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The thoracolumbar spinal nerves consist of the 12 pairs of thoracic (T1–T12) and 5 pairs of lumbar (L1–L5) nerves that originate from the spinal cord segments of the same name [7]. These nerves are responsible for the sensory and motor innervation of the trunk, the anterolateral abdominal wall, and parts of the lower extremities [9]. Crucially, the thoracolumbar region provides the sole source of preganglionic sympathetic fibers for the autonomic nervous system, which travel through white rami communicantes to regulate visceral organs [3, 5]. Pathological conditions such as herniated discs, spinal stenosis, or traumatic injury can compress these nerves, resulting in radiculopathy, chronic pain, and motor deficits [1, 6]. Although not a single molecular entity, they are targeted in clinical practice using regional anesthesia techniques, such as the transversus abdominis plane (TAP) block, to provide perioperative analgesia [7, 11]. Drugs such as local anesthetics (e.g., bupivacaine) interact with these nerves by blocking voltage-gated sodium channels, effectively halting the transmission of nociceptive signals [4, 5]. Additionally, systemic treatments like gabapentinoids modulate the activity of these nerves by targeting voltage-gated calcium channels to alleviate neuropathic pain [8]. Recent advancements in neuromodulation also utilize magnetic or electrical stimulation of the thoracic spinal nerves to treat gastrointestinal disorders like gastroparesis by restoring autonomic balance [3, 6].
Voltage-gated sodium channel blockade to inhibit axonal conduction [5]; modulation of voltage-gated calcium channels to decrease excitatory neurotransmitter release [3, 8]; and electrical or magnetic neuromodulation to alter nerve excitability [6].
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