With over 40 years of clinical experience in pain management, the author has relieved tens of thousands of patients from painful disorders and lifted their quality of life. Still, numerous patients with chronic or neuropathic pain fail to achieve adequate pain relief and live in constant agony.

Postherpetic neuralgia (PHN) frequently afflicts elderly people; risk rises sharply with age. Although drugs and minimally invasive therapies for PHN have matured globally over the past decade, many patients remain treatment-refractory, leaving clinicians with limited solutions.

PHN pathogenesis varies individually: some patients suffer primarily from abnormal calcium channel activity, others from sodium channel dysfunction, and a subset from opioid receptor irregularities. This explains inconsistent therapeutic outcomes with identical drugs or minimally invasive interventions.

I. Neuropathic Pain (NP, including PHN)

1. Overview

Definition: Pain caused by lesions or disorders of the somatosensory system.

Classification: Peripheral and central neuropathic pain.

Pathogenesis

Dysregulated ion channels: Peripheral nerve injury disturbs sodium, calcium and potassium channels, lowering stimulation thresholds and triggering ectopic discharges that cause spontaneous pain.

Peripheral & central sensitization: Nerve injury induces inflammation and peripheral neuronal hyperexcitability, which may persist under persistent irritation such as diabetes. Central sensitization amplifies nociceptive responses and impairs descending inhibitory pathways. Neuronal dysfunction disrupts the balance between inhibition and excitation, leading to pain, anxiety, depression and sleep disturbance.

Clinical manifestationsProlonged refractory pain persists even after the primary lesion heals, severely impairing quality of life and triggering mood disorders. Four core pain presentations:(1) Spontaneous pain: Pain without external stimuli(2) Allodynia: Pain induced by normally innocuous stimuli(3) Hyperalgesia: Exaggerated pain from standard painful stimuli due to reduced pain threshold(4) Paresthesia: Unpleasant abnormal sensations, spontaneous or evoked

Treatment principlesEarly etiological intervention to ease pain, restore function, improve life quality, lower recurrence and facilitate nerve repair.

Pharmacotherapy as first-line basic treatment

Minimally invasive intervention, neuromodulation or surgery for drug-resistant cases

Multimodal combined therapy integrating rehabilitation, psychology and physical therapy

2. Pharmacotherapy Guidelines (per 2024 Chinese Guidelines for Neuropathic Pain Assessment and Management)

First-line agents(1) Anticonvulsants

Calcium channel blockers (Gabapentin, Pregabalin): Bind presynaptic voltage-gated calcium channels in the spinal dorsal horn to reduce excitatory neurotransmitters, effective for PHN, painful diabetic peripheral neuropathy and post-traumatic neuralgia.

Sodium channel blockers (Carbamazepine, Oxcarbazepine): Suppress neuronal hyperexcitability via sodium channel inhibition.(2) Antidepressants

Tricyclic antidepressants (Amitriptyline): Block multiple ion channels and inhibit serotonin/norepinephrine reuptake to activate descending inhibitory pathways, indicated for PHN and diabetic neuropathy.

SNRIs (Venlafaxine, Duloxetine): Selectively boost synaptic serotonin and norepinephrine for painful diabetic neuropathy.

Second-line agents (for insufficient pain relief or intolerable adverse reactions to first-line drugs)

Opioids (Tramadol, Morphine, Oxycodone, Fentanyl): For PHN, diabetic neuralgia, chronic postoperative neuralgia, sciatica and spinal cord injury pain.

Topical analgesics: 5% lidocaine patch (sodium channel blocker)

Capsaicin (<1%, 8%): Target TRPV1 receptors on Aδ and C fibers to trigger transient depolarization.

Adjuvant medications

Bulleyaconitine A: Domestic proprietary Chinese raw material drug

Extracts from Rabbit Skin Inflamed by Vaccinia Virus for Injection: Activates spinal descending pain inhibitory pathways via noradrenergic, serotonergic and GABAergic systems.Note: Formerly named Extracts from Rabbit Skin Inflamed by Vaccinia Virus; domestic commercial name: Lizaisi.

II. Avoiding Therapeutic Deadlocks in PHN Treatment

Based on 40 years of clinical practice, PHN is notoriously hard to manage. Flexible rational combinations of first-line, second-line and adjuvant drugs are recommended from initial treatment.Combining first-line agents with Extracts from Rabbit Skin Inflamed by Vaccinia Virus for Injection yields unexpected efficacy for severe pain accompanied by cold numbness and formication, greatly reducing treatment dilemmas for clinicians.

This injection serves as an effective adjuvant therapy for PHN with favorable safety profiles, prominently relieving spontaneous burning/stabbing pain, tightness, coldness and numbness. It is rarely used alone; combined with gabapentin or pregabalin to enhance efficacy and cut side effects.

1. Mechanisms of Extracts from Rabbit Skin Inflamed by Vaccinia Virus for Injection

Its complex composite ingredients regulate abnormal central and peripheral nerve function through multi-pathway effects:

Analgesia: Activate central descending pain inhibitory noradrenergic pathways

Alleviate cold sensation and numbness

Inhibit neuronal apoptosis by downregulating caspase-9 to mitigate nerve damage

Immunomodulation: Reduce neuroinflammation to relieve neuralgia

Promote nerve repair: Improve autonomic nerve function, accelerate axon and Schwann cell proliferation, and modulate neurotransmitter release to optimize nerve conduction.

Its unique pathways differ from NSAIDs, opioids and calcium channel modulators, offering an alternative therapeutic approach.

2. Clinical Evidence

Randomized controlled trials, observational studies and long-term clinical practice verify its efficacy:

Significant reduction in VAS/NRS pain scores as monotherapy or combined with gabapentin/pregabalin

Superior relief of subjective neurogenic symptoms: burning pain, tightness, coldness and formication, widely recognized by clinicians and patients

Improve sleep, mood and daily activity to raise quality of life

Onset: Obvious efficacy after 1–2 weeks of continuous administration; treatment course ranges weeks to months

Research Status

Clinical trials on this injection for PHN remain limited, yet preclinical and animal studies demonstrate promising potential.

Advantages & limitations

Strengths: Multi-target mechanisms to comprehensively repair nerve injury with distinct action sites and milder side effects versus conventional drugs

Limitations: Insufficient large-scale randomized controlled trials; incompletely clarified molecular mechanisms requiring further research

Comparison with mainstream treatments

Versus anticonvulsants (gabapentin, pregabalin): Anticonvulsants stabilize neuronal membranes to reduce abnormal discharges, while this injection prioritizes anti-apoptosis, immunoregulation and nerve regeneration

Versus antidepressants (amitriptyline): Antidepressants modulate neurotransmitters with slow onset and side effects including dry mouth, constipation and drowsiness; the injection excels at nerve functional recovery

Extracts from Rabbit Skin Inflamed by Vaccinia Virus holds promising value for PHN treatment, yet more clinical research is needed to validate its efficacy and safety for optimized patient care.

This popular science article is compiled from public professional resources for reference only. Please contact us for revision or removal if any content causes unintended offense.

December 5, 2025

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