Mechanism of pain in the acute phase of herpes zoster.
Invasion of the virus, secondary inflammatory changes in the skin, peripheral nerves, dorsal root ganglia of the spinal cord, nerve roots, soft meninges and spinal cord activating primary nociceptive afferent nerves – herpes zoster acute phase pain.
Principles of herpes zoster treatment: antiviral, pain reduction, prevention of posterior pain, prevention of secondary infection, and shortening the course of the disease.
1.Anti-viral drugs
2, analgesics: mild pain section to choose non-steroidal drugs; moderate pain: weak opioid drugs; severe pain, strong opioid drugs.
3, anti-inflammatory drugs: corticosteroids can significantly reduce the duration of acute neuralgia and improve the quality of life. They can be injected locally (e.g. intravertebral injection) or used systemically.
4.Antidepressants: tricyclics alone can significantly reduce pain and improve sleep in elderly patients.
5, anticonvulsants and antiarrhythmic drugs are not commonly used in acute herpes zoster.
6, local infiltration; somatic nerve block; sympathetic nerve block – to prevent posterior pain; central nerve block – epidural block is effective, usually without the use of arachnoid block – its effect is not more specific than epidural block.
7, nerve destruction: acute herpes zoster is not applied to nerve destruction.
Principles of management of postherpetic neuralgia.
The pathogenesis is unknown, and it is generally believed that there are both peripheral and central mechanisms.
Injury to the segmental nociceptive modulation system may play a role – accompanied by a decrease in the function of the thick fibers resulting in increased transmission of nociceptive information from the dorsal horn to the spinal cord.
Tactile pain – damage or regeneration of nociceptive afferent fibers.
Soreness, tingling – related to injury to sensory nerve endings.
Herpes zoster neuralgia treatment goals: analgesia, reduce depression and anxiety, reduce insomnia, and improve quality of life.
1, tricyclic antidepressants, which may require long-term or lifelong treatment
2. anticonvulsants, topical medications (capsaicin), antiarrhythmic drugs
Intravenous lidocaine is advocated for a variety of chronic neuralgia, including herpes zoster neuralgia, oral antiarrhythmic drugs (mexiletine)
3, strong opioids
4, local infiltration, cortisol, or local ozone injection; somatic nerve block; sympathetic block; central block (epidural block advocated, subarachnoid block not advocated)
5, nerve destruction: diagnostic treatment is effective on the basis of the previous use of chemical destruction, now more use of radiofrequency physical destruction.
Stratified treatment of pain in the acute phase of herpes zoster.
(i) Young immunocompetent patients
Objective: To relieve pain and prevent inflammation from damaging tissue.
1. antiviral treatment within 72 hours of onset and use of anti-inflammatory drugs (hormones).
2. sympathetic or epidural block for severe pain.
3.Non-steroidal drugs, weak opioid drugs.
4, antidepressants.
(ii) Immunologically sound elderly patients
Objective: To prevent postherpetic neuralgia
1, antiviral, anti-inflammatory (short-term hormone use)
2, narcotic analgesics in combination with nerve blocks (epidural and sympathetic or local anesthetics plus corticosteroid subcutaneous infiltration).
(iii) Young immunocompromised patients
Treatment focus: limiting viral infections
Early inpatient intervention, various therapeutic approaches can be used
(iv) Immunocompromised elderly patients
Objective: To prevent both the spread of the virus and the occurrence of posterior pain.
1.Anti-viral treatment without hormone therapy
2.Nerve block is most effective in relieving pain.
The role of ozone in the treatment of herpes zoster pain
Herpes zoster is an acute inflammatory skin disease caused by varicella-zoster virus (VZV). It is believed that the development of HZ is associated with a decrease in CD4+ T and an imbalance of Th1/Th2 cells (helper T cells), mainly manifested by hypo-Th1 cell function and hyper-Th2 cell function.
In HZ patients Th1 cell hypofunction leads to decreased IL-2 levels, making IL-2 function reduced and predisposing to herpes zoster.
The hyperactivity of Th2 cells is not conducive to disease recovery and tends to be a constant amplification of the inflammatory response. Among the cytokines secreted by Th2 cells, IL-6 is particularly closely related to HZ, and some studies have concluded [7] that serum IL-6 levels in HZ patients are positively correlated with the occurrence of PHN, the degree of nerve damage, and the degree of cold sensory deficit in painful areas.