep disturbances were frequently reported by all groups. Similar levels of anxiety and depression were reported by participants in all groups, however TBI participants reported higher stress levels. All groups achieved mean FIM scores > 100. The dual diagnosis and SCI groups received more daily care and support than TBI participants. Similar levels of community reintegration were achieved by all groups with a high level of productive engagement in work, study, or volunteer activities. CONCLUSIONS: The findings of this study do not support the hypotheses. Postrehabilitation functioning was better than anticipated in adults with dual diagnosis. The contribution of rehabilitation factors, such as longer admission time to develop compensatory techniques and strategies for adaptation in the community, may have contributed to these positive findings.

Computerised pinch dynamometry in the assessment of adult hand spasticity.

BACKGROUND/AIM: The hand engages with the environment through the grasp, stabilisation, manipulation and release of objects during everyday tasks, activities and routines. Upper motor neuron syndrome following acquired brain injury may negatively impact hand function, reducing strength, range of motion and motor control. It is important for clinicians to reliably measure such impacts, particularly for the impact of intervention and to monitor change in performance over time. Therefore, the aim of this study was to investigate the test-retest reliability and construct validity of Dynamic Computerised pinch Dynamometry for measuring fine hand motor performance following acquired brain injury. METHODS: The Dynamic Computerised pinch Dynamometry protocol was completed by 36 community dwelling adults and 27 healthy adults using a simulated pinch and release task in lateral and pincer grip positions. Measurements were conducted over two testing occasions approximately five weeks apart. Dynamic Computerised pinch Dynamometry output was evaluated to determine the test-retest reliability and construct validity of the measure. RESULTS: Test-retest reliability scores using Kendall coefficient of concordance ranged from W = 0.61-0.94. Dynamic Computerised pinch Dynamometry discriminated between participants with and without acquired brain injury (z = 4.97-6.50, P < 0.05) and between the affected and non-affected hand of participants with acquired brain injury (z = 3.37-5.22, P < 0.001). CONCLUSIONS: Dynamic Computerised pinch Dynamometry in both lateral and pincer positions had fair to excellent test-retest reliability, and had good construct validity for discrimination between participants with and without acquired brain injury as well as between the affected and non-affected hand of participants with acquired brain injury.

Outcomes of ambulatory rehabilitation programmes following botulinum toxin for spasticity in adults with stroke.

OBJECTIVE: To examine the benefits of high intensity ambulatory rehabilitation programmes over usual care following botulinum toxin A (BoNT-A) for post-stroke spasticity in Australian adults. DESIGN: Prospective single centre, controlled clinical trial. PARTICIPANTS: Fifty-nine adults, median 61 years old and 2.5 years following stroke. METHODS: PARTICIPANTS were dichotomised into high intensity ambulatory rehabilitation programmes (≥ 3 × 1-h weekly sessions for approximately 10 weeks) or usual care programmes (≤ 2 × 1-h weekly sessions) following BoNT-A injections for spasticity. A blinded assessor completed outcomes at 0 (baseline), 6, 12 and 24 weeks. Primary endpoints: proportion of participants achieving ≥ 50% of their goals (using Goal Attainment Scaling: GAS) and GAS T-score change at 12 weeks. SECONDARY OUTCOMES: Modified Ashworth Scale (MAS), participant satisfaction, activity/participation measures and caregiver burden. RESULTS: Both groups showed significant improvement in goal attainment and participant satisfaction up to 24 weeks, with no overall between-group significant differences. There was, however, a statistical trend (p = 0.052) for participants to achieve more upper limb goals in the high intensity therapy group. GAS and satisfaction benefits persisted beyond the duration of spasticity reduction as measured by MAS. CONCLUSIONS: While patient-centred outcomes following BoNT-A injections for post-stroke spasticity were not influenced by intensity of ambulatory rehabilitation programmes, there was a trend for high intensity therapy to be associated with greater upper limb goal attainment. This suggests that the effects of more intensive therapy may be a modifier of the 'black box' of rehabilitation; however, further research is required to evaluate this effect and determine which elements of therapy programmes optimise post-BoNT-A outcomes.