Spasticity is a consequence of dysfunction of the central nervous system and is characterized by muscles overactivity, high tone spasms and may lead to muscle and soft tissue contracture and limb deformity, if untreated. It is defined as “velocity dependent increase in muscle tone with exaggerated tendon jerks resulting in hyper-excitability of the stretch reflex in association with other features of the upper motor neurone syndrome1”.
It may present as a focal problem, where there is impairment and activity limitation around one joint, or as multi-focal problems around a number of joints. This is distinguished from regional spasticity, where treatment is aimed at a whole limb or a number of limbs and generalised problems affecting the whole body 2.
This article will concentrate on the management of focal and multifocal spasticity with particular reference to pharmacological treatment with phenol and botulinum toxin (BoNT). The sole indication for the treatment of spasticity is when it causes harm.
Successful treatment strategies have now been developed and there is good evidence of treatment effectiveness 3. Physical management (good nursing care, physiotherapy, occupational therapy) through postural management, exercise, stretching and strengthening of limbs, splinting and pain relief is the basis of spasticity management4.
The aim of treatment in all cases is to reduce abnormal sensory inputs, in order to decrease excessive a-motor neuron activity5. All pharmacological interventions are adjunctive to a program of physical intervention. ‘Stretching plays an important part in physical management, but needs to be applied for several hours per day6.
This is of course impossible to do on a one-to-one basis with a therapist and limb casting has been developed in this field to provide a prolonged stretch.
A Guide to Clinical Practice for the Treatment of Adults with Spasticity using Botulinum Toxin’ was produced in April 20013 and is currently the most useful document highlighting clinical practice and the evidence base for treatment with this agent.
Successful spasticity management is a multidisciplinary activity. It is first necessary to manage any underlying provocative factors, such as any nociceptive stimulus, such as poor posture, constipation, incontinence, limb pain and skin or tissue damage.
Even tight clothing can cause an increase in sensory stimulation and the role of the nurse in managing these factors is crucial. Once it is recognized that spasticity may still require more active management, the team can then discuss with the patient and care-giver the available treatment options.
Some will be physical and some will be pharmacological or medical/surgical interventions. A management plan is therefore devised for each patient, but may incorporate a number of activities at the same time.
The pharmacological options depend on the pattern of the presenting problem. The figure shows the drugs of choice for generalized, regional and focal spasticity and these are guides. One does not see focal spasticity as such.
One sees a focal problem in the context of a generalized impairment. Managing spasticity involves dealing with the patient’s problems and not simply the impairments seen. However, oral drugs are more useful for generalized problems than focal problems, for which BoNT is the pharmacological treatment of choice.
It is important to develop a treatment plan as soon as possible, so as to be clear about the intended outcomes. It is important to state at the stage that antispastic drugs treat spasticity and not contractures, for which other measures will need to be adopted. With this in mind, the treatment plan follows a standard pathway:
- Define goals for treatment;
- Identify expected outcomes;
- Treat patient according to current guidelines;
- Review & record details of treatment outcomes.
It is therefore important to develop a system of assessment and of clinical examination for spasticity. The first point to find out is what the patient wants and their view of what is wrong. Outcome expectations can be then be discussed and the team can evaluate any unrealistic goals.
Chemodenervation is a suitable way to decrease the focal effects of the upper motor neurone syndrome. This article will confine a description of phenol chemonucleolysis and botulinum toxin.
Phenol Nerve Blockade
Phenol produces a chemical neurolysis, which is a destructive process of a nerve. It is different from the ion channel blockade of local anaesthetics7. Intrathecal 2-5% phenol was first described to carry out regional blockade8,9 and has enjoyed a little revival.
Motor point injections were then used to reduce the morbidity associated with spinal injections, but were time consuming and had a variable effect. As a result, a perineural injection was developed using a 3-6% aqueous solution, which has allowed groups of muscles to be blocked, when more proximal nerves are injected.
This provides an initial local anaesthetic effect, which is later followed by blockade one hour later by as protein coagulation and inflammation occur10. Wallerian degeneration then occurs later on before healing by fibrosis starts after about 4-6 months.
This leaves the nerve with about 25% less function than before, but does not disadvantage people with little or no residual function, as a mild progressive denervation can be beneficial in reducing spasticity10.
Khalili et al first pioneered nerve blockade11 and re-growth of most axons is seen with preservation of γ-neurones10. This means that, unlike BoNT, phenol can reduce spasticity without reducing strength to the same extent.
The effect is concentration and volume dependent12 and concentrations above 3% are more likely to result in histological change13.
The indications for use are as an alternative to BoNT or surgery in the treatment of focal problems and it has about the same efficacy as BoNT 14. The effect can last for 4-6 months, which is slightly longer than that of BoNT and the renewal of muscle overactivity is probably due to nerve regeneration15.
It can also be a useful addition to BONT in allowing a wider distribution of chemodenervation, as described above. It is not really a first line alternative because of its potential for harm.
The main problems are that it takes time to give and therefore can only be done where suitable facilities exist. As it can cause tissue necrosis, great care is required to give as little phenol as possible.
Placement of the needle is therefore critical. Nerves are located by stimulation at 1-2Hz and a muscle twitch responds to it.
When the stimulus intensity is <1 mAmp, the needle is optimally placed and the smallest amount of phenol is injected perineurally so that the muscle stimulation ceases. The patient feels a burning sensation, which may be unpleasant16.
The main problems occur later with vascular problems, reported as producing local oedema and venous thrombosis17. This can produce a localised tissue necrosis, which may take considerable efforts to treat.
Dysaesthesia is perhaps one of the most distressing complications and will occur if the phenol is place in proximity to sensory nerve fibres. As a result, only certain nerves are recommended for phenol chemoneurolysis. These are the obturator nerve (purely a motor nerve), which will treat adductor and gracilis spasticity and the musculocutaneous nerve, which supplies the biceps brachii, brachialis and coracobrachialis muscles.
It has a small sensory component, for which gabapentin is very effective in treating. It is worth giving the patient a prescription for this drug, as one gives the phenol, so that patients can start treatment the moment they notice the complication.
The tibial nerve may also be treated in experienced hands for triceps surae spasticity by blocking the nerve in the popliteal fossa. The nerve has separate sensory and motor bundles and the latter can be isolated after training.
Although phenol is cheap and a lot cheaper than BoNT, its total cost is about the same as that of BoNT, if the clinician’s time (it may take up to 45-60 minutes to perform a nerve block compared to a few minutes for a BoNT injection) and the need for more specialised facilities are taken into account.
To this must be added the considerable cost of gabapentin and the potential cost of ulcer treatment. On top of this is, of course, the human misery of these complications.
5% intrathecal phenol in glycerol is given on infrequent occasions for the management of paraplegia.
With the patient lying on one side and with the foot of the bed down, 1-2ml are instilled via a lumbar puncture needle and the patient lies on one side for 2-4 hours afterwards. The phenol is heavier than cerebrospinal fluid (specific gravity 1.25 compared to 1.007 for CSF) and the phenol will sink distally to a proportion of 4:1.
The patient may notice a tingling sensation. One to two days later, the procedure is repeated with the patient lying on the other side. The procedure is only indicated for people with progressive disease, who are refractory to other antispastic treatments and who have no ambulatory function. It is also only indicated for those already rendered incontinent, as the phenol will otherwise lead to permanent urinary and faecal incontinence.
Terminally-ill multiple sclerosis patients are the main group of patients for whom this treatment is given, when they have severe spasticity and do not have the ability to resilience to cope with intrathecal baclofen treatment.
In addition, the surgical placing of a pump designed to last for eight years has to be counterbalanced by the risks to the patient and logistics of living with a pump. The block is usually painless, as the phenol exerts a local anaesthetic effect and the procedure can be repeated as required.
Doctors, who wish to inject BoNT must be trained, as gaining the necessary skills requires time and commitment. The placing of the injection accurately is straightforward, but to get good results does require careful thought and planning. BoNT has a great propensity to seek neuromuscular junctions, but placing the toxin as near as practical to them may achieve better results and may possibly allow a smaller dose of the drug to be achieve the same clinical outcome.
A sound knowledge of anatomy is therefore necessary. Dilution is also an important factor and more dilute solutions have a greater ability to be taken up in neuromuscular junctions.
A recent study showed a good response in the neuromuscular junction uptake of BOTOX® when 5ml dilutions (20U/ml) were injected in a four point pattern in biceps brachii muscle compared to 1ml dilutions (100u/ml). These were both compared to motor point injections of 1ml dilutions (100u/ml)18.
Four preparations of botulinum toxin are commercially available in clinical practice in Europe and three in the USA. These are BOTOX®, Dysport® and Myo/Neurobloc throughout the world and, additionally, Xeomin® in Europe.
They are not the same and their differences have been highlighted in a book, which is shortly to be published19. It is thus better for a clinician to learn the individual characteristics of each rather than try to create notional inaccurate conversion ratios.
In addition, the drug should be place in different locations of the muscle to obtain an optimal effect. It is unwise to inject more that 50U Botox® or 200U Dysport® or 2,500U Myo/Neurobloc in any one site, as too much local denervation may occur with saturation of the nearest neuromuscular junctions7,8. Table 8.1 gives a list of dosages for individual muscles.
Electromyography & Muscle Stimulation
The use of EMG guidance and muscle tion is generally favoured to locate muscles accurately for injection. This is not necessary for large, superficial, easily visible muscles, but is advisable for smaller and deep inaccessible muscles, e.g. forearm and lower leg muscles.
The aim is to record muscle action potentials and their interference pattern on muscular activation. Muscle stimulation is particularly useful in flexor digitorum profundus muscle, which is organised in muscular fascicles supplying each digit. Correct placement of the needle can therefore allow neuromuscular blockade for each fascicle and thereby a very accurate result.
The procedure is carried out using a hollow Teflon-coated EMG needle with a sideport for syringe attachment. Motor point stimulation can also be carried out to activate small intramuscular fascicles, but this is time-consuming. Its advantage, however, is that it places the toxin as closely as possible to the motor end plate, the binding area, but increased effectiveness has not been shown in human studies.
It is possible that accurate localisation through EMG guidance can reduce the dose of toxin. This is obviously important for patients with progressive disorders, such as multiple sclerosis and for patients requiring repeated injections.
Computerised Tomography & Ultrasonography
Computerised tomographic (CT) radiography location of muscles is not justifiable from a safety point of view and confers no greater accuracy than other techniques. Ultrasound, on the other hand, has a useful place in locating both superficial and deep muscles.
It is safe, non-invasive and does not distress patients. It is accurate, but does require the injector to learn the technique and to orientate him or herself to the expected findings. Alternately, a radiographer/radiologist is required, which increases both the cost and technical organisation of the procedure.
Clinical Scenarios for Botulinum Toxin Treatment
Certain typical clinical patterns lend themselves well to botulinum toxin treatment.
i) Spastic Shoulder & Upper Arm
Treatment should be aimed at reversing the typical hemiplegic arm pattern of adduction and medial rotation of the arm at the shoulder, flexion of the elbow, forearm pronation and flexion of the wrist and hand.
With adduction of the arm, axillary hysgiene and loss of distal function is a problem and BoNt treatment should be considered for the pectoralis and teres groups and subscapularis muscle. The contribution of pronator teres and pronator quadratus muscles to pronationare small in comparison to the effect of brachialis muscle. Elbow flexors are powerful and are essentially three in number.
The first action of biceps brachii is the supinate the forearm before flexing the elbow. Brachioradialis flexes in a neutral position and brachialis has a pronatory contribution in flexion.
If biceps alone in injected with BONT, the tendency to supinate will be reduced and the forearm will be more likely to pronate, which of course is the reverse of the rehabilitative aim.
Therefore, injecting both biceps and brachialis is useful and will take 80-120U and 60-100U Botox® respectively. Alternately, a musculo-cutaneous nerve block with phenol will achieve as good a result.
ii) The clawed hand and flexed wrist
Flexor spasticity is frequently responsible for this deformity. Flexor carpi radialis and ulnaris muscles act on the wrist with flexor digitorum superficialis muscle flexing the fingers at the proximal interphalangeal joints and flexor digitorum profundus muscle flexing the terminal phalanges.
The lumbrical muscles flex the fingers at the metacarpophalangeal joints. It is important to differentiate between the action of these muscle. Good hand function is impossible with a thumb in palm deformity, i.e. an adducted flexed thumb in the palm and it is important to assess this.
The deformity is caused by overactivity in opponens pollicis muscle and thumb flexion is due to a combination of flexor pollicis longus and brevis muscle shortening. Finally, it may be useful to note that in patients with coarse hand function, it is sometimes better to leave a flexed stiff thumb terminal digit, as this will assist pincer grip.
iii) Hip flexor and thigh adductor spasticity
Scissoring of the legs is a common feature in non-ambulant severely disabled people with paraplegia. Injecting the adductor muscles with BoNT is useful in patients with true adductor spasm, but is not the sole treatment of choice for some people.
It is necessary to address hip flexor spasticity and shortening in addition. The psoas major and rectus femoris muscles are the two main flexors responsible for this. Psoas major can be injected with 50U Botox® at L2, L3 and L4 to a total of 150U Botox® per muscle.
Injecting the rectus femoris muscle is straightforward, as the muscle is easily identified and 100U Botox® is a reasonable dose. Patients should be warned that knee stability may be transiently altered for a couple of weeks after the procedure due to mild weakening of the muscle.
iv) Talipes equino-varus foot
A common feature of a spastic lower limb is an inverted plantar-flexed foot and it is important to demonstrate that this is due to spasticity rather than to imbalance between plantar flexor/inverter and dorsiflexor/everter muscles before treating it.
BoNT will not be effective if the deformity is simply due to weakness. Where spasticity is the major feature, injecting tibialis posterior and the posterior calf muscles is used to achieve a straight foot for weight bearing or to fit an orthosis.
It thus facilitates standing transfers and allows the patient to stand on a flat foot, which is essential for safe walking. If the patient cannot achieve proper base of support, because the foot itself is flexed and inverted, it is necessary to inject the short toe flexors (flexor digitiorum and hallucis brevis muscles).
The treatment of spasticity is enhanced by a programme of physical treatment after BONT injections or nerve blockade20 and physiotherapy in the form of stretching and strengthening is thus required for a period following the procedure
. The effect of a single dose of BONT-A may be prolonged beyond its action duration and repeat injections, which are necessary for MS patients can be reduced to a minimum.
Limbs should be stretched to a functional position, but should not be traumatised, as this will provide a nociceptive stimulus to increase spasticity in non-injected muscles. Stretching should be carried out for several hours every day and night-resting splints/casts can get round this by providing a stretch for several hours without interfering with daily activities.
Follow-up is important to identify whether or not the treatment objectives have been met and to plan further treatment. Patients may require further injections and it is important to have clear documentation of what has been previously done. A trend may thus be observed to aid further management.
Phenol and BoNT are useful drugs to add to the physical management of patients with spasticity producing focal problems. Their characteristics are as below in Table 1.
Table 1 Current Proven Effective Treatment
|Phenol Nerve Block||Cheap drug
Time consuming to give
Need trained clinician to treat
Effect lasts four – six months<
|Expensive to administer in clinical time.
Potentially painful to give.
Potential for severe complications.
|Botulinum Toxin||Effective for focal spasticity
Simple to prescribe
Simple intramuscular injection.
Need trained clinician to treat.
Effect lasts four months
|Regarded as expensive, but good value.
Considerable benefit to management.
However, before considering these treatments, it is important to ask the following questions.
- What are the problems and will BoNT or phenol help?
- Is there a significant component of muscle overactivity to treat effectively with BoNT?
- Is the problem localised to a number of muscles?
- Is there a clear aim for treatment?
- Are the advantages of BoNT or phenol treatment clear?
- Are there any contraindications to BoNT or phenol injection?
- How will treatment outcomes be evaluated and are there appropriate measures to use?
Anthony B Ward, BSc
Consultant in Rehabilitation Medicine/Director
North Staffordshire Rehabilitation Centre, Stoke on Trent, UK
Senior Lecturer in Rehabilitation Medicine, University of Keele, UK
North Staffordshire Rehabilitation Centre
The Haywood, High Lane, Burslem, Stoke on Trent, ST6 7AG, UK
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