Tick Paralysis

V. Vedanarayanan, M.D.; W.H. Sorey, M.D.; S.H. Subramony, M.D.


Semin Neurol. 2004;24(2) 

In This Article

Abstract and Introduction

Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. It is a relatively uncommon neuromuscular disease with a higher prevalence among young girls, although older men who get exposed to ticks may also be affected. It typically presents as an acute ascending paralysis occurring a few days after tick attachment and may result in respiratory failure and death. Patients may report minor sensory symptoms but constitutional signs are usually absent. Deep tendon reflexes are usually hypoactive or absent and ophthalmoplegia and bulbar palsy can occur. Children may be ataxic. Electromyographic studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials. Removal of the tick results in the very rapid reversal of clinical and physiologic deficits, quicker with North American ticks than with the Ixodes species seen in Australia.

Tick paralysis, also known as tick toxicosis, is a relatively uncommon form of human neuromuscular disorder; it is more of a problem in veterinary medicine.[1] The first case of tick paralysis was reported in 1912 and the topic has been reviewed from time to time.[1,2,3]


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