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Conduction block and impaired axonal function in tick paralysis
Author(s) -
Krishnan Arun V.,
Lin Cindy S.,
Reddel Stephen W.,
Mcgrath Robert,
Kiernan Matthew C.
Publication year - 2009
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21395
Subject(s) - refractory period , medicine , electromyography , anatomy , weakness , paralysis , anesthesia , neuroscience , biology , surgery , physical medicine and rehabilitation
Tick paralysis (TP) is an uncommon disorder caused by a neurotoxin secreted by engorged female ticks. The cause of TP remains unclear, although alterations in axonal ion channel function and neuromuscular transmission have been proposed. In the present case, nerve excitability techniques, which provide information regarding axonal ion channel function, were used to elucidate the mechanism underlying weakness in a 45‐year‐old man who presented with weakness following a tick bite in the lateral aspect of the left axilla. Standard clinical nerve conduction studies were undertaken during the acute phase of symptoms and following clinical recovery. Nerve excitability studies were performed to investigate possible changes in ion channel properties distal to the site of conduction failure. Nerve conduction studies and electromyography suggested the possibility of a lesion involving the lower trunk of the left brachial plexus. Nerve excitability studies distal to the site of the tick bite demonstrated an abrupt increase in refractoriness, a marker of recovery from inactivation of Na + channels. There was normalization of both nerve conduction and nerve excitability parameters associated with clinical recovery. The alteration in refractoriness is similar to that noted in disorders involving the terminal portion of the motor nerve. The changes raise the possibility that TP may cause weakness through impairment of distal neural transmission. Muscle Nerve, 2009