bubble_chart Overview

Shingles (herpes zoster) is a viral skin disease caused by the varicella-zoster virus, characterized by clusters of blisters distributed along peripheral nerves and neuralgia. Traditional Chinese medicine refers to it as "herpes zoster."

bubble_chart Epidemiology

This disease causes primary infection in individuals with no or low immunity, such as infants and young children, which is known as chickenpox. After viral infection, the virus remains latent in the ganglion cells of the spinal or cranial nerves for a long time. When activated by certain factors, the virus travels along the corresponding peripheral nerves from one or several ganglia to the skin, causing recurrent infection, known as herpes zoster. After experiencing primary chickenpox, one can develop herpes zoster, but recurrence of herpes zoster is rare. This is related to the incomplete immunity (IgM response) produced after the former and the complete, persistent immunity (IgM response) produced after the latter.

The disease often occurs sporadically and is related to the body's immune function. In the elderly, individuals with local trauma, systemic lupus erythematosus, lymphoma, leukemia, as well as those undergoing long-term corticosteroid, immunosuppressive, or radiation therapy, are significantly more susceptible than normal individuals. Moreover, the course of the disease is prolonged, the condition is more severe, and postherpetic neuralgia is also more prominent.

bubble_chart Pathogen

The pathogen of this disease belongs to the herpesvirus DNA group and is identical to the chickenpox virus, also known as the varicella-zoster virus (VZV).

bubble_chart Pathological Changes

The pathological changes in the skin primarily occur in the epidermis, with blisters located in the deep layers of the epidermis. Notably swollen balloon-like epidermal cells can be observed within the blisters and at their edges. Eosinophilic intranuclear inclusion bodies are visible in the degenerated cell nuclei. Corresponding lesions are also found in the ganglia associated with the rash, manifesting as segmental poliomyelitis in the posterior columns of the spinal cord, along with intense inflammatory reactions in the ganglia and posterior nerve roots. Shortly after the appearance of the rash, significant degeneration of sensory nerve fibers in the dermis also becomes evident.

bubble_chart Clinical Manifestations

Often, there are precursor symptoms of grade I, such as fever, lack of strength, general malaise, loss of appetite, local lymph node swelling and pain, as well as skin burning, hypersensitivity, or neuralgia at the affected area.

The typical skin lesions are clusters of non-fusing foxtail millet-sized to soybean-sized papules on an inflammatory base. These papules then turn into blisters with clear fluid, tense walls, and surrounded by erythema. The lesions are distributed along peripheral nerves, arranged in a band-like pattern, which is highly characteristic and diagnostically valuable. The skin between clusters of blisters remains normal. Without secondary infection, the blisters dry and crust over within a few days, leaving temporary pigmentation and usually no scarring. Due to variations in immune status, the manifestations can be atypical and are given different names. Cases with neuralgia but no rash are called zoster sine herpete; those with only erythema and papules that do not progress to blisters are termed abortive zoster; those with large blisters are called bullous zoster; those with hemorrhage are hemorrhagic zoster; those with significant necrosis are gangrenous zoster; lesions due to hematogenous spread of the virus are termed generalized zoster; and involvement of internal organs such as the lungs, liver, or brain is called zoster pneumonia, hepatitis, or encephalitis. Rarely, more than two ganglia may be affected, producing bilateral or ipsilateral lesions involving multiple nerve distributions.

Neuralgia is one of the hallmark features of this disease and has diagnostic value. It often appears before the rash or during the eruption and may gradually worsen. Pain is milder or absent in children but is often severe in elderly patients, presenting as paroxysmal exacerbations that are difficult to tolerate and may persist for months or longer after the skin lesions resolve.

The varicella-zoster virus most commonly affects the intercostal nerves. Among the spinal nerves, except for the thoracic nerves, which alone form the intercostal nerves to innervate the skin of the chest and abdomen, most other spinal nerves combine with adjacent spinal nerves to form the cervical, brachial, lumbar, and sacral plexuses. From these plexuses, numerous peripheral nerves branch out to innervate the skin of the neck, upper and lower limbs, and perineum. Therefore, when thoracic nerves are affected, the segmental pathology can be clearly reflected by the intercostal nerves. In contrast, lesions of the cervical or lumbosacral nerves can only be localized to the region of spinal nerve involvement based on the skin lesions.

Cranial nerves have specific distributions, with the trigeminal and facial/auditory nerves being the most commonly affected. Among the trigeminal branches, the ophthalmic branch is most frequently involved, especially in the elderly, often accompanied by severe pain. Lesions are distributed on one side of the forehead and face; if the nasal tip is involved, ocular inflammation may occur, and severe cases can lead to blindness. Therefore, when the ophthalmic branch is affected, careful examination of the cornea is essential for early intervention. When the maxillary branch is involved, blisters appear on the uvula and tonsils; when the mandibular branch is affected, blisters appear on the anterior tongue and buccal mucosa. When the facial and auditory nerves are invaded by the virus, blisters may appear in the external auditory canal or on the tympanic membrane, accompanied by tinnitus, deafness, vertigo, nausea, vomiting, nystagmus, and ipsilateral facial deviation, loss of taste in the anterior two-thirds of the tongue, etc. This is also known as herpes zoster oticus, and the triad of facial deviation, ear pain, and external auditory canal blisters is called Ramsey-Hunt syndrome.

If the virus spreads upward after invading cranial or cervical ganglia, it can cause zoster meningoencephalitis, leading to symptoms such as headache, vomiting, and convulsions, which require vigilance.

Additionally, if the virus spreads from the dorsal root ganglia to the visceral autonomic nerve fibers, it can produce symptoms corresponding to the affected systems, such as gastroenteritis, cystitis, peritonitis, pleuritis, etc.

The course of the disease generally lasts about 2–3 weeks. Generalized or recurrent cases often indicate immune dysfunction, and the possibility of underlying immunodeficiency or malignancy should be considered.

bubble_chart Diagnosis

The diagnosis is not difficult based on unilateral clusters of vesicular lesions distributed along peripheral nerves accompanied by neuralgia. This condition should be differentiated from herpes simplex, which typically occurs at mucocutaneous junctions, is unrelated to peripheral nerve distribution, tends to recur, and causes minimal pain. During the prodromal stage of herpes zoster or in cases of zoster sine herpete, misdiagnosis as intercostal neuralgia, pleuritis, or acute abdominal conditions may occur and should be noted.

bubble_chart Treatment Measures

The treatment mainly focuses on antiviral, anti-inflammatory, analgesic, and local symptomatic management.

(1) Systemic Therapy

1. Antiviral drugs: Acyclovir (acycloguanosine) taken orally or intravenously, or cytarabine administered intravenously (refer to "Herpes Simplex"). Poly I:C, 2mg per dose, injected intramuscularly 2-3 times a week.

2. Analgesics: Options include indomethacin, carbamazepine (0.1g, three times daily), cimetidine, etc. Chinese patent drug scandent schefflera stem and leaf tablets (wild Floweringquince Fruit) can also be used. For severe cases, procaine local block may be performed, and vitamin B₁, B₁₂ can also be applied as appropriate.

3. Immunomodulators: Transfer factor, α-interferon, thymosin, or gamma globulin may be selected as needed to alleviate symptoms and shorten the course of treatment. Zoster immune globulin is a specific high-titer immunoglobulin containing high concentrations of neutralizing antibodies, with significant efficacy, but it is scarce and expensive.

4. Corticosteroids: For elderly patients and those with ocular involvement, early administration of moderate-dose prednisone (20-40mg/day) can shorten the disease course and alleviate neuralgia.

5. Acupuncture: For cases affecting the upper limbs and chest, Hegu (LI4) and Quchi (LI11) are selected; for lower limb involvement, Yanglingquan (GB34), Zusanli (ST36), and Sanyinjiao (SP6) are used. Ear acupuncture can also be employed. All methods have analgesic effects.

(2) Local Therapy: The focus is on drying and anti-inflammatory measures. If the blisters are unruptured, sulfur calamine lotion can be applied multiple times daily, or acyclovir cream 2-3 times daily. If the blisters have ruptured, 3% boric acid solution wet compresses, adhesive membrane ulcer paste, or neomycin ointment may be applied 2-3 times daily as appropriate.

(3) Physical Therapy: Helium-neon laser irradiation, ultraviolet irradiation, and frequency spectrum electrotherapy all have certain anti-inflammatory and analgesic effects.