E-23 Spasticity management
Spasticity, slowness, and stiffness of muscles associated with upper motor neurone damage and muscle spasms are frequently encountered in most rehabilitation. Competence in managing spasticity and its related problems has become essential for rehabilitation experts. Other specialities play a part, such as orthopaedic surgeons who may operate to reduce contractures or neurosurgeons who may insert an intrathecal baclofen pump, but rehabilitation experts usually lead on overall patient management. Surprisingly, spasticity’s exact nature and genesis still need to be fully understood and control over spasticity is rarely achieved. The most effective direct treatments, intramuscular botulinum toxin injections and the baclofen pump have significant practical and financial limitations and other treatments, though used, have limited evidence to support them. This page will introduce you to some aspects of spasticity management.
Table of Contents
The rehabilitation expert shall be “Able to identify spasticity and its complications, to determine its causes, and to formulate a goal-directed, patient-centred plan, including pharmacological, surgical and non-pharmacological aspects.” Given the limited ability to control spasticity in most patients, the practical emphasis is on alleviating the consequences of spasticity and its associated problems. You may download a description of the indicative behaviours, knowledge and skills associated with this competency and some general references.
Defining spasticity is challenging because it is associated with other impairments of the motor control system, and the types and areas of neurological damage associated with spasticity vary considerably. A review published in 2009 was titled “Spasticity, an impairment that is poorly defined and poorly measured.” The most used definition, first proposed in 1980, is “Spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.”
Another definition from 2005 is “Spasticity is a disordered sensorimotor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles.” This followed a detailed review of the clinical and neurophysiological aspects of spasticity by Anand Pandyan and colleagues, and it recognises that hyperreflexia is not the only factor contributing to muscle stiffness.
However, many definitions start from the premise that spasticity arises from an overactive stretch reflex, and many measures focus on that. However, the theory is debated, and spasticity can be present without hyper-reflexivity, as demonstrated by O’Dwyer et al. in 1996. There is continuing interest in spastic dystonia, which Jakob Lorentzen and colleagues have also defined as “tonic, chronic, involuntary muscle contraction in the absence of any stretch or any voluntary command.”
Most research and teaching emphasise treatments aimed at reducing spasticity as measured, often by quite different techniques. More research needs to be done into other aspects of spasticity. One exception has been the measurement of care burden related to arm spasticity. This arose because, although botulinum toxin demonstrably reduced spasticity, arm use had no associated functional gain. There is, however, a reduction in the negative features associated with spasticity.
Spasticity is one part of the upper motor neurone syndrome, a collection of losses observed in people with disturbance in the central mechanisms controlling motor function. There are also the effects of more comprehensive associated features such as sensory disturbance, central neurogenic pain, and joint pain, especially in the shoulder. The term is usually used about the arms and legs.
The central clinical feature is an increased resistance to passive movement by the muscle secondary to an increase in the muscle’s contraction from the usual baseline of no contraction.
The features associated with spasticity include reduction in:
- voluntary muscle strength
- fine motor control
- sensory feedback and sensation
And an increase in:
- stretch-reflex sensitivity
- spasms (involuntary, sudden muscle contractions)
Spasticity is absent in the early days and weeks after acute damage; the central nervous system adapts such that spasticity arises. As I pointed out in the introduction, it is only an assumption that an abnormal stretch reflex is the primary cause of spasticity, and the failure of treatments aimed at the reflex pathway to exert much control over spasticity suggests other mechanisms are at work.
Thus, rehabilitation experts must avoid assuming that spasticity is synonymous with hyperactive stretch reflexes and consider other neurophysiological processes that may contribute to the phenomenon. Second, they must always consider the other associated impairments and that the person’s function is determined by the combination of impairments affecting the particular patient; spasticity is only one part of the explanation and often only a minor part.
Prevention of spasticity.
First, can we stop spasticity from developing? A recent trial of routine botulinum toxin shortly after stroke by Lindsay Cameron et al. suggests it might. Research into other techniques, such as positioning or stretching, is inconclusive.
Second, can we prevent the consequences of spasticity, especially contractures? A systematic review and meta-analysis of 8 studies (332 patients) by Laura Gomez-Cuaresma and colleagues did not give evidence of effectiveness.
Treatment of spasticity
Treatments aimed at spasticity are primarily based on the supposition that hyperreflexia is the predominant underlying mechanism causing spasticity. Many drugs have been tried such as baclofen, tizanidine, gabapentin, nabiximols, and dantrolene. Overall, the evidence is weak, with small trials and minimal long-term data. Moreover, the effect sizes are small. The drug with the most published data is nabiximols.
The one specific treatment that is well-proven to reduce measured spasticity is botulinum toxin. For example, a systematic review by Aukje Andringa and colleagues in 2016 showed this to be sufficiently confident that no further trials were needed. There is also reasonable evidence that effectiveness is further increased by additional therapy given after the injection. For example, Patricia Mills and colleagues undertook a systematic review that found this, but, although generally true, there were many adjunct therapies, and their relative efficacy needs further study.
However, the practical or functional benefits are less well-established. It is essential to consider not only an improvement in function but also a reduction in the burden of care, which has been demonstrated for the arm after stroke.
Intrathecal baclofen is also undoubtedly effective. There are few trials on account of the considerable expense of the intervention. A recent study by Michael Creamer and an international group of colleagues studied 60 people after stroke; it reduced spasticity and pain.
Another non-pharmacological treatment to consider is transcutaneous electrical nerve stimulation (TENS); a review by Miriam Marcolino and colleagues provides provisional evidence of effectiveness. A systematic review of all non-pharmacological interventions found little evidence to support using any of them.
Management of a person with spasticity
The management of the patient with spasticity will need to be considered holistically. The approach should be to focus on the person, not their spasticity. In doing this, one should recognise that controlling spasticity is problematic, with no substantial evidence suggesting that most pharmacological treatments are beneficial. The only effective interventions are botulinum toxin and intrathecal baclofen. Cost and practical issues limit the use of these.
Thus, for most people with spasticity, the clinician should focus on reducing the direct adverse effects of spasticity, such as pain, difficulty in undertaking activities secondary to difficulties in moving the affected limb passively, and troublesome spasms.
One particular area of concern that must always be considered is the adverse effects associated with drugs prescribed for spasticity. Most of the medications impair cognition, cause drowsiness and fatigue, may worsen swallowing and constipation, and other difficulties. Whatever the original benefits, one must always review whether the drugs are still helping. A gradual withdrawal over 8-10 weeks is the best approach, asking the person whether their spasticity is getting any more troublesome as the drug is reduced.
This competency would be better entitled, managing the person who has troublesome spasticity, because the spasticity itself can rarely be alleviated to a significant degree, and few significant functional benefits arise from the reduction in spasticity achieved. Management should focus on reducing the effects of spasticity with a particular focus on the adverse effects of long-term drug treatment, which may no longer be helping the patient.