Varicella-zoster virus (VZV) initial infection causes chickenpox, and after healing the residual virus lurks in the ganglia of the posterior spinal nerve roots and cranial nerves, and when VZV-specific cellular immunity decreases, the virus is revived and herpes zoster occurs. Herpes zoster has the highest incidence of any neurological disorder. The basic characteristic of the development of herpes zoster is that its incidence tends to increase significantly with age and with the impairment of cellular immunity by disease, drugs, etc. The quality of life may be significantly reduced in patients with herpes zoster over 50 years of age and in immunocompromised individuals. The clinical course of herpes zoster is variable. Symptoms are usually milder in children and young adults. Typical herpes zoster has prodromal symptoms; headache, photophobia, discomfort, and usually rarely fever may occur, and abnormal skin sensation and varying degrees of pain are the most common symptoms. These symptoms can occur days to weeks before the onset of shingles. Pain can be burning, stabbing, throbbing, or electric shock-like. Altered tactile sensitivity, pain triggered by minor irritation, and intense itching are also not uncommon. Herpes zoster lesions are usually unilateral, occurring in one or two adjacent skin areas, with normal skin between herpes clusters and a tendency for the entire lesion to be distributed in bands without crossing the midline of the torso. Rarely, lesions may occur outside of the main dermatome or adjacent dermatomes. Rarely, several dermatomes are involved asymmetrically, i.e., both sides of the body are affected. The rash initially presents as asymmetric, unilateral erythema or maculopapular rash, usually appearing as clusters of small, clear blisters containing high concentrations of VZV within 12-24 h. After 2-4 days, the blisters fuse. On the third day, the blisters become cloudy and dry up after 7-12 days. In immunocompetent individuals, the duration of lesions until crusting disappears is usually 2-3 weeks. Local lymph nodes are often enlarged and painful to pressure. Occasionally, immunodeficient individuals have a chronic course, with skin changes that can last for months and may recur as small blisters. Most patients have a rash on the infected skin area. Those who have only erythema and papules that resolve without blistering are referred to as “strophic herpes zoster”. Some people who do not have painful skin areas may develop pain at the onset of the rash or within a few days after the onset of the rash. A very small number of patients have only pain in the skin area after the prodromal phase without a rash, called “rashless herpes zoster”. Herpes zoster can occur in any dermatomes, but most commonly in the dermatomes innervated by the thoracic and cranial nerves. The thoracic nerve is involved in about 50-56% of cases. Cranial nerves, such as the trigeminal nerve and other cranial nerves (VII and VIII cranial nerves), are involved in about 20% of cases. The lumbar and sacral segments are rarely involved (in decreasing order of frequency, 15% and 2%, respectively). Treatment is mostly based on antiviral, immune system improvement, pain reduction, nerve nutrition and local medication, depending on the patient’s condition.