Botulinum toxins (BTX) have revolutionised the management of focal post-stroke spastic hypertonia. Published literature has supported the efficacy and safety of BTX in reducing spastic hypertonia but has not convincingly demonstrated the ability to enhance function. While clinicians and stroke survivors have reported impressive clinical outcomes, randomised, controlled trials (RCTs), have demonstrated only significant improvement in muscle tone but not functional changes. This paper will review the evidence supporting the efficacy of BTX for spastic hypertonia and discuss current clinical practice.
Botulinum toxins (BTX) have revolutionised the management of focal spastic hypertonia in a variety of neurologic diseases. Prior to the introduction of BTX for this purpose in the early 1990s, clinicians were limited to oral spasmolytic agents and nerve blocks using phenol or alcohol. All these interventions are effective in controlling spasticity, but side effect profiles vary. Oral drugs lack treatment target specificity and are associated with a multitude of adverse events, such as drowsiness and sedation. Phenol and alcohol require expertise in technique and are, like BTX, desirable for focal intervention. However, they have associated complications, such as swelling and dysaesthesia. Due to its relative effectiveness and safety compared to other spasmolytic options, the popularity of BTX in the management of spastic hypertonia has grown significantly over the last 2 decades. The literature has supported the effectiveness of BTX in reducing hypertonia but has not convincingly demonstrated functional improvement. While both clinicians and patients report impressive clinical outcomes, this has not been reflected in randomised, controlled trials (RCTs). This paper will review the evidence supporting the efficacy of BTX for spastic hypertonia and discuss current clinical practice.
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