The frequency of abnormal CSF findings in 40 children, ages 3-19 years, with new onset facial palsy and Lyme disease was determined at the State University of New York at Stony Brook. CSF white cell count, protein, or both were elevated in 68% of cases. The majority (89%) had markers of B burgdorferi CNS invasion or immune involvement. Lyme disease-associated facial nerve palsy was related to CNS involvement and occult meningitis. Of 22 with CSF pleocytosis, none had meningeal signs and only one third had headache. [1]

COMMENT. The diagnostic value of CSF examination in children with peripheral facial palsy and suspected Lyme borreliosis was reported from Zurich, Switzerland, in Neurology [2] (see Ped Neur Briefs Oct 1997). Analysis of CSF for specific antibodies to B burgdorferi in children with acute facial palsy may facilitate eary diagnosis and prompt antibiotic treatment.

There are more questions than answers, according to an editorial comment by Shapiro ED of Yale University, New Haven, CT, and Gerber MA, University of Connecticut, Farmington. They consider that the clinical significance of CSF abnormalities in Lyme disease-associated facial palsy has not been established, and routine spinal tap and parenteral antibiotic therapy, recommended by some authorities in cases with CSF pleocytosis, is unnecessary and not justified.

Facial palsy in Kawasaki syndrome is reported from Children's Hospital, Boston, MA [3]. A 12-week-old-boy with coronary artery aneurysms and Kawasaki syndrome (KS) developed a facial palsy which resolved after treatment with IV immunoglobulin. KS is a vascular inflammatory disease of young children of unknown cause, presenting with unexplained fever, conjunctivitis, red lips, tongue and pharynx, skin rash, cervical adenopathy, erythematous hands and feet, and 25% have coronary aneurysms. Encephalopathy, seizures, stroke, ataxia, myositis, and facial palsy are rare neurological complications.