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health prof v24_Layout 1 28/10/2011 17:12 Page 3 MS: an overview
Diagnosis
Types of MS
Prognosis
Clinical measures
A multidisciplinary approach to MS care
Self-management
Relapse and drug therapies
Relapse
Steroids
Disease modifying drug therapies
Symptoms, effects and management
Vision
Fatigue
Cognition
Depression
Women’s health
Bladder
Bowel
Sexuality
Mobility
Spasticity
Tremor
Pain
Communication and swallowing
Pressure ulcers
Advanced MS
Complementary and alternative medicine
Index
Fourth Edition
Spasticity
Spasticity is one component of the upper motorneurone syndrome9 that occurs as a result of Spasticity
acquired damage to any part of the CNS,including the spinal cord. It has a range of effects, Spasticity can be a complex and chal enging which can be categorised into positive and symptom to manage in neurological conditions and is negative features (Table 1). Most people wil a common symptom experienced by people with present with a combination of features. One or multiple sclerosis. The ongoing management of several of the positive features wil influence the spasticity requires teamwork between the person with resistance to passive movement. Often people are spasticity, their regular carers, and members of the described as having spasticity, but it is likely they multidisciplinary team1,2. In a survey 84% of people wil also have other features of the upper motor with MS reported symptoms of spasticity with one third rating it as moderate or severe3.
Table 1. Features of the upper motor neurone What is spasticity?
The true nature of spasticity is stil not clearlyunderstood. The most common definition used is: Positive
Negative
‘a motor disorder characterised by a velocity features
features
dependent increase in tonic stretch reflexes withexaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex, as one component of the upper motor neurone syndrome’4. Moresuccinctly spasticity has been defined as ‘the velocity dependent increase in resistance of a More recently these definitions have been chal enged by a European working group asnarrow and limiting. Specifical y this group identified that the term spasticity is used differentlyby clinical and research communities and concluded that spasticity is not a pure motor disorder, or just a result of the hyper-excitablestretch reflex or dependent on the velocity of the stretch. They suggested a new definition as, ‘Disordered sensorimotor control, resulting from an upper motor neurone lesion, presenting asintermittent or sustained involuntary activation Why does spasticity occur?
The control and regulation of normal skeletal muscleactivity involves a complex combination of The resistance to passive movement caused by descending motor commands, reflexes and sensory spasticity is generated by abnormalities in the control feedback from the brain, spinal cord and peripheral of movement by the central nervous system (CNS).
sensation. During normal movement, influences from As wel as this neural involvement of spasticity there the cerebral cortex, basal ganglia, thalamus and are also biomechanical changes, which occur both in cerebel um, travel ing via upper motor neurones muscles and connective tissue, which through disuse adjust, reinforce and regulate the lower motor and immobility can lead to reduced range of neurone which connects directly via peripheral nerves movement or contractures7. Increased resistance to to the muscle to form smooth, coordinated muscle passive movement felt by the clinician, often referred activity and maintenance of posture.
to as hypertonia, may be caused by a combination of spasticity, which is neural y generated, and In simple terms spasticity occurs when there is biomechanical changes in the muscle and connective damage to these descending upper motor neurone tissue. Together these changes can significantly tracts (eg a plaque in MS) which interrupts the regulation of spinal cord and lower motor neurone Multiple Sclerosis Information for Health and Social Care Professionals Spasticity
activity. This can result in enhanced lower motor A multidisciplinary approach
neurone activity and an increase in muscle activity, Effective communication between disciplines is vital in response to peripheral stimuli (eg muscle stretch, to enhance the management of an individual’s a urinary tract infection or pressure ulcer)10,11.
spasticity. Each discipline can be seen to havespecific expertise within the team. However this is Consequences of spasticity
not exclusive and teamwork is essential1,2.
Spasticity can affect physical activities such aswalking, transferring, picking up objects, washing, Nurses have a significant role in educating a
dressing and sexual activity. It can also have an person on managing trigger factors and about the emotional impact, on for example, mood, self-image available treatments to manage spasticity. They and motivation12-14. Safety in sitting and lying can also can provide ongoing support and advice to abe compromised due to spasms or persistent poor person and their family as they live with and adjust positioning15,16 which can lead to the development of to managing spasticity and spasms over time. contractures. This can potential y lead to restrictedmobility and social isolation.
Physiotherapists can carry out specific treatments
to assist an individual to manage muscle tone
Symptoms of the upper motor neurone syndrome are particularly the biomechanical changes. Treatment not always detrimental and they may even be may include appropriate exercise programmes that positive in improving vascular flow and assisting in may encompass stretches, active exercises or transfers and even walking17. Therefore the treatment standing. Advice can also be given regarding of spasticity needs to be careful y selected and posture and positioning throughout the day.
reviewed over time in order to meet the individual’saims and to maintain and promote function.
Occupational therapists can play a key role in
assessing and recommending appropriate
Management and treatment
adaptations to an individual’s environment and of spasticity
advising on how to maximise activities of daily Two core principles of spasticity management living within the context of spasticity. Appropriate seating is of particular importance in spasticitymanagement. Optimising an individual’s posture and
movement through use of appropriate seating,
Occasional y the expertise of speech and language therapists can be sought when spasticity affectsneck and facial muscles18. Preventing or managing factors that may
increase spasticity and spasms. Primarily
Medical management is important in terms of exacerbations can occur from cutaneous stimuli assessing, prescribing and evaluating the use of such as skin irritation, pressure sores, ingrown antispasticity drugs. In conjunction with other toenails, tight fitting orthoses. Visceral stimuli members of the team, doctors can decide the appropriate timing and selection of more constipation, bowel impaction and infections, for example urinary tract infections, can be triggers2, 10.
Patterns of movement in function and sustained Inpatient rehabilitation may be appropriate to postures throughout the day and night can also individual’s spasticity throughout a 24 hour periodand to al ow a more detailed management These principles need to be regularly considered and reviewed over time and used in conjunctionwith medical treatments. Pivotal to their success is Sometimes despite optimal physical management ongoing multidisciplinary teamwork across hospital programmes and optimisation of trigger factors and community settings working col aboratively pharmacological measures are necessary.
with the person with spasticity to effectively Depending on the pattern of spasticity these can Spasticity
Generalised treatments19
MS wil respond to Sativex; whether someone is aresponder can be identified after a four week trial of Baclofen acts on the CNS and is the most
the drug. The dose of Sativex is then control ed by commonly used antispasticity drug. To avoid side varying the number of sprays taken each day.
effects it needs to be started at low doses, slowlyincreased and stopped at a dose that does not Focal treatments
cause unwanted side effects. The effect of an oralbaclofen dose can last between 4-6 hours so doses Botulinum toxin can be injected into muscles and
need to be taken regularly to ensure adequate acts as a neuromuscular block which causes the control of symptoms. Side effects can include targeted muscle to become temporarily weak. It can take 10-14 days for the ful effect to be felt. It mustbe used in conjunction with physiotherapy/ Gabapentin is useful for treating spasticity
occupational therapy and an exercise programme to and spasms. It is particularly helpful in managing maximise effect and to promote an ongoing change spasticity when pain is associated with it. in the spasticity once the toxin has worn off (approx.
Side effects can include drowsiness, dizziness Phenol or alcohol motor point injections. The injection
The NICE clinical guideline states that the permanently destroys nerve fibres in the injected muscle.
fol owing should only be given if treatment with Some nerves may partial y regrow, causing the effect to baclofen or gabapentin is unsuccessful or side wear off after several weeks or months. Injections can Tizanidine also works on the CNS and needs to be
Intrathecal therapies
introduced slowly to avoid side effects. Regularblood tests should be performed to ensure there is Intrathecal baclofen acts by binding to gamma
no adverse effect on liver function. Side effects can aminobutyric acid (GABA) receptors and results in include weakness, drowsiness and dry mouth.
inhibition of mono and polysynaptic spinal reflexes24with associated reduction in spasm, clonus and pain.
Diazepam or clonazepam can be used alone or in
A concentration of GABA receptors is situated in the combination with other drugs. Their daytime use is intrathecal space of the spinal cord. Delivering limited by sedative side effects, but if taken prior to baclofen intrathecal y accentuates its antispasticity sleep they can be very useful in managing effect whilst minimising the troublesome systemic nocturnal spasms. Side effects can include side effects associated with oral intake. An implanted pump can deliver baclofen directly to this Dantrolene is the only antispasmodic drug that
area and can be used to treat generalised lower limb works directly on the muscles rather than on the spasticity25-27. It requires commitment from the person CNS. It can be used in combination with other with MS, not only during the trial and implant phase, drugs. Often it is not wel tolerated and can cause but also for its ongoing maintenance of regular reservoir nausea, vomiting, diarrhoea and weakness. Regular refil s and pump replacements2. It is however an blood tests need to be completed to ensure no extremely effective treatment and is being used earlier in people with MS to improve their walking28.
Sativex is a cannabis extract which works on the
Intrathecal phenol is a permanent destructive
cannabinoid receptors in the brain and spinal cord.
procedure29. It can be helpful for some people, It is licensed in MS as an add-on therapy for those to treat very severe spasms that do not respond people whose spasticity and spasm has not to other drug treatments. The effects of an injection can responded to the other available drugs20, 21. It is sometimes wear off but can be repeated if necessary.
available as an oral spray. Side effects can includedizziness, sleepiness and feelings of light Negative effects on lower limb sensation, sexual headedness. Occasional y the spray can cause function, bladder and bowel management can occur so soreness in the mouth so it is important to change appropriate patient selection is critical to ensure effective the spray site regularly. About half of people with strategies are in place to manage these30. Multiple Sclerosis Information for Health and Social Care Professionals Spasticity
Intrathecal treatments require a detailed clinical 16. Jarrett L. The role of the nurse in the management of administration, an example of guidelines and nursing spasticity. Nurs Residential Care 2004;6(3):116-9. care plans from one service have been published2.
17. Losseff N, Thompson AJ. The medical management of increased tone. Physiotherapy 1995;81(8):480-4. 18. Leary S, Jarrett L, Lockley L, et al. Intrathecal baclofen therapy Occasional y orthopaedic or neurosurgical procedures improves functional intel igibility of speech in cerebral palsy.
Clin Rehabil 2006;20(3):228-31. may be recommended. These can include myelotomy 19. Beard S, Hunn A, Wright J. Treatments for spasticity and pain (severing of tracts in the spinal cord) and rhizotomy in multiple sclerosis: a systematic review. Health Technol Assess (resection of posterior roots)31,32.
20. Novotna A, Mares J, Ratcliffe S, et al. A randomized, double Complementary therapies
blind, placebo-control ed, paral el-group, enriched-design Some individuals with spasticity report that study of nabiximols (Sativex) as add-on therapy, in subjectswith refractory spasticity caused by multiple sclerosis. Eur J complementary therapies such as acupuncture can 21. Col in C, Ehler E, Waberzinek G, et al. A double-blind randomized placebo-control ed paral el-group study of Sativexin subjects with symptoms of spasticity due to multiple References
sclerosis. Neurol Res 2010;32(5):451-9.
1. Thompson AJ, Jarrett L, Lockley L, et al. Clinical management of 22. Turner-Stokes L, Ashford S. Serial injections of botulinum toxin spasticity. J Neurol Neurosurg Psychiatry 2005;76(4):459-63. for muscle imbalance due to regional spasticity in the upper 2. Stevenson VL, Jarrett L. Spasticity management: a practical limb. Disabil Rehabil 2007;29(23):1806-12.
multidisciplinary guide. Oxford: Informa Health Care; 2006. 23. Royal Col ege of Physicians. Spasticity in adults: management 3. Rizzo, MA, Hadjimichael OC, Preiningerova J, et al. Prevalence using botulinum toxin. National guidelines. London: RCP; 2009.
and treatment of spasticity reported by multiple sclerosis 24. Davidoff RA, Sears ES. The effects of Lioresal on synaptic activity in the isolated spinal cord. Neurology 4. Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Koel a WP, editors. Spasticity, disordered motor control.
25. Penn RD, Savoy SM, Corcos D, et al. Intrathecal baclofen for Chicago: Year Book Medical Publishers; 1980. p485-94. severe spinal spasticity. N Engl J Med 1989;320(23):1517-21. 5. Brown P. Pathophysiology of spasticity. J Neurol Neurosurg 26. Porter B. A review of intrathecal baclofen in the management of spasticity. Br J Nurs 1997;6(5):253-62. 6. Pandyan AD, Gregoric M, Barnes MP, et al. Spasticity: clinical 27. Jarrett L, Leary S, Porter B, et al. Managing spasticity in people perceptions, neurological realities and meaningful with multiple sclerosis - a goal-oriented approach to intrathecal measurement. Disabil Rehabil 2005;27(1/2):2-6. baclofen therapy. Int J MS Care 2001;3(4):10-21.
7. Carr J, Shepherd R. The upper motor neurone syndrome. In: 28. Erwin A, Gudesblatt M, Bethoux F, et al. Intrathecal baclofen in Neurological rehabilitation: optimizing motor performance.
multiple sclerosis: too little, too late? Mult Scler 2011:17(5):623-9.
Oxford: Butterworth-Heinemann; 1998. p85-203. 29. Bonica JJ. Neurolytic blockade and hypophysectomy. In: Bonica 8. Dietz V. Spastic movement disorder: what is the impact of JJ. The management of pain. 2nd edition. Philadelphia: Lea & research on clinical practice? J Neurol Neurosurg Psychiatry 30. Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb 9. Greenwood R. Introduction: spasticity and upper motor spasticity in multiple sclerosis: does intrathecal phenol have a neurone syndrome. In: Sheean G, editor. Spasticity role? J Neurol Neurosurg Psychiatry 2002;73(6):705-9. rehabilitation. London: Churchil Communications; 1998. 31. Lazorthes Y, Sol JC, Sal erin B, et al. The surgical management 10. Sheean G. Neurophysiology of upper motor neurone of spasticity. Eur J Neurol 2002;9(Suppl 1):35-41.
syndrome and spasticity. In: Barnes MP, Johnson GR, editors.
32. Mittal S, Farmer JP, Al-Atassi B, et al. Long-term functional Upper motor neurone syndrome and spasticity: clinical outcome after selective posterior rhizotomy. J Neurosurg management and neurophysiology. Cambridge: Cambridge 11. Stevenson VL, Marsden JF. What is spasticity? In: Stevenson V, Jarrett L, editors. Spasticity management: a practicalmultidisciplinary guide. Oxford: Informa Health Care; 2006. p3-14. 12. Ward N. Spasticity in multiple sclerosis. J Community Nursing MS Trust resources
13. Porter B. Nursing management of spasticity. Primary Health 14. Currie R. Spasticity: a common symptom of multiple sclerosis.
15. Keenan L, Stevenson V, Jarrett L. Care Pathway: The role of the health care professional in the management of spasticity.
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