Spasticity is a word that is often heard when someone’s movement problems after a stroke are being described. Yet strangely there is little or no agreement as to what spasticity actually is!
Here are a few quotes gleaned from medical sites on the internet:
“Spasticity is a condition in which certain muscles are continuously contracted. This contraction causes stiffness or tightness of the muscles and can interfere with normal movement, speech and gait”
“Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia.”
“Spasticity is a muscle control disorder that is characterized by tight or stiff muscles and an inability to control those muscles. In addition, reflexes may persist for too long and may be too strong (hyperactive reflexes)”.
From these quotes spasticity might be: continuously contracting muscles, or paralysed muscles, might be stiff muscles, or there may be changes in reflex activity, or a combination of all of these features! Not very helpful if you don’t agree on what you are describing! This failure to clearly describe/define spasticity is problematic for clinicians and stroke survivors. If spasticity isn’t clearly defined or described:
- it can’t be Identified or distinguished from other muscle responses which may occur after stroke (such as stiffness, hyperreflexia etc),
- it can’t be Measured objectively, and importantly
- interventions for spasticity cannot be shown to be effective (or ineffective) because of the uncertainty as to what is being measured.
There are many theories and rationales about just what spasticity is and why it occurs (eg Lance 1980, Pandyan 2005). The lack of consensus about the definition of spasticity only adds to the confusion for clinicians and more importantly, for stroke survivors.
What is the incidence of spasticity?
The ongoing preoccupation with spasticity is surprising when the incidence of spasticity after stroke is actually quite low. The incidence of spasticity (depending on how it is defined and measured) seems to be somewhere between 17% (Lundstrom 2008) to 38% (Watkins 2002) (see Sommerfield 2012 for a review). However, it must be acknowledged that for some individual stroke survivors, the consequences of spasticity can have profoundly adverse consequences for their activities of daily living such as being unable to open their hand to be able to clean it.
Is there a relationship between spasticity and function?
Even more surprising, the research that has measured the relationship between spasticity and function has found that spasticity is not correlated with loss of functional ability (Dietz et al 1981, Ada et al Upper Limb 2006, Ada et al Lower Limb 1998, Williams et al Lower Limb – in traumatic brain injury – 2015, Fayazi 2014, Shaw et al 2011). So even if spasticity is present, it does not appear to be the main problem limiting stroke survivors’ ability to move. Weakness, on the other hand, is very strongly correlated with loss of function. (Look for future blogs to discuss the relationship between weakness and poor function in blogs on the StrokeEd website over the coming months.)
This is the first in a series of blogs about spasticity in an attempt to try to make sense of what continues to be a very fraught issue – despite the strong evidence that spasticity is not the main problem preventing stroke survivors from moving. These blogs will present some of the problems with the prevailing beliefs about spasticity and importantly, provide some evidence based strategies clinicians may use to assist stroke survivors learn to move even in the presence of spasticity.
Your comments, both from clinicians, researchers and stroke survivors, are very welcome. This blog is intended to help, not hinder, clinical decision making. So if you want to comment please keep the contributions about spasticity open and informative to progress the discussion for the benefit of all. Comments will be moderated to ensure a civil conversation!
Canning C, Ada L, Adams R & J O’Dwyer N (2004) Loss of strength contributes more to physical disability after stroke than loss of dexterity. Clinical Rehabilitation. 18: 300-308
Dietz V, Quintern J & Berger W (1981) Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia. Brain : a Journal of Neurology. 104(3):431-449]
Fayazi M, Dehkordi SN, Dadgoo M, Salehi M (2014) The relationship between spasticity and lower extremity strength with functional mobility following chronic stroke. Int J Phys Med Rehabil. 2: 218.
Lance J. Spasticity: Disordered Motor Control. Chicago. Year Book Medical Publishers, 1980; 485–495.
Louise Ada L, Vattanasilp W, J O’Dwyer N, Crosbie J (1998) Does spasticity contribute to walking dysfunction after stroke? J Neurol Neurosurg Psychiatry. 64: 628–635
Lundström E, Terént A, Borg J (2008) Prevalence of disabling spasticity 1 year after first-ever stroke. Eur J Neurol. 15(6): 533-9.
Pandyan A, Gregoric M, Barnes M, et al. (2005) Spasticity: clinical perceptions, neurological realities and meaningful measurement. Disabil Rehabil. 27: 2–6.
Shaw L et al (2011). BoTULS: a multicentre randomised controlled trial to evaluate the clinical effectiveness and cost-effectiveness of treating upper limb spasticity due to stroke with botulinum toxin type A. Stroke. 42(5): 1371-9.
Sommerfeld D, Gripenstedt U, Welmer A (2012) Spasticity after stroke: an overview of prevalence, test instruments, and treatments. American Journal of Physical Medicine & Rehabilitation. 91(9): 814–820.
Watkins C et al (2002) Prevalence of spasticity post stroke. Clin Rehabil. 16(5):515-22.
Williams G, Banky M, Olver J (2015) Distribution of lower limb spasticity does not influence mobility outcome following traumatic brain injury: an observational study. J Head Trauma Rehabil. 30(5): 49-57.