12 Management of spasticity in children Rachael Hutchinson and H. Kerr Graham Introduction Spasticity can be defined as a velocity-dependent resistance to passive movement of a joint and its associated musculature (Lance, 1980; Rymer & Pow- ers, 1989; Massagli, 1991). Although spasticity is usu- ally present before contracture in children with cere- bralpalsy, true muscle shortening or contracture also appears at an early stage. The majority of children will have a mixture of spasticity and contracture. Dis- tinguishing spasticity from contracture is important from a management point of view. 1. ‘Dynamic’ shortening is most commonly caused by spasticity but may also be associated with dystonia and mixed movement disorders. Typ- ically, ‘dynamic’ contracture is recognized in younger children with cerebral palsy or spas- ticity of recent onset. Such children are likely to exhibit hyperreflexia, clonus, co-contraction and a velocity-dependent resistance to passive joint motion. Children who exhibit ‘dynamic’ calf shortening may walk on their toes with an equinus gait, but on the examination couch the range of passive ankle dorsiflexion may be full or almost full. 2. ‘Fixed’ shortening or ‘myostatic’ contracture describes the typical stiffness found in mus- cles of older children with cerebral palsy or spasticity of longer duration. The stiffness is much less velocity dependent and is still present during couch examination and under anaesthesia. Causes of spasticity in children With the eradication of poliomyelitis and the dra- matic fall in the prevalence of spina bifida, the most common motor disorder in children in developed countries is cerebral palsy. The incidence of cere- bral palsy in developed countries is static or even ris- ing. The reductions in the prevalence of kernicterus due to neonatal jaundice has been overshadowed by improved survival of very low birth weight and premature infants, many of whom suffer from spas- tic diplegia and quadriplegia (Stanley & Alberman, 1984; Petterson et al., 1993a,b; Pellegrino & Dor- mans, 1998; Marlow et al., 2005). Other common causes of spasticity in children are acquired brain injury and spinal cord injury. Table 12.1 shows the cause of spasticity in a consecutive sample of 341 children seen in a variety of clinics at the Royal Chil- dren’s Hospital in Melbourne in 1998. Spasticity in children will continue to be a com- mon and challenging problem for the foreseeable future. While reduction in the incidence of cerebral palsy would have the most impact in reducing the overall incidence of spasticity in children, preven- tion of traumatic brain injury and spinal cord injury is probably more realistic (Glasgow & Graham, 1997). The pathology of spasticity Given that the most common cause of spasticity in our clinics is cerebral palsy, subsequent discussion 214 Management of spasticity in children 215 Table 12.1. Aetiology of spasticity in 341 children (cerebral palsy, orthopaedic and spasticity clinics) Cerebral palsy 79% Acquired brain injury 6% Spina bifida 5% Spinal cord injury 2% Miscellaneous 8% on pathology and management focuses mainly but not exclusively on spasticity in the context of juve- nile cerebral palsy. The effects of spasticity cannot be separated from the overall effects of the upper motor neurone (UMN) syndrome (Fig. 12.1). The child with diplegia who walks on his toes because of calf spas- ticity may also be unable to voluntarily control the dorsiflexors of the ankle during gait. No matter how effective management of the calf spasticity is, gait may remain impaired because toe clearance cannot be achieved during the swing phase of gait (Perry, 1985, 1992). Indeed there is virtually always an effec- tive solution to calf spasticity/stiffness/shortening, but inability to control the ankle dorsiflexors dur- ing swing phase may mean life-long dependence on an orthosis. Weakness and impaired selective motor control have a much greater impact on gait and func- tion than spasticity. They are also more difficult to manage. Fixed musculoskeletal pathology in cerebral palsy is acquired during childhood. Children with cere- bral palsy do not have contractures, dislocated hips or scoliosis at birth. These common deformities are acquired during childhood. Muscle growth in chil- dren is a race between the pacemakers (i.e. the phy- ses of the long bones) and the muscle tendon units, in which the muscles are doomed to second place (Graham & Selber, 2003). The prerequisites for nor- mal muscle growth is frequent stretching of relaxed muscle. In children with cerebral palsy, the muscles do not readily relax because of spasticity, and they are infrequently stretched because of reduced activ- ity. Spasticity plus reduced activity leads to failure of longitudinal muscle growth, contractures and fixed deformities (Ziv et al., 1984; Cosgrove & Graham, 1994). The limb pathology can be considered in three stages (Fig. 12.2): In stage 1, typically the younger child with cerebral palsy, the deformities are all dynamic or reversible. This is the phase when spasticity management, gait training and the use of orthoses may be most useful. Orthopedic surgery is not indicated. In stage 2, there are fixed contractures, which may require surgical lengthening of muscles or tendons. In stage 3, there are changes in bones and joints, including torsionofthelongbonesand joint instabil- ity. The most common torsional problems are medial femoral torsion and lateral tibial torsion. Joint insta- bility problems include hip subluxation and subtalar collapse in the hindfoot (Graham & Selber, 2003). Spasticity, dynamic and fixed contractures coexist in varying proportions in most children. The tran- sition from dynamic to fixed contracture occurs at different rates in different topographical types of cerebral palsy and at different rates in different limb segments and even in different muscle groups in the same limb segment. There appears to be a ‘biolog- ical clock’ running at different speeds for different muscles in children with cerebral palsy, governing the timing of the transition from dynamic to fixed contracture (Eames et al., 1999; Preiss et al., 2003). In hemiplegia, there is an earlier transition from dynamic to fixed contracture than in diplegia. The dynamic component can be exploited by spasticity management (Eames et al., 1999). In spastic hemi- plegia, fixed contracture usually develops in the lower limb earlier than in the upper limb. Spastic- ity management may be appropriate in the upper limb at an age when surgery is required for a fixed equinus deformity. In the hemiplegic upper limb, the first muscle to develop a fixed contracture is almost invariably the pronatorteres (Preiss et al., 2003). This may result more from the absence of active supina- tion than increased spasticity in the pronator teres. A useful strategy may be to combine a lengthening or rerouting of the pronator teres, with spasticity management of the wrist and finger flexors using botulinum toxin A (BoNT-A). Recognition of these types of patterns may greatly improve the outcome of both spasticity and contracture management and 216 Rachael Hutchinson and H. Kerr Graham Progressive musculo-skeletal pathology in CP CNS pathology PVL Loss of inhibition LMN Positive features of UMN syndrome Neural Musculoskeletal pathology Muscle shortening Bony torsion Joint instability Degenerative arthritis Mechanical • Weakness • Fatiguability • Poor balance • Sensory deficits • Spasticity • Hyperreflexia • Clonus • Co-contraction Negative features of UMN syndrome Loss of connections to LMN (and other pathways) Figure 12.1. Progressive musculoskeletal pathology in cerebral palsy. (From Graham & Selber, 2003. Reproduced with permission. Copyright C  British Editorial Society of Bone and Joint Surgery.) Management of spasticity in children 217 Figure 12.2. The stages of lower limb pathology in the child with cerebral palsy. (Modified after Rang, 1990.) lead to the development of creative strategies to deal with common clinical presentations (Preiss et al., 2003)(Fig. 12.3). Measuring spasticity in children: clinical The Ashworth scale There are few useful clinical measures of spastic- ity and none validated for use in children. The Ash- worth and modified Ashworth scales are blunt and unresponsive tools in the assessment of the child with cerebral palsy (Ashworth, 1964; Bohannon & Smith, 1987). Their evaluations are subjective and reliability between investigators may be a problem. Most muscles in most children are grade 1+ to grade 3. Most useful clinical responses to spasticity man- agement are within and not across a single Ashworth grade. Of much greater utility is the measurement of dynamic joint range, which can be used across most major joints as a quantitative measure of spasticity (Tardieu et al., 1954; Fosang et al., 2003). The dynamic and static joint range of motion The range of motion of joints in both the upper and lower limbs is classically used as a proxy measure of the length of muscles crossing that joint. In the upper limb, the range of elbow extension is taken to be a measure of the length of the elbow flexors, the biceps and brachialis. Loss of elbow extension (fixed flexion deformity) is taken to mean shortening of the elbow flexors, although it should be noted that other factors such as intrinsic joint contractures must be excluded. In the lower limb, the range of dorsiflex- ion at the ankle is considered to be a measure of the calf muscle length. A further refinement is that the range of ankle dorsiflexion with the knee flexed is a measure of soleus length, and the range of ankle dorsiflexion with the knee extended is a measure of gastrocnemius length (Silfverskiold, 1924). This is 218 Rachael Hutchinson and H. Kerr Graham Age 3 Age 7 Age 11 Age 19 Figure 12.3. The pathology in the lower limbs in children with cerebral palsy is progressive as this sequence of hip X-rays shows. At the age of 3 the hip X-ray is normal; at age 7 there is a very mild uncovering of the right hip. At age 11 the hip is subluxed and more than 50% is outside the acetabulum. At age 19 there is painful degenerative arthritis with few management options remaining. the basis for the Silfverskiold test, and although it may be only completely reliable under anaesthesia, it is of great value as a simple test to differentiate between gastrocnemius versus gastrocnemius and soleus contracture. Typically, in hemiplegia there is usually shortening of both the gastrocnemius and soleus but in diplegia, isolated gastrocnemius shortening is common. The criticism of the Sil- fverskiold test (Silfverskiold, 1924) by Perry has in our view led to an unwarranted devaluation of this most useful clinical test (Perry et al., 1974, 1976, 1978). Dynamic joint range of motion is measured by provoking a stretch reflex if it is present. Typically this first catch, or R1, comes in at a repeatable joint angular position. This is usually 20 to 50 degrees prior to R2, the static muscle length (Tardieu et al., 1954). The variation is due to the proportion of the deformity, which is dynamic, and not fixed. R2 approximates to the degree of ‘myostatic contrac- ture’ or fixed shortening, which may require tendon Example 1 A 3-year-old child with spastic diplegia has an equinus gait affecting both lower limbs equally. R1: −35 degrees (35 degrees of equinus) R2: +5 degrees (5 degrees of dorsiflexion) R2 − R1 = 40 degrees Spasticity management is likely to be beneficial because there are 40 degrees of dynamic shortening to be exploited by spasticity management. Surgical lengthening of the heel cord is contraindicated because the degree of fixed contrac- ture is so small. Example 2 A 10-year-old boy with hemiplegia walks with an equinus gait on the affected side. R1: − 30 degrees (30 degrees of equinus) R2: −20 degrees (20 degrees of equinus) R2 − R1: 10 degrees Surgical lengthening of the Achilles tendon is indicated because R2 minus R1 = 10 degrees. This is not enough dynamic shortening for spasticity management and there would be too much residual contracture. Management of spasticity in children 219 lengthening and R1 the degree of spasticity or dynamic shortening, which may respond to spas- ticity management. These simple clinical tests of R1 and R2, static and dynamic muscle length can be per- formed to assess the length of the adductors of the hip, the hamstrings, quadriceps and the calf mus- cles, some of the most important lower limb muscle groups to be affected by spasticity. The measurement of R2 and R1 are of great prac- tical relevance in the management of spasticity because they help to: r Differentiate between spasticity and contracture r Quantify the degree of spasticity present r Select which muscles might respond to spasticity management r Serve to monitor the response to spasticity man- agement Measuring spasticity in children: instrumented Although we believe that dynamic joint range of motion is a useful clinical tool in the measurement of spasticity in children, there is a clear need for objec- tive measurements with a greater degree of valid- ity and repeatability. A number of techniques have been described, and although most are useful within research settings, none have become popular in clin- ical practice. Measurements of muscle stiffness address the biomechanical rather than the neurophysiologi- cal components of spasticity. These measurements may also be obtained on the examination couch or during walking. Static measurements include measurements of muscle torque and resonant fre- quency (Walsh, 1988; Corry et al., 1998; McLaugh- lin et al., 1998). In a placebo-controlled clinical trial, resonant frequency was found to be an objective means to quantify muscle stiffness in the hemiplegic upper limb. Reductions in resonant frequency were recorded after injecting the forearm muscles with BoNT-A (Corry et al., 1997). Video recording of gait and aspects of the static couch examination are very useful in clinical prac- tice. Utility is further enhanced by split-screen, two- dimensional recording with freeze-frame facilities (Keenan et al., 2004). Careful editing and archiving of patient records is also important. Various scoringsystems or‘physician rating scales’ have been devised to increase the sensitivity and objectivity of information gained from video record- ings of children’s gait (Koman et al., 1993, 1994; Corry, 1994). Although some have been tested for repeatability, few have been tested for validity (Corry, 1994). Instrumented gait analysis, including kine- matics and kinetics, provide the clinician with valu- able information regarding the effects of spastic- ity, contractures and other manifestations of the UMN syndrome on gait (Gage et al., 1995). Typical kinematic and kinetic patterns can be recognized and interpreted in the light of the patient’s history and clinical examination. Instrumented gait anal- ysis is considered by many clinicians to be essen- tial to plan such interventions as multilevel injec- tions of BoNT-A and selective dorsal rhizotomy. The dilemma is that only instrumented gait analysis gives valid,repeatableand accurate measuresofthe effects of spasticity and associated limb pathology on gait. Instrumented gait analysis is limited in clinical utility because of cost and availability. Furthermore, many of the children who may need and benefit most from spasticity management are too small and lacking in co-operation for instrumented gait analysis using current techniques. Managing spasticity in children In our preliminary open label study into the use of BoNT-A in the lower limbs of children with cere- bral palsy, the indications were summarized as ‘chil- dren with dynamic deformities which were interfer- ing with function, in the absence of fixed, myostatic deformities’ (Cosgrove et al., 1994). Although we believe that this statement remains valid, we increasingly recognize the twin difficul- ties in differentiating between dynamic and fixed deformities and in measuring functional outcomes in motor disabled children. Spasticity should not be treated just because it is present. The natural 220 Rachael Hutchinson and H. Kerr Graham history of spasticity in children is not sufficiently well known nor are our present methods of manage- ment sufficiently safe and effective to warrant such an approach. Children with severe, ‘whole body’ involvement frequently use spasticity in functional activities. A total extensor pattern may aid stand- ing transfers. In this scenario, ‘successful’ spasticity management, if measured by reduction in tone and improved range of motion, might reduce rather than enhance function. Hence the prime goal of spasticity management must be improved function. Understanding of motor development and meth- ods of assessing function in children is also crucial. A major characteristic of children who have cere- bral palsy is the delayed acquisition of motor skills (Rosenbaum et al., 2002). Given that spasticity man- agement must often be undertaken against a back- ground of growth and motor development, it is clear that only controlled clinical trials can reliably sepa- ratethe effects ofspasticity management on function from gains made as part of normal motor develop- ment. It is relatively straightforward to demonstrate reduction in tone, improved joint range of motion and improved muscle length after spasticity man- agement, but evidence of functional gains is much more demanding. The Gross Motor Function Classification System (GMFCS) is the most useful tool to stratify children with cerebral palsy into five major groups (Palisano et al., 1997). The Functional Mobility Scale is a use- ful measure of functional mobility and is sensitive to change after major interventions (Graham et al., 2004). The Gross Motor Function Measure (GMFM) is the most useful validated tool to measure func- tional outcomes in children with cerebral palsy (Rus- sell et al., 1989; Ketalaar et al., 1998; Wei et al., 2006). The best candidates for spasticity management are children who share the following features: r Mild to moderate spasticity r Good cognitive ability r No fixed contractures or deformities r Good selective motor control r Good general health r Stable supportive home environment r Access to appropriate physiotherapy Management of spasticity General tnenamrePelbisreveR Botulinum toxin A SDRITB Oral therapy Focal Figure 12.4. The four-way compass of spasticity management with general versus focal (north and south) and reversible versus permanent (west versus east). r Access to appropriate orthotics Spasticity management may fail for a variety of reasons including: r Spasticity, too severe and generalized r Poor cognitive ability r Fixed deformity r Poor selective motor control r Associated medical disease r Inadequate home support r No access to appropriate physiotherapy or orthotics Methods of spasticity management can be clas- sified on a four-way compass (Fig. 12.4) according to whether they are focal or general in effect and as to whether the effects are permanent or temporary. Within this four-way matrix (permanent-temporary, focal-general) practical clinical guidelines may be derived. The child with acquired spasticity sec- ondary to acquired brain injury may have a relatively short period of severe spasticity in a hemiplegic dis- tribution. This could be managed by a program, which may include intramuscular BoNT-A to large muscle groups on the affected side including the elbow flexors, the forearm muscles and the gas- trosoleus. In this scenario the focal and temporary nature of BoNT-A may be advantageous. Selective dorsal rhizotomy (SDR) would be contraindicated because it is permanent and bilateral. Management of spasticity in children 221 A child with spastic diplegia who demonstrates lower limb spasticity may respond favorably to SDR; the permanence and generalized effects on the lower limbs may be advantageous. Multiple, repeated injections of BoNT-A would be less effec- tive and risk systemic side effects. The spasticity team and the spasticity clinic Successful spasticity management in children depends as much on teamwork as it does on tech- niques and technology. Given that options in spastic- ity management in children include administration of drugs by oral and intrathecal routes, neurosurgi- cal procedures and orthopaedic surgery, it should be self-evident that spasticity management is a multi- disciplinary exercise. In many centres, the concept of a spasticity team and a spasticity clinic are well developed. At the Royal Children’s Hospital in Mel- bourne, the members of the team are drawn from the following backgrounds: r Physical Medicine and Rehabilitation r Child Development and Rehabilitation r Physiotherapy r Occupational Therapy r Clinical Nurse Coordinators r Orthotics r Neurosurgery r Orthopaedic Surgery r Motion Analysis Laboratory Many children are managed successfully by individ- ual clinicians. However, there are a sufficient num- ber of very difficult management problems to justify a monthly spasticity clinic where the management of a small number of problem children is discussed in detail. Often investigations such as gait analysis or examination under anaesthesia are requested to aid decision making. We find the multidisciplinary discussions stimulating and the communication between specialties invaluable and management is frequently altered with benefit to our patients. The most frequent management issue is the interplay between spasticity management and orthopaedic surgery for deformity correction. Are the deformities dynamic or fixed? To resolve this common dilemma, an examination under the full relaxation of a general anaesthetic may be invaluable. Oral medications: generalized temporary Oral medications for the management of spasticity in children are in the temporary/generalized cat- egory of the treatment compass. The agents most frequently used are diazepam (Valium), baclofen (Lioresal) and dantrolene sodium (Dantrium). In general oral medications have a rather narrow ther- apeutic window between efficacy and side effects. Individual responses vary greatly, and a careful clin- ical trial is necessary for many children to deter- mine the individual response/side-effect profile.The advantages and disadvantages of oral agents have recently been discussed (Ried et al., 1998); see also Chapter 7). Diazepam Most clinicians are familiar with the role of diazepam as an anxiolytic agent. However evidence from ani- mal work suggests that it possesses both muscle relaxant and spinal reflex blocking properties. The spinal actions of diazepam are the result of poten- tiation of the presynaptic inhibitory effects of GABA at GABA A receptors on spinal afferent presynaptic terminals. Central effects in the brainstem reticular formation result in sedation (Costa & Guidoffi, 1979; Young & Delwaide, 1981a; Davidoff, 1989; Blackman et al., 1992). Diazepam is rapidly and almost com- pletely absorbed following oral or rectal adminis- tration. Intravenous administration is occasionally used to gain rapid control of muscle spasms in a child who is excessively anxious and in pain after orthopaedic procedures, but there is a risk of res- piratory depression, and this route is not recom- mended for routine use. Intramuscularinjections are painful, rarely required and erratic in their absorp- tion profile. Rectal administration is ideal when chil- dren are fasting, nauseated or unable to take medi- cation orally. The half-life in children is shorter than in adults but still long at 18 hours. There tends to be a cumulative effect of diazepam and it may take 222 Rachael Hutchinson and H. Kerr Graham some time to reach the appropriate levels in body tissues and optimal clinical effect. The drug’s vol- ume of distribution is large, reflecting its extensive tissue penetration within the body. It is metabolized by the liver to pharmacologically active metabo- lites, including nordiazepam and oxazepam (Green- blatt et al., 1980). The most common side effects are excessive sedation, respiratory depression, fatigue and ataxia. Paradoxical effects may occur, including hallucinations and increased spasticity. These must be recognized and not managed by increasing the dose. Many children with cerebral palsy and other forms of spasticity demonstrate increased spasticity when theyare anxious and especiallywhen they arein pain. Anxiety and pain seem to interact in a vicious cycle to increase muscle tone after painful interventions such as orthopaedic surgery (Baillieu et al., 1997). Thecentral tranquilizingeffects and peripheral tone- reducing effects of diazepam are extremely useful in this situation. However, this means equally that there is a very small threshold between effective reduction in spasticity and sedation, invalidating diazepam for chronic spasticity management in the vast major- ity of children. We use diazepam almost routinely in children with cerebral palsy who are facing painful invasive procedures, including orthopedic surgery, SDR, etc. Addiction and withdrawal symptoms are reported in patients who use diazepam in the long term (Young & Delwaide, 1981b). We have noted a ‘rebound’ phenomenon in children who have high doses of diazepam postoperatively if it is stopped suddenly. We routinely recommend that children be ‘weaned’ slowly from diazepam use after short- term/high-dose use. Dantrolene Dantrolene is valuable in the treatment and preven- tion of malignant hyperthermia (Arens & McKinnon, 1971; Waterman et al., 1980). The main effect on skeletal muscle appears to be direct muscle relax- ation rather than a central or a spinal level of action. Dantrolene inhibits the release of calcium from the sarcoplasmic reticulum of muscle cells (Van- Winkle, 1976; Desmedt & Hainaut, 1979; Molnar & Kathirithamby, 1979). All muscles, both spastic and normal, tend to be affected, ranging from relax- ation through to weakness. Dantrolene is rapidly and extensively absorbed, but there is a lack of pharma- cokinetic data in children and especially in children who have spasticity (Lietman et al., 1974; Young & Delwaide, 1981a; Lerman et al., 1989). The utility of dantrolene has been limited by the potential for hep- atotoxicity (Utili et al., 1977; Wilkinson et al., 1979; Chan, 1990). Fatal dantrolene-induced hepatitis has been reported in adults but not in children. In chil- dren, transaminase levels may rise, leading to a with- drawal of therapy. Liver function should be assessed prior to starting dantrolene therapy and at frequent intervals thereafter (Ried et al., 1998). A number of studies have been reviewed by Black- man and colleagues, who note that the numbers of patients within the published files are small and the outcome measures not particularly objective (Black- man et al., 1992). However, most studies do report that in comparison with placebo, dantrolene has a positive effect in reducing muscle tone but not nec- essarily in improving function. Tizanidine Tizanidine is a benzothiodozol derivative of cloni- dine and acts centrally as an alpha-2-adrenergic agent. It may reduce spasticity by decreasing the release of excitatory neurotransmitters from affer- ent terminals and interneurones (Albright & Neville, 2000). Experience in children is limited and use is limited by sedation. Baclofen Baclofen was introduced in the mid-1970s and appears to act as a GABA agonist on the GABA B receptors (Rice, 1987). Baclofen inhibits transmit- ter release by competitive inhibition of excitatory neurotransmitters at the spinal level. There may be actions in the spinal cord or more centrally which are not yet fully described or understood (Pedersen et al., 1974; Calta & Santomauro, 1976; Milla & Jack- son, 1977; McKinlay et al., 1980; Young & Delwaide, 1981a; Dolphin & Scott, 1986; Fromm & Terrence, Management of spasticity in children 223 1987). Pharmacokinetic data in respect of baclofen children are lacking. Although baclofen is rapidly absorbed after oral administration, levels in the cere- brospinal fluid (CSF) are low because of its low lipid solubility and 30% binding to plasma proteins. This limits its transport across the blood–brain barrier (Knutson et al., 1974; Gilman et al., 1990). It can be administered orally or intrathecally but not par- enterally. The response to baclofen in children varies widely (Milla & Jackson, 1977). In general the thresh- old between effective reduction in spasticity or mus- cle tone and side effects such as dizziness, weakness and fatigue is rather small. However, individual chil- dren can respond well, and a careful trial of various dose levels is worthwhile, although the majority will have their medication discontinued because of side effects. Hallucinations and seizures may occur with abrupt withdrawal of baclofen; therefore, as with diazepam, children who have become habituated to larger doses should be weaned off the drug slowly. A double-blind crossover trial of oral baclofen admin- istration in children documented a decrease in spas- ticity with little change in functional abilities, such as ambulation and the performance of activities of daily living (ADLs)(Milla & Jackson, 1977; Molnar & Kathirithamby, 1979). Much interest has been raised by the intrathe- cal administration of baclofen (Knutson et al., 1974; Penn & Kroin, 1985). Using this technique, the low lipid solubility and binding to plasma proteins is avoided by administration of the drug directly to the target tissues. As will be seen in a later section, this introduces a new ‘risk–benefit’ profile with specific advantages and disadvantages. Casting and orthoses: temporary/focal The use of casting and orthoses can be classified as focal/temporary. Casting, orthoses, neurolytic injec- tions and physiotherapy are often used in vari- ous combinations to manage spasticity in younger children with cerebral palsy (see also Chapter 6). The efficacy and duration of casting are related to the proportions of dynamic and fixed contracture before treatment and the responsiveness to the con- nective tissue to stretching forces. Many clinicians combine casting with intramuscular injections of botulinum toxin. It is still unclear as to whether the combined effect of injection and casting may be better than either intervention on its own (Boyd & Graham, 1997; Corry et al., 1997; Booth et al., 2004; Kay et al., 2004); however, the evidence remains anecdotal. Spasticityof the gastrosoleus,resulting in dynamic equinus, is usually treated by serial below-knee cast- ing for periods of 1 to 4 weeks. Given the very widespread utilization of the technique by phys- iotherapists, there have been few outcome studies (Corry et al., 1998; Brouwer et al., 2000). In a ran- domized clinical trial, Corry and colleagues com- paredserial casting with injection of botulinum toxin in the management of dynamic equinus in chil- dren with cerebral palsy. They concluded that both interventions were effective but that the effects of botulinum toxin lasted longer (Corry et al., 1998). Flett et al. (1999) reported the inconvenience of cast- ing and child and family preference for botulinum toxin over serial casting. Orthoses such as the ankle-foot orthosis (AFO) are widely used in the management of younger children who have calf spasticity. The effects of AFOs are dif- ficult to study in younger children, but there are def- inite biomechanical benefits, confirmed by motion analysis (Rose et al., 1991; Ounpuu et al., 1993). Intramuscular injections: chemoneurolysis: temporary/focal Intramuscular injections are focal in nature. The duration depends on the agent, the concentration used and the site of injection. ‘Chemoneurolysis’ refers to a nerve block resulting in impaired neu- romuscular conduction by the destruction of neural tissue, either temporarily or permanently (see Chap- ter 8). Injection can be performed at many levels in the peripheral nervous system from nerve root to motor end plate (Glenn, 1990). The more proximal the injection site, the more general and prolonged the effect. Sciatic nerve block results in a variable degree of weakness of all of the muscles supplied by the sciatic nerve in the distal thigh and leg. Injec- tion of the gastrocnemius muscle affects small local [...]... surgery The use of BoNT-A in other forms of childhood spasticity is less well defined than in cerebral palsy There do not appear to be any intrinsic differences between the responses of large skeletal muscles to BoNT-A in relation to the underlying cause of the spasticity, but the natural history of the spasticity is of great importance BoNT-A has been of great value in the management of spasticity secondary... osteotomy of the femur in the intertrochanteric region will change the effective line of pull of muscle whose origins and insertion points cross the line of the osteotomy These include the iliopsoas, hip adductors and hamstrings Computer modeling indicates that some of these muscles may be relaxed by the rotational osteotomy, but others may have their tension increased As described above, spasticity may increase... practice following a trial in which we demonstrated alarming degrees of inaccurate needle placement using palpation and distal joint movement (Chin et al., 2005) The conclusions from our first clinical trial were that large doses of BoNT-A in children were safe and that reduction in tone was reasonably predictable but short lived Some improvements in the kinematics of gait were noted and, in some children, ... Figure 12.7 The pain/spasm vicious circle in the child with cerebral palsy after hip-release surgery Muscle tone increases postoperatively because of the combination of incisional pain and postoperative hip abduction in plasters or splints The incisional pain is managed by a various combination of analgesics and the hip abduction is considered to be essential The cycle of spasm increasing pain which produces... pronator teres with BoNT-A injections to the wrist and finger flexors Other uses of BoNT-A in the hemiplegic upper limb include pain relief and protection of upper limb tendon transfers from post-operative spasm RCT 2: BoNT-A vs casting for dynamic equinus In this study we compared the effects of BoNT-A and casting in the management of dynamic equinus (Fig 12.6) in a group of younger children with cerebral... and appropriate measures of functional activity, should be the focus of our efforts in spasticity management research in children REFERENCES Albright, A L (1996) Baclofen in the treatment of cerebral palsy J Child Neurol, 11: 77–83 Albright, A L., Barron, W B., Fasick, M P Polinko, P & , Janosky, J (1993) Continuous intrathecal baclofen infusion for spasticity of cerebral origin JAMA, 270: 2475–7 Albright,... (1993) Intrathecal baclofen for severe spasticity of spinal origin: results of a long-term multicenter study J Neurosurg, 78: 226–32 Corry, I S (1994) Use of a Motion Analysis Laboratory in Assessing the Effects of Botulinum Toxin A in Cerebral Palsy Thesis Belfast: Queen’s University Corry, I S., Cosgrove, A P Duffy, C M et al (1995) ., Botulinum toxin A as an alternative to serial casting in the... Botulinum toxin A in the hemiplegic upper limb: a double blind trial Dev Med Child Neurol, 39: 185–93 Corry, I S & Graham H K (1997) Botulinum toxin A as an alternative to serial casting in the management of dynamic equinus in cerebral palsy – a randomised prospective trial J Bone Joint Surg Br, 79(suppl IV): 418 Cosgrove, A P., Corry, I S & Graham, H K (1994) Botulinum toxin in the management of the... 709–12 Graham, H K (1995) Management of spasticity associated with cerebral palsy In: O’Brien, C O & Yablon, S (eds.), Management of Spasticity with Botulinum Toxin: A Clinical Monograph Englewood: Colorado Postgraduate Institute for Medicine, pp 17–23 Graham, H K., Aoki, K R., Autti-Ramo, I et al (2000) Recommendations for the use of botulinum toxin type A in the management of cerebral palsy Gait Posture,... bearing may initiate a chain of events that lead to progressive fixed contractures, torsional deformities in long bones and eventually joint instability and even frank degenerative arthritis Because spasticity seems to play a key role in the development of deformity, spasticity management is very important in the growing child There is now a range of options from which the clinician can choose in order . causes of spasticity in children are acquired brain injury and spinal cord injury. Table 12.1 shows the cause of spasticity in a consecutive sample of 341 children. Managing spasticity in children In our preliminary open label study into the use of BoNT-A in the lower limbs of children with cere- bral palsy, the indications