Peripheral neuropathy in patients at the onset of blood diseases: etiology, pathogenesis clinical features, and diagnosis

This review focuses on the investigation of peripheral neuropathy in patients during the initial stages various hematological diseases, alongside an analysis of its diverse clinical manifestations, the complexity of its pathogenetic mechanisms, and the necessity for an interdisciplinary approach to diagnosis. The article provides a classification of peripheral neuropathies based on multiple criteria, including etiology (paraneoplastic, drug-induced, and metabolic), the extent of damage, the type of pathological process (axonal degeneration, demyelination), and clinical manifestations (sensory, motor, and autonomic forms). Emphasis is placed on neuropathies associated with vitamin B12 deficiency, as well as nervous system pathologies linked to monoclonal gammopathies, such as multiple myeloma, Waldenström’s macroglobulinemia, AL amyloidosis, and POEMS syndrome. The review examines the key pathogenetic mechanisms underlying neuropathy in blood cancer diseases with paraprotein secretion, as well as the diagnostic principles for these conditions. In cases of suspected hematological disorders, it is essential to conduct a comprehensive diagnostic evaluation involving both hematologists and neurologists, including electrophysiological studies. For the diagnosis of paraproteinemic neuropathies, protein electrophoresis and immunofixation are necessary, while suspected vitamin B12 deficiency requires the assessment of methylmalonic acid and homocysteine blood levels. In certain cases, neuroimaging techniques with tomography scan methods are indicated to rule out neoplastic processes. The results obtained during the conducted literature review underscore the importance of a consensus-based approach to the evaluation and management of this patient population, heightened clinical vigilance, and the application of modern differential diagnostic techniques, which can enhance patient quality of life and mitigate the risk of irreversible neurological damage.