Painful diabetic neuropathy (PDN), a prevalent complication of diabetes, has become a significant public health concern. It is characterized by nerve damage induced by chronic hyperglycemia, leading to pain, tingling, and numbness, predominantly in the hands and feet. This review comprehensively explores the neural mechanisms underlying PDN, emphasizing the dorsal root ganglion (DRG) as a central hub for pain initiation and transmission. In the periphery, dysregulated pathways in the DRG, including ion channel dysfunction, mitochondrial abnormalities, impaired glucose metabolism, and inflammatory disturbances, contribute to the hyperexcitability of nociceptors and the amplification of pain signals. In the central nervous system, PDN is characterized by structural and functional changes in the spinal dorsal horn and higher brain centers, leading to central sensitization and altered pain processing. The review also highlights the role of epigenetic regulation and emerging insights from single-cell RNA sequencing in understanding PDN. By integrating these peripheral and central mechanisms, future research can focus on developing targeted therapies and multimodal treatment strategies to improve patient outcomes.

A 63-year-old woman with a history of left basal ganglia and paraventricular infarcts, type II diabetes, and hypertension presented with recurrent dizziness when turning her head to the right. These episodes, lasting for eight months, were often accompanied by nausea and vision disturbances but resolved spontaneously. Dynamic digital subtraction angiography (DSA) revealed significant blood flow slowdown in the left vertebral artery (VA) with a 90° right neck turn, showing narrowing in the V3 segment of the left VA. The patient was diagnosed with Bow Hunter's Syndrome (BHS) and underwent atlantoaxial fusion surgery. On day three post-surgery, she developed sudden weakness in the left upper limb, visual field hemianopia, impaired sensation, and slurred speech. Emergency CT and MRI revealed acute infarcts in the basal ganglia and periventricular area. Following antiplatelet therapy and volume expansion, her symptoms improved, and by day seven, her speech and left upper limb strength had partially recovered, though residual symptoms persisted at discharge. One year post-surgery, the dizziness had resolved, but residual symptoms from the infarction remained. Cervical fusion effectively treated the symptoms of BHS; however, surgery should be considered with caution in patients with thromboembolic risk factors.