ABOUT RADIATION NEUROPATHY
Radiation neuropathy is a delayed, often progressive nerve injury that occurs in patients who have received therapeutic radiation, typically to the head, neck, pelvis, or limbs, and can manifest months to years after treatment.
It is characterized by focal or multifocal neuropathic pain, sensory loss, muscle weakness, and sometimes paralysis, depending on which nerves or plexuses are exposed, such as brachial‑plexus neuropathy after breast or head‑neck irradiation or lumbosacral plexopathy after pelvic radiotherapy. The underlying pathophysiology involves radiation‑induced damage to Schwann cells, vascular endothelium, and neurons, leading to impaired nerve‑blood supply, hypoxia, fibrosis around nerves, and axonal degeneration; these changes are closely linked to mitochondrial dysfunction and oxidative stress, as ionizing radiation generates reactive oxygen species that overwhelm endogenous antioxidant systems and disrupt mitochondrial energy production and mtDNA integrity.
In the US, radiation neuropathy is relatively uncommon in the general population but is a clinically significant problem in cancer survivors exposed to high‑dose or re‑irradiation regimens, particularly around the brachial or lumbosacral plexus.
At present, there are no approved disease‑modifying therapies that reliably prevent or reverse the neuropathic damage; treatment is therefore limited to symptom control (e.g., analgesics, neuromodulators), rehabilitation, pain‑modulating procedures, and optimization of radiation planning to minimize dose to critical nerves.[1][2][3][4][5][6][7][8][9][10]