Spasticity and the use of Botulinum toxin
MBBCH, FAFRM
Spasticity causes significant long-term disabilityquality of life and carer burden.
Spasticity is defined as “a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motor neuron syndrome”. 1
Spasticity occurs because of an insult to the central nervous system or motor neurons. Interruption of descending inhibitory modulation of the alpha motor neurons causes hyperexcitability, increased muscle tone and spasms.2
This is commonly seen in stroke, multiple sclerosis, brain and spinal injuries. It is estimated to affect 38% of stroke survivors after 12 months and up to 90% of persons with MS.3
On clinical examination spasticity can manifest by exaggerated reflexes, clonus, clasp-knife phenomenon, dystonia and flexor/extensor spasms.4 These are also known as the “negative effects” of spasticity because they result in unwanted effects like pain, decreased mobility, contractures, and muscle spasms, all of which can cause major limitation in functional activities and mobility.
Spasticity may have “positive effects”. Some patients may rely on spasticity to maintain use of their non-functional limb 5. For example, a patient with severe leg weakness, may be able to utilise his spastic leg for weight bearing to assist in transfers, a function that could not be possible in the absence of spasticity. Therefore, diminishing spasticity in some situations could be detrimental.
Prior to the commencement of treatment, a thorough assessment is required to identify the cause and the type (focal, regional or generalised). Identification of goals for treatment during the patient consultation, allows for an agreed treatment plan to address functional impairment.
Nonpharmacologic treatments include physical modalities, regular stretching regimens and the use of splints/braces. Those methods can help maintain range of movement of joints around spastic muscles and prevent contractures, though there is only limited proof that they have significant benefit on important clinical outcomes.6
Commonly used pharmacologic agents like Baclofen, Dantrolene and Tizanidine, though often prescribed for spasticity, their efficacy is not substantial and in many instances dose titration is limited by side effects which include sedation, dry mouth, dizziness, and weakness.
Intramuscular injection of Botulinum toxin (BoNT-A) plays a significant role in the management of spasticity as one of the most efficient ways to combat localised spasticity. It provides localized treatment within a muscle or muscle group and hence ideally used for focal or segmental spasticity. Rehabilitation physicians or neurologists usually perform the procedure in the outpatient setting. Topical anaesthetic could be used, and accurate muscle localisation is done using either ultrasound or neuro-stimulation/EMG machine.
Botulinum toxin (BoNT-A) acts at the neuromuscular junction, preventing acetylcholine release and thus causing flaccid paralysis. Post injection effects are seen within a few days, peak at four to six weeks, and typically last for few months; ongoing injections are required to control tone. Common side effects include flu-like symptoms and injection site reaction which usually settle with simple analgesia, other adverse effects include muscle weakness.
In general Botulinum toxin treatment is safe and effective as was evident in a randomized study that compared Botulinum toxin injections with Tizanidine for upper limb spasticity following stroke or traumatic brain injury. This study showed that Botulinum toxin treatments were more effective in reducing tone and were associated with fewer adverse effects than Tizanidine. 7
Treatment of upper and lower limb spasticity by Botulinum toxin (BOTOX and Dysport) is now approved under PBS. However, there is still no consensus on dosage or dilution. It largely depends on the physician’s expertise.
Botulinum toxin treatments alone in most instances would result in suboptimal outcomes. It requires a comprehensive management by a team of experts in clinical assessment and muscle selection when using BoNT-A for treatment of spasticity. 8
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References:
1. Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenbeg Lecture. Neurology. 1980;30(12):1303-1303.
2. Mukherjee A, Chakravarty A. Spasticity mechanisms–for the clinician. Frontiers in neurology. 2010;1
3. Watkins C, Leathley M, Gregson J, Moore A, Smith T, Sharma A. Prevalence of spasticity post stroke. Clinical rehabilitation. 2002;16(5):515-522.
4. Dromerick AW. Clinical features of spasticity and principles of treatment. Clinical evaluation and management of spasticity. Springer; 2002:13-26.
5. Martin A, Abogunrin S, Kurth H, Dinet J. Epidemiological, humanistic, and economic burden of illness of lower limb spasticity in adults: a systematic review. Neuropsychiatric disease and treatment. 2014;10:111.
6. Amatya B, Khan F, La Mantia L, Demetrios M, Wade DT. Non pharmacological interventions for spasticity in multiple sclerosis. Cochrane database of systematic reviews. 2013;(2)
7. Intiso D. Therapeutic use of botulinum toxin in neurorehabilitation. Journal of toxicology. 2012;2012
8. Varvarousis DN, Dimopoulos D, Vasileiadis GI, Manolis I, Ploumis A. Do gait parameters improve after botulinum toxin injections in post stroke patients? A prospective study. Toxicon. 2021;200:189-197.