Peripheral Neuropathy

Abstract

Abstract Peripheral neuropathy describes the clinical syndrome of weakness, sensory loss, diminished tendon reflexes, or some combination of these findings caused by lesions of peripheral nerves. It may symmetrically involve the distal extremities, usually lower extremity greater than upper extremity (distal sensory, motor, or sensorimotor polyneuropathy), or may involve one or more named nerves (mononeuritis or mononeuritis multiplex). Peripheral neuropathy can also involve nerve roots (polyradiculopathy). From a pathophysiologic perspective, peripheral neuropathies are commonly divided into axonal and demyelinating types. Axonal neuropathy primarily destroys the axon, with secondary loss of the myelin sheath. Nerve conduction velocities are commonly normal with axonal neuropathy, but the sensory or motor amplitudes are low. Demyelinating neuropathy is associated with loss of the myelin sheath but preservation of the axon. Nerve conduction velocities are slowed, but the amplitudes are normal with this type of neuropathy. From a clinical standpoint, four main types of peripheral neuropathy occur among HIV-infected persons: (1) distal sensory polyneuropathy (DSPN), (2) acute and chronic inflammatory demyelinating polyneuropathy (AIDP and CIDP), (3) mononeuritis or mononeuritis multiplex (MM), and (4) lumbosacral polyradiculopathy (LSPR). With HIV-infected patients, the type of neuropathy depends in part on the degree of their immunodeficiency. Patients with AIDP and CIDP more often have early stage HIV disease. Distal sensory neuropathy, the most common form of neuropathy, generally develops in patients with more advanced, or late stage HIV disease. Similarly, LSPR predominantly occurs in patients who have progressed to AIDS. Mononeuritis or limited MM can develop in early stage HIV disease; extensive neuritis is seen in late stage HIV disease and may resemble CIDP.