Article Text
Abstract
Spasticity is common in many neurological disorders, such as stroke and multiple sclerosis. It is part of the upper motor neurone syndrome manifesting as increased tone, clonus, spasms, spastic dystonia and co-contractions. The impact of spasticity varies from it being a subtle neurological sign to severe spasticity causing pain and contractures. Existing spasticity can be worsened by external factors such as constipation, urinary tract infections or pressure ulcers. Its management involves identification and elimination of triggers; neurophysiotherapy; oral medications such as baclofen, tizanidine and dantrolene; focal injection of botulinum toxin, alcohol or phenol, or baclofen delivered intrathecally through a pump; and surgical resection of selected dorsal roots of the spinal cord. This article reviews the current understanding of pathophysiology, clinical features and management of spasticity.
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Introduction
Spasticity is defined as ‘disordered sensorimotor control resulting from an upper motor neurone (UMN) lesion, presenting as intermittent or sustained involuntary activation of muscles’.1 It is a frequent symptom of common neurological disorders, such as multiple sclerosis and stroke. Spasticity seldom exists in isolation and is usually accompanied by one or more components of UMN syndrome (table 1).
Spasticity varies from being a clinical sign with no functional impact to being a gross increase in tone interfering with mobility, transfers and personal care. Untreated, it can cause shortening of muscles and tendons, leading to contractures (figure 1). Some patients depend on their spasticity to stand, walk and transfer or sit upright. The optimum management of spasticity requires a co-ordinated approach with rehabilitation professionals.
Pathophysiology
Tone is the resistance of resting muscle to passive movements. Normal tone results from visco-elastic properties of muscle and neural drive from spinal motor neurones. Viscosity is the resistance of tissue to deforming forces whereas elasticity is the ability of a tissue to return to its original position after being stretched. Viscosity resists stretch; elasticity pulls the muscle back to its original position. When stretched, muscle spindle Ia afferents excite spinal motor neurones; this results in contraction of agonist and relaxation of antagonistic muscles. This stretch reflex is modulated by supraspinal and spinal pathways, activity, posture and sensations.
Increased tone initially results from the excessive neural drive of spinal motor neurones, and later is partly because of visco-elastic changes in immobilised muscles and joints. In spasticity, motor neurones respond to stretch at a lower threshold than normal, with long discharges: the ‘plateau potentials’.2 This results from a change in balance between inhibitory and excitatory inputs to spinal motor neurones in favour of excitation (table 2). After immobilisation, connective tissue and fat can replace sarcomeres. Left unchecked, this process can end in contractures and permanent loss of joint mobility.3
As well as increased tone spasticity has other features, such as clonus, spasms, spastic dystonia and spastic co-contractions.
Clonus is the phenomenon of involuntary rhythmic contractions in response to sudden sustained stretch. It is due to alternate loading and off-loading of muscle spindles. A sudden stretch activates muscle spindles, resulting in the stretch reflex. Tension produced by the muscle contraction activates the Golgi tendon organs, which in turn activate an ‘inverse stretch reflex’, relaxing the muscle. If the stretch is sustained, the muscle spindles are again activated, causing a cycle of alternating contractions and relaxations. It can be triggered by active or passive stretch and can interfere with walking, transfers, sitting and care.
Spasms are sudden involuntary movements that often involve multiple muscle groups and joints. They can be repetitive and sustained. These represent an exaggerated reflex withdrawal response to nociceptive stimuli and are mediated by polysynaptic intersegmental spinal cord circuits.
Spastic dystonia is tonic muscle overactivity that occurs without any triggers.4 It is due to an inability of motor units to cease firing after a voluntary or reflex contraction, resulting in sustained muscle contractions. The postures characteristic of spastic dystonia are shoulder adduction and internal rotation, elbow flexion, forearm pronation, wrist and elbow flexion, hip adduction and ankle plantar flexion and inversion. Spastic dystonia can lead to contractures and deformities causing pain, discomfort and high-care needs.
Spastic co-contraction is the inappropriate activation of antagonistic muscles during voluntary activity.4 It is due to loss of reciprocal inhibition during voluntary contraction. Normal voluntary activity involves selective and sequential contraction of agonists and synergistic muscles, with antagonist muscle inhibition. In spastic co-contraction, there are instead mass contractions of both agonist and antagonistic muscles, resulting in loss of dexterity and slowed movements.
Clinical evaluation
Clinical assessment of spasticity includes the following steps:
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Differentiation of spasticity from other causes of increased tone
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Identification of potential triggers
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Measurement of spasticity
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Assessment of impact on function.
Complete assessment requires input from patients, carers, therapists and other rehabilitation professionals.
Is it spasticity?
Clinically, spasticity needs to be differentiated from other causes of increased tone, such as rigidity, catatonia, gegenhalten or contractures.
Spasticity has several characteristic features:
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Velocity dependence: The increased tone of spasticity is velocity dependent, that is, the faster the stretch, the greater the muscle resistance.
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‘Clasp-knife’ phenomenon: This is where the spastic limb initially resists movement and then suddenly gives way, rather like the resistance of a folding knife blade. During initial movement, the tone is high due to overactive stretch. On sustained movement, the inverse stretch reflex kicks in, relaxing the muscles with a ‘give away’ feel. In the later stage, as contractures set in, this is replaced by a non-elastic solid resistance.
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Stroking effect: Stroking the surface of the antagonistic muscle may reduce the tone in spasticity, though it does not affect contracture.
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Distribution: Spasticity has a differential distribution with antigravity muscles being more affected.
Rigidity is a non-selective increased tone throughout the range of muscle movements and is not velocity dependent.
Gegenhalten, or ‘counter hold’ is an increase in muscle tone proportional to the force applied. When the limb is moved passively, the muscles stiffen in proportion to the force applied, as if the patient is actively opposing movement.
Catatonia is a neuropsychiatric syndrome accompanying a wide range of psychiatric, neurological and medical conditions with motor, behavioural, affective and autonomic features.5 The clinical features include abnormal posturing, waxy flexibility and gegenhalten. In waxy flexibility, patients maintain limbs in positions placed by others for a long time.
What causes spasticity?
Neurologists encounter spasticity either as a presenting feature of a neurological illness or as a feature of an established condition. Spasticity could be the initial manifestation of any pathology affecting UMN. Table 3 lists some conditions that can present predominantly as spasticity.
Spasticity can worsen because of exacerbating factors—nociceptive, visceral or somatic stimuli—or it can increase through progression of the underlying disease, through delayed complications of the primary pathology such as post-traumatic syrnigomyelia, or through coincidental new pathology.
What is the impact of spasticity?
Spasticity often causes discomfort. Any trivial sensory stimulus may trigger painful spasms. Spasticity restricts joint motion and limits mobility. The asymmetric pull of overactive muscles can alter posture and cause deformities, for example, kyphoscoliosis, flexion contractures at the elbow, hip and knee, or talipes equinovarus at the ankle. Untreated, spasticity leads to contractures, which are often difficult to correct (figure 1). Spasticity affects positioning and pressure area care, resulting in pressure ulcers (figure 2). It makes hygiene tasks, especially cleaning of hands, axillae, elbows and genital areas particularly difficult. Spasticity can interfere with bowel and bladder care and sexual relationships.
Spasticity is not always detrimental and has some benefits. Trunk muscle stiffness helps with sitting upright and with transfers. Spasticity of hip and knee extensors aids standing, transfering and walking. An overactive soleus facilitates toe push-off and helps walking in children with cerebral palsy. Finger flexor spasticity enables people to hold objects, such as cutlery and a toothbrush. Clinicians must therefore weigh up the positive and negative aspects of spasticity when advising on its treatment.
Measurement of spasticity
Before advising intervention, it is essential to obtain a baseline measurement of the spasticity, to enable objective assessment of the impact of treatment. Note that the degree of spasticity varies with ambient temperature, time of the day, fatigue, posture and position of the limb.4 Assessment of spasticity should include recording of any exacerbating or relieving factors. There are several scales that quantify different aspects of spasticity, but no one scale is universally clinically acceptable (table 4).
The modified Ashworth score is the most frequently used clinical measure (table 5). It is a good clinical tool, especially for repeated measurements by the same assessor. It does not require any instruments and can be done easily in different clinical settings. It is an ordinal scale but has several limitations.14
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It does not differentiate between spasticity and soft tissue contractures.
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There is poor inter-rater reliability, as the applied force varies between examiners.
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It is a six-level ordinal scale that is not sensitive to change.
Documentation of spasticity assessment should also include:
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assessment of other UMN syndrome components, such as weakness and loss of dexterity
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the response to antispasticity drugs, and their adverse effects
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contractures, as these do not respond to pharmacological interventions
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the patient's need for mobility aids and assistive devices, such as wheelchairs, seats, hoists and orthoses.
Management
The aim of management is to reduce the impact of spasticity and to prevent secondary complications. The first step is to set treatment goals, which must be agreed upon by the patient and the therapy team. Goals need to be meaningful for the patient and easily understood. Examples of spasticity management goals are the relief of discomfort, improved sitting, standing and walking, facilitated activities of daily living, reduced burden of care, improved body image and self-esteem and prevention of complications. Goal attainment scaling is a measure of the extent to which treatment goals are achieved. The intended outcome is graded as12
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−2: much worse than expected
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−1: somewhat worse than expected
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0: achieved the expected outcome
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+1: somewhat better than expected
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+2: much better than expected outcome.
The patient is actively involved in setting goals and in measuring the outcome of interventions.
Some key elements of spasticity management are identification and elimination of triggers, non-pharmacological interventions and medications.
Identifying and eliminating triggers and aggravating factors (table 6)
Common causes of spasticity exacerbation are urinary tract infections and constipation. Bladder stones may rarely present through worsening of spasticity (figure 3). Patient and carer education to recognise these triggers is an important part of management.
Non-pharmacological interventions
Passive movements
Passive stretching decreases the excitability of motor neurones and maintains the visco-elastic properties of muscles and joints.15 Manual stretching delivered by therapists, therapy assistants or carers is time and labour intensive. The intensity of force applied, the duration of a stretch and the number of repetitions per session may vary with the person applying stretch and within and between treatment sessions. Machines such as the isokinetic dynamometer deliver standardised passive stretches. However, they are expensive and not widely available. Muscles and joints can be kept stretched for hours or days using casts or splints, sometimes used together with botulinum toxin injections. Prolonged stretching can help to treat contractures. Patients often report exacerbation of spasticity on waking up: stretching and taking a morning dose of antispasticity medication before getting out of bed may help to reduce this. However, a recent systematic review failed to show evidence for regular stretching in neurological conditions.16 The effect of stretching on spasticity and contractures is still largely evidence free; however, there is no evidence that it is harmful.
Exercises
Exercises improve motor control and cardiovascular fitness in people with UMN disorders. Strong trunk, pelvic and shoulder girdle muscles provide stability required for accurate control of the distal movements.17 Whereas exercises improve strength and overall function in people with spasticity, there is only very limited evidence that they directly reduce spasticity.18 Exercises that help people with spasticity include cycling, strengthening exercises and treadmill training.18–20 In contrast to previous ideas, exercises do not aggravate spasticity.18 Exercises may be inappropriate if patients are not otherwise fit, have osteoporosis, coagulation disorders or severe limitation of passive range of movement, or in the immediate postoperative period.17 Biofeedback uses visual or auditory cues to help patients judge their performance. This technique helps patients to recognise and promote muscular activity that is not otherwise obvious to them. It also helps to avoid unwanted activity such as spastic co-contractions.15
Posture and standing
Standing for about half an hour a day may help to reduce spasticity.21 As well as its effect on spasticity, weight bearing and standing also help to improve psychological wellbeing, to improve bone mineral density, facilitate pulmonary drainage and helps bowel and bladder functions. Tilt tables and standing frames help with proper positioning of the joints and trunk while standing. Therapists often use tilt tables to initiate standing and than progress to standing frames.
Proper positioning of limbs and trunk during standing, sitting or lying is essential to prevent aggravation spasticity and development of contractures. Incorrect standing, for example, with ankles plantar flexed, knees flexed and hip flexed and adducted, can facilitate spasticity and contractures. Devices such as T-rolls and splints help to position limbs properly and thereby prevent contractures. A wheelchair and seating assessment also help to position the trunk and limbs properly during sitting and is an essential component of management of late stage spasticity. Splints such as wrist–hand orthosis and ankle–foot orthosis may help in managing spasticity. They provide a prolonged stretch and inhibit motor neurone excitability. However, there is little evidence to support their ability to inhibit motor neurones.22
Physical modalities
Physical modalities used to treat spasticity include ultrasound, cryotherapy (application of cold), vibration, shockwave therapy, magnetic stimulation, transcutaneous electrical nerve stimulation (TENS) and functional electrical stimulation. These physical modalities work through either modulating the visco-elastic properties of muscles and tendons (cryotherapy, ultrasound and shock wave therapy), inducing long-term depression at the spinal level, stimulating cortico-cortical inhibitory pathways (magnetic stimulation), inducing short-term plasticity in injured spinal motor systems or activation of proprioceptive inputs (TENS).15 There is only a limited evidence base to support the use of these modalities and no current guidance about their use in clinical practice.
Medications
Before starting antispasticity drugs, it is essential to decide the treatment goals: for example, to reduce pain and discomfort, to facilitate a good night's sleep, to achieve proper position on the chair or in bed, to facilitate hygiene or to improve functions such as gait. The choice of treatment and the timing of doses depend largely on these goals. Weakness is a side effect of all antispasticity drugs, usually due to unmasking of underlying UMN weakness, rather than from a direct drug effect. Inappropriate dose escalation often leads to side effects and hence to poor compliance. A ‘start low and go slow’ policy limits these unwanted functional effects.
Spasticity is often undertreated. Drugs are too quickly labelled as ineffective without a fair trial of maximal tolerated doses. It is essential to try to reach the maximal tolerated dose for a sufficiently long period before stopping a drug. Patients not responding to one drug may respond to another. Sudden stopping of even an apparently ‘ineffective’ drug may cause a rebound increase in spasticity. It is better to taper initial drug while simultaneously introducing the second drug.
A combination of two drugs should be tried if the spasticity does not respond to a single agent, or if the patient can tolerate only low doses. It is important to time the doses according to the patient's activity, care and therapy. Ambulant patients often require lower doses during the daytime as they may be using spasticity to facilitate their walking. A dose may be required immediately after awakening in the morning to facilitate care.
Oral agents
The commonly used antispasticity drugs are those acting on a gamma aminobutyric acid (GABA)ergic system (baclofen, gabapentin and benzodiazepines), α-2 adrenergic system (tizanidine) and those that block calcium release into the muscles (dantrolene). Even though these drugs have been used for several decades, there are no evidence-based guidelines for the choice, titration rates and withdrawal of these drugs.23 Our recommendations (below) are based on both a literature review and clinical pragmatism.
Baclofen
Baclofen is the most widely used oral antispasticity drug. It is a GABA-B receptor agonist. Baclofen reduces calcium influx and suppresses release of excitatory neurotransmitters, including glutamate and aspartate. It down-regulates activity of 1a sensory afferents, spinal interneurones and motor neurones. The usual starting dose is 5 mg thrice daily, increased by 5–10 mg weekly, until there is an optimal effect. The maximum dose is 90–120 mg per day. Its side effects include weakness, drowsiness and dizziness; some people report sexual dysfunction and urinary incontinence. Baclofen can reduce the seizure threshold and should be used with caution in people with seizures. Stopping baclofen can provoke rebound spasticity within 48 h, though it usually settles after another 48 h. Sudden withdrawal may also cause seizures and hallucinations. Baclofen should be used with caution during pregnancy: although there are no reports of baclofen directly causing human fetal malformations, animal studies using high doses show that it causes impaired sternal ossification and omphalocele.24 Withdrawal from maternal baclofen occasionally provokes neonatal convulsions25 and so newborns of mothers taking baclofen should receive oral baclofen 0.5 mg per kg per day, weaned off over 9 days.26 Baclofen appears in breast milk and this must be considered when advising mothers about breast feeding.
Benzodiazepines
Benzodiazepines act on GABA-A receptors. They have similar efficacy to other antispasticity drugs, but more troublesome side effects. Drowsiness and behavioural side effects limit its use during the daytime. They are particularly useful to treat spasticity that interferes with sleep. Clonazepam is particularly useful to treat nocturnal spasms. The usual starting dose is 500 µg at night, with a maximum dose of 1 mg.
Gabapentin and pregabalin
A few small trials show the efficacy of these GABAergic drugs in treating spasticity.27 ,28 They are particularly useful as adjuncts in treating spasticity associated with pain. Their side effects include weight gain, gastro-intestinal disturbances, confusion, depression, hostility and sleep disturbance. Gabapentin should start at 300 mg once daily on day 1, 300 mg twice daily on day 2, then 300 mg thrice daily on day 3, then increased according to the patient's response in steps of 300 mg every 2–3 days to maximum of 3600 mg daily. The dose of pregabalin is 75 mg twice a day and it can be titrated up to 300 mg twice daily.
Tizanidine
Tizanidine is an α-2 receptor agonist which enhances noradrenergic activity in the spinal cord and brain. It inhibits excitatory spinal interneurones and tracts from locus coeruleus. Its side effects include dry mouth, gastrointestinal disturbance, hypotension and acute hepatitis. It is essential to monitor liver enzymes during the first 4 months of treatment. Sudden stopping of tizanidine can lead to a hyperadrenergic syndrome, characterised by anxiety, tremor, hypertension and tachycardia. The usual starting dosage is 2 mg at bedtime, increased by 2 mg weekly to a maximum of 36 mg, divided into 3–4 daily doses.
Dantrolene
Dantrolene blocks calcium release from the sarcoplasmic reticulum and interferes with excitation–contraction coupling of the skeletal muscle. Unlike other antispasticity drugs, it acts directly on the muscle and so is less sedative. The starting dose is 25 mg daily for the first week, increased in steps of 25 mg per week to a top dose of 100 mg 3–4 times daily. The most important side effect is hepatotoxicity, and so liver function must be monitored carefully.
Cannabinoids
There are cannabinoid receptors in dorsal spinal cord, basal ganglia, hippocampus and cerebellum, and these modulate spasticity.29 Tetrahydrocannabinol, an agonist of cannabinoid 1 and 2 receptors, reduces spasticity but causes sedation and psychotropic side effects. Cannabidiol has lower affinity for both these receptors and reduces the psychotropic and sedative effects of tetrahydrocannabinol. Recently, nabiximols (Sativex) oromucosal spray, a 1:1 mixture of 9-δ-tetrahydrocannabinol and cannabidiol, was licensed for use in spasticity in multiple sclerosis in the UK. An independent review noted improvement in patient reported outcome measures, but found no significant reduction in objective measures of spasticity.30 Side effects include taste disturbance, dry mouth, oral ulcers, dizziness, depression, mood changes, cognitive impairment, drowsiness, dysarthria and blurred vision.29 ,30 Nabiximols currently has only a limited role in managing treatment-resistant spasticity. It may be worth trying a 4-week trial in patients with spasticity from multiple sclerosis who are not responding to a combination of two drugs in adequate doses. As only 30–40% of people show a response, the treatment effect should be reviewed at 4–6 weeks and continued only if there is an objective improvement. There are still concerns about its long-term effects on cognition, behaviour and mental health.
Botulinum toxin
All therapeutically used botulinum toxins are prepared from the bacterium Clostridium botulinium, which causes botulism, a potentially fatal neuromuscular paralysis. The heavy chain of botulinum toxin binds to and becomes internalised into presynaptic nerve endings. There, it degrades synaptosomal-associated protein 25, a protein required for fusion of acetylcholine vesicles to the presynaptic membrane. This inhibits release of acetylcholine, thereby blocking neuromuscular transmission. The effect is reversed by nerve sprouting and reinnervation which develops over a few months. When injected into skeletal muscle, botulinum toxin causes selective weakness of the target muscle. It is particularly useful in the treatment of focal spasticity. It has the advantage of achieving selective reduction in spasticity without the side effects of global weakness or sedation.
Before considering botulinum toxin, it is important first to address all triggers factors have and to ensure that there are no significant contractures. The next step is to agree with members of the multidisciplinary team the treatment goals, the target muscles and postinjection interventions. Before giving the injections, these goals and the treatment plan must be discussed and agreed with the patient and carer, with informed consent. Electromyography, nerve stimulator or ultrasound can be used to identify the target muscle. Postinjection interventions such as physiotherapy, splinting and serial casting help to maximise benefits of botulinum toxin injections. The patient should be reassessed 4–6 weeks after the initial injections to assess the efficacy of the injections and whether the treatment goals have been attained. If required, further injections should be planned after 3–4 months.12 Adverse events of botulinum toxin include respiratory tract infections, muscle weakness, urinary incontinence, falls, fever and pain.31 Rarely, the toxin can cause transient dysphagia, even requiring nasogatric feeding.
Intrathecal baclofen
Oral baclofen has only very low bioavailability to GABAergic neurones in the spinal cord. When administered intrathecally, however, a relatively small dose of baclofen can give a high concentration of drug within the spinal cord. This helps to achieve good muscle relaxation and to avoid troublesome side effects. Intrathecal baclofen (ITB) is relatively well-tolerated and is effective in spasticity secondary to spinal cord disorders, stroke, cerebral palsy and multiple sclerosis.32–35 It is indicated for significant lower-limb spasticity which persists despite adequate treatment with at least two oral antispasticity drugs concomitantly. A recent review in multiple sclerosis suggested that ITB pumps were under used.36
The ITB system comprises a subcutaneous pump which stores and delivers programmable doses of baclofen through a catheter into the spinal subarchnoid space (figure 4). The pumps can be adjusted to vary the doses delivered, depending on the level of patient activity and needs. Although ITB has a greater effect on lower-limb spasticity and spasms, it also helps to reduce upper-limb tone. ITB is usually first tested using a temporary catheter with an initial test dose is 50 µg, and subjects are monitored for side effects and efficacy. One should proceed to baclofen pump implantation if the screening test succeeds in meeting the goals previously agreed with the patient and multidisciplinary team.
Patients must be warned about potentially life-threatening complications and the need for regular long-term monitoring. Implants may lead to procedure related complications such as infection, skin erosions, cerebrospinal fluid leak and seroma formation around the pump. The frequency of complications varies from zero to 2.24 per implant.37 Abruptly stopping ITB can cause high fever, confusion, rebound spasticity and muscle rigidity, similar to neuroleptic malignant syndrome. Common causes include pump failure, battery failure, catheter block and non-adherence. Patients who cannot attend regular monitoring visits should not be offered this intervention. Treatment of acute ITB withdrawal should be aimed at reducing muscle tone and treating central nervous system (CNS) effects such as delirium and seizures. If possible, ITB should be restarted with a temporary external catheter at the same dose and rate. Large oral doses of baclofen, for example, 120 mg per day are often used, but may still not be adequate, as the penetration into CNS is poor and oral baclofen takes as it takes 3–4 days to become effective. Adjuvant drugs to treat acute baclofen withdrawal include dantrolene, benzodiazepines, propofol, tizanidine and cyproheptadine.38
Phenol
Phenol injected directly into peripheral nerves cause destruction of neural tissue by protein coagulation. This chemical neurolysis has long been in use to treat spasticity.39 Muscle near the injection site is usually damaged along with the target nerves. These agents are effective in treating spasticity that occurs in large, powerful muscle groups close to the trunk, such as the thigh adductors. The most commonly applied blocks are to the medial popliteal muscles to aid spastic foot drop, or obturator nerve blocks either in patients with scissoring gait or to improve perineal hygiene and seating posture. It should be done only under the guidance of an ultrasound scan or nerve stimulator (figure 5). Nerve sprouting may lead to recurrence of spasticity. A single injection often has effects lasting many months and can be repeated if necessary. The most trouble some side effect is pain and dysaesthesia; it is therefore used usually only in people with loss of sensation. Other side effects are peripheral oedema, skin sloughing and wound infection.39 Phenol also increases the risk of deep venous thrombosis and leukaemia. However, there are no reports of leukaemia in those who received it as spasticity treatment.
In selected people whose spasticity is resistant to conventional treatment, intrathecal injection of 0.5–4.0 ml of 5% phenol in glycerine may be an alternative.40 As phenol indiscriminately damages motor and sensory nerve roots, it should be reserved for people who have no functional movement in their legs, lost bladder and bowel functions and lost sensation to their legs.
Selective dorsal rhizotomy
This procedure involves a surgical section of dorsal nerve roots of the lumbosacral spinal cord. This reduces the sensory input into spinal motor neurone pools, reducing their excitability. It is usually used to treat spasticity associated with cerebral palsy, with good long-term outcomes.41 Patients with spastic dystonia or co-contractions are unlikely to benefit from this procedure. It is an invasive surgical procedure and requires multiple-level laminectomies and must be followed by an intensive rehabilitation programme. Side effects include sensory loss, urinary incontinence, low-back pain and spinal deformity. Recently, less invasive percutaneous radiofrequency ablation of dorsal root ganglion showed promising results.42
Summary
Spasticity is one component of UMN syndrome and its effects are often compounded by other deficits in motor function. The impact of spasticity varies between patients. Treatment strategies should be selected keeping in mind the useful effects of spasticity. Untreated, it can cause significant discomfort and problems to mobility and care. An important aspect of management is to eliminate trigger factors and to try non-pharmacological approaches. Oral antispasticity drugs should be started at a low dose and gradually titrated. Once started, no single drug should be discarded until its maximum dose is reached or if patient develops intolerable side effects. In patients whose spasticity is resistant to oral treatments, surgical interventions such as ITB pump should be tried.
Acknowledgement
Authors would like to thank Mr Martin McClleland, Consultant in Spinal Injuries, Princess Royal Spinal Injuries and neurorehabilitation Centre, Northern General Hospital, Sheffield for permission to reproduce figures 2, 3 and 5.
References
Footnotes
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Contributors Both Dr A Kheder and Dr KPS Nair made substantial contributions to this article; Dr Ammar Kheder: Literature search, review of literature, writing; Dr KPS Nair: Idea, review of literature, writing, correspondence.
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Competing interests KPSN was a site investigator for a clinical trial of Sativex for spasticity funded by GW Pharma Ltd UK.
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Provenance and peer review Commissioned. Externally peer reviewed. This paper was reviewed by Diane Playford, London, UK.
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