Involvement of the optic nerve, either because of inflammation or increased
intracranial pressure, is a rare manifestation of Lyme disease. Of the 4 c
hildren reported here with optic nerve abnormalities, 2 had decreased visio
n months after disease onset attributable to optic neuritis, and 1 had head
ache and diplopia early in the infection because of increased intracranial
pressure associated with Lyme meningitis. In these 3 children, optic nerve
involvement responded well to intravenous ceftriaxone therapy. The fourth c
hild had headache and visual loss attributable to increased intracranial pr
essure and perhaps also to optic neuritis. Despite treatment with ceftriaxo
ne and steroids, he had persistent increased intracranial pressure leading
to permanent bilateral blindness. Clinicians should be aware that neuro-oph
thalmologic involvement of Lyme disease may have significant consequences.
If increased intracranial pressure persists despite antibiotic therapy, mea
sures must be taken quickly to reduce the pressure.