Abstract
Aim of the review — to summarize current data on the pathogenesis, clinical manifestations, diagnosis, and treatment of peripheral neuropathy in patients with rheumatoid arthritis. Peripheral neuropathy (PN) is a common complication of rheumatoid arthritis (RA), significantly impairing patients’ quality of life and leading to disability. This article provides an overview of current data on the pathogenesis, clinical manifestations, diagnosis, and treatment of PN in RA. Mechanisms involved in the pathogenesis of PN include vasculitis, autoimmune responses, neurogenic inflammation, and nerve compression. Clinical manifestations of PN are diverse and include sensory, motor, and autonomic disorders. Diagnosis involves clinical examination, electroneuromyography, ultrasound, magnetic resonance imaging (MRI), and nerve biopsy. MRI, including magnetic resonance neurography, functional MRI, and MRI spectroscopy, allows visualization of affected nerves, assessment of their structure and function, as well as detection of brain changes associated with pain. Treatment of PN in RA includes control of the underlying disease with disease-modifying antirheumatic drugs (DMARDs) and biologic therapy, as well as symptomatic treatment of neurological manifestations. In cases of vasculitic neuropathy, more aggressive therapy with high doses of glucocorticoids and/or cytotoxic drugs may be required. Conservative methods and surgical intervention are used to treat compressive neuropathies. Additional therapy includes drugs affecting neurotransmitters, B vitamins, and α-lipoic acid. In recent years, data have emerged on the effectiveness of palmitoylethanolamide and pterostilbene in the treatment of PN in RA, but further research is needed to confirm their efficacy and safety. Despite the progress made in understanding PN in RA, questions remain that require further study, including the development of more effective treatments and the identification of predictors of the development of neuropathy.