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Tick paralysis usually occurs in the spring and summer months, and most often in young children, especially girls as their long hair conceals the embedded tick. Tick paralysis occurs when the female tick attaches to a host and releases a neurotoxin that can produce cerebellar dysfunction or ascending paralysis. Symptoms begin 4 to 7 days after the tick attaches. Initial manifestations include restlessness and irritability, followed by ascending flaccid paralysis, acute ataxia, or a combination of the two. Deep tendon reflexes are almost always lost. Treatment consists of simply removing the tick. Improvement is seen typically within a few hours and complete recovery within 48 hours.
Botulinum toxin (A) binds to the presynaptic terminus of neuromuscular and autonomic synapses resulting in a decrease of acetylcholine release. Flaccid paralytic symptoms ensue, first in a bulbar distribution then descending. Ciguatera poisoning (B) is associated with ingestion of ciguatoxin, a substance with anticholinesterase and cholinergic properties that also lowers the threshold for opening of voltage-gated sodium channels. The latter results in depolarization and heightened neurologic response with symptoms that include dyesthesias and paresthesias around the throat and perioral area, a burning sensation in the feet and distortion of temperature sensation. The Miller-Fisher variant of Guillian Barre syndrome (C) is associated with a descending paralysis. It usually affects the eye muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia. The ataxia predominantly affects the gait and trunk, with the limbs relatively spared.
Bolgiano EB, Sexton, J: Tick-Borne Illnesses, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch)132:p 1791-1792
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