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Williams G.1, Bankly M.2, Olver J.3
1Epworth Healthcare & University of Melbourne, Physiotherapy, Melbourne, Australia, 2Epworth Healthcare, Physiotherapy, Melbourne, Australia, 3Epworth Healthcare, Rehabilitation Medicine, Melbourne, Australia
Background: The presence of spasticity in people with neurological disorders has been associated with significant mobility limitations, reduced motor function, increased pain levels and longer inpatient rehabilitation admission times. However, recent findings suggest that lower limb spasticity may not have as great an impact on mobility as originally thought. A disparity between clinical measures of spasticity, how spasticity may manifest during gait, and whether clinical measures of gait relate to gait disorders has major implications for clinical practice given the widespread use of neuro-muscular agents such as botulinum toxin and baclofen.
Purpose: The main aim of this project was to determine the impact of plantarflexor spasticity on muscle performance for ambulant people with traumatic brain injury (TBI).
Methods: Seventy-two ambulant people with TBI who were attending physiotherapy for mobility limitations. Twenty-four participants returned for a six month follow-up reassessment. All patients who consented to participate in this study underwent three-dimensional gait analysis (3DGA) and a routine neurological clinical assessment which included the measurement of lower limb spasticity and muscle strength. The Tardieu scale was used to assess spasticity. All Tardieu assessments were performed using previously described standardised testing positions. Hand held dynamometry (HHD) was selected as the modality to quantify clinical measures of ankle plantarflexor muscle strength. To quantify APG at push-off, three-dimensional gait analysis (3DGA) was performed using the Vicon 512 motion analysis system (Oxford Metrics, Oxford, UK), with eight cameras sampling at a rate of 120 Hz.
Results: Participants with ankle plantarflexor spasticity had significantly lower self-selected walking speed, however there was no significant difference in ankle plantarflexor strength or APG. Participants with ankle plantarflexor spasticity were not restricted in the recovery of self-selected walking speed, ankle plantarflexor strength or APG, indicating equivalent ability to improve their mobility over time despite the presence of spasticity.
Conclusion(s): Following TBI, people with ankle plantarflexor spasticity have significantly greater mobility limitations than those without spasticity, yet retain the capacity for recovery of self-selected walking speed, ankle plantarflexor strength and APG.
Implications: Spasticity may not have a great an impact on mobility following TBI as originally believed. Other features of the upper motor neurone lesion may have a greater impact on mobility, or it may be the combination of spasticity and muscle weakness (for example) that may be most disabling. Further consideration needs to be given to the prescription of anti-spasticity agents when the primary goal is to improve mobility outcomes.
Funding acknowledgements: Nil
Topic: Neurology
Ethics approval: This project was approved by Epworth Hospitals HREC (study number 34006) and by the University of Melbourne (Ethics ID: 060496.1).
All authors, affiliations and abstracts have been published as submitted.
