Botulinum Toxin Injection Therapy

12 Botulinum Toxin Injection Therapy








Mechanism of Action


Depending on the serotype of the organism, Clostridium botulinum, seven distinct BoTNs can be produced by the bacterium (types A, B, C1, D, E, F, and G), all with similar mechanisms of action. At the present time, only BoTN A (Botox [Allergan, Irvine, CA] or Dysport [Medicis, Scottsdale, AZ]) and BoTN B (Myobloc or Neurobloc [Solstice Neuroscience, Louisville, KY]) are commercially available for clinical use. BoTN acts by cleaving a specific site (specific to each BoTN serotype) of a protein complex (soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor [SNARE] complex) responsible for exocytosis of neurotransmitter vesicles from the neuron. In the case of BoTN A, the most well-studied toxin subtype, the specific substrate is the synaptosomal associated protein of 25 kD (SNAP-25), a component of SNARE complex, which results in the inhibition of synaptic release of acetylcholine from the peripheral motor neuron end plate at the neuromuscular junction and ensuing muscle paralysis (Figure 12-1). More recent experience also suggests toxin effect on neurotransmitters related to sensory (afferent) function in the lower urinary tract.



At therapeutic doses of 100 to 300 units, BoTN A induces paralysis in the detrusor muscle. However, BoTN A may additionally inhibit sensory nerve activity directly and modulate bladder sensory transmission to the central nervous system. In the cases of bladder overactivity (both neurogenic and idiopathic) and in bladder compliance abnormalities, both mechanisms of action are exploited.


BoTN A specifically is a noncompetitive agonist, and as such the effects are irreversible, yet also temporary as well. After administration of BoTN A, neuromuscular function is regained primarily through a process of motor neuron end plate regeneration and sprouting of the distal motor nerve. The duration of the effect is variable, but in the bladder, the clinical response to BoTN A injections lasts approximately 6 months.


The most common adverse event is increased post-void residual volume, which can occur in 10% to 20% of patients undergoing injection. Catheterization may be required, and secondary urinary tract infection may ensue. More recent changes in BoTN A labeling, in response to systemic effects associated with toxin use in skeletal muscle, include warnings regarding systemic absorption of toxin and respiratory effects resulting from disseminated toxin effects.


May 29, 2016 | Posted by in GASTOINESTINAL SURGERY | Comments Off on Botulinum Toxin Injection Therapy

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