Mechanisms, characteristics, prevention and treatment of drug-induced peripheral neuropathy

Abstract

Drug-induced peripheral neuropathy (DIPN) is a disease caused by drug′s direct or indirect damage on the structure or function of peripheral nerve. The main clinical characteristics are the dysfunctions of sensory, motor and autonomic nerves in the area of the affected nerves. The sensory nerve abnormality includes paresthesia, burning sensation, and tactile sensitivity reduction. The motor nerve abnormality includes limited mobility, and weakened or disappeared deep tendinous reflect. The autonomic nervous′ symptoms include constipation, abdominal pain, frequent micturition, and sexual dysfunction. The mechanism of DIPN includes the drug′s direct injury on the peripheral nerves, the immune-mediated nerve injury and the inflammatory damage of the neurotrophic vessels. The pathological nerve fibers show that the changes of segmental demyelination, axonal degeneration, dense granule and vacuole. The results of neuroelectrophysiological examinations show that the decrease of the amplitude and conduction velocity of sensory nerve action potential, and the normal or light change of the amplitude and conduction velocity of motor nerve action potential. The diagnosis of DIPN are mainly on the basis of the history of drug exposure, clinical characteristics and the results of neuroelectrophysiological examination. The causality between the drugs and the peripheral neuropathy is evaluated by Naranjo. The treatment of DIPN includes drug withdrawal or decreasing of the dosages of suspected drugs, taking anticonvulsants, antidepressants or opioid drugs, local anesthetics, and lipophilic antioxidants-zinc sulfate at the same time. Key words: Peripheral nervous system diseases; Drug therapy; Diagnosis