Management of Spasticity Revisited

Laura A. Graham


Age Ageing. 2013;42(4):435-441. 

In This Article


Physical Therapies

Before considering pharmacological agents, the mainstay of spasticity management depends on adequate 24-h positioning and consideration of trunk, head and limb posture.[13]

The contribution of compensatory muscle actions in combating postural weakness leading to global increases in tone is now well recognised.[14] The concept of restoring 'good' normal movement patterns after neurological injury versus quick mobilisation using abnormal muscle patterns which increase tone further and potentially limit long-term rehabilitation outcomes is a challenge to neurophysiotherapists aiming to meet early hospital discharge targets.

The incorporation of an active or passive movement programme into the patient's daily care package is crucial to the maintenance of range of joint movement preventing contracture.

Good posture may be maintained in bed using a range of positioning tools including 'TBar' or trunk wedge to aid trunk stability and combat adductor spasticity (Figure 1). The principles of adequate pelvic and trunk support, allowing lowering of resting tone, also apply to providing adequate head and neck support whilst sitting. Satisfactory seating systems may include using a tilt in space wheelchair and suitable head rest or cervical collar (Figure 2). These postural aids allow trunk stability, alleviating compensatory limb spasticity and maximising motor control.

Figure 1.

Correct positioning in side lying.

Figure 2.

Correct Wheelchair Positioning.

Standing (using a standing frame) or weight-bearing on a tilt table (with blood pressure monitoring) allows stretch of the ankle joint complex using body weight and helps to combat contracture development.

Thermoplastic splinting and serial plaster casting are both used as adjuncts to passive stretching to maintain range of movement, but there is insufficient high- quality evidence to support any specific method.[15] The potential for skin pressure damage may be a particular issue for older people. A combined approach using casting with botulinum toxin injections to specific muscle groups has makes clinical sense and has shown some benefit in post-stroke spasticity.[16]

Pharmacological Treatments

The evidence base for benefits of drug treatment for spasticity has not had significant expansion in terms of high-quality randomised controlled trials of particular relevance to functional outcomes since Professor Mike Barnes' review in this journal 15 years ago.[17] The rationale for the use of oral medication relies on practical expert experience.

Oral Medication

Baclofen is the commonest systemic agent used to treat spasticity. Side effects occur in half of all cases and are more common in older people and those with cognitive impairment. Drowsiness, weakness, parasthesia, nausea and vomiting, and dry mouth limit its usefulness. More cautious commencement and a lower dosage are required. Lowering of the seizure threshold also occurs. Sudden withdrawal may precipitate seizures, confusion, anxiety and hallucinations.

Baclofen's mechanism of action is incompletely understood, but it works at the spinal level to inhibit monosynaptic and polysynaptic reflexes. Functional benefit has not been studied in detail. In stroke patients, a benefit in Ashworth scores was shown but no change on the incapacity status scale.[18] Baclofen's half life is 3–4 h, requiring dosing three times daily to retain effectiveness. The recommended maximum dose is 120 mg per day but decreased dosage is required in those with renal impairment.

Tizanidine acts as a potent selective alpha two adrenergic receptor agonist which acts to reduce stretch reflexes and co-contraction. Studies in stroke patients have shown a reduction in tone and spasms compared with placebo and equal to baclofen.[19] Side effects are similar to baclofen and more likely to affect older people. Liver function tests need to be monitored as fulminant hepatic necrosis can occur. Like baclofen, tizanidine has a short half-life, requiring three or four times daily dosing to a maximum of 36 mg.

Dantrolene works directly on skeletal muscle to reducing calcium ion release to reduce muscle fibre excitation. Moderate beneficial effects are seen in stroke and it may be used as an adjunct to centrally acting agents.[20] No studies have demonstrated improvement in function. The risk of hepatotoxicity requires on-going monitoring of liver function tests and severely limits its use.

Benzodiazepines act to reduce spasticity through modulation of GABAergic transmission. Diazepam and clonazepam are the most common agents, but their usefulness is limited by side effects.[21] Clonazepam may be particularly helpful in low dose (0.25–1 mg) for nocturnal spasm.

Gabapentin, a GABAergic drug-modulating intracellular calcium channels, was introduced as an anti-epilepsy drug in the 1990s and found to be beneficial for neuropathic pain. Randomised-controlled trial data support a beneficial effect.[22] Gabapentin is generally well tolerated. Side effects of drowsiness, somnolence and dizziness may be avoided by using a starting dose of 100 mg a day, gradually increasing to three times daily and increasing in 100 mg increments to a maximum dose of 2400 mg.

Cannabis has been noted to relieve pain and spasticity, particularly in MS and spinal cord injury for many years In the UK an oromucosal spray—'Sativex' (Delta 9-tetrahydrocannabinol THC) is now available, but reserved for patients with severe spasticity in MS, refractory to other treatments.[23]

Focal Treatments. Focal therapies have the advantage of targeting specific muscle groups or patterns of spasticity without the risk of systemic side effects such as drowsiness, cognitive impairment and generalised weakness which are particularly relevant to the elderly population.

Botulinum Toxins. Botulinum toxin is a powerful neurotoxin produced by Clostridium botulinum. There are seven distinct subtypes—Types A and B are used for medical purposes.[24] Acetyl choline release is blocked at the neuromuscular junction, causing temporary paralysis and allowing stretching of muscle fibres. Three Types of botulinum Type A (Dysport®, Botox® and Xeomin®) and one of Type B (Neurobloc®) are currently available in the UK. These drugs are not interchangeable, having different dosing ranges. Adverse effects are related to anticholinergic effects and local injection site irritation. Swallowing muscles may be affected and disabling generalised weakness may occur rarely, especially in the frail with small muscle bulk, where reduced dosage should be considered. Side effects are transient, as are the treatment effects, which last for 3–4 months. An advantage over oral agents is the lack of systemic side effects, in particular generalised CNS effects which may limit active movement and cognition.

The pattern of injections depends on the degree and dynamic nature of spasticity. The muscle groups targeted and dosages depend on the outcome of multi-disciplinary assessment focused on the patient's functional goals (Table 2). Identification of muscle groups is carried out using anatomical landmarks and palpation, or by using EMG guidance.[25] There are no randomised-controlled trials comparing these methods. Use of ultrasound is becoming more common, but whether this improves outcomes is not yet clear.

After stroke, there is evidence that botulinum toxin reduces muscle tone, but evidence for functional gain is limited. The recent BoTULs trial[26] showed significant improvement in Ashworth scores (as well as improved facilitation of dressing and hand hygiene) in stroke patients, but no benefit in active upper limb function. The methodology of available trials is diverse and differs from current clinical practice. Variable doses and different preparations of botulinum toxin are used and consideration of the need for repeat injections as well as how to measure meaningful improvement is some of the challenges in the literature. A Cochrane systematic review of botulinum toxin for adult spasticity after stroke is on-going.[27]

For patients with lower limb spasticity after stroke, there is an even smaller body of evidence which suggests there is improvement of gait speed. Combination treatments with functional electrical stimulation and targeted botulinum injections have not yet shown convincing benefit.

Chemical Neurolysis. Local injection of ethanol or phenol results in irreversible destruction of neural tissue by protein coagulation. The procedure is carried out percutaneously, using EMG for nerve identification.[28] Targets include the tibial nerve (correction of equinus deformity), obturator nerve (adductor spasticity aiding personal hygiene and catheter care) and the musculocutaneous nerve to reduce elbow spasticity. The procedure has largely been superseded by botulinum toxin injection where botulinum is available.

Intrathecal Therapies. These interventions are usually reserved for severe widespread spasticity that does not respond to oral or focal treatments.

Intrathecal Baclofen. Intrathecal baclofen directly acts on the GABA receptors in the lumbar spinal cord where a high concentration of receptors allows small doses to be used to good effect without systemic side effects. Originally used in spinal injury patients, it has also been successful in treating MS and hemiplegia, including post-stroke spasticity.[29] Patients are selected after thorough multi-disciplinary assessment and inpatient trial via lumbar puncture. Regular outpatient review by the specialist team is required for pump refills. Pump failure or catheter fracture, kinking or displacement may result in under-dosage and withdrawal syndrome which is potentially life-threatening.

Intrathecal Phenol. This therapy is appropriate for a small number of patients with severe painful spasticity and may be a highly effective treatment.[30] Application is limited because it is neuro-destructive and not reversible. Painful parasthesia, incontinence and loss of sexual function may occur. The aim is to improve seating, hygiene and personal care and pain.