International Journal of Clinical Case Reports 2024, Vol.14, No.4, 175-188 http://medscipublisher.com/index.php/ijccr 179 Figure 1 Central and peripheral mechanisms contributing to neuropathic pain in diabetic neuropathy (Adopted from Feldman et al., 2019) Image caption: a, Alterations in peripheral and central neurons significantly contribute to the pathophysiology of painful diabetic neuropathy. At the nociceptor terminals, glycation of ion channels through methylglyoxal forms advanced glycation end-products (AGEs), leading to enhanced channel function and neuronal hyperexcitability. Increased expression of voltage-gated sodium channels, such as Nav1.8, at the perikaryon also promotes hyperexcitability. Additionally, in myelinated axons, a reduction in shaker-type potassium (Kv) channel expression further exacerbates hyperexcitability, resulting in increased stimulus responses and ectopic neuronal activity, which in turn generates excessive nociceptive input to the spinal cord. Within the spinal cord, activated microglia amplify excitability in the dorsal horn. b, Multiple ascending pathways, including the spinothalamic tract (1) and spinoreticular tract, play roles in pain perception and the associated psychological responses. Pathways ascending through the parabrachial nucleus (2) to the hypothalamus and amygdala (3) are involved in autonomic regulation, fear, and anxiety. Descending pathways modulate nociceptive transmission at the spinal level (4), either facilitating or inhibiting pain signals. Peripheral neuropathy-induced changes are highlighted in the accompanying boxes (Adapted from Feldman et al., 2019)
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