bubble_chart Overview

Burning neuralgia is a persistent post-traumatic neuropathic pain symptom. Statistics from scholars in various countries show that its incidence rate varies, ranging from 1% to 38%.

bubble_chart Pathogenesis

1. Ischemic Factors ① The nerve is embedded in scar tissue. ② Injury to the major blood vessels accompanying the nerve. ③ Disruption of the nerve's own microcirculation, severe crush injuries such as drug-induced nerve injury.

Experiments show that ischemia can cause demyelination of myelinated fibers, exposing nerve fibers and causing them to lose their insulating components. Stimulation from tissue metabolic chemicals such as acidic ions, Black Catechu phenols, and local scar constriction directly affect the axon, leading to causalgia.

Axoplasmic transport requires ATP for energy, with mitochondria in the axoplasm serving as the energy source, dependent on oxygen metabolism. Experiments indicate that hypoxia induced by sodium azide or cyanide rapidly halts fast axoplasmic transport within 15 minutes. Insufficient oxygen supply results in abnormal conduction. Under normal oxygen conditions, sensory fiber conduction is fast, precise in localization, and appropriately scoped. Under hypoxia, fast sensory fiber conduction is blocked, and slow fiber conduction (which requires less oxygen) takes over, leading to prolonged pain conduction, vague localization, broad scope, and a burning pain sensation.

2. Sympathetic Nerve Factors

(1) Sympathetic nerves: Small, unmyelinated fibers exhibit greater tolerance to ischemia.

(2) Sympathetic nerve terminals release large amounts of serotonin.

(3) Sympathetic fibers ultimately enter the central reticular formation (an anti-pain structure), exerting an inhibitory effect on it.

Clinical evidence supporting the sympathetic nerve factor theory includes: ① Nerves rich in sympathetic fibers (e.g., median, ulnar, and sciatic nerves) are commonly affected. ② Sympathectomy can alleviate symptoms. ③ The distribution of causalgia aligns with the vascular distribution of sympathetic nerves.

3. Cerebral Cortex Factors

(1) The incidence rate is significantly higher during wartime than in peacetime.

(2) The cerebral cortex generates excitatory foci for causalgia, consistent with the recent "reeducation theory" of nerves.

bubble_chart Clinical Manifestations

Pain begins 2 weeks after nerve injury, with a widespread burning sensation that lasts for a long time. In severe cases, it can disrupt sleep and eating, cause emotional fluctuations, and even lead to pathological personality and unusual behaviors. Incidence: The male-to-female ratio is 5:1, most commonly seen in individuals aged 20–40 (rare in children). The most frequently affected sites, in order, are the brachial plexus, sciatic nerve, median nerve, tibial nerve, and digital nerve.

bubble_chart Diagnosis

1. Temporality Persistent for months or even years after injury, lasting for hours daily or even without interruption.

2. Nature Indescribable burning pain.

3. Scope Extends beyond the innervation area of the injured nerve.

4. Severity Mild cases affect mood, while severe cases cause unbearable suffering, leading to loss of appetite and sleep.

Epidemiology The male-to-female ratio is 5:1, most commonly seen in individuals aged 20–40 (rare in children). Predilection sites, in order, include the brachial plexus, sciatic nerve, median nerve, tibial nerve, and digital nerves.

bubble_chart Treatment Measures

1. Conservative Treatment

Short duration of onset, within 3 months. For individuals with significant emotional fluctuations, conservative treatment is preferred.

(1) Systemic Block Therapy: Intravenous block with 0.5% procaine 500ml, or 0.05% procaine injected via the cervical stirred pulse, 150–250ml.

(2) Stellate Ganglion Block: Injection between the two heads of the sternocleidomastoid muscle above the clavicle. Accurate injection results in Horner's sign. After the block, effectiveness can last for 3 hours, after which the stellate ganglion may be surgically removed.

(3) For lower limbs, lumbar sympathetic ganglion block therapy is used. Early comprehensive treatment is emphasized.

(4) Medications: Librium 10mg, 3 times/day; Tardan 25mg, 3 times/day.

(5) Other methods: Physical therapy, electrostimulation, resonant spark therapy, acupuncture, music therapy, etc.

2. Surgical Treatment

(1) Vascular Surgery: If the major blood vessels accompanying the nerves are injured, they should be repaired. Hypoxia of the nerves within the blood vessels is undoubtedly one of the factors contributing to causalgia.

(2) Nerve Surgery: The painful neuroma should be sharply excised and allowed to retract into well-vascularized soft tissue.

After neuroma excision, the nerve is divided into two bundles, and end-to-end anastomosis is performed to facilitate balanced axoplasmic flow.

Excise nerve trunks with extensive scarring or tension and replace them with nerve grafts.

(3) Central Pain Neuron Surgery: Procedures such as electrode implantation in the caudate nucleus.

(4) Sympathetic Nerve Surgery: Stellate ganglionectomy, cervicothoracic or lumbar sympathetic ganglionectomy.