Six children aged 3.3 to 5.5 years (5 girls and 1 boy), of 26 admitted with acute muscle weakness to the University of Mississippi Medical Center, Jackson, over a 5 year period (1992-97), were diagnosed with tick paralysis. The initial diagnosis in 3 of the 6 children was Guillain-Barre syndrome, the clinical and electrodiagnostic findings being indistinguishable from tick paralysis. Treatment with IV immunoglobulin was not of benefit, and the diagnosis of tick paralysis was established by finding a tick on the scalp or nape of the neck, and a rapid recovery within 24 hours following its removal. Clinical findings included leg, arm, and trunk weakness (6), facial weakness (4), bulbar weakness (1), eye muscle weakness (1), respiratory failure (1), and areflexia (5). Cranial nerves were normal in 2. Vibratory sense was mildly diminished in patients tested. CSF studies were normal in 4 tested. Low CMPA amplitudes found on initial electrodiagnostic studies increased rapidly after removal of the tick and in parallel with clinical improvement. Distal latencies and motor conduction velocities were normal, but the H reflex was absent. Repetitive nerve stimulation at both slow and fast rates was normal. Sensory nerve action potentials were within normal limits but showed a consistent increase in amplitude on recovery. [1]

COMMENT. A child admitted with acute, rapidly progressive muscle weakness should be examined for a tick. The incidence of tick paralysis among children admitted with acute muscle weakness is 25%. Unless the tick is considered as the cause, found by examination of scalp and neck, and removed, the clinical and electrodiagnostic findings may be difficult to distinguish from those of Guillain-Barre syndrome, leading to misdiagnosis and inappropriate therapy. The tick causing paralysis in N America is the Dermacentor species, and the illness is milder and shorter than that in Australia, caused by Ixodes holocyclus [2]. A toxin is secreted by the female tick salivary gland which is presumed to cause an interference with transmission at motor nerve terminals. Removal of the tick is followed by a rapid recovery. Previous reports have cited Guilain-Barre syndrome in the differential diagnosis [3], but the present article emphasizes the similarities of clinical and electrodiagnostic findings. Alternative causes of acute paralysis to be considered include organophosphate pesticide poisoning and shellfish poisoning. [4]

Lyme disease neurologic manifestations. A more common and well known illness and neurologic syndrome caused by tick bite is Lyme disease or Lyme neuroborreliosis. The infecting organism is a spirochete, B burgdorferi, that may be isolated from its vectors, Ixodes scapularis and pacificus, and from a patient’s blood, skin lesions, or CSF (AAP Red Book 25th ed. 2000). A Guillain-Barre syndrome can occur with Lyme disease but is rare, reported in only 1 of 96 patients, ages 3 to 19 years, and sometimes atypical, with mild lymphocytic pleocytosis in the CSF as well as the characteristic elevated protein [5]. Most common neurologic symptoms and complications of Lyme disease include headache (71%), facial palsy (14%), aseptic meningitis, and pseudotumor cerebri. Meningoradiculitis (Bannwarth’s syndrome) and peripheral neuropathy are rare in children and occur more commonly in adult Lyme disease. Diagnosis of neuroborreliosis requires characteristic neurologic signs and either erythema migrans, arthritis or heart involvement, positive spinal fluid serology for anti-B burgdorferi antibodies, or seroconversion [6]. See Progress in Pediatric Neurology III 1997, pp484-5, for review of Lyme disease neurologic syndromes.