Krishnan Arun V, Lin Cindy S, Reddel Stephen W, McGrath Robert, Kiernan Matthew C
Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, Barker Street, Randwick, Sydney, NSW, Australia.
Muscle Nerve. 2009 Sep;40(3):358-62. doi: 10.1002/mus.21395.
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.
