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.