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Autonomic Zoster - An Overview

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Herpes zoster is a DNA-based human herpes virus. Read below to learn more about Zoster.

Medically reviewed by

Dr. Abhishek Juneja

Published At October 27, 2023
Reviewed AtOctober 27, 2023

Introduction

Herpes zoster or shingles is an inflammatory viral disease. Structurally varicella-zoster virus is similar in appearance to the herpes simplex virus. The word zoster comes from Latin, which means a belt, as the lesion occurs in a belt-like distribution. Pathogenesis transmission is predominantly through the inhalation of contaminated droplets and is highly contagious, and rarely may occur due to direct contact. The incubation period is two weeks; during that period virus proliferates in macrophages, with viremia and dissemination to the skin and other organs. Humoral and cell-mediated immunity are also triggered against it. As the viremia overlaps, body defense systemic signs and symptoms appear. The host can recover in two-three weeks with a normal immune response. During the disease process, it may progress along the sensory nerves to the sensory ganglia, where it resides in latent form. Varicella zoster virus is cytopathic to the skin and mucosa epithelial cells with sensory nerve involvement. Herpes zoster - reactivation of latent VZV is uncommon but characteristically occurs in immunosuppressive patients.

What Is an Autonomic Zoster?

Zoster is also called 'shingles' or 'zona.’ It is an acute viral infection of extremely painful and incapacitating nature, characterized by the formation of dorsal root ganglion, associated with vesicular eruptions of skin and mucous membrane of the area supplied by the affected sensory nerve.

Being aware of autonomic dysfunction brought on by VZV is crucial because such patients may initially attend a gastrointestinal or urology clinic. Neurologists, dermatologists, gastroenterologists, and urologists must work closely together to initiate early antiviral medicines and maximize bowel and bladder care in such patients.

Herpes zoster (HZ) can be brought on by the latent varicella-zoster virus (VZV) reactivating. Ramsay Hunt syndrome (RHS) is brought on by the reactivation and growth of VZV in the geniculate ganglion, which can result in neurological problems and a vesicular rash on the mouth or ear mucosa.

How Is the Lesion of the Zoster Manifests?

  • It involves adults, and there is no gender prediction.

  • The prodromal period of two to four days in which shooting and burning pain, paraesthesia, burning, and tenderness appear along the course of the affected nerve. The reason for shooting pain is the occurrence of active ganglions with resultant neuronal necrosis and severe neuralgia. The pain is present in the area supplied by the involved nerve, the dermatome.

  • Unilateral blisters on an erythematous floor occur in groups along the course of the nerve and give a picture of a stage dermatome involvement. This is called the 'zoster-form' pattern.

  • Nerves typically involved are C3, T5, L1, L2, and the first division of the trigeminal nerve, which may lead to corneal scarring, lesion of the scalp, and blindness, presumably linked to viral spread, neural harm, vasculitis, and inflammatory immune reaction. In addition, it may affect the motor nerve.

  • Zoster sine eruptions or zoster sine herpete is a zoster infection without the appearance of a dermatomal lesion.

  • Hutchinson's sign is a cutaneous zoster infection of the side of the nose.

  • Retinal necrosis is a serious and occasional complication of zoster infection.

  • In immunocompromised patients, the infection is atypically manifested with bilateral lesions that appear involving multiple dermatomes where varicella zoster infection (VZI) may involve dorsal root ganglion as anterior horn cells resulting in paralysis complications.

What Is Postherpetic Neuralgia?

This is a complication of zoster infection.

  • Peripheral Injury: Zoster virus injures the peripheral nerve by demyelination, Wallerian degeneration, and sclerosis.

  • Central Injury: There is also atrophy of dorsal horn cells in the spinal cord.

  • Low-grade persistent infection of trigeminal ganglion also causes postherpetic neuralgia.

The distribution of postherpetic neuralgia affects the older age group. The incidence of postherpetic neuralgia is more in women as compared to men. Initially, there is the presence of a rash, which is followed by pain. Pain may continue for weeks to months. If pain occurs for more than six months, the duration is usually called postherpetic neuralgia. Other symptoms: There may be paresthesia and hyperesthesia, sensory deficit, and allodynia.

The syndrome is a zoster infection of the geniculate ganglion with the involvement of the external ear and oral mucosa. The clinical manifestation of it is facial paralysis and pain of the external auditory meatus and pinna of the ear, with the vesicular eruption occurring in the oral cavity and oropharynx with hoarseness of voice, tinnitus, vertigo, and occasional other disturbances.

How to Manage Herpes Zoster Infection?

  • The antiviral drug should be given in the early course of the disease. Acyclovir 800 mg, Famciclovir 250 mg TDS, and Valacyclovir 1 gram TDS.

  • Topical Therapy: Use of topical agents like lidocaine to reduce pain.

  • Drug Therapy: The use of tricyclic antidepressants like amitriptyline, nortriptyline, doxepin, and desipramine have been used to minimize the painful sequelae of this infection. For patients who cannot tolerate tricyclic antidepressants (TCA) due to cardiovascular side effects, other drugs, Gabapentin, and Pregabalin, can also be given to minimize the pain. Compared with a placebo, these drugs may reduce pain at up to eight weeks in people with established postherpetic neuralgia.

  • Surgery: When drug therapy is ineffective, surgery should be carried out at the peripheral nerve level or dorsal root indicated. In some cases, a sympathetic nerve block is also effective.

  • Steroid Therapy: Steroid injections can be given to patients older than 60 to treat postherpetic neuralgia. This will help in reducing the pain of the patient.

  • Control of Pruritus: Warm baths with soap or baking soda and calamine lotion should be applied. Systemic diphenhydramine is also given to control pruritus.

  • Varicella Zoster Immune Globulin: This is given in the case of the immunocompromised patient. This will help to reduce the severity of the lesion.

Conclusion

Varicella zoster is a DNA-based (deoxyribonucleic acid) virus that produces prodromal symptoms like fatigue, hyperesthesia, and pain. Development of lesions initiates as edema and erythema, papulovesicular and vesiculopustular lesions, and erosions limited to a dermatome, which are unilateral. In the older age group, zoster arises as a complication of severe pain postherpetic neuralgia manifest as unilateral with vesicular eruption along the course of the trigeminal fifth cranial nerve due to the nature of the virus to reactivate within the body. Thus it is always better to consult the doctor for any abrupt changes as soon as possible to treat the diseases at their mild stage to have a good outcome.

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Dr. Abhishek Juneja
Dr. Abhishek Juneja

Neurology

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