Herpes zoster is caused by varicella-zoster virus, a neurophilic double-stranded DNA virus; herpes zoster is the result of latent infection and reactivation of the virus, which is latent in the sensory ganglia of the dorsal roots of the spinal cord after the initial infection and can be reactivated when the body is immunocompromised or under certain circumstances, replicating in the sensory ganglia and causing nerve necrosis, inflammation and neuralgia, and spreading along the sensory nerve fibers to the corresponding dermatomes. The virus can replicate in the sensory ganglia, causing nerve necrosis, inflammation and neuralgia, and spread along the sensory nerve fibers to the corresponding innervated cortical areas. It is characterized by clusters of small blisters distributed along unilateral peripheral nerves, often accompanied by significant neuralgia and what we call postherpetic neuralgia (PHN for short). The main factors affecting the incidence of PHN are.
1. age The incidence of PHN is positively correlated with age. PHN hardly occurs in patients under 40 years of age.
2. the degree of pain in the acute phase of herpes zoster. The more severe the pain in the acute phase, the greater the likelihood of PHN.
The more severe the lesions, the longer the duration of new blisters and the time of rash remission in the acute phase, the more blisters and the more extensive the lesions, the easier it is to develop PHN.
4. Humoral and cellular immunity level. Surgery, trauma, radiation, application of immunosuppressive agents, malignancy, infection, tuberculosis, syphilis, malaria, and acquired immunodeficiency syndrome are all predisposing factors for herpes zoster. Increased stress stress can also activate underlying viral activity.
Clinical observations suggest that herpes zoster occurring in specific sites, such as the head and neck and perineum, are more likely to develop into PHN.
PHN has both peripheral and central nervous mechanisms. Nociceptive hyperalgesia and touch-induced pain are characteristic manifestations common to neuropathic pain syndromes and are particularly prominent in PHN.
Clinical manifestations of this disease are higher in summer and autumn. In the pre-onset phase, there are often symptoms of hypothermia and malaise, which will be painful and burning at the site of the rash, and trigeminal herpes zoster may present with toothache. The disease is most commonly known as herpes zoster of the thoracoabdominal or lumbar region, accounting for about 70% of the entire lesion, followed by herpes zoster of the trigeminal nerve, accounting for about 20%, with damage distributed along the three branches of the trigeminal nerve. However, the trigeminal nerve is more susceptible than the spinal nerve in elderly people over 60 years of age. Herpes begins as an irregular or oval-shaped erythematous patch on the facial skin, and after a few hours, blisters develop on the erythematous patch, which gradually increase and can merge into large blisters – in severe cases, they can be hemorrhagic, or pustules if there is secondary infection. After a few days, the blister pulp is cloudy and absorbed, and finally a crust is formed, and the crust is removed in 1 to 2 weeks, and the pigment left behind gradually fades away, generally leaving no scar, and the damage does not go beyond the midline. The duration of the disease in the elderly is often 4 to 6 weeks, with some exceeding 8 weeks. Damage to the oral mucosa is more dense with herpes and larger ulcerated surfaces, and lesions of the lips, cheeks, tongue, and palate are limited to unilateral. The first branch can involve the corneal mucosa and even blindness, in addition to the first branch; the second branch involves the lip, palate and lower temporal, zygomatic and infraorbital skin; the third branch involves the tongue, lower lip, cheek and chin skin. In addition, viral invasion of the geniculate ganglion may result in herpes of the external auditory canal or tympanic membrane. When the geniculate ganglion is involved and the motor and sensory nerve fibers of the facial nerve are also invaded, it manifests as a triad of facial palsy, otalgia and herpes of the external auditory canal, called Ramsay-Hunt syndrome. Herpes zoster is often accompanied by neuralgia, but it mostly disappears within 1 month after the complete resolution of the skin mucosal lesions, and may persist for more than 1 month in a few patients, called postherpetic neuralgia (PHN). Patients with PHN are often accompanied by anxiety and depressive states and symptoms of autonomic dysfunction. The local skin manifests as nociceptive hypersensitivity and touch-triggered pain. the duration of PHN is long, ranging from several years to decades.
Disease diagnosis
The diagnosis is usually easy based on the characteristic unilateral cutaneous-mucosal herpes, distribution along the nerve branches and severe pain.
Differential diagnosis
Differentiation from herpes simplex and herpetic pharyngitis should be noted.
Treatment of disease: Herpes zoster itself is clinically self-limiting and can heal spontaneously in 2-4 weeks; however, 20% of patients with herpes can develop PHN. treatment of PHN begins with the acute phase of herpes zoster, with antiviral, anti-anxiety-depression, anti-epileptic drugs, nerve nutrition, nerve repair, and pain relief therapy. The pain relief treatment options are highlighted here
1. Antiviral drugs
They should be applied as early as possible. Commonly used drugs: acyclovir, ganciclovir, famciclovir.
2. Pain relief
Commonly used drugs: mainly non-steroidal anti-inflammatory drugs, anti-anxiety and depression drugs, anti-epileptic drugs, and mild to moderate opioid drugs. In particular, tricyclic antidepressants and antiepileptic drugs are mainly used.
3. Nutritional drugs
Commonly used drugs: vitamin B1; vitamin B12; neurotropine; ganglioside, rat nerve growth factor, etc.
4. Special treatment
(1) Nerve block treatment: In the early stage, especially in January, the treatment effect is very good. The pain department of our hospital applies the characteristic treatment tools in the early stage: minimally invasive interventional nerve block therapy and intradermal encapsulation injection therapy are effective in the treatment of herpes zoster pain in the early stage, avoiding the development of the disease into PHN.
(2) For recalcitrant PHN that cannot be relieved by blocking methods, nerve/ganglion destruction can be used to selectively destroy painful afferent nerve fibers. Chemical destruction has a high chance of neuritis. Our pain department uses radiofrequency destruction by neurothermal coagulation for treatment with few complications, such as radiofrequency destruction of the dorsal horn ganglion of the spinal nerve, which can achieve long-term pain relief.
(3) Intrathecal continuous target-controlled infusion system: used for persistent disruption to treat PHN that is difficult to relieve.
(4) Spinal cord electrical stimulation: stimulation electrodes are placed in the epidural cavity of the spinal canal to treat pain by stimulating and posterior spinal cord conduction bundle and posterior horn sensory neurons by electric current.
5. Physical therapy.
(1) Ultraviolet light: Irradiate the lesions with medium-wave ultraviolet light (UVB ) to promote the drying and crusting of the lesions.
(2) Infrared or ultrashort wave: irradiate the affected area to help relieve the pain.
In conclusion, the pain in the acute phase of shingles must be treated promptly to avoid the development of post-herpetic neuralgia. Finally, we wish all shingles patients early and timely correct and standardized treatment to stay away from pain and ensure quality of life.
Related links: Our pain department strictly follows the three principles of standardized treatment for herpes zoster pain: antiviral, nerve nutrition and pain relief treatment. We have very mature clinical experience in treating herpes zoster pain and post-herpetic neuralgia using medication, various minimally invasive neurointerventional procedures and responsible nerve/ganglion disruption surgery.