Download as a PDFClick here for patient information


Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Loh E, Sproule S, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0: p 1-135.

We would like to acknowledge previous contributors: Jo-Anne Aubut, Keith Sequeira, Jeffrey Blackmer.



Spasticity is traditionally defined as “[…] a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflexes, as one component of the upper motoneuron syndrome” (Lance 1980). Spasticity is quite commonly confused with tremor, rigidity, clonus, dystonia and various movement disorders (i.e., athetoid, ballisms, and chorea). One of the earliest examples of this confusion is the term “spastic rigidity” used to refer to “excessive muscular contraction” first published in 1843 (Little WJ). Attempts to clarify this confusion have resulted in the most recent definition published by Pandyan et al. (2005) (adapted from Tardieau et al. 1954) as follows: “disordered sensori-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscle”. This definition is intended to be more inclusive of clinical signs and symptoms of “spasticity” but has yet to be validated for clinical relevance.

Regardless of the definitions presented, each eludes to various inter-related components of the upper motor neurone syndrome (i.e., tone, clonus, spasms, spastic dystonia and co-contractions). Therefore, a thorough clinical assessment of spasticity should always be undertaken as follows (Kheder & Nair 2012): 1) differentiate spasticity from other causes of increased tone, 2) identify potential triggers, 3) measure spasticity, 4) assess spasticity’s impact on function, and 5) gather input from patients, caregivers, therapists and other rehabilitation professionals. Spasticity is not static and therefore, assessments should be done regularly and combined with establishing goals of treatment to make decisions regarding treatment strategy (Rekand et al. 2012).


Recent studies indicate that, besides changes in motoneuron activation (involuntary supraspinal descending inputs and inhibited spinal reflexes etc.), changes in muscle properties also contribute to the clinical appearance of limb spasticity and rigidity, which are frequently linked symptoms. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are generally thought to be responsible for spastic movement disorders. Therefore, most antispastic treatments are directed at the reduction of reflex activity. In recent years, researchers have noticed a discrepancy between spasticity as measured in the clinic and functional spastic movement disorders, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behaviour of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organisation. Antispastic drugs can accentuate paresis and therefore should be applied with caution in mobile patients (Dietz & Sinkjaer 2007).

Phadke et al. (2013) completed a review of articles published between 1989 and 2012 (n=24) using the EMBASE, CINAHL, and PEDro databases. The review examined the effect of triggers on spasticity. The authors found that the quality of the studies was moderate and included non-randomized trials, randomized trials with no effect and/or low study subject numbers or case reports. The authors found that factors increasing spasticity included pregnancy, posture, cold, circadian rhythm, and skin conditions as measured via objective clinical tests. Studies that relied on patient self-reports, revealed that bowel and bladder related issues, menstrual cycle, mental stress, and tight clothing were suspected to increase spasticity. There was no literature that reported on the increase in spasticity in response to heterotopic ossification, hemorrhoids, deep vein thrombosis, fever, sleep patterns and pain and conditions, even though these are thought to increase spasticity.


It has been estimated that 53% (Walter et al. 2002) to 78% (Adams & Hicks 2005; Maynard et al. 1990; Levi et al. 1995) of individuals report spasticity secondary to chronic SCI. Spasticity has been reported to be more frequent in cervical and incomplete injuries (Mumtaz et al. 2014). Approximately 41% (Levi et al. 1995) of individuals with spasticity secondary to SCI list it as one of the major medical obstacles to community and workplace re-integration (Canadian Paraplegic Association 1996). Although, spasticity is not typically thought to get worse with age and time, uncontrolled spasticity is thought to have an impact on emotional adaptation, dependency, secondary health problems and environmental integration (Krause 2007).

Determining Impact of Treatment

During initial inpatient rehabilition, spasticity that was not optimally managed was found to be, after pain and fatigue, a primary medical reason for increased length of stay (Dijkers & Zanca 2013; Hammond et al. 2013). Van Cooten et al. (2015) postulate that early, active rehabilitation would serve to reduce functional hindrance due to spasticity. Identification of specific spasticity components, during the subacute and chronic stages of SCI, that impact directly on gait, lower limb muscle function and activities of daily living could also be helpful in the refinement and customization of ongoing neurorehabilitation treatment strategies (Bravo-Esteban et al. 2013).

Spasticity in SCI varies with location and degree depending on the injury pathophysiology. Not all spasticity is bad and for this reason, an assessment of treatment goals must be considered with various management strategies and cost factors in mind. Sometimes, increased spasticity is beneficial for transfers and mobility, and the reduction of tone may negatively impact those activities of daily living. For example, in the acute rehabilitation setting, the absence of spasticity was an independent risk factor for the development of deep vein thrombosis (Do et al. 2013).

The goal should not be to modify the excitability and rigorousness of reflexes, but to overcome functional impairments related to “spasticity” (Dietz 2000). Therefore, the decision to treat “spasticity” should not only be based on the findings gained by the examination in passive (lying bed, sitting in the wheelchair) but also in active conditions (like walking, doing transfer etc.). As well, spasticity can be protective against skeletal muscle atrophy that in turn could indirectly affect functional independence, ambulation and incidence of fracture (Gorgey & Dudley 2008). Spasticity has also been reported to increase glucose uptake and thereby reduce the risk of diabetes in SCI (Bennegard & Karlsson 2008). Furthermore, recent reports identifying spasticity related enhancement/detraction of sexual activity in males/females respectively (Anderson et al. 2007a; Anderson et al. 2007b), again exemplifies the importance of individualized treatment choices. Incrementally applying the less invasive and cost-efficient treatments, as is common practice (Kirshblum 1999), will likely lead to a combination of treatments necessary to achieve the most successful outcome specific for each individual. Simultaneously with the completion of an assessment that clearly delineates the treatment goals, objective measures of spasticity that include patient reported outcomes are important to identify in order to confidently monitor the success of treatment choice(s). Spasticity treatment as it pertains to the various domains of everyday life should be considered (Mahoney et al. 2007).

Outcome Measurement and Spasticity

The studies reviewed in this chapter involve a variety of outcome measures that have been summarized into four categories: 1) Known Clinical Measures; 2) Other Measures; 3) Electrophysiological Measures and 4) Quality of Life Measures. Among the known measures, some are validated and only a subset of those is used frequently by clinicians. It will be important to develop agreement as to well-defined, clinically meaningful outcome measures for demonstrating the efficacy of an experimental therapeutic intervention (Steeves et al. 2007). The abundance of outcome measures in the other categories are not well understood by the majority of clinicians and increases the difficulties encountered when comparing studies and treatments. Outcome measure feasibility is another important consideration given that clinicians commonly do not have consistent access to equipment, nor have sufficient time to administer highly technical methods in a clinical setting (e.g. Cybex; Franzoi et al. 1999). Very few studies included measures addressing quality of life despite the need to ensure that treatments are well tolerated as well as functionally and practically effective for patients. However, Balioussis et al. (2014) provided a review of psychometric data for SCI specific spasticity outcome measures that assess its impact on quality of life. These authors conclude that PRISM (Patient Reported Impact of Spasticity Measure) is the current best option because it accounts for more affective reactions in the presence of spasticity compared to SCI-SET (SCI Spasticity Evaluation Tool) that also has less available psychometric data. Balioussis et al. (2014) also put forth that despite good clinical feasibility, the Ashworth Scale and Modified Ashworth Scale’s (MAS) known poor inter-rater and intersession reliability may shed doubt on their applicability for SCI, especially with respect to quality of life. Having a psychometrically-validated outcome assessment for spasticity related quality of life will be beneficial, especially for understanding of interactions between the clustering of spasticity with chronic pain and depression in people with SCI.

Table 1 Summary of Outcome Measures used in Spasticity Intervention Studies

The gold-standard for clinical testing is the double-blind, randomized, placebo-controlled study design, particularly for the measurement of short term treatment effects. However, the results of a well-designed trial are more easily interpreted if the outcome measures used follow outcome measure standards as outlined by Pierson (1997). In summary, effective outcome measures should be selected based on 1) understandability for administration/scoring/interpretation and validity/reliability; 2) relevancy to the clinical situation and population measured; 3) having a reasonable risk-benefit ratio; 4) requirement for strict adherence to test conditions and procedures; and 5) practicality in terms of personnel, time, equipment, cost, space and impact on the subject. No single outcome measure can capture the multi-dimensional nature of spasticity. Therefore, it is important, not only to choose an effective outcome measure but also to choose effective outcome measures to monitor the range of medical outcomes as suggested by Goldberg (1991): 1) technical outcome (i.e., reduction of spasm frequency); 2) functional outcome; 3) patient satisfaction and; 4) cost effectiveness. Consensus has not yet been reached on clinically meaningful, feasible and effective outcome measures relevant to the treatment of spasticity and patient reported outcomes.

Some of the measures that have been tested for various aspects of spasticity and for validity and/or reliability include the Ashworth (Ashworth 1964) and MAS (Bohannon & Smith 1987; Haas et al. 1996) spasticity scales, the Spasm Frequency scale (Penn 1988; Priebe 1996), the Pendulum test (Nance 1994), the Spinal Cord Assessment Tool for Spasticity (SCATS; Benz et al. 2005), the Spastic Paraplegia Rating scale (Schϋle et al. 2006), and the Spinal Cord Injury Spasticity Evaluation Tool (SCI-SET; Adams et al. 2007). Please refer to the SCIRE Outcome Measures for a more in-depth discussion on these measures.

  • Although consensus has not yet been reached on clinically meaningful, feasible and effective outcome measures relevant to the treatment of spasticity and patient reported outcomes, development and inclusion of such a multidimensional test battery is required for understandable interpretations of and between future studies.

Overview of Treatments

Physical therapy, surgery, and pharmacotherapy including neurolysis are among the most common treatment options currently employed to manage spasticity in SCI. Physical therapy is initiated during rehabilitation and usually continues post-discharge either formally or through patient education and caregiver administration. Pharmacotherapies are thought to be the most efficacious for treatment of the velocity-dependent increase in hyperexcitable tonic stretch reflexes, one component of the upper motor neuron syndrome defined by Lance (1980). Surgery and neurolysis may be appropriate choices to treat focal spasticity. A combination treatment regimen can be individualized and appears to be a common approach in clinical practice.