Clinical management of spasticity
http://www.100md.com
神经科学杂志 2005年第4期
1 National Hospital for Neurology and Neurosurgery, Queen Square, London WC1, UK
2 Institute of Neurology, Queen Square
Physical and pharmacological treatments can reduce pain and discomfort without compromising function
Abbreviations: FES, functional electrical stimulation; UMN, upper motor neurone
Keywords: spasticity; treatment; management
Spasticity is a common symptom seen in many neurological conditions, notably head injury, spinal cord injury, stroke, cerebral palsy, and multiple sclerosis. It is also the dominant feature in several rarer conditions such as tropical and hereditary spastic paraparesis. The fact that it is relevant to many chronic neurological conditions and that the absence of multidisciplinary input can result in progressive disability makes it an ideal model to reflect service provision In the future more long term care for such patients will be done in primary care and the community. It is therefore essential that a multidisciplinary approach is used with successful liaison between secondary, primary, and social care.
Optimum management of spasticity is dependent on an understanding of its underlying physiology, an awareness of its natural history, an appreciation of the impact on the patient, and a comprehensive approach to minimising that impact which is both multidisciplinary and consistent over time. Regrettably, these essential requirements are rarely met; consequently, inadequately managed spasticity results in a range of painful and disabling sequelae which, with the right approach, are for the most part preventable.
PATHOPHYSIOLOGY OF SPASTICITY AND SPASMS
Stretch reflexes in healthy subjects are complex. At rest the reflex response is mediated through IA afferents that connect monosynaptically with the parent motor neurone. However, with the muscle activated other reflex components may also be elicited through group II spindle afferents and transcortical pathways. Stretch reflexes are normally modulated by task and during the different phases of walking. Such modulation reflects changes in motoneuronal and spinal cord inhibitory interneuronal activity. This inhibitory influence is in turn controlled by descending and peripheral inputs. In spasticity an enhanced and prolonged response to muscle stretch is seen at rest. Here both group IA and group II afferents may play a role in eliciting the response, which may be processed by monosynaptic and polysynaptic circuits. Additionally, decreased task and phase dependent modulation of stretch reflexes occurs, reflecting abnormalities of supraspinal control.
Although spasticity is seen after an upper motor neurone (UMN) lesion, the relative importance of individual descending pathways remains unclear.1 A lack of descending control over spinal cord interneuronal circuits results in a decrease in the effectiveness of spinal inhibitory circuits such as those mediating reciprocal, presynaptic, and recurrent inhibition. However, the slow clinical development of spasticity following a neurological insult argues against it simply being a release phenomenon.2,3 Recent studies suggest that intrinsic changes in the motor neurone develop over time following a lesion. These result in abnormally long plateau-like potentials that prolong motor neurone discharge and thus muscle contraction in response to synaptic inputs.4–8 Although prolonged motor neurone discharge can occur in healthy subjects, the paucity of inhibitory spinal cord control in people with spasticity means that this activity could, once triggered, continue relatively unabated.
As well as hyperexcitable stretch reflexes, connective tissue changes and abnormal co-contraction can contribute significantly to stiffness.9 Connective tissue changes can occur without any contracture and the resulting stiffness may vary in a velocity dependent manner similar to spasticity, making it difficult to distinguish clinically between hypertonia of neural and non-neural origin. This distinction is, however, clinically important as the treatment of such stiffness is through physical adjuncts such as stretching and splinting rather than through pharmacological interventions.
Abnormal co-contraction can be seen after stroke during tasks that do not require any joint movement and thus stretch related activity.10 Co-contraction and excessive muscle activity during movements may therefore reflect deficits in coordination that are independent of any abnormalities in stretch related muscle activation.11
Spasms or sudden involuntary, often painful, movements are often included under the umbrella term of spasticity. However, physiologically these appear to be an independent entity. Spasms can be triggered not only by muscle stretch but also through a variety of peripheral, noxious, and visceral afferents. Spasms may be caused by disinhibited polysynaptic reflexes such as the flexor withdrawal reflex,12 or they may reflect abnormal activity within spinal cord circuits which have the effect of synchronising the discharge of motor neurones supplying multiple muscles.13
Spasticity and spasms are, however, only two of the symptoms of the UMN syndrome; other symptoms such as muscle weakness, decreased postural responses, and reduced dexterity all have an impact on an individual’s function. These features may be independent of each other but it is often difficult to assess the relative contribution each has to reduction in function. For example, in hereditary spastic paraparesis it was often thought that spasticity was the main factor contributing to the abnormal gait, but if spasticity is effectively reduced—for example by intrathecal baclofen—there is often evidence of profound underlying weakness which is clearly contributing to the disability.14
THE IMPACT OF SPASTICITY
Spasticity can cause discomfort and stiffness, while spasms can be annoying and painful and may interfere with function. Physical activities such as walking, transferring, picking up objects, washing, dressing, and sexual activity can all be affected. Likewise the ongoing presence of spasticity and spasms can have an emotional impact on, for example, mood, self image, and motivation. Poorly managed spasticity can also be responsible for muscle shortening and the development of tendon and soft tissue contractures, which together with spasms can lead to compromised safety in lying and sitting.15 Once contractures are present these are often very difficult to treat and can have major functional implications, including difficulties with personal hygiene or dressing, positioning, and at times the inability to sit, which may lead to restricted community mobility and social isolation. In addition, such difficulties can lead to the development of pressure sores, which may increase the severity of spasticity and spasms. A further problem—particularly in children with spasticity, which is often secondary to cerebral palsy—is the failure of normal muscle growth, resulting in torsion of long bones and consequent joint instability and degeneration.16 Early identification and intervention to treat spasticity and associated symptoms such as spasms can minimise the development of these long term secondary complications.
However, it must not be forgotten that spasticity can also be useful, perhaps allowing a person to stand or walk when weakness would not otherwise permit it. With these issues in mind it is imperative that management is always patient and function focused rather than aimed at the reduction of spasticity per se.
EFFECTIVE MANAGEMENT MUST BE SEAMLESS AND MULTIDISCIPLINARY
There is no agreed evidence based model available for the management of spasticity and much of what is done is based on a logical and pragmatic approach. A key component of management is the education of all involved, including the patient, family, carers, and health professionals. Continuity of care—particularly across the interfaces of primary and secondary care, involving community rehabilitation teams and care agencies—combined with documentation of the evolving impact of spasticity, is necessary to enable ongoing assessment of change and the appropriate choice and timing of any management intervention (fig 1). Whether the impact of spasticity on an individual is mild or severe, it is important that patients are knowledgeable about spasticity, its associated features, and how they can help themselves to manage and prevent symptoms. The trigger and aggravating factors detailed in fig 1 are particularly important as they can exacerbate spasticity and its associated features. Far too often pharmacological treatment is escalated before appropriate strategies to manage bladder and bowel function, skin integrity, soft tissue length, and positioning are instigated. Attention to these simple but essential areas is paramount at all stages of management.
It is often helpful to approach spasticity management according to the level of severity, including points at which intervention is essential to prevent secondary complications (table 1). However, regardless of the level of severity, it is always important to consider triggers and aggravating factors at each stage and determine whether the spasticity is predominantly focal or generalised (fig 1).
MOVEMENT, EITHER PASSIVE OR ACTIVE, IS ESSENTIAL AT ALL STAGES OF MANAGEMENT
Maintaining muscle length through passive or active exercise and stretching regimens including standing or splinting can be key to managing spasticity both in the short and the long term. Likewise, attention to posture and positioning, which may include the provision and regular review of seating systems, is paramount in managing severe spasticity. Doctors, physiotherapists, occupational therapists, and nurses across primary and secondary care can play key roles in working with the individual and their carers to assess the degree and impact of spasticity, identify goals of treatment, initiate referrals for specialist advice, implement management programmes, and monitor the effects of such interventions.17 Effective spasticity management requires clear communication and documentation between the individual and all the services involved in their care.
Short periods of inpatient rehabilitation can also be useful for individuals experiencing changes in their level of function; this may be increasing difficulty with walking or it could be the transition to the safe use of a wheelchair.
Functional electrical stimulation (FES) is an adjunct to physiotherapy that can be of benefit to selected individuals who are predominantly affected by UMN pathologies resulting in a dropped foot. In theory this should benefit both the neural (by reciprocal inhibition in antagonistic muscles) and non-neural (lengthening of soleus and gastrocnemius) aspects of spasticity. In a small randomised controlled trial in patients following stroke, the use of FES in combination with physiotherapy was statistically superior to physiotherapy alone.18
PHARMACOLOGICAL TREATMENT OF SPASTICITY
Drug treatment can be used for generalised spasticity or targeted to focal problems, and can include agents such as botulinum toxin or intrathecal baclofen and phenol. Botulinum toxin is the most widely used treatment for focal spasticity. The effect of the toxin is to inhibit the release of acetylcholine at the neuromuscular junction. Although this blockade is permanent, the clinical effect of injecting botulinum toxin is reversible because of nerve sprouting and muscle reinnevation, leading to functional recovery of the muscle in a few months.19 It is essential that botulinum toxin injections be given in conjunction with physiotherapy to obtain the maximum benefit. The toxin is injected directly into the targeted muscle and takes 10 to 14 days to have a visible effect. As it is a reversible treatment it may have to be repeated after a few months. Despite randomised controlled trials showing that botulinum toxin is effective in reducing tone,20 there have been few that have shown an improvement in active function, although improvement in passive functions—ease of hygiene, dressing, and so on—has been demonstrated. A notable exception is the study by Brashear and colleagues, which demonstrated a reduction in spasticity in the wrist and fingers of patients following stroke, together with an improvement in their disability assessment scale.21 The lack of evidence of functional improvement in some studies may be related to poor trial design and the lack of function based outcome measures.22
Local injection of phenol is an alternative option for focal spasticity management. This can be used alone or in combination with botulinum toxin, particularly in children, where small body size restricts the available treatment dose of botulinum toxin. Chemical neurolysis by phenol is irreversible and can be used at several sites. The most commonly used are medial popliteal blocks in the management of children with developing foot deformities, and obturator nerve blocks in ambulatory patients with scissoring gait or for improving sitting posture and ease of perineal hygiene.23
The oral agents most commonly used to treat spasticity are baclofen, tizanidine, benzodiazepines, dantrolene, and gabapentin. There is limited evidence of efficacy in clinical trials. The first four appear to be of similar benefit in multiple sclerosis, although diazepam is less well tolerated than the others. Gabapentin has only been studied in a few short term trials (two to six days).24 With the exception of tizanidine and dantrolene, these drugs act by potentiating the action of the inhibitory neurotransmitter gamma amino butyric acid (GABA). Tizanidine, however, is predominantly an 2 agonist and thus decreases presynaptic activity of the excitatory interneurones. Dantrolene is the only antispasticity treatment that acts primarily on muscle. Through inhibiting calcium release from the sarcoplasmic reticulum it decreases the excitation–coupling reaction involved in muscle contraction.
Unfortunately all drug treatments for spasticity can have side effects, the commonest of which are drowsiness and weakness. Of course it is important to recognise that a perceived increase in weakness may actually be a result of unmasking the impairment by removing tone which was functionally useful. To optimise the effects of oral drug treatment it is important to identify appropriate dosage regimens. For instance, if getting out of bed is difficult, the drugs should be left next to the bed and taken immediately on waking, preferably 10 to 20 minutes before getting up. If nocturnal spasms are a particular problem, then increasing night-time doses can be useful.
If oral drug treatment is inadequate at controlling lower limb spasticity or is not tolerated, then intrathecal delivery of baclofen should be considered. The concentration of GABA receptors in the lumbar spinal cord allows very small dosages of baclofen to be effective without causing any systemic side effects. The programmable pump is implanted into the abdomen, from where a catheter conveys the baclofen into the intrathecal space. This is obviously an invasive and relatively expensive treatment which requires careful selection of patients, a trial using a bolus dose of baclofen through a lumbar puncture needle, and significant commitment from patient, not only during the trial and implant phase but also for the ongoing maintenance of regular refills and replacements.
Occasionally the measures outlined above are not sufficient to manage severe spasticity causing contractures and preventing carers from seating or hoisting the patient safely, and such patients may be considered for intrathecal phenol treatment. As phenol is a destructive agent which indiscriminately damages motor and sensory nerves, it is reserved for those individuals who do not have any functional movement in the legs, who have lost bladder and bowel function, and who have impaired sensation to the legs. Phenol is injected intrathecally and is prepared in glycerin, which renders it hyperbaric and viscous, thus limiting its spread. Intrathecal phenol can be an effective treatment which, though it requires expert administration, does not have the long term maintenance or cost issues that go with intrathecal baclofen treatment. The effect of a single injection often lasts many months and can be repeated if necessary.25
MONITORING SPASTICITY
It is clearly helpful to adopt a management approach that is linked to the severity of the spasticity. However, this implies an accurate and reliable assessment of severity, which is in itself a challenging area. Research is ongoing into different assessment strategies, including gait analysis and biomechanical, neurophysiological, and clinical measurements. The first and best known scale for measuring the degree of spasticity was the Ashworth scale, first developed in 1964 for use in a multiple sclerosis therapeutic trial.26 However, this is a single item scale with poor validity, reliability, and responsiveness.27 Neither is the Ashworth grade influenced by associated features including pain or spasms, or by impact on function; all of which are important issues for the patient. Other clinical scales have been used, including clinician visual analogue scales or self report scales for spasm severity and frequency, though none has been shown to be reliable.28,29 There is thus still a need for development of a valid, responsive, and reliable scale to assess both the severity and the functional impact of spasticity and its associated features.30 In addition to clinical scales, more complex techniques including pendulum tests or gait analysis can be employed, as well as simple goniometers allowing ranges of movement in relevant joints to be recorded and monitored.31 In our experience several measures are necessary to complete a thorough evaluation of the severity and impact of an individual’s spasticity. Our battery includes the Ashworth scale, range measures at rest, active movement and full stretch using a goniometer at joints, and measuring the distance between the knees. We also use subjective severity scores of stiffness, clonus, spasms, pain, and overall comfort, a sitting tolerance score, and recordings of a timed 10 metre walk and frequency of falls. Functional difficulties are outlined in a patient tailored goal of treatment form.
CONCLUSIONS
Spasticity is one of the components of the UMN syndrome but should not be considered in isolation when it comes to management strategies. It is essential that management targets function and is always patient focused rather than aimed at reducing the degree of spasticity. A management strategy is required, such as that prepared by the Multiple Sclerosis Council for their clinical practice guidelines,32 which incorporates an understanding of spasticity in the context of the UMN syndrome with its associated features, aggravating factors, and trigger factors. This is of paramount importance for the patient, family, carers, and health teams. This allows self management strategies to be employed, but also the knowledge essential to identify when further treatment strategies are needed to prevent secondary complications. There is a wide range of physical and pharmacological treatments available which, if used in a timely and appropriate fashion, can be very useful at reducing pain and discomfort without compromising function.
REFERENCES
Brown P . The pathophysiology of spasticity. J Neurol Neurosurg Psychiatry 1991;238:131–9.
Burke D . Spasticity as an adaptation to pyramidal tract injury. Adv Neurol 1988;47:401–23.
Wilson LR, Gandevia SC, Inglis JT, et al. Muscle spindle activity in the affected upper limb after a unilatreral stroke. Brain 1999;122:2079–88.
Aymard C, Katz R, Lafitte C, et al. Presynaptic inhibition and homosynaptic depression. A comparison between lower and uppper limbs in normal human subjects and patients with hemiplegia. Brain 2000;123:1688–702.
Zijdewind I, Thomas CK. Spontaneous motor unit behavior in human thenar muscles after spinal cord injury. Muscle Nerve 2001;24:952–62.
Zijdewind I, Thomas CK. Motor unit firing during and after voluntary contractions of human thenar muscles weakened by spinal cord injury. J Neurophysiol 2003;89:2065–71.
Bennett DJ, Li Y, Harvey PJ, et al. Evidence for plateau potentials in tail motoneurons of awake chronic spinal rats with spasticity. J Neurophysiol 2001;86:1972–82.
Nickolls P, Collins DF, Gorman RB, et al. Forces consistent with plateau-like behaviour of spinal neurons evoked in patients with spinal cord injuries. Brain 2004;127:660–70.
Dietz V . Spastic movement disorder: what is the impact of research on clinical practice? J Neurol Neurosurg Psychiatry 2003;74:820–6.
Dewald JP, Pope PS, Given JD, et al. Abnormal muscle coactivation patterns during isometric torque generation at the elbow and shoulder in hemiparetic subjects. Brain 1995;118:495–510.
Canning CG, Ada L, O’Dwyer NJ. Abnormal muscle activation characteristics associated with loss of dexterity after stroke. J Neurol Sci 2000;176:45–56.
Schmit BD, Benz EN, Rymer WZ. Reflex mechanisms for motor impairment in spinal cord injury. Adv Exp Med Biol 2002;508:315–23.
Norton JA, Marsden JF, Day BL. Spinally generated electromyographic oscillations and spasms in a low-thoracic complete paraplegic. Mov Disord 2003;18:101–6.
Richardson D, Thompson AJ. Management of spasticity in hereditary spastic paraplegia. Physiother Res Int 1999;4:68–76.
Jarrett L . The role of the nurse in the management of spasticity. Nurs Resident Care 2004;3:116–19.
Koman LA, Smith BP, Shilt JS. Cerebral palsy. Lancet 2004;363:1619–31.
Richardson D . Physical therapy in spasticity. Eur J Neurol 2002;9:17–22.
Burridge J, Taylor P, Hagan S, et al. The effects of common peroneal stimulation on the effort and speed of walking: a randomised controlled clinical trial with chronic hemiplegic patients. Clin Rehabil 1997;11:201–10.
Davis EC, Barnes MP. Botulinum toxin and spasticity. J Neurol Neurosurg Psychiatry 2000;69:143–9.
Richardson D, Sheean G, Werring D, et al. Evaluating the role of botulinum toxin in the management of focal hypertonia in adults. J Neurol Neurosurg Psychiatry 2000;69:499–506.
Brashear A, Gordon MF, Elovic E, et al. Botox Post-Stroke Spasticity Study Group. Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. N Engl J Med 2002;347:395–400.
Sheean GL. Botulinum treatment of spasticity: why is it so difficult to show a functional benefit? Curr Opin Neurol 2001;14:771–6.
Barnes MP. Local treatment of Spasticity. Baillieres Clin Neurol 1993;2:55–71.
Beard S, Hunn A, Wright J. Treatments for spasticity and pain in multiple sclerosis: a systematic review. Health Technol Assess 2003;7:1–111.
Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb spasticity in multiple sclerosis: does intrathecal phenol have a role? J Neurol Neurosurg Psychiatry 2002;73:705–9.
Ashworth B . Preliminary trial of carisoprodal in multiple sclerosis. Practitioner 1964;192:540–2.
Hobart J . Rating scales for neurologists. J Neurol Neurosurg Psychiatry 2003;74 (suppl IV) :iv705–9.
Pomeroy VM, Dean D, Sykes L, et al. The unreliability of clinical measures of muscle tone: the implications for stroke therapy. Age Ageing 2000;29:229–33.
Riazi A, Fox P, Vickery J, et al. Developing a patient-based measure of the impact of spasticity in multiple sclerosis. Multiple Sclerosis 2003;9:S151.
Priebe MM, Sherwood AM, Thornby JI, et al. Clinical assessment of spasticity in spinal cord injury: a multidimensional problem. Arch Phys Med Rehabil 1996;77:713–16.
Johnson GR. Outcome measures of spasticity. Eur J Neurol 2002;9 (suppl 1) :10–16.
Multiple Sclerosis Council for Clinical Practice Guidelines. Spasticity management in multiple sclerosis: evidence based management strategies for spasticity treatment in multiple sclerosis. Paralyzed Veterans of America/Consortium of Multiple Sclerosis Centres 2003:27pp.(A J Thompson, L Jarrett, )
2 Institute of Neurology, Queen Square
Physical and pharmacological treatments can reduce pain and discomfort without compromising function
Abbreviations: FES, functional electrical stimulation; UMN, upper motor neurone
Keywords: spasticity; treatment; management
Spasticity is a common symptom seen in many neurological conditions, notably head injury, spinal cord injury, stroke, cerebral palsy, and multiple sclerosis. It is also the dominant feature in several rarer conditions such as tropical and hereditary spastic paraparesis. The fact that it is relevant to many chronic neurological conditions and that the absence of multidisciplinary input can result in progressive disability makes it an ideal model to reflect service provision In the future more long term care for such patients will be done in primary care and the community. It is therefore essential that a multidisciplinary approach is used with successful liaison between secondary, primary, and social care.
Optimum management of spasticity is dependent on an understanding of its underlying physiology, an awareness of its natural history, an appreciation of the impact on the patient, and a comprehensive approach to minimising that impact which is both multidisciplinary and consistent over time. Regrettably, these essential requirements are rarely met; consequently, inadequately managed spasticity results in a range of painful and disabling sequelae which, with the right approach, are for the most part preventable.
PATHOPHYSIOLOGY OF SPASTICITY AND SPASMS
Stretch reflexes in healthy subjects are complex. At rest the reflex response is mediated through IA afferents that connect monosynaptically with the parent motor neurone. However, with the muscle activated other reflex components may also be elicited through group II spindle afferents and transcortical pathways. Stretch reflexes are normally modulated by task and during the different phases of walking. Such modulation reflects changes in motoneuronal and spinal cord inhibitory interneuronal activity. This inhibitory influence is in turn controlled by descending and peripheral inputs. In spasticity an enhanced and prolonged response to muscle stretch is seen at rest. Here both group IA and group II afferents may play a role in eliciting the response, which may be processed by monosynaptic and polysynaptic circuits. Additionally, decreased task and phase dependent modulation of stretch reflexes occurs, reflecting abnormalities of supraspinal control.
Although spasticity is seen after an upper motor neurone (UMN) lesion, the relative importance of individual descending pathways remains unclear.1 A lack of descending control over spinal cord interneuronal circuits results in a decrease in the effectiveness of spinal inhibitory circuits such as those mediating reciprocal, presynaptic, and recurrent inhibition. However, the slow clinical development of spasticity following a neurological insult argues against it simply being a release phenomenon.2,3 Recent studies suggest that intrinsic changes in the motor neurone develop over time following a lesion. These result in abnormally long plateau-like potentials that prolong motor neurone discharge and thus muscle contraction in response to synaptic inputs.4–8 Although prolonged motor neurone discharge can occur in healthy subjects, the paucity of inhibitory spinal cord control in people with spasticity means that this activity could, once triggered, continue relatively unabated.
As well as hyperexcitable stretch reflexes, connective tissue changes and abnormal co-contraction can contribute significantly to stiffness.9 Connective tissue changes can occur without any contracture and the resulting stiffness may vary in a velocity dependent manner similar to spasticity, making it difficult to distinguish clinically between hypertonia of neural and non-neural origin. This distinction is, however, clinically important as the treatment of such stiffness is through physical adjuncts such as stretching and splinting rather than through pharmacological interventions.
Abnormal co-contraction can be seen after stroke during tasks that do not require any joint movement and thus stretch related activity.10 Co-contraction and excessive muscle activity during movements may therefore reflect deficits in coordination that are independent of any abnormalities in stretch related muscle activation.11
Spasms or sudden involuntary, often painful, movements are often included under the umbrella term of spasticity. However, physiologically these appear to be an independent entity. Spasms can be triggered not only by muscle stretch but also through a variety of peripheral, noxious, and visceral afferents. Spasms may be caused by disinhibited polysynaptic reflexes such as the flexor withdrawal reflex,12 or they may reflect abnormal activity within spinal cord circuits which have the effect of synchronising the discharge of motor neurones supplying multiple muscles.13
Spasticity and spasms are, however, only two of the symptoms of the UMN syndrome; other symptoms such as muscle weakness, decreased postural responses, and reduced dexterity all have an impact on an individual’s function. These features may be independent of each other but it is often difficult to assess the relative contribution each has to reduction in function. For example, in hereditary spastic paraparesis it was often thought that spasticity was the main factor contributing to the abnormal gait, but if spasticity is effectively reduced—for example by intrathecal baclofen—there is often evidence of profound underlying weakness which is clearly contributing to the disability.14
THE IMPACT OF SPASTICITY
Spasticity can cause discomfort and stiffness, while spasms can be annoying and painful and may interfere with function. Physical activities such as walking, transferring, picking up objects, washing, dressing, and sexual activity can all be affected. Likewise the ongoing presence of spasticity and spasms can have an emotional impact on, for example, mood, self image, and motivation. Poorly managed spasticity can also be responsible for muscle shortening and the development of tendon and soft tissue contractures, which together with spasms can lead to compromised safety in lying and sitting.15 Once contractures are present these are often very difficult to treat and can have major functional implications, including difficulties with personal hygiene or dressing, positioning, and at times the inability to sit, which may lead to restricted community mobility and social isolation. In addition, such difficulties can lead to the development of pressure sores, which may increase the severity of spasticity and spasms. A further problem—particularly in children with spasticity, which is often secondary to cerebral palsy—is the failure of normal muscle growth, resulting in torsion of long bones and consequent joint instability and degeneration.16 Early identification and intervention to treat spasticity and associated symptoms such as spasms can minimise the development of these long term secondary complications.
However, it must not be forgotten that spasticity can also be useful, perhaps allowing a person to stand or walk when weakness would not otherwise permit it. With these issues in mind it is imperative that management is always patient and function focused rather than aimed at the reduction of spasticity per se.
EFFECTIVE MANAGEMENT MUST BE SEAMLESS AND MULTIDISCIPLINARY
There is no agreed evidence based model available for the management of spasticity and much of what is done is based on a logical and pragmatic approach. A key component of management is the education of all involved, including the patient, family, carers, and health professionals. Continuity of care—particularly across the interfaces of primary and secondary care, involving community rehabilitation teams and care agencies—combined with documentation of the evolving impact of spasticity, is necessary to enable ongoing assessment of change and the appropriate choice and timing of any management intervention (fig 1). Whether the impact of spasticity on an individual is mild or severe, it is important that patients are knowledgeable about spasticity, its associated features, and how they can help themselves to manage and prevent symptoms. The trigger and aggravating factors detailed in fig 1 are particularly important as they can exacerbate spasticity and its associated features. Far too often pharmacological treatment is escalated before appropriate strategies to manage bladder and bowel function, skin integrity, soft tissue length, and positioning are instigated. Attention to these simple but essential areas is paramount at all stages of management.
It is often helpful to approach spasticity management according to the level of severity, including points at which intervention is essential to prevent secondary complications (table 1). However, regardless of the level of severity, it is always important to consider triggers and aggravating factors at each stage and determine whether the spasticity is predominantly focal or generalised (fig 1).
MOVEMENT, EITHER PASSIVE OR ACTIVE, IS ESSENTIAL AT ALL STAGES OF MANAGEMENT
Maintaining muscle length through passive or active exercise and stretching regimens including standing or splinting can be key to managing spasticity both in the short and the long term. Likewise, attention to posture and positioning, which may include the provision and regular review of seating systems, is paramount in managing severe spasticity. Doctors, physiotherapists, occupational therapists, and nurses across primary and secondary care can play key roles in working with the individual and their carers to assess the degree and impact of spasticity, identify goals of treatment, initiate referrals for specialist advice, implement management programmes, and monitor the effects of such interventions.17 Effective spasticity management requires clear communication and documentation between the individual and all the services involved in their care.
Short periods of inpatient rehabilitation can also be useful for individuals experiencing changes in their level of function; this may be increasing difficulty with walking or it could be the transition to the safe use of a wheelchair.
Functional electrical stimulation (FES) is an adjunct to physiotherapy that can be of benefit to selected individuals who are predominantly affected by UMN pathologies resulting in a dropped foot. In theory this should benefit both the neural (by reciprocal inhibition in antagonistic muscles) and non-neural (lengthening of soleus and gastrocnemius) aspects of spasticity. In a small randomised controlled trial in patients following stroke, the use of FES in combination with physiotherapy was statistically superior to physiotherapy alone.18
PHARMACOLOGICAL TREATMENT OF SPASTICITY
Drug treatment can be used for generalised spasticity or targeted to focal problems, and can include agents such as botulinum toxin or intrathecal baclofen and phenol. Botulinum toxin is the most widely used treatment for focal spasticity. The effect of the toxin is to inhibit the release of acetylcholine at the neuromuscular junction. Although this blockade is permanent, the clinical effect of injecting botulinum toxin is reversible because of nerve sprouting and muscle reinnevation, leading to functional recovery of the muscle in a few months.19 It is essential that botulinum toxin injections be given in conjunction with physiotherapy to obtain the maximum benefit. The toxin is injected directly into the targeted muscle and takes 10 to 14 days to have a visible effect. As it is a reversible treatment it may have to be repeated after a few months. Despite randomised controlled trials showing that botulinum toxin is effective in reducing tone,20 there have been few that have shown an improvement in active function, although improvement in passive functions—ease of hygiene, dressing, and so on—has been demonstrated. A notable exception is the study by Brashear and colleagues, which demonstrated a reduction in spasticity in the wrist and fingers of patients following stroke, together with an improvement in their disability assessment scale.21 The lack of evidence of functional improvement in some studies may be related to poor trial design and the lack of function based outcome measures.22
Local injection of phenol is an alternative option for focal spasticity management. This can be used alone or in combination with botulinum toxin, particularly in children, where small body size restricts the available treatment dose of botulinum toxin. Chemical neurolysis by phenol is irreversible and can be used at several sites. The most commonly used are medial popliteal blocks in the management of children with developing foot deformities, and obturator nerve blocks in ambulatory patients with scissoring gait or for improving sitting posture and ease of perineal hygiene.23
The oral agents most commonly used to treat spasticity are baclofen, tizanidine, benzodiazepines, dantrolene, and gabapentin. There is limited evidence of efficacy in clinical trials. The first four appear to be of similar benefit in multiple sclerosis, although diazepam is less well tolerated than the others. Gabapentin has only been studied in a few short term trials (two to six days).24 With the exception of tizanidine and dantrolene, these drugs act by potentiating the action of the inhibitory neurotransmitter gamma amino butyric acid (GABA). Tizanidine, however, is predominantly an 2 agonist and thus decreases presynaptic activity of the excitatory interneurones. Dantrolene is the only antispasticity treatment that acts primarily on muscle. Through inhibiting calcium release from the sarcoplasmic reticulum it decreases the excitation–coupling reaction involved in muscle contraction.
Unfortunately all drug treatments for spasticity can have side effects, the commonest of which are drowsiness and weakness. Of course it is important to recognise that a perceived increase in weakness may actually be a result of unmasking the impairment by removing tone which was functionally useful. To optimise the effects of oral drug treatment it is important to identify appropriate dosage regimens. For instance, if getting out of bed is difficult, the drugs should be left next to the bed and taken immediately on waking, preferably 10 to 20 minutes before getting up. If nocturnal spasms are a particular problem, then increasing night-time doses can be useful.
If oral drug treatment is inadequate at controlling lower limb spasticity or is not tolerated, then intrathecal delivery of baclofen should be considered. The concentration of GABA receptors in the lumbar spinal cord allows very small dosages of baclofen to be effective without causing any systemic side effects. The programmable pump is implanted into the abdomen, from where a catheter conveys the baclofen into the intrathecal space. This is obviously an invasive and relatively expensive treatment which requires careful selection of patients, a trial using a bolus dose of baclofen through a lumbar puncture needle, and significant commitment from patient, not only during the trial and implant phase but also for the ongoing maintenance of regular refills and replacements.
Occasionally the measures outlined above are not sufficient to manage severe spasticity causing contractures and preventing carers from seating or hoisting the patient safely, and such patients may be considered for intrathecal phenol treatment. As phenol is a destructive agent which indiscriminately damages motor and sensory nerves, it is reserved for those individuals who do not have any functional movement in the legs, who have lost bladder and bowel function, and who have impaired sensation to the legs. Phenol is injected intrathecally and is prepared in glycerin, which renders it hyperbaric and viscous, thus limiting its spread. Intrathecal phenol can be an effective treatment which, though it requires expert administration, does not have the long term maintenance or cost issues that go with intrathecal baclofen treatment. The effect of a single injection often lasts many months and can be repeated if necessary.25
MONITORING SPASTICITY
It is clearly helpful to adopt a management approach that is linked to the severity of the spasticity. However, this implies an accurate and reliable assessment of severity, which is in itself a challenging area. Research is ongoing into different assessment strategies, including gait analysis and biomechanical, neurophysiological, and clinical measurements. The first and best known scale for measuring the degree of spasticity was the Ashworth scale, first developed in 1964 for use in a multiple sclerosis therapeutic trial.26 However, this is a single item scale with poor validity, reliability, and responsiveness.27 Neither is the Ashworth grade influenced by associated features including pain or spasms, or by impact on function; all of which are important issues for the patient. Other clinical scales have been used, including clinician visual analogue scales or self report scales for spasm severity and frequency, though none has been shown to be reliable.28,29 There is thus still a need for development of a valid, responsive, and reliable scale to assess both the severity and the functional impact of spasticity and its associated features.30 In addition to clinical scales, more complex techniques including pendulum tests or gait analysis can be employed, as well as simple goniometers allowing ranges of movement in relevant joints to be recorded and monitored.31 In our experience several measures are necessary to complete a thorough evaluation of the severity and impact of an individual’s spasticity. Our battery includes the Ashworth scale, range measures at rest, active movement and full stretch using a goniometer at joints, and measuring the distance between the knees. We also use subjective severity scores of stiffness, clonus, spasms, pain, and overall comfort, a sitting tolerance score, and recordings of a timed 10 metre walk and frequency of falls. Functional difficulties are outlined in a patient tailored goal of treatment form.
CONCLUSIONS
Spasticity is one of the components of the UMN syndrome but should not be considered in isolation when it comes to management strategies. It is essential that management targets function and is always patient focused rather than aimed at reducing the degree of spasticity. A management strategy is required, such as that prepared by the Multiple Sclerosis Council for their clinical practice guidelines,32 which incorporates an understanding of spasticity in the context of the UMN syndrome with its associated features, aggravating factors, and trigger factors. This is of paramount importance for the patient, family, carers, and health teams. This allows self management strategies to be employed, but also the knowledge essential to identify when further treatment strategies are needed to prevent secondary complications. There is a wide range of physical and pharmacological treatments available which, if used in a timely and appropriate fashion, can be very useful at reducing pain and discomfort without compromising function.
REFERENCES
Brown P . The pathophysiology of spasticity. J Neurol Neurosurg Psychiatry 1991;238:131–9.
Burke D . Spasticity as an adaptation to pyramidal tract injury. Adv Neurol 1988;47:401–23.
Wilson LR, Gandevia SC, Inglis JT, et al. Muscle spindle activity in the affected upper limb after a unilatreral stroke. Brain 1999;122:2079–88.
Aymard C, Katz R, Lafitte C, et al. Presynaptic inhibition and homosynaptic depression. A comparison between lower and uppper limbs in normal human subjects and patients with hemiplegia. Brain 2000;123:1688–702.
Zijdewind I, Thomas CK. Spontaneous motor unit behavior in human thenar muscles after spinal cord injury. Muscle Nerve 2001;24:952–62.
Zijdewind I, Thomas CK. Motor unit firing during and after voluntary contractions of human thenar muscles weakened by spinal cord injury. J Neurophysiol 2003;89:2065–71.
Bennett DJ, Li Y, Harvey PJ, et al. Evidence for plateau potentials in tail motoneurons of awake chronic spinal rats with spasticity. J Neurophysiol 2001;86:1972–82.
Nickolls P, Collins DF, Gorman RB, et al. Forces consistent with plateau-like behaviour of spinal neurons evoked in patients with spinal cord injuries. Brain 2004;127:660–70.
Dietz V . Spastic movement disorder: what is the impact of research on clinical practice? J Neurol Neurosurg Psychiatry 2003;74:820–6.
Dewald JP, Pope PS, Given JD, et al. Abnormal muscle coactivation patterns during isometric torque generation at the elbow and shoulder in hemiparetic subjects. Brain 1995;118:495–510.
Canning CG, Ada L, O’Dwyer NJ. Abnormal muscle activation characteristics associated with loss of dexterity after stroke. J Neurol Sci 2000;176:45–56.
Schmit BD, Benz EN, Rymer WZ. Reflex mechanisms for motor impairment in spinal cord injury. Adv Exp Med Biol 2002;508:315–23.
Norton JA, Marsden JF, Day BL. Spinally generated electromyographic oscillations and spasms in a low-thoracic complete paraplegic. Mov Disord 2003;18:101–6.
Richardson D, Thompson AJ. Management of spasticity in hereditary spastic paraplegia. Physiother Res Int 1999;4:68–76.
Jarrett L . The role of the nurse in the management of spasticity. Nurs Resident Care 2004;3:116–19.
Koman LA, Smith BP, Shilt JS. Cerebral palsy. Lancet 2004;363:1619–31.
Richardson D . Physical therapy in spasticity. Eur J Neurol 2002;9:17–22.
Burridge J, Taylor P, Hagan S, et al. The effects of common peroneal stimulation on the effort and speed of walking: a randomised controlled clinical trial with chronic hemiplegic patients. Clin Rehabil 1997;11:201–10.
Davis EC, Barnes MP. Botulinum toxin and spasticity. J Neurol Neurosurg Psychiatry 2000;69:143–9.
Richardson D, Sheean G, Werring D, et al. Evaluating the role of botulinum toxin in the management of focal hypertonia in adults. J Neurol Neurosurg Psychiatry 2000;69:499–506.
Brashear A, Gordon MF, Elovic E, et al. Botox Post-Stroke Spasticity Study Group. Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. N Engl J Med 2002;347:395–400.
Sheean GL. Botulinum treatment of spasticity: why is it so difficult to show a functional benefit? Curr Opin Neurol 2001;14:771–6.
Barnes MP. Local treatment of Spasticity. Baillieres Clin Neurol 1993;2:55–71.
Beard S, Hunn A, Wright J. Treatments for spasticity and pain in multiple sclerosis: a systematic review. Health Technol Assess 2003;7:1–111.
Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb spasticity in multiple sclerosis: does intrathecal phenol have a role? J Neurol Neurosurg Psychiatry 2002;73:705–9.
Ashworth B . Preliminary trial of carisoprodal in multiple sclerosis. Practitioner 1964;192:540–2.
Hobart J . Rating scales for neurologists. J Neurol Neurosurg Psychiatry 2003;74 (suppl IV) :iv705–9.
Pomeroy VM, Dean D, Sykes L, et al. The unreliability of clinical measures of muscle tone: the implications for stroke therapy. Age Ageing 2000;29:229–33.
Riazi A, Fox P, Vickery J, et al. Developing a patient-based measure of the impact of spasticity in multiple sclerosis. Multiple Sclerosis 2003;9:S151.
Priebe MM, Sherwood AM, Thornby JI, et al. Clinical assessment of spasticity in spinal cord injury: a multidimensional problem. Arch Phys Med Rehabil 1996;77:713–16.
Johnson GR. Outcome measures of spasticity. Eur J Neurol 2002;9 (suppl 1) :10–16.
Multiple Sclerosis Council for Clinical Practice Guidelines. Spasticity management in multiple sclerosis: evidence based management strategies for spasticity treatment in multiple sclerosis. Paralyzed Veterans of America/Consortium of Multiple Sclerosis Centres 2003:27pp.(A J Thompson, L Jarrett, )