Botulinum Toxin Use in Movement Disorders and Spasticity
Ever since botulinum toxin was first used as a treatment for strabismus in 1980, it has become instrumental in the treatment of a myriad of conditions with focal muscle overactivity including cosmetic uses to treat wrinkles. Botulinum toxin use in the tre
- PDF / 203,425 Bytes
- 9 Pages / 504.567 x 720 pts Page_size
- 21 Downloads / 189 Views
37
Karen Frei and Daniel Truong
Botulinum toxin was first used as a treatment for strabismus by Alan Scott published in 1980 [23]. Soon thereafter, botulinum toxin was developed as a treatment for many different conditions including strabismus, hemifacial spasm, blepharospasm, and cervical dystonia. Over time botulinum toxin injections have been considered to treat any condition with focal muscle overactivity including cosmetic uses to reduce wrinkles. Botulinum toxin is the protein product of the bacterium Clostridium botulinum. There are seven serotypes of botulinum toxin denoted as A through G. However, only serotypes A and B have been developed commercially. Commercially available forms of botulinum toxin in the USA include Botox (onabotulinum toxin), Dysport (abobotulinum toxin), Xeomin (incobotulinum toxin), and Myobloc (rimabotulinum toxin). Botox, Dysport, and Xeomin are all serotype A, and Myobloc is serotype B.
K. Frei, MD Department of Neurology, Loma Linda University Medical Center, 11370 Anderson St. Suite B-100, Loma Linda, CA, USA e-mail: [email protected] D. Truong, MD (*) Parkinson’s and Movement Disorder Institute, 9940 Talbert Avenue, Suite 204, Fountain Valley, CA 92708, USA e-mail: [email protected]
Botulinum toxin acts to inhibit the release of acetylcholine from the neuromuscular synapses. There are three steps to this process. The toxin first binds to the receptors on the presynaptic chain. The toxin is internalized into the neuron, and then an enzymatic cleavage takes place. The toxin’s light chain cleaves proteins involved in the acetylcholine transport protein cascade also known as SNARE proteins. SNARE proteins act to regulate fusion of the vesicle containing acetylcholine to the plasma membrane, Botulinum toxin type A cleaves SNAP 25, and botulinum toxin type B cleaves synaptophysin-2 also known as VAMP (vesicle-associated membrane protein). The vesicles containing acetylcholine are prevented from binding to the membrane, and acetylcholine is not released. The reduced acetylcholine release results in muscle weakness, the expected therapeutic result. After 3 months, the presynaptic neuron forms sprouts restoring the neuromuscular synapse which then can act at the muscle restoring the acetylcholine activity to normal [10, 16]. In the majority of cases, the botulinum toxin is injected into muscles that are overly active, usually the muscles producing the aberrant movement. The toxin’s beneficial effect takes up to 2 weeks to begin and lasts up to 3 months. Recurrent injections are required to produce and maintain optimum effect. Time intervals between injections are generally 3 months. It is thought that giving doses at 3-month intervals will prevent
© Springer-Verlag Wien 2017 C. Falup-Pecurariu et al. (eds.), Movement Disorders Curricula, DOI 10.1007/978-3-7091-1628-9_37
375
K. Frei and D. Truong
376
antibody production against the toxin. Antibodies to the toxin render the toxin inactive, and a patient will appear not to respond to the injections. Antibody tests or a simple forehead
Data Loading...
