JRSM >
Volume 98, Number 2 >
Pp. 63
Leigh Infirmary, Greater Manchester WN7 1HS, UK
Correspondence to: Dr T GaberE-mail: tarek.gaber{at}wwl.nhs.uk
Despite routine immunization, tetanus is still occasionally seen in the UK. After the acute episode, long-term neurological and musculoskeletal sequelae are common.1
CASE HISTORY
An intravenous drug user aged 28 sought advice because of trismus and then quickly deteriorated, developing generalized muscle spasms. Respiratory failure required artificial ventilation. Tetanus was diagnosed and he was treated with antibiotics and tetanus human immunoglobulins, together with diazepam and dantrolene to reduce muscle tone. After three weeks he was weaned off the artificial ventilation and transferred to a general medical ward where he improved slowly. However, he continued to have severe muscular rigidity with restriction of movements in the left elbow and both ankles, especially in dorsiflexion. For this we treated him with botulinum toxin (Dysport), a total of 1000 units injected into the left biceps brachii and brachioradialis and both gastrocnemius muscles. By the next day he had regained a full range of movement in both ankles, and elbow movements improved over the next few days. No side-effects were noted. Dantrolene was slowly withdrawn and within two weeks the patient was independently mobile with full movement in both elbows.
COMMENT
Like the tetanic neurotoxin tetanospasmin, botulinum toxin is the product of a clostridial species (Clostridium botulinum). The toxins are similar in structure and in mechanisms of action; the difference in clinical effects is attributable to their neurospecificities. Tetanus neurotoxin binds to the presynaptic membrane of the neuromuscular junction. It is internalized and transported retro-axonally to the spinal cord. The spastic paralysis induced by tetanus toxin is due to blockade of neurotransmitter release from spinal inhibitory interneurons. In contrast, the seven serotypes of botulinum neurotoxin act at the periphery, inhibiting acetylcholine release at the neuromuscular junction and inducing a flaccid paralysis.2
Benzodiazepines and dantrolene are the drugs customarily used for muscle rigidity in tetanus3 but they act generally and are less useful for localized muscle rigidity of the sort experienced by our patient. The successful use of botulinum toxin to manage trismus in cephalic tetanus has been reported by Andrade et al.4 In our patient, use of this agent in peripheral muscle groups appeared to speed return to mobility and may well have helped prevent long-term joint deformities. More than half the survivors of tetanus have evidence of joint damage, which is thought to be due to repeated traction on the periosteum and violent stress on the joint.5
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