Approach to spasticity in General practice

Ganesh Bavikatte and Tarek Gaber

Spasticity is a common symptom seen as a consequence of an injury to the brain (stroke, trauma, hypoxia, infection, cerebral palsy and post surgery), spinal cord injury or multiple sclerosis. It is a complex problem, which can cause profound disability alone or in combination with other features of upper motor neuron syndromes (figure 1). The word “spasticity” is derived from the Greek word “spasticus”, which means “To pull or To Tug”. Spasticity is defined¹ as “Disordered sensori-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”. Simply stated, spasticity is stiffness of muscles that occurs after injury to the spinal cord or brain. Awareness of the implications and associated symptoms can minimise development of long term secondary complications (table 1). The impact of spasticity can be devastating. If not managed early and appropriately it may result in progressive disability, resulting in secondary complications such as contractures and pressure sores. This significant impact has ensured that spasticity management is a prominent feature in the national management guidelines for long term neurological conditions, promoting coordination of care between primary, secondary and social care providers. Symptoms Spasticity can range from mild muscle stiffness to severe, painful and uncontrollable muscle spasms. It is associated with both positive and negative components of upper motor neuron syndromes. Positive components include muscle overactivity, flexor and extensor spasm, hyperreflexia, athetosis, spastic dystonia, clonus, and an extensor plantar response. Common negative symptoms comprise weakness/ paralysis, early hypotonia, fatigue and loss of dexterity. Spasticity can be distinguished from rigidity by its dependence on the speed of muscle stretch and characteristic distribution in antigravity muscle groups. Spasticity does not always cause harm and can occasionally assist in the rehabilitation process by enabling a patient to stand when their limb weakness would not otherwise allow it Table 1 Clinical and functional problems associated with severe Spasticity

 Figure 1 Vicious cycle of spasticity   Assessment of spasticity Before any intervention is undertaken to modulate hypertonicity, it is important to attempt to assess the severity of spasticity. Many grading scales are used to quantify spasticity. These address the degree of muscle tone, the frequency of spontaneous spasms and the extent of hyperreflexia. Goniometry, Ashworth scale, Tardieu Scales, Goal attainment scale are only a few of these scales. One of the most widely used scales is the modified Ashworth scale². Table 2 Modified Ashworth scale

  It is also important to remember that not every “tight” muscle is spastic. The clinically detectable increase in muscle tone may be due to spasticity, rigidity or a fixed muscle contracture. Management  The key to successful spasticity management is education of the patient and carers with both verbal and written information. This allows them to understand, appreciate and be fully involved in the management plan. All patients with spasticity should be followed up by a coordinated multidisciplinary team, which allows more timely intervention and close monitor of the progress. Liaison between health and social services in both primary and secondary care is essential in long term management. This helps to deliver a more consistent approach to the individual over time (figure 2). Table 3 Aims of spasticity management.

 The first step in the management of spasticity is to identify the key aims and realistic goals of therapy. Understanding the underlying pathology and possible prognosis is helpful in planning these goals (table 3). Other key points to consider are: ·          Identification and management of any trigger or aggravating factors-Initial assessment should exclude any co morbidity that may worsen spasticity such as pressure sores, chronic pain, infection (commonly urinary tract infection), constipation or in-growing toe nails.·          Instigation of an effective and realistic physical programme including attention to posture and positioning Figure 2
Approach to spasticity assessmentComprehensive assessment of spasticityRecognition of underlying provocative factorsImpact on the individualMeasurement of spasticityPotential goals- individualised and person focussed 
Initial approachEducation to patient/ and their family /carersMultidisciplinary team assessmentIdentification of clear treatment goalsEstablish mechanism for monitoring and review  Management Manage triggering factorsBalance between positioning and movementPosture and seatingPhysical therapy and active exercise programmeSplinting and use of orthoticsPharmacotherapy A)      Physical modalities·          Stretching- this intervention has the benefit of being benign and non-invasive. Maintaining muscle length through passive or active exerciseand stretching regimens including standing or splinting canbe key to managing spasticity both in the short and the longterm.·          Cooling of muscles- this inhibits mono synaptic stretch reflex and lowers the receptor’s sensitivity, different techniques such as quick icing and evaporating spray like ethyl chloride are occasionally used.·          Heat-heat may increase the elasticity of the muscles. Techniques used include ultrasound, fluidotherapy, paraffin, superficial heat and whirlpools. These techniques should be combined with stretching and exercise.·          Orthosis/equipment/ aids – an orthosis or splint is an external device designed to apply, distribute or remove forces to or from the body in a controlled manner to control body motions and /or alter the shape of body tissues. E.g. ankle foot orthosis, insoles, ankle supports, wrist/ hand/ elbow splints, knee splints, spinal brace, hip brace, neck collar. Some equipment can also aid positioning e.g. T roles, wedges, cushions and foot straps.These are usually used in combination with other modalities like botox therapy. Attention to posture and positioning, whichmay include the provision and regular review of seating systems,is paramount in managing severe spasticity·          Massage– althoughvarious techniques are in use there is no evidence to support this·          Dynamic physiotherapy technique- many schools of physiotherapy claim that particular technique has antispastic and functional benefits, particularly for the more mobile person. E.g. Bobath technique, proprioceptive neuromuscular facilitation, Brunnstrom technique. B) Electrical therapy·          Functional Electrical stimulation –Thisis an adjunct to physiotherapythat can be of benefit to selected individuals who are predominantlyaffected by upper motor neuron pathologies resulting in a foot drop. Randomised controlled trial by Burridge et al in patients following stroke found that the use of functional electrical stimulation in combination with physiotherapy was statistically superior to physiotherapy alone³·          Transcutaneous electrical nerve stimulation – this has been found to reduce spasticitythrough its nociceptive action and reduction of pain. C) PharmacologicalMedicationshould always be used as adjunct to good general management and education. Identification of treatment goals will help optimise drug therapy not only in terms of choice of agent, but also in timing and dose. Aims of medication should be to improve function or relieve troublesome symptoms rather than to simply reduce the degree of spasticity. Table 4 Useful things to remember to optimise medication effects

 Table 5 Different methods of delivery of medication

 The oral agentsAlthough different categories of drugs are available, those most commonly used to treat spasticity are baclofen,tizanidine, benzodiazepines, dantrolene, and gabapentin^{4, 5, 6}. Different agents act through different mechanisms (table 6 and 7) for e.g. GABA-like (baclofen, benzodiazepine), central alpha 2 agonists (tizanidine, clonidine) and peripheral anti-spastics (dantrolene). Antispastic drugs act in the CNS either by suppression of excitation (glutamate), enhancement of inhibition (GABA, glycine) or a combination of the two. Table 6 Mechanism of action of commonly used oral antispasticity medication

  Baclofen remains the most commonly used anti-spastic agent. The preferential indication is spasticity caused by spinal cord disease especially in multiple sclerosis. Many studies including the pilot study by Scheinberg et al ⁷ demonstrated that oral baclofen has an effect beyond placebo in improving goal-oriented tasks (such as transfers), in children with spastic quadriplegic cerebral palsy. In open-label studies of oral baclofen, the drug improved spasticity in 70-87 per cent of patients; additionally improvement in spasms was reported in 75-96 per cent of patients. In double-blind, crossover, placebo-controlled trials, baclofen was reported to be effective, producing statistically significant improvements in spasticity⁸. The main adverse effects of oral baclofen include sedation or somnolence, excessive weakness, vertigo and psychological disturbances. The incidence of adverse effects is reported to range from 10 to 75 per cent. The majority of adverse effects are not severe; most are dose related, transient and/or reversible. The main risks of oral baclofen administration are related to withdrawal; seizures, psychic symptoms and hyperthermia. These symptoms improve after the reintroduction of baclofen, usually without sequelae. When not related to withdrawal, these symptoms mainly present in patients with brain damage and in the elderly. The limited data on baclofen toxicity in patients with renal disease suggest that administration of the drug in these persons may carry an unnecessarily high risk. Tizanidine is an efficient and well tolerated antispastic. It is predominantlyan alpha 2 agonist and thus decreases presynaptic activity of theexcitatory interneurones. There is a large body of evidence for the effective use of tizanidine monotherapy in the management of spasticity ¹⁵. Tizanidine is the antispasticity drug that has been most widely compared with oral baclofen. Studies have generally found the two drugs to have equivalent efficacy, although tizanidine has better tolerability; in particular weakness was reported to occur less frequently with tizanidine than with baclofen.Dantrolene has a peripheral mechanism of action and acts primarily on muscle through inhibitingcalcium release from the sarcoplasmic reticulum. It decreasesthe excitation–coupling reaction involved in muscle contraction and can be prescribed in the different forms of spasticity. The efficacy of benzodiazepines (diazepam, tetrazepam, clonazepam) is comparable with baclofen. Although there is no evidence to suggest any difference in effectiveness between them, diazepam and dantrolene are associated with more side effects than baclofen and tizanidine. There are other compounds with anti-spastic properties (gabapentine, cyproheptadine, piracetam). Their advantage is

Table 7

rather limited when used alone. Generally, they are administrated in combination with usual anti-spastic drugs. A few short term trials have trialed gabapentin with good results ¹⁹ .Pregabalin may be of value as a systemic agent in the treatment of spasticity, although properly controlled studies with clearly defined outcome measures are required to confirm this finding ²². The Sativex Spasticity in MS Study Group²³ concluded that oromucosal whole plant cannabis-based medicine (CBM) containing delta-9 tetrahydrocannabinol (THC) and cannabidiol (CBD) may represent a useful new agent for treatment of the symptomatic relief of spasticity in MS. 
Intrathecal pump·          Baclofen- If oral drug treatment is inadequate in controlling lower limb spasticity or is not tolerated, intrathecal delivery of baclofen should be considered. This has been found to be a cost-effective strategy when compared to conventional medical management alone by Bensmail et al ²⁰ .The benefits of continuous intrathecal baclofen infusion have been demonstrated in more than 80 percent and over 65 percent of patients report an improvement in tone and spasms respectively. The main risks of intrathecal baclofen infusion are symptoms related to overdose or withdrawal. These are mostly related to catheter disruption, failure to refill the pump reservoir or failure of the pump's power source. Abrupt disruption of intrathecal baclofen can be a serious scenario with continuous spasms, tremors, temperature elevation, seizure and death having been reported.·          Phenol- As phenol is a destructive agent which indiscriminately damagesmotor and sensory nerves, it is reserved for those individualswho do not have any functional movement in the legs, who havelost bladder and bowel function and who have impaired leg sensation. Intrathecal phenol can be an effective treatmentwhich, though it requires expert administration, does not havethe long term maintenance or cost issues that are associated with intrathecalbaclofen treatment. The effect of a single injection often lastsmany months and can be repeated if necessary ²⁴. D) Nerve blockPeripheral nerve blockade/ Regional blocks/ Neurolytic blockade²⁵ are another therapeutic possibility in the treatment of spasticity. This can be done with the help of fluoroscopy or nerve stimulation. Chemical neurolysis by phenol/ alcohol is irreversible and can be used at several sites. Blocks are applied most often to 4 peripheral sites: the pectoral nerve loop, median, obturator, and tibial nerves. The main indication is debilitating or painful spasticity. Peripheral blocks with local anaesthetics are used as tests to mimic the effects of motor blocks and determine their potential adverse effects. Peripheral neurolytic blocks are easy to perform, effective, and inexpensive³⁰. E) Botulinum toxin injectionBotulinum toxin is the most widely used treatment for focal spasticity^27,28,29. The effect of the toxin is to inhibit the release of acetylcholine at the neuromuscular junction. The clinical effect of injecting botulinum toxin is reversible due to nerve sprouting and muscle reinnervation, leading to functional recovery of the muscle in a few months. It is essential that botulinum toxin injections are given in conjunction with physiotherapy in order to obtain the maximum benefit. The toxin is injected directly into the targeted muscle and an effect can be noticed from as early as 2-3 days with a maximum effect seen by about 3 weeks, lasting at least 3 months. As it is not a permanent treatment it may have to be repeated after a few months.Many randomisedcontrolled trials show that botulinum toxin is effectivein reducing muscle tone in various conditions ^{28, 29}. Brashear and colleaguesdemonstrated a reduction in spasticity in the wrist andfingers of patients following stroke with the use of botulinum toxin, together with an improvementin their disability assessment scale²⁹.E) Surgical techniqueMost surgical procedures are irreversible. This means that realistic goal setting between the health care provider, family and patient is critical. Neurosurgical techniques have been proven useful in conditions like cerebral palsy ^{32, 33}.·          Neurosurgical techniques- Anterior and posterior rhizotomy, peripheral neurotomy ³¹, Drezotomy, percutaneous radiofrequency rhizotomy, spinal cord and deep cerebellar stimulation of the superior cerebellar peduncle ³², functional neurosurgery ³³·          Orthopaedic procedures- directly act on muscles and tendons e.g. lengthening operation, tenotomy, neurectomies, and transfer of tendons. 

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