The Use of Botulinum Toxin in Children with Muscle Stiffness: An UpdateThis Keeping Current is one of a series of reports that discuss the effectiveness of rehabilitation interventions for children and youth with brain injury. When reading this Keeping Current, you will notice that the research reviewed is often taken from studies involving children and youth with a variety of neurological conditions and diagnoses. Be critical when deciding what information relates to your situation. The most relevant information will come from studies that specifically address the diagnosis in question. However, be aware that research findings from studies involving children with one specific diagnosis may be relevant for children with other diagnoses when their functional difficulties are similar, even if the causes are different.Support for the research to conduct this critical review comes from a grant from The Economical Insurance Group
When injected into a muscle, Clostridium botulinum toxin type A (BTA) produces a local, temporary weakness that is associated with a decrease in muscle stiffness (spasticity). Over the last 25 years, BTA has been used to treat many neuromuscular conditions including strabismus (crossed eyes) and vocal cord spasm. In the last ten years, BTA has been used in children with cerebral palsy and traumatic brain injury who have muscle stiffness. It is thought that decreasing the children’s muscle stiffness will allow for better stretching of shortened muscles, increased range of motion and opportunities to strengthen muscles that work opposite to the muscle that has been injected.These changes should allow the children to learn better control of their movement and to improve their motor function.
(The following section presents a brief overview of the technical and biological aspects of BTA. Some readers may wish to skip this section.) Botulinum neurotoxins are produced by certain strains of Clostridium bacteria and are classified into 7 serotypes, A through G (Shantz & Johnson, 1992). Most clinical work has been done with serotype A. The biological effects of BTA are well understood. An injection of BTA into the muscle creates a localized muscle paralysis by causing a highly specific binding to presynaptic cholinergic peripheral nerve terminals. The toxin is then internalized into the nerve terminal and inhibits the release of acetylcholine at the neuromuscular junction. Neurotransmission recovers when the axon terminal sprouts new nerve endings and forms new synaptic contacts on adjacent muscle fibers (Jankovic & Brin, 1991). Over time the original neuromuscular junction starts to work again highlighting the reversible nature of the treatment (De Paiva et al., 1999). In humans within two to three days of the injection, the muscle becomes weak with a reduction in tone, reaching a maximum effect at two weeks. The reduction in muscle tone lasts an average of three months with gradual increase in tone and gain in muscle strength occurring after this time. Effects from BTA can still be noted up to 6 months after the injection.
BTA injections are well tolerated with few serious side effects. The primary side effect is weakening of nearby muscles. The impact this has on the individual depends on the muscle group that has been injected. For instance when injecting neck muscles, the most frequent side effect is difficulty swallowing which generally improves after two weeks. In children receiving leg muscle injections, BTA can lead to short-term stumbling when walking. Temporary urinary incontinence has been reported following hip muscle injections in 1% of the children (Bakheit et al., 2001). Whole body side effects have been rare, with generalized weakness and fatigue reported in less than 1% of children injected (Bakheit et al., 2001). The individual experiences some pain at the time of the injection (similar to receiving an immunization needle) and can develop mild soreness at the injection site.The effects of BTA injections are temporary and repeated injections are often required. The individual can develop antibodies to the toxin and become resistant to its effect. Repeated BTA injections may not be as effective in these individuals (Hermann et al., 2000). Antibody formation has been observed in a small number of patients (less than 10%) who have received repeated injections of BTA. The dosage and frequency of the injection are felt to be the two important factors affecting antibody formation (Jankovic & Brin, 1991).
