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Management of spasticity in multiple sclerosis (MS)

Management of spasticity in multiple sclerosis (MS)
  • Neurology

Serafin Beer, Department of Neurorehabilitation, Valens Clinic Rehabilitation Center, Valens, Switzerland


Spasticity can be defined as a “disordered sensorimotor control resulting from an upper motor neuron (UMN) lesion, presenting as intermittent or sustained involuntary activation of muscles” as one component of upper neuron syndrome [1]. Reflex (tonic and phasic reflexes) and non-reflex (loss of viscoelastic properties of muscles) mediated mechanisms contribute to this increased muscle tone [2].

Clinical features of UMN syndrome can be divided into ‘Plus` and ‘Minus` components (see Table 1). It is important to note, that pharmacological interventions are targeting only “Plus” components, whereas “Negative” symptoms (such as weakness, dexterity) cannot directly be improved by any medication. Another important aspect to note is that certain ‘Plus` symptoms (such as increased muscle tone) may be useful and even indispensable for some patients in compensating for minus symptoms.




 Exaggerated tendon reflexes


 Released reflexes, Babinski sign 

 Slowed movements

 Increased tone

 Loss of dexterity

 Muscle spasms

 Loss of selective motor control


 Reduced range of motion (ROM) 

 Spastic co-contraction

 Impaired postural control

Table 1. Components of upper motor neuron (UMN) syndrome.


Spastic syndromes in MS

Due to the widespread affection of descending motor pathways, spastic syndromes are very common in multiple sclerosis (MS). In the long-term up to 80% of people with MS report some degree of spasticity, one third suffering from moderate to severe spasticity significantly affecting their daily activities [3]. These spastic syndromes have a negative impact not only on motor functions and mobility (motor control, ROM, gait, defective joint position, biomechanical stress) but often lead to sleep disturbances, bladder/bowel dysfunctions and pain, increasingly affecting daily activities and social participation, and often increasing the burden of care. On the other side spasticity may have a positive impact in compensating weakness thus allowing patients with MS to stand and walk and also reducing ataxic movements.


Evaluation of spasticity and goal setting

 The first issue before starting any treatment is to evaluate the negative or possible positive impact of spasticity. Treatment should only be considered in patients with clear negative impact. Another important aspect is to evaluate possible factors triggering or increasing spasticity. The most common reasons for increased spasticity are infections (especially urinary infections) and pain. Other triggering factors are obstipation, pressure sores, thrombosis and fatigue. Ambient temperature can influence the degree of spasticity in different ways: heat can increase spasticity by Uhthoff’s phenomenon, whereas cold ambient temperature can increase the sensitivity of muscle spindles thus increasing reflex activity. Other important contributing factors are sitting in a wheel-chair, lying in supine position and emotional stress. All these factors must be considered and should be excluded/treated if possible [4].

Assessment of spasticity can be done with the Modified Ashworth Scale [5](see Table 2). Even though the interrator reliability is acceptable, this scale is only recommended as a first assessment measure and it is not useful as follow-up measure. Due to different variable distribution of spasticity in different muscle groups (upper and/or lower limbs, trunk muscles) it is important to test and record distribution and impact of spasticity in different parts of body. Another problem grading severity of spasticity is the changing degree depending on different factors (activity, posture, mood, fatigue). Assessment therefore should be done in a standardised manner.




 No increase of muscle tone


 Minimal increase of muscle tone (release at the end of ROM)


 Minimal increase of muscle tone, minimal resistance during the < 50% of ROM


 Marked increase of muscle tone during the major part of ROM, affected extremities  can be moved easily


 Severe increase of muscle tone, passive movements difficult


 Affected extremities rigid in flexion or extension

Table 2. Modified Ashworth spasticity scale.

Possible goals of treatment are improving movement and functions, reducing functionally impairing malposition, improving mobility and independence, reducing spasticity related pain and painful spasms, avoiding long-term complications (i.e. mechanical strain, contractures, pressure sores), and facilitating personal care / hygiene thus reducing need of care. It is important to note that reducing muscle tone alone is not a relevant goal.


Non-pharmacological treatment

Physiotherapy is generally accepted as a basic treatment option for spasticity even though the evidence for different interventions is generally low (physiotherapy, aquatic therapy, structured exercise programme) or lacking (TENS, sports climbing, vibration) [6]. In addition to active training and measures to reduce muscle tone, patients with MS should be instructed to limit spasticity triggering postures as sitting and perform regular standing. In patients with severe spasticity or fixed contractures serial casting (with or without Botulinum toxin) is beneficial especially in respect of ROM [7-9]. Neurosurgical interventions (dorsal rhizotomies, dorsal root entry zone DREZtomies) and orthopaedic interventions (tendon release/transfer) are generally not recommended in patients with MS.


Oral antispastics

 In patients with spastic syndromes with a clear negative impact on daily life and who are not responding to general measures and physical therapy, the first treatment option is oral antispastics (see Table 3). Due to different modes of action, combining these agents may have an additive effect. Even though reduction of muscle tone can be achieved, the impact on function and activity remains unclear. The practical use, however, is often limited due to systemic side effects and their generalized non-selective effect on all muscle groups including hypotonic trunk muscles. In addition some of these agents may increase weakness thus leading to a negative effect on strength, postural stability and gait. Tolperisone, an agent inhibiting afferent inputs to spinal reflex arc, seems to have lower risks in this respect. Due to sleepiness diazepam should only be given in the evening in patients with painful nocturnal spasms during night. After starting oral antispastic therapy careful evaluation of possible side effects and negative impact is necessary. Treatment should also be stopped if no beneficial effect is detectable.


 Dose  range

 Mode of action

 Adverse events



 Inhibition of reflex activity by stimulation of GABA-A receptors

 sleepiness, somnolence



 Spinal inhibition of reflex activity by stimulation of GABA-A receptors

 tiredness,  dizziness, weakness, hypotension



 Spinal and supraspinal inhibition of spasticity by stimulation of alpha-adrenergic  receptors

 tiredness,  dizziness, dryness of mouth,  hypotension


 3x150-  300mg

 Presynaptic inhibition of spinal reflex activity via sodium and calcium channels

 hypersensitivity, rarely: hypotension



 Inhibition of muscle contraction by inhibition of Ca-release from the  sarcoplasmatic reticulum

 severe hepatopathy, weakness, nausea

 Table 3. Antispastic drugs.


After some promising anecdotal reports, some randomised trials investigated the value of different cannabinoids in treatment of spasticity in patients with MS [10, 11]showing no improvement of spastic muscle tone. Rog and co-workers, however, could show a significant improvement of central pain in patients with MS treated with cannabinoids [12]. In recent years there have been some studies indicating at least some benefits of phytocannabinoids for spasticity: in a meta-analysis Wade and co-workers showed that spasticity (assessed by a self-assessment numerical rating scale) can be improved by nabiximols (Sativex®) [13]. The use of this compound, however, is[dl1]  restricted to a subgroup of Patients with MS with moderate-severe generalized spasticity not responding to oral antispastics. The main drawbacks are possible adverse effects on cognitive functions and on the developing brain (especially in younger patients), the high costs and an absence of  approval in different countries.


Botulinum toxin

Botulinum toxin (BOTX) is a useful treatment for focal spasticity [14]. In patients with MS spasticity usually is more generalized than in stroke: therefore BOTX treatment in MS is restricted to a selected group of patients. In a randomized trial Hyman and co-workers showed that BOTX reduces the degree of hip adductor spasticity without major side effects [15]. Treatment effect and duration can be enhanced by additional physical therapy [16]. Severely disabled patients with MS with uncontrollable flexor leg spasticity may benefit from BOTX in combination with serial casting. Use of BOTX treatment, however, is expensive and its effect is limited to a relatively short time period (3-6 months).


Intrathecal baclofen therapy

In patients with severe spasticity of the lower limbs not responding to oral antispastics, intrathecal baclofen therapy (ITB) may be a reasonable treatment option [4, 17, 18]. In contrast to oral baclofen, systemic side effects can be avoided, and negative impact on strength of upper limbs and trunk muscles minimized by delivering the drug directly intrathecally. Intrathecal baclofen, therefore, in general is well tolerated and very effective in spasticity of spinal origin [19]. The ITB system consists of a subcutaneously implanted programmable pump with a reservoir and a catheter inserted into the spinal subarachnoid space. The dosage can be adjusted to the patient’s activities and requirements. Careful selection of patients and a positive test injection, as a regular follow-up by experienced ITB-users, are crucial for a successful long-term benefit and limitation of possible complications [4]. There might be potentially life-threatening complications which should be recognized and treated as they arise. Overdose with flaccid paralysis, respiratory failure, epileptic seizures and coma can be caused by errors in dosing and programming, whereas withdrawal with massive increase of muscle tone, fever and confusion is seen due to battery failure, disruption of catheter or an empty reservoir after missed refilling. After successful implantation and a first time period finding the optimal individual dose, ITB has a long-lasting benefit in patients with MS.



Spastic syndromes are very common and disabling in patients with MS affecting not only motor functions but also different activities and social participation. Before starting the treatment careful evaluation of spasticity and possible triggering factors should be done, starting pharmacological treatment only in patients with a negative functional impact. Possible negative effects of treatment should be considered, especially deterioration of postural stability due to loss of compensating spastic muscle groups and increased weakness of trunk muscles.



1.    Kheder, A. and K.P. Nair, Spasticity: pathophysiology, evaluation and management. Pract Neurol, 2012. 12(5): p. 289-98.

2.    Zhang, L.Q., et al., Characterizations of reflex and nonreflex changes in spastic multiple sclerosis. J Neurosci Methods, 2014.

3.    Rizzo, M.A., et al., Prevalence and treatment of spasticity reported by multiple sclerosis patients. Mult Scler, 2004. 10(5): p. 589-95.

4.    Beer, S., et al., Intrathekale Baclofen (ITB)-Therapie der schweren Spastik bei Multipler Sklerose Übersicht und praktische Empfehlungen. Schweiz Arch Neurol Psychiatr, 2005. 156: p. 333–42.

5.    Bohannon, R.W. and M.B. Smith, Interrater reliability of a modified Ashworth scale of muscle spasticity. Phys Ther, 1987. 67(2): p. 206-7.

6.    Amatya, B., et al., Non pharmacological interventions for spasticity in multiple sclerosis. Cochrane Database Syst Rev, 2013. 2: p. CD009974.

7.    Pohl, M., et al., Effectiveness of serial casting in patients with severe cerebral spasticity: a comparison study. Arch Phys Med Rehabil, 2002. 83(6): p. 784-90.

8.    Preissner, K.S., The effects of serial casting on spasticity: a literature review. Occup Ther Health Care, 2002. 14(2): p. 99-106.

9.    Farina, S., et al., Combined effects of botulinum toxin and casting treatments on lower limb spasticity after stroke. Funct Neurol, 2008. 23(2): p. 87-91.

10.  Zajicek, J., et al., Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial. Lancet, 2003. 362(9395): p. 1517-26.

11.  Vaney, C., et al., Efficacy, safety and tolerability of an orally administered cannabis extract in the treatment of spasticity in patients with multiple sclerosis: a randomized, double-blind, placebo-controlled, crossover study. Mult Scler, 2004. 10(4): p. 417-24.

12.  Rog, D.J., et al., Randomized, controlled trial of cannabis-based medicine in central pain in multiple sclerosis. Neurology, 2005. 65(6): p. 812-9.

13.  Wade, D.T., et al., Meta-analysis of the efficacy and safety of Sativex (nabiximols), on spasticity in people with multiple sclerosis. Mult Scler, 2010. 16(6): p. 707-14.

14.  Baker, J.A. and G. Pereira, The efficacy of Botulinum Toxin A for spasticity and pain in adults: a systematic review and meta-analysis using the Grades of Recommendation, Assessment, Development and Evaluation approach. Clin Rehabil, 2013. 27(12): p. 1084-96.

15.  Hyman, N., et al., Botulinum toxin (Dysport) treatment of hip adductor spasticity in multiple sclerosis: a prospective, randomised, double blind, placebo controlled, dose ranging study. J Neurol Neurosurg Psychiatry, 2000. 68(6): p. 707-12.

16.  Giovannelli, M., et al., Early physiotherapy after injection of botulinum toxin increases the beneficial effects on spasticity in patients with multiple sclerosis. Clin Rehabil, 2007. 21(4): p. 331-7.

17.  Nielsen, J.F. and T. Sinkjaer, Guided intrathecal baclofen administration by using soleus stretch reflex in moderate-severe spastic multiple sclerosis patients with implanted pump. Mult Scler, 2004. 10(5): p. 521-5.

18.  Ben Smail, D., et al., Intrathecal baclofen for treatment of spasticity of multiple sclerosis patients. Mult Scler, 2006. 12(1): p. 101-3.

19.  Erwin, A., et al., Intrathecal baclofen in multiple sclerosis: too little, too late? Mult Scler, 2011. 17(5): p. 623-9.

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Valens, Switzerland
Sep 25 - 26, 2014
Target audience
Neurologists, Physiatrists
by Excemed