Lyme disease is a tick-borne illness that has protean
neurologic manifestations involving both the central and peripheral nervous system. The peripheral nervous system manifestations of
Lyme borreliosis can be divided chronologically into acute and chronic forms. Within weeks after disease onset, approximately 15% of untreated patients develop an acute Lyme meningoradiculoneuritis with
headache,
fever, radicular
pain, weakness, and sensory loss, often associated with
cranial neuropathy, usually
facial palsy. Cerebrospinal fluid typically shows lymphocytic
pleocytosis, high
protein, and normal
glucose. Diagnosis is made by recognition of characteristic clinical features with a history of preceding exposure and confirmed by serologic evidence of exposure to B. burgdorferi or by antibody or PCR evidence of cerebrospinal fluid
infection. Months to years after onset, rare patients may develop chronic
polyradiculoneuropathy presenting with sensory symptoms or radicular
pain. Diagnosis is confirmed by a history of exposure, previous systemic or acute
neurologic manifestations of
Lyme borreliosis, and serologic evidence of
infection. Pathology of acute or chronic Lyme radiculoneuropathy reveals axonal degeneration with perivascular mononuclear infiltration. Eradication of the organism can be achieved with 2 to 4 weeks of
ceftriaxone for both acute and chronic
Lyme neuroborreliosis. Isolated
facial palsy without evidence of cerebrospinal fluid
infection can be treated with oral
antibiotics such as
doxycycline. Prognosis after
therapy is good, but neurologic recovery is slower for chronic than acute Lyme radiculoneuropathy.