Leprosy and Other Infections Sometimes Causing Peripheral Neuropathies

LYME

Lyme disease in the United States is caused by Borrelia burgdorferi infection transmitted by the Ixodes tick. In the majority of infected individuals, Lyme disease manifests first with erythema migrans, a painless and nonpruritic skin lesion that evolves over days to weeks. Patients typically have flulike symptoms and may have infection of large joints, meninges, heart, or peripheral nerve. Approximately 15% of patients develop neurologic complications days to weeks after untreated infection. The most typical neurologic manifestations are one or more elements of the triad of polyradiculoneuritis, lymphocytic meningitis, accompanied by cranial neuritis. The polyradiculopathy or polyradiculoneuropathy is typically sensorimotor, painful, asymmetric, and non–length-dependent due to involvement of nerve roots. Approximately 5% of untreated patients develop a chronic axonal neuropathy, with symptoms of relatively symmetric, distal paresthesias. Serologic testing may be negative early in the course and should be repeated if the clinical suspicion is high. Positive serologies should be confirmed by a Western blot. Cerebrospinal fluid (CSF) in acute disease typically shows modest lymphocytic pleocytosis and mild increase in protein. In chronic infection, the immunoglobulin G (IgG) synthesis rate should be increased, and oligoclonal bands may be present. CSF Lyme polymerase chain reaction (PCR) has 40% to 50% sensitivity and 97% specificity.

HUMAN IMMUNODEFICIENCY VIRUS (HIV)

Symptomatic neuropathies occur in approximately 10% to 15% of HIV-1–infected patients, and the incidence increases as the immunodeficiency worsens. Distal symmetric sensory polyneuropathy (DSPN) is the most common HIV neuropathy manifestation. DSPN presents with distal pain, paresthesias, and numbness in a symmetric length-dependent manner. It involves sensory or sensorimotor nerve fibers and is gradually progressive. The neuropathy is similar to that associated with nucleoside-analog reverse-transcriptase inhibitors (NRTIs: dideoxyinosine [ddI], dideoxycytodine [ddC], 2′-3′-didehydro-2′-3′-dideoxythymidine [d4T/Stavudine]), used in the treatment of HIV. Polyradiculopathy is a much less common presentation for neuropathy in an HIV-infected patient. Acute inflammatory demyelinating polyradiculopathy (AIDP) can rarely occur at the time of seroconversion (CD4 counts ≥ 500). Polyradiculopathy can also be seen in moderately advanced HIV (CD4 counts 200-500) as a CIDP phenotype. In both cases, cerebrospinal fluid (CSF) examination typically demonstrates lymphocytosis of 10 to 50 cells/mm³. Mononeuritis multiplex is infrequent complication of HIV (0.1%-3% of patients). In advanced HIV (CD4 counts < 50), co-infection with cytomegalovirus (CMV) can cause painful mononeuritis multiplex, polyradiculoneuropathy, or polyradiculopathy. In these cases, CSF demonstrates polymorphonuclear pleocytosis in 5%; CMV PCR in CSF is positive in 90% of cases.

HEPATITIS C VIRUS

Hepatitis C virus (HCV) is the most common chronic blood-borne viral infection in the United States. Neuropathy associated with HCV may affect approximately 10% of patients, with a higher prevalence (up to 30%) in those also positive for type II or type III cryoglobulins. Different pathophysiologic mechanisms have been suggested, including virus-triggered nerve microvasculitis and intravascular deposits of cryoglobulins, leading to disruption of the vasa nervorum microcirculation. The peripheral neuropathy may present as a distal, asymmetric sensory or sensorimotor polyneuropathy or as multiple mononeuropathies. Patients often have prominent symptoms of pricking, burning, or pain. Palpable purpura, for example, on the ankles, is common and should be looked for during the examination.

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