2.2 Neuroanatomy & Nerve Physiology for Wound Care

2.2 Neuroanatomy & Nerve Physiology for Wound Care

Core Clinical Principle: Nerves protect tissue by warning of injury, control sweating and skin blood flow, and release mediators that help wounds heal. Neuropathy removes all three functions at once. Knowing which fibers each bedside test examines, and which nerve supplies each skin territory, helps you locate a lesion and predict risk.

The CWSP outline lists neurological anatomy and physiology in the Wound Healing Environment domain. This section provides the foundation for neuropathy assessment, pain assessment, and spinal cord injury wounds covered elsewhere in the guide.

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Structure of a Peripheral Nerve

• Axon surrounded, in myelinated fibers, by a myelin sheath made by Schwann cells; gaps (nodes of Ranvier) allow fast saltatory conduction.
• Endoneurium surrounds each fiber, perineurium wraps each fascicle and forms the blood-nerve barrier, and epineurium encloses the whole nerve.
• Vasa nervorum supply the nerve. Microvascular disease and hyperglycemia-driven metabolic injury (polyol pathway, advanced glycation end-products, oxidative stress) damage both the vessels and the axons.

Fiber Types and What Bedside Tests Measure

A normal monofilament exam does not exclude small-fiber neuropathy, which can cause burning pain while touch and vibration remain intact. Loss of the 10-g monofilament indicates loss of protective sensation, a major ulcer risk factor.

Diabetic Neuropathy: A Length-Dependent Process

The longest axons fail first, so distal symmetric polyneuropathy begins in the toes and ascends in a stocking distribution; by the time it reaches the mid-calf, the fingertips may be affected (stocking-glove pattern).

• Sensory: Loss of pain and pressure warning allows repetitive trauma from shoes and gait to go unnoticed; loss of position sense impairs balance.
• Motor: Intrinsic foot muscle weakness allows claw and hammer toes and prominent metatarsal heads.
• Autonomic: Loss of sweating produces dry, cracked skin; arteriovenous shunting produces a warm foot with distended dorsal veins, even when capillary nutrition is poor.

Other neuropathy patterns matter for the differential: mononeuropathies (such as peroneal nerve palsy from compression), radiculopathies (dermatomal), and entrapments such as tarsal tunnel syndrome (tibial nerve under the flexor retinaculum behind the medial malleolus). Other causes of neuropathy include alcohol use, vitamin B12 deficiency (including with long-term metformin), chemotherapy, chronic kidney disease, hypothyroidism, HIV, and leprosy.

Sensory Territories of the Lower Limb

Knowing these territories helps place ankle blocks for debridement, distinguish a peripheral nerve lesion from polyneuropathy, and recognize injury to the sural nerve during harvest or the superficial peroneal nerve during lateral leg surgery.

Nerves and Wound Healing

Sensory nerve endings release substance P and calcitonin gene-related peptide (CGRP), which cause vasodilation, recruit inflammatory cells, and stimulate keratinocytes, fibroblasts, and angiogenesis (neurogenic inflammation). Denervated skin, as in diabetic neuropathy or spinal cord injury, shows blunted inflammation and slower closure. The sympathetic system controls skin blood flow and sweating, which keep skin supple and resistant to fissuring.

Pain Pathways in Brief

Tissue injury activates nociceptors (A-delta and C fibers) that synapse in the dorsal horn and ascend in the spinothalamic tract. Inflammatory mediators lower nociceptor thresholds (peripheral sensitization), and sustained input increases dorsal horn excitability (central sensitization), producing allodynia (pain from normally painless stimuli, such as a dressing change) and hyperalgesia. Nerve damage itself causes neuropathic pain, which is burning, shooting, or electric and responds better to gabapentinoids, SNRIs, or tricyclics than to opioids alone.

Spinal Cord Injury and Autonomic Dysreflexia

After spinal cord injury, skin below the lesion lacks sensation and normal vasomotor control, so pressure injuries are common. In injuries at T6 or above, a noxious stimulus below the level of injury can trigger autonomic dysreflexia: massive sympathetic discharge below the lesion causes severe hypertension, while the body's attempt to compensate produces bradycardia, headache, and flushing and sweating above the lesion.

• Common triggers: Bladder distension or blocked catheter, constipation, pressure injuries, ingrown toenails, tight clothing or shoes, and wound care procedures.
• Immediate management: Sit the patient upright, loosen clothing and devices, check and drain the bladder, look for and remove the trigger, and give a rapid-acting antihypertensive if blood pressure stays high. Topical anesthetic before wound procedures below the lesion can prevent episodes.

Clinical Traps

Trap 1: Equating a Normal Monofilament With Normal Nerves

The monofilament tests large A-beta fibers. A patient with burning feet and a normal monofilament exam may still have small-fiber neuropathy and impaired warning of heat injury.

Trap 2: Treating a Hypertensive Crisis During Wound Care as Anxiety

A patient with tetraplegia whose blood pressure spikes during sacral wound debridement is having autonomic dysreflexia until proven otherwise. Stop the stimulus and sit the patient up.