Content » Vol 43, Issue 9

Commentary on ”Spasticity or Reversible Muscle Hypertonia?”

The article by Bakheit et al. (1) on the terminology of spasticity is very useful at this time, particularly in attempting to capture this aspect within the domains of the International Classification of Functioning, Disability and Health (ICF) (2). There has been a lot of work over many years in trying to clarify what we mean by the term spasticity, and I agree with the authors that using the nomenclature of spasticity to describe muscle hypertonia is inaccurate, and not always helpful in daily clinical practice and research. For instance, post-stroke spasticity shows considerable variability and often does not conform to any of the standard definitions, particularly with regard to the role of muscle tone in producing loss of activity. Malhotra et al. (3) found that a substantial proportion of post-stroke patients exhibiting involuntary muscle activity consistent with spasticity, as measured by biomechanical and neurophysiological measures, did not exhibit scores on the Modified Ashworth Scale (which measures muscle tone) that were diagnostic for spasticity. Eighty-seven out of 100 patients were diagnosed with abnormal muscle activity using biomechanical and neurophysiological measures. Spasticity was then measured in the same set of patients using the 6-point Modified Ashworth Scale, and 56 out of the 87 previously identified patients scored a 0, indicating no detectable spasticity (3). The Ashworth and Modified Ashworth Scales are frequently-used clinical methods for evaluating muscle tone. At best, such incongruity between common measures of spasticity and standard definitions of the condition (4) complicate the diagnosis, and, at worst, result in sub-optimal treatment of the patient with spasticity.

The question now is whether the alternative term “reversible hypertonia” proposed by Bakheit et al. (1) is more valuable. They make a good case for it, but again their emphasis on hypertonia may be relevant for what one is treating in some patients, but not in all. Young people with relatively mild spasticity due to cerebral palsy have problems with motor control rather than the phasic and tonic aspects of hypertonia (5). The attempt to separate the very different presentations of the upper motor neurone syndrome is important, but will it make a difference to the treatments currently employed? The reason for asking this question is that most people demonstrate a multiplicity of features and no single term will capture all of them. Will changing the terminology change the treatment approach? All manner of manifestations of upper motor neurone syndrome are addressed in clinical practice, and these have been included in the term, “spasticity” because it is easy to do so. The product licences for the pharmaceutical interventions are for spasticity and the clinician does not then have to make a separate justification for treating associated reactions, reciprocal inhibition, mass synergy effects, etc. It is thus important to keep a watchful eye on practical issues, such as this, but my experience from examining data from post-stroke patients, who had rehabilitation goals to improve function, indicates that, where they were not achieved for walking, it may have been because they did not have true spasticity. The outcomes were thus diminished in terms of the goal of treatment, but the patients nonetheless improved to a degree. However, Bakheit et al. (1) suggest the terminology change on the basis that anti-spastic treatment is given for a range of findings in upper motor neurone syndrome. This is true, but there does not appear to be an advantage in dropping the term “spasticity” in favour of “reversible hypertonia”, which does not describe the impairments any better.

On the other hand, the operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (6, 7). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. Tonic stretch reflex does not always contribute to clinical hypertonia in spinal cord dysfunction. Other reflex mechanisms must contribute to hypertonia, as assessed clinically and contrasts with similar studies of cerebral spasticity after stroke. Comparable low-frequency stretch perturbation produced clear evidence of a gain in increased tonic stretch reflex that was correlated with the hypertonia at rest, and low-frequency stretch perturbation clearly distinguished between spasticity after stroke and spinal cord injury. The conclusion was that spasticity in the two conditions was not equivalent, and care should be taken in generalizing results between them.

The authors make the point that the impairments change over time after an insult to the upper motor neurone. This is true, but changing the terminology may not change our thinking about the recognition of these changes or their treatment. Being more specific in determining the patient’s problem may help, and identifying ways of teasing out the therapeutic challenges will clarify our thinking. Quantification has focused mainly on hypertonia, i.e. increased resistance at rest to passive movement. This could be caused by a combination of spasticity, spastic dystonia, soft tissue stiffness and thixotropy (8). Most attempts at quantification (measures, such as the Ashworth/Modified Ashworth, and Tardieu Scales) are very poor at distinguishing between spasticity and soft tissue stiffness, and all that can be said is that quantification of the spasticity portion of hypertonia remains difficult, at least in a clinical setting (9).

The aim of the article is to distinguish the neurogenic component of upper motor neurone syndrome from its mechanical consequence, i.e. fixed contracture. These are really two different things, and the treatment required for the neurogenic component of the clinical picture is different from that for the biomechanical consequences. While I accept the shortcomings of the term “spasticity”, I do not think that changing the terminology will really help this distinction. I will keep an open mind about this, but I wonder whether a name change will really catch on. The article does not offer new treatment strategies for treating patients with “reversible hypertonia” as opposed to “spasticity”. Similar pharmacological agents are used to treat a variety of physiological features in “spasticity management” and it probably makes sense not to change a simple term, like spasticity, just yet until we propose different treatments for those different features.

References

Anthony Ward, BSc, MD, FRCPEd, FRCP

North Staffordshire Rehabilitation Centre, University Hospital of North Staffordshire (Haywood Hospital), High Lane, Burslem, Stoke on Trent, UK-ST6 7AG, UK. E-mail: anthony@bward2.freeserve.co.uk

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