Tetanus toxin, the product of Clostridium tetani, is the cause of
tetanus symptoms.
Tetanus toxin is taken up into terminals of lower motor neurons and transported axonally to the spinal cord and/or brainstem. Here the toxin moves trans-synaptically into inhibitory nerve terminals, where vesicular release of inhibitory
neurotransmitters becomes blocked, leading to disinhibition of lower motor neurons.
Muscle rigidity and
spasms ensue, often manifesting as
trismus/
lockjaw,
dysphagia, opistotonus, or rigidity and
spasms of respiratory, laryngeal, and abdominal muscles, which may cause
respiratory failure.
Botulinum toxin, in contrast, largely remains in lower motor neuron terminals, inhibiting
acetylcholine release and muscle activity. Therefore,
botulinum toxin may reduce
tetanus symptoms.
Trismus may be treated with
botulinum toxin injections into the masseter and temporalis muscles. This should probably be done early in the course of
tetanus to reduce the risk of pulmonary aspiration, involuntary tongue biting,
anorexia and
dental caries. Other muscle groups are also amenable to
botulinum toxin treatment. Six
tetanus patients have been successfully treated with
botulinum toxin A. This review discusses the use of
botulinum toxin for
tetanus in the context of the pathophysiology, symptomatology, and medical treatment of
Clostridium tetani infection.