Herpes zoster is an acute infectious disease caused by the varicella virus belonging to the DNA virus group, which mainly affects the dorsal root ganglia of the spinal cord. Modern medicine has known that this virus is invaded by respiratory infection and latent in the nerve cells of the posterior root ganglion of the spinal nerve or other sites of morbidity. The virus may not usually develop, but the elderly and people who have been ill for a long time are prone to develop the disease due to a decrease in systemic resistance, and then encounter physical exertion, colds, and other triggers. The incidence is mainly unilateral, with a bilateral incidence of less than 1%, with 1-8% recurrence, and about half occurring in the same location.
I. Pathogenesis.
Viral infection with no immunity or low immunity (mostly children) can occur as primary infection, i.e. chickenpox. When the immunity of the body decreases (e.g. trauma, cold, cancer, immune system diseases, etc.), the latent virus can replicate in the sensory ganglion in large numbers, causing inflammation and necrosis of the ganglion, causing neuralgia in the patient, while the virus travels down the nerve pathway to the nerve The virus also travels down the nerve pathway to the area dominated by that nerve causing segmental herpes. The virus can also infect motor neurons, causing muscle weakness and motor paralysis in patients, but this is rare.
II. Mechanisms 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 activate primary nociceptive afferent nerves and acute phase pain of herpes zoster. 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: tricyclic drugs 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.
Third, the 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-along with a decrease in the function of the thick fibers to increase the transmission of nociceptive information from the dorsal horn to the spinal cord. Tactile pain – damage or regeneration of nociceptive afferent fibers. Soreness, tingling, and injury to sensory nerve endings are related. 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 nerve block; central block (epidural block is advocated, subarachnoid block is 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.
IV. Stratified treatment of pain in the acute phase of herpes zoster.
(a) immunologically sound young patients Aim: to relieve pain and prevent inflammatory damage to tissue.
1, antiviral therapy within 72 hours of onset, anti-inflammatory drugs (hormones) use ;
2. Sympathetic or epidural block can be used for severe pain;
3 non-steroidal drugs, weak opioid drugs ;
4, antidepressants.
(B) Immunologically sound elderly patients Purpose: Prevention of 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: to limit the early hospital intervention of viral infection, various treatment methods can be used (iv) Immunocompromised elderly patients purpose: to prevent both the spread of the virus and the occurrence of posterior pain.
(1) Antiviral therapy without hormonal therapy.
(2) Nerve block is most effective in relieving pain.
V. 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 occurrence of HZ is related to the decrease of CD4+T and the imbalance of Th1/Th2 cells (helper T cells), mainly manifested as 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 the level of serum IL-6 in HZ patients is positively correlated with the occurrence of PHN, the degree of nerve damage, and the degree of cold sensory deficit in the pain area.
1, the systemic effect of ozone: ozone has a bidirectional effect on the immune system, low concentration of ozone can stimulate immunity, while medium and high concentrations of ozone suppress immunity, 20-40 μg/ml of ozone has the effect of regulating the balance of the number of immune cells. after HZ patients treated with O3-AHT, the immune balance of the body is regulated, so that IL-2, which is beneficial to disease recovery, is elevated to a greater extent and The IL-6, which is unfavorable to the recovery of the disease, was reduced to a greater extent.
2. Possible mechanisms of local ozone treatment for herpes zoster pain.
(1) Local ozone injection can reduce the neuropathic pain caused by CCI in rats.
(2) Ozone can inhibit microglia activation at the spinal cord level.