Tick paralysis

Revision as of 13:56, 17 October 2018 by Kxl328 (talk | contribs) (Clinical Features)
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Background

  • Caused by neurotoxin produced by certain ticks (e.g. Ixodes holocyclus) in the US and Australia
  • Most cases reported in children

Pathophysiology

  • Paralysis results from the neurotoxin “ixobotoxin,” which inhibits the release of acetylcholine at the neuromuscular junction and autonomic ganglia, very similar to botulinum toxin.

Clinical Features

  • Symptoms begin 2-6d after attachment of tick
    • Ataxia → symmetric ascending flaccid paralysis with loss of DTRs
  • Presentation can be identical to Guillain-Barre including progression to respiratory paralysis
    • Unlike GBS, may have ocular signs (e.g. fixed and dilated pupils)
    • Also unlike GBS, autonomic dysfunction is not typical in tick paralysis

Differential Diagnosis

Tick Borne Illnesses

Weakness

Evaluation

  • Clinical diagnosis
  • Sensory abnormalities and elevation of CSF protein level do not occur
  • Progression and resolution of symptoms (with tick removal) is faster than in Guillain-Barre

Management

  • Removal of tick is curative, but resolution may take days-weeks.
    • Proper removal of the tick is important.
      • Tick should be grasped as close to the skin surface as possible with blunt curved forceps, tweezers, or gloved hands. Steady pressure without crushing the body should be used. After tick removal, the site should be disinfected.
      • Traditional methods of tick removal using petroleum jelly, topical lidocaine, fingernail polish, isopropyl alcohol, or a hot match head are ineffective and may induce the tick to salivate or regurgitate into the wound.
  • Supportive care (resolves on its own)

See Also

References