What is the prognosis of herpes zoster (shingles)?

Author

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Joseph S Eastern, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Dermatology, University of Medicine and Dentistry of New Jersey; Clinical Assistant Professor, Seton Hall University School of Graduate Medical Education

Joseph S Eastern, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH Physician, San Antonio Infectious Diseases Consultants; Adjunct Professor of Medicine, Department of Medicine, University of Texas Health Science Center at San Antonio

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Infectious Diseases Society of America, International Society for Human and Animal Mycology, International Society for Infectious Diseases, International Society of Travel Medicine, Medical Mycological Society of the Americas, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

James E Moon, MD, FACP, FIDSA Director, Center for Enabling Capabilities, Walter Reed Army Institute of Research; Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences

James E Moon, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

Wayne E Anderson, DO Assistant Professor of Internal Medicine/Neurology, College of Osteopathic Medicine of the Pacific Western University of Health Sciences; Clinical Faculty in Family Medicine, Touro University College of Osteopathic Medicine; Clinical Instructor, Departments of Neurology and Pain Management, California Pacific Medical Center

Wayne E Anderson, DO is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Law, Medicine & Ethics, California Medical Association, and San Francisco Medical Society

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Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI

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Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

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Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

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Maria M Diaz, MD Staff Physician, Department of Emergency Medicine, Memorial Hospital

Maria M Diaz, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Andrea N Driano, MD Consulting Staff, Department of Emergency Medicine, Children’s Hospital and Medical Center, Seattle WA

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Franklin Flowers, MD Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

webmd.com”>Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

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C Stephen Foster, MD, FACS, FACR, FAAO Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution

C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi

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Kilbourn Gordon III, MD, FACEP Urgent Care Physician

Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan I Huffman, MD, Staff Physician, Department of Ophthalmology, Yale-New Haven Hospital

webmd.com”>Disclosure: Nothing to disclose.

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

webmd.com”>Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

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Cynthia Haeshin Moon, MD Staff Physician, Department of Emergency Medicine, SUNY Downstate Medical Center/Kings County Hospital Center

Disclosure: Nothing to disclose.

Barbara L Roque, MD Full Partner, Ophthalmic Consultants Philippines Co; Service Chief, Pediatric Ophthalmology and Strabismus, Department of Ophthalmology, Asian Hospital and Medical Center; Active Staff, International Eye Institute, St Luke’s Medical Center Global City; Visiting Ophthalmologist, AMC Eye Center, Alabang Medical Center

Barbara L Roque, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Cataract and Refractive Surgery, Philippine Academy of Ophthalmology, Philippine Society of Cataract and Refractive Surgery, and Philippine Society of Pediatric Ophthalmology

webmd.com”>Disclosure: Nothing to disclose.

Manolette R Roque, MD, MBA General Manager, Full Partner, Ophthalmic Consultants Philippines Co.; President and CEO, Chief Refractive Surgeon, EYE REPUBLIC Ophthalmology Clinic; Section Chief, Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief, Ocular Immunology and Uveitis, International Eye Institute, St Luke’s Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic; Director, AMC Eye Center, Alabang Medical Center; President, Philippine Ocular Inflammation Society

Manolette R Roque, MD, MBA is a member of the following medical societies: American Academy of Ophthalmic Executives, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery

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Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

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Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

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Florian P Thomas, MD, MA, PhD, Drmed Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, and Sigma Xi

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

webmd.com”>Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

webmd.com”>R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

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Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Shingles: MedlinePlus Genetics

Shingles (also known as herpes zoster) results from infection by the varicella zoster virus. This common virus causes chickenpox (also known as varicella), which is characterized by itchy spots on the skin that cover the whole body and usually occurs in childhood or adolescence. After the body fights the initial infection, the varicella zoster virus remains in nerve cells for the rest of a person’s life. Because the virus is controlled by immune system cells called T cells, it is generally inactive (latent) and typically causes no health problems. However, in some people, the virus becomes active again (reactivates) and causes shingles. Shingles can occur at any age, although it is rare in childhood and becomes more common after age 50.

Shingles is characterized by a severely painful, itchy, or tingling rash, most commonly on one side of the torso, although it can occur anywhere on the body. Reactivation of the virus usually occurs in a single nerve, leading to the symptoms of shingles in just the region of skin connected to that nerve. When the nerve connected to the eye and the skin surrounding it is affected, the condition is called herpes zoster ophthalmicus. This form of shingles, which accounts for about 20 percent of cases, can cause permanent vision impairment.

Some individuals with shingles feel throbbing or tingling in the affected region shortly before the rash appears. Blisters form in the rash area, break open, and scab over in a few days. Healing usually takes 2 to 4 weeks. Most people have only one episode of shingles, although it can recur in rare cases.

In 5 to 20 percent of people with shingles, severe pain continues in the affected region after healing of the rash, which is known as postherpetic neuralgia (PHN). PHN is the most common complication of shingles. It can also involve severe itchiness or an overactive pain response to things that do not usually cause pain (allodynia), such as a light touch. PHN can last weeks, months, or even years. The likelihood of developing PHN after shingles and its severity increase with age. The pain caused by shingles and PHN can disrupt day-to-day activities and reduce a person’s quality of life.

Shingles (for Parents) – Nemours KidsHealth

What Is Shingles?

Shingles, also called zoster or herpes zoster, is a skin rash caused by a viral infection of the nerves right below the skin.

What Causes Shingles?

The varicella zoster virus causes shingles and chickenpox. Anyone who has had chickenpox can later develop shingles — even children. That’s because the virus stays dormant (resting) in the nervous system for the rest of a person’s life.

In many people, the virus never comes back. But in others, it flares up and causes shingles. It’s uncommon for someone to get shingles more than once.

People of all ages can get shingles, but most cases are in people over 50 years old.

What Are the Signs & Symptoms of Shingles?

Often the first shingles symptoms happen in the area where the rash will appear. A person may have tingling, itching, or pain in this area. When the rash shows up, the pain may be mild or severe.

The rash starts as groups of tiny pimples on one side of the body or the face. It’s often in the shape of a band or belt. The pimples change to pus-filled blisters that break open and scab over in about 7–10 days. The scabs usually heal and fall off about 2–4 weeks after the rash starts.

Some kids with shingles also may have a fever and a headache, and might feel tired and achy. Rarely, a child has the pain of shingles without the rash. More severe symptoms can happen, but usually in people over age 50.

What Problems Can Happen?

Most cases of shingles heal on their own, with or without treatment, and won’t lead to any other problems. In rare cases, shingles can lead to complications, including:

• Ongoing pain (post-herpetic neuralgia): Damaged nerve fibers in the skin send confused messages to the brain, leading to pain. Pain can go on for a long time after the shingles rash is gone. This is the most common shingles complication.
• Vision problems: Shingles near or in an eye can lead to vision loss.
• Skin infections: A shingles rash can become infected with bacteria, leading to impetigo or cellulitis.
• Nervous system problems: Shingles on the face can involve different nerves that connect to the brain. This can lead to nerve-related problems such as facial paralysis, hearing problems, and problems with balance. In very rare cases, shingles can lead to encephalitis (inflammation of the brain).

How Is Shingles Diagnosed?

Doctor usually can diagnose shingles by looking at the rash. Rarely, a doctor may send a small sample of infected skin to be checked in a laboratory.

If you think your child might have shingles, call your doctor. If your child might have shingles on the face, it’s important to get a doctor’s help right away to keep the infection from spreading to the eyes.

How Is Shingles Treated?

Not all kids who get shingles need treatment. If a doctor decides a treatment may help, it should start right away. Treatment usually includes an antiviral medicine and pain-control medicines.

Antiviral medicines like acyclovir (Zovirax) or valcylovir (Valtrex):

• help heal the skin rash
• stop the virus from multiplying
• help control pain

Pain medicines (over-the-counter or prescription creams, sprays, or skin patches):

• help control pain
• ease inflammation (swelling and redness)

Medicines can’t rid the body of the virus, but they can lower the chances of complications and help speed healing. Ask your doctor if treatment might help your child.

As the rash heals, keep the area clean. Wash it with water and a mild soap, and apply cool, wet compresses to the blisters several times a day to ease pain and itching. Oatmeal baths also can bring relief.

To prevent the virus from spreading to other people, keep the rash covered at all times.

Can Shingles Be Prevented?

It’s not always possible to prevent shingles. But the chickenpox vaccine can make a case of shingles less serious. If your child hasn’t had chickenpox, ask your doctor about getting the chickenpox vaccine.

There is a shingles vaccine, but it’s mostly given to older adults. The older someone is, the more severe shingles can be. Kids are unlikely to be seriously affected by shingles.

What Else Should I Know?

Children whose shingles rash that can’t be completely covered should not go to school or childcare until the blisters scab over and are dry.

Newborn babies, pregnant women, people with weakened immune systems, and anyone who is not immune to chickenpox should avoid close contact with anyone who has shingles until the rash is gone.

Shingles

Shingles (herpes zoster) is an outbreak of rash or blisters on the skin that is caused by the same virus that causes chickenpox — the varicella-zoster virus. The first sign of shingles is often burning or tingling pain, or sometimes numbness or itch, in one particular location on only one side of the body. After several days or a week, a rash of fluid-filled blisters, similar to chickenpox, appears in one area on one side of the body. Shingles pain can be mild or intense.  Some people have mostly itching; some feel pain from the gentlest touch or breeze.  The most common location for shingles is a band, called a dermatome, spanning one side of the trunk around the waistline. Anyone who has had chickenpox is at risk for shingles.  Scientists think that in the original battle with the varicella-zoster virus, some of the virus particles leave the skin blisters and move into the nervous system.  When the varicella-zoster virus reactivates, the virus moves back down the long nerve fibers that extend from the sensory cell bodies to the skin.  The viruses multiply, the tell-tale rash erupts, and the person now has shingles.

Treatment

The severity and duration of an attack of shingles can be significantly reduced by immediate treatment with antiviral drugs, which include acyclovir, valcyclovir, or famcyclovir. Antiviral drugs may also help stave off the painful after-effects of shingles known as postherpetic neuralgia. Other treatments for postherpetic neuralgia include steroids, antidepressants, anticonvulsants (including pregabalin and gabapentin enacarbil), and topical agents.In 2006, the Food and Drug Administration approved a VZV vaccine (Zostavax) for use in people 60 and older who have had chickenpox. In March 2011, the FDA extended the approval to inlcude adults 50 to 59 as well.  Researchers found that giving older adults the vaccine reduced the expected number of later cases of shingles by half. And in people who still got the disease despite immunization, the severity and complications of shingles were dramatically reduced. The shingles vaccine is a preventive therapy and not a treatment for those who already have shingles or postherpetic neuralgia.

Prognosis

For most healthy people who receive treatment soon after the outbreak of blisters, the lesions heal, the pain subsides within 3 to 5 weeks, and the blisters often leave no scars.  However, shingles is a serious threat in immunosuppressed individuals — for example, those with HIV infection or who are receiving cancer treatments that can weaken their immune systems.  People who receive organ transplants are also vulnerable to shingles because they are given drugs that suppress the immune system.  A person with a shingles rash can pass the virus to someone, usually a child, who has never had chickenpox, but the child will develop chickenpox, not shingles.  A person with chickenpox cannot communicate shingles to someone else.  Shingles comes from the virus hiding inside the person’s body, not from an outside source.

Research

The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct shingles research in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Current research is aimed at finding new methods for treating shingles and its complications.

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Organizations

American Chronic Pain Association (ACPA)
Provides self-help coping skills and peer support to people with chronic pain. Sponsors local support groups throughout the U.S. and provides assistance in starting and maintaining support groups.

P.O. Box 850
Rocklin, CA 95677-0850
[email protected]
http://www.theacpa.org
Tel: Rocklin
Fax: 916-652-8190

National Shingles Foundation
[For Research on Varicella Zoster]
Non-profit organization solely combating VZV infections: chickenpox, shingles and post-herpetic neurgalia (PHN). Supports research that may lead to a better understanding of VZV infections and to advances in their prevention, treatment and cure.

603 W. 115 Street
Suite 371
New York, NY 10025
[email protected]
http://www.vzvfoundation.org
Tel: New York
Fax: 212-838-0380

National Institute on Aging (NIA)

National Institutes of Health, DHHS
31 Center Drive, Rm. 5C27 MSC 2292
Bethesda, MD 20892-2292
http://www.nia.nih.gov
Tel: Bethesda

National Library of Medicine (NLM)

National Institutes of Health, DHHS
8600 Rockville Pike, Bldg. 38, Rm. 2S10
Bethesda, MD 20894
http://www.nlm.nih.gov
Tel: Bethesda

Content Provided By

NINDS Disorders is an index of neurological conditions provided by the National Institute of Neurological Disorders and Stroke. This valuable tool offers detailed descriptions, facts on treatment and prognosis, and patient organization contact information for over 500 identified neurological disorders.

Neurological Disorders and Stroke »

Shingles Overview: Symptoms, Causes, Treatment, and More

The varicella zoster virus — the virus that causes chickenpox and shingles — is part of a group of viruses called herpes viruses. This group also includes the viruses that cause cold sores (oral herpes) and genital herpes.

But the varicella zoster virus is not the same virus that causes cold sores and genital herpes. The viruses that cause oral and genital herpes are herpes simplex 1 and herpes simplex 2.

If you’ve had chickenpox, you can get shingles. After the chickenpox is over, varicella zoster lies inactive, mainly in spinal or cranial nerves. Sometimes the virus reactivates, and that’s when it travels along the nerves to erupt as a rash on your skin, causing shingles.

But the cause of the reactivation is still unknown, according to the National Institute of Neurological Disorders and Stroke.

Risk Factors

The risk of shingles increases as you age, which may be due to lowered immunity to infections as you grow older.

The following may also put you at increased risk for shingles, according to the CDC.

• Certain cancers, such as leukemia and lymphoma
• HIV or AIDS
• Immunosuppressive medications, such as corticosteroids, which are used in the treatment of cancer and autoimmune conditions like rheumatoid arthritis, as well as drugs that are given to people who have undergone an organ transplant

Some research suggests that genetics may play a part, according to MedlinePlus.

If you have a first-degree relative — meaning a parent or sibling — who has had shingles, it may increase your risk of having it. A study published in the Journal of Clinical Virology found that nearly 44 percent of those with shingles had family members who had also developed it.

Is Stress a Risk Factor for Shingles?

You may have heard that someone got shingles because they were stressed, perhaps after the death of a relative, soon after a divorce, or at the end of a difficult semester at school.

But studies haven’t definitively proved that stress is a risk factor for shingles. Some research suggests that it is, according to MedlinePlus, while other research suggests that it’s not at all.

In a study published in March 2015 in Clinical Infectious Diseases, researchers reviewed the medical records of more than 39,000 people to see if cases of shingles increased after a difficult life event, and the authors found no evidence that stress is a trigger.

“There’s some controversy about the matter,” says Safdieh. “We know for a fact that stress can have an impact on the function of the immune system. If there’s stress, immunity is depressed, and I certainly see patients who tell me they were having a lot of stress when they got shingles.” But, he adds, “there are many people who are stressed and don’t get shingles, and many people who get them while they’re on vacation.”

If there is a link between stress and shingles, it’s probably not that the stress itself is putting a strain on the immune system — it may be that stress creates conditions that lower immunity. “Keep in mind,” says Safdieh, “that when you’re stressed, you don’t sleep and you don’t eat, and all these factors can play a role.”

RELATED: How Stress Affects Your Body, From Your Brain to Your Digestive System

Disseminated Herpes Zoster – an overview

Epidemiology of Herpes Zoster in Men and Women

Primary varicella-zoster virus (VZV) infection typically occurs in childhood and may result in clinical chickenpox; however, reactivation of latent VZV within the dorsal root ganglia decades later leads to herpes zoster, a dermatomal vesicular eruption often associated with painful post-herpetic neuralgia. The clinical course of acute zoster is variable. The rash usually lasts 7–10 days with complete healing within 2–4 weeks. Post-herpetic neuralgia (PHN) is manifested by persistent pain that may last months or years following rash resolution and occurs in 10–18% of patients with zoster.³⁴ Other complications associated with zoster include herpes zoster ophthalmicus, occurring in 10–25% of persons with zoster, and which can result in loss of vision and other complications of the eye.^35,36 Reactivation of VZV in the geniculate ganglion of the facial nerve results in the uncommon Ramsay Hunt syndrome, a peripheral facial nerve palsy accompanied by zoster vesicles on the ear, hard palate, or tongue.³⁷ Uncommonly, herpes zoster is associated with neurologic complications that include myelitis, aseptic meningitis, meningoencephalitis, cranial palsies, motor weakness in noncranial nerve distributions called zoster paresis, autonomic dysfunction causing urinary retention, and rarely acute focal stroke-like neurologic deficits termed granulomatous angiitis.³⁸ Immunocompromised persons are at increased risk for cutaneous and visceral dissemination and neurologic zoster complications.³⁹

Approximately 1 in 3 persons will develop zoster during their lifetime, resulting in an estimated 1 million episodes in the United States annually.⁴⁰ In the United States, approximately 99.5% of the population age 40 years and older has serologic evidence of prior VZV infection, thus predisposing almost all older adults to develop zoster.⁴¹

Among varicella vaccine recipients, zoster may also develop from reactivation of the attenuated Oka/Merck VZV strain in the vaccine, and although longer follow-up is needed, studies suggest this risk to be considerably lower than the incidence of zoster following wild-type VZV infection.^42–44

Age is the most important risk factor for development of zoster. Zoster incidence has been shown to increase with age by a factor of >10 with much of the increase in incidence beginning around 50–60 years old.⁴⁵ It is estimated that 50% of persons who live to age 85 years will have experienced zoster.^46,47

Several studies have also demonstrated a higher incidence of zoster among women after controlling for age, other zoster risk factors such as immunodeficiency and co-morbidities, and gender differences in medical consultation rate.^48–50 In a large, randomized controlled vaccine trial in the US, the incidence of confirmed zoster cases was 11% higher among women in a cohort of immunocompetent persons 60 years and older.⁴⁸ However, some researchers did not find a difference in incidence by gender.^46,51

The epidemiology of zoster is directly related to the biology underlying the virus–host relation that allows reactivation of latent VZV. As cell mediated immunity plays a key role in controlling the development of zoster and its severity, persons who are immunocompromised with deficiencies in cell mediated immunity (such as among persons with hematologic malignancies and solid tumors, stem cell transplants and solid organ transplants, and HIV infection) have a substantially higher incidence of zoster and its severe manifestations.^52–62

Shingles – symptoms, treatment, vaccination

Shingles is a viral infection, the first symptom of which is usually a tingling, sharp, burning pain under the skin. This is followed 1 – 14 days later by a red rash and blisters. Early treatment can help to shorten the duration of infection and reduce the risk of complications.  Vaccination can help to reduce the risk of developing shingles.

Shingles is caused by the same virus as chickenpox. After a bout of chickenpox the virus remains in the body for life and can be reactivated at a later stage as shingles. Anyone who has had chickenpox can go on to develop shingles.

Signs and symptoms

Shingles can occur at any age but usually occurs in adults over the age of 50 years.  Females appear to be more frequently affected than males.
 Groups at an increased risk of developing shingles include people whose immune systems have been impaired due to ill health, medications or diseases that lower the immunity.

The initial tingling, sharp, burning pain under the skin can occur anywhere on the body but usually affects the face, upper abdomen or back.  It almost always occurs on one side of the body only. The pain can be mild or it can be quite severe. The older the person is, the more severe the pain is likely to be.  Pain can be accompanied by other symptoms including: 

• A feeling of being generally unwell
• Mild chills and fever
• Headache
•  An upset stomach
• Enlarged lymph nodes.

After 1 – 14 days a red rash appears over the painful area of skin followed quickly by the development of small, fluid-filled blisters. The rash can be quite itchy. Within a few days of appearing the blisters dry and crust over. It is possible for the blisters to cause mild scarring.

Because shingles affects the nerve cells it is common for the rash to appear as a band across the body or down the leg along the path of a nerve.   Occasionally the rash does not eventuate after the initial pain has developed.  The pain and other symptoms of shingles gradually resolve as the skin rash and blisters disappear. Full recovery from the condition usually occurs within 2 – 3 weeks, or up to 4 weeks in older adults.

Causes

Only people who have had chickenpox in the past (usually in childhood) can get shingles.  The reason why the chickenpox virus reactivates as shingles is not fully understood. It is thought that the following factors influence the development of shingles:

• Emotional stress
• Lowered immunity eg: due to medications or chemotherapy that suppress the immune system
• A recent illness or major surgery
• Injury or sunburn to the skin
• Older age.

However, in most people there is no identifiable cause for shingles occurring.

Diagnosis

A doctor is usually able to make a diagnosis of shingles based on its characteristic symptoms. A full medical history will be taken and the doctor may take a sample of the fluid from within the blister so that it can be tested in a laboratory for presence of the chickenpox virus.

Treatment

As shingles is caused by a virus and cannot be cured with antibiotics, treatment focuses on relieving symptoms. Getting adequate rest is an important factor in the treatment of shingles.  Other treatment may include: 

• Pain relief medications such as paracetamol
• Cool compresses applied to the affected area
• Lotions and creams may be prescribed for the rash
• Antiviral medications may be prescribed. They don’t kill the virus but can help to reduce the duration of the symptoms
• Corticosteroids medications may be prescribed if the rash and pain are severe
• Antibiotics may be required if the skin rash develops a bacterial infection.

If the shingles rash has affected the eyes, treatment by an ophthalmologist (eye specialist) may be required to prevent damage to the cornea (the transparent part of the eyeball that covers the iris and pupil).

Transmission

The virus that causes shingles is present in the fluid within the blisters of people suffering from shingles. Transmission of this virus mainly occurs through direct or indirect contact with the fluid in the blisters. Rarely, the virus can be transmitted in droplets of saliva from the nose and mouth.

A person with shingles is contagious from when the blisters first develop until after all of the blisters have crusted over.  If the virus is transmitted from a person who has shingles to a person who has not had chickenpox, that person will develop chickenpox, not shingles.

Complications

The most common complication of shingles is a condition called post-herpetic neuralgia. Symptoms include persistent pain at the site of the shingles rash that lasts for more than one month.  Anti-seizure and anti-depressant medications are sometimes used to treat the pain caused by post-herpetic neuralgia.  Other less common complications of shingles include: 

• Bacterial skin infections
• Harm to anunborn foetus if the mother develops shingles in the early months of pregnancy
• Damage to the eye if shingles affecting the eye is left untreated. In rare cases, blindness can occur
• Ramsay Hunt’s syndrome caused by facial shingles. This condition can cause ear pain, facial paralysis, and loss of taste and hearing.

Most complications of shingles are very rare, but it is still important to consult a doctor as soon as shingles is suspected so that an accurate diagnosis and appropriate treatment can be given. This is especially important for those people with a weakened immune system.

Prevention / vaccination

Although shingles is less contagious than chickenpox, you should still take the following steps to prevent spreading the virus: 

• Keep the rash covered
• Avoid scratching or touching the rash
• Wash your hands thoroughly and often
• Avoid contact with people at risk, including women who are pregnant, premature or low birth-weight babies, and people with weakened immune system. 

A shingles vaccine is available in New Zealand for immunisation of people aged 50 years and older and free from GPs for adults at age 65 years. The vaccine reduces the risk of shingles developing and may help to reduce the severity and duration of shingles if it does occur. 

Further information

If you believe you may have shingles or you want to know if the shingles vaccine is suitable for you, contact your GP or practice nurse, or call Healthline on 0800 611 116 (24 hours a day, 7 days a week).

References

Immunisation Advisory Centre (2018). Herpes zoster (shingles) Fact Sheet (PDF). Auckland: University of Auckland. http://www.immune.org.nz/sites/default/files/resources/Written%20Resources/DiseaseHerpesZosterImac20180426V02Final.pdf
Mayo Clinic (2018). Shingles (Web Page). Rochester, NY: Mayo Foundation for Medical Education and Research. https://www.mayoclinic.org/diseases-conditions/shingles/symptoms-causes/syc-20353054 [Accessed: 18/06/19] 
Ministry of Health (2018). Shingles (Web Page). Wellington: New Zealand Ministry of Health. http://www.health.govt.nz/your-health/conditions-and-treatments/diseases-and-illnesses/shingles [Date Accessed: 18/06/19] 
Oakley, A. (2015). Herpes zoster (Web Page). Hamilton: DermNet New Zealand. https://www.dermnetnz.org/topics/herpes-zoster/ [Accessed: 18/06/19
Reid, J.S., Ah Wong B (2014). Herpes zoster (shingles) at a large New Zealand general practice: incidence over 5 years. N Z Med J. 2014;127(1407):56-60. 
O’Toole, M.T. (Ed.) (2017). Herpes zoster. Mosby’s Dictionary of Medicine, Nursing & Health Professions (10th ed.). St Louis, MI: Elsevier.

Last Reviewed – June 2019

90,000 Publications in the media

Shingles is a sporadic disease that reactivates a latent viral infection. The causative agent is the varicella-zoster virus of the Alphaherpesviruses subfamily of the Herpetoviridae family (herpes simplex virus type 3). Outside of exacerbation, the localization of the virus is the roots of the spinal ganglia. It proceeds with damage to the posterior roots of the spinal cord and intervertebral ganglia, fever, intoxication and vesicular rash along the sensory nerves.

Epidemiology • The main routes of transmission of the virus are similar to those in chickenpox – airborne and contact (through vesicle discharge) • The disease is seasonally inherent (an increase in the incidence in cold months) • Contact with a patient with shingles can infect children with chickenpox.

Pathogenesis • The development of the disease is considered as a result of the reactivation of the virus circulating in the sensitive ganglia of persons who have had chickenpox; the triggers of reactivation remain unexplored, but the risk group includes patients with immunodeficiencies, malignant growth diseases and injuries, and drug addicts. • On average, the overall incidence is less than 10% of primarily infected persons.

Clinical picture
• Gangliocutaneous form of the disease. Characterized by an acute onset, fever, symptoms of intoxication, severe burning pains at the site of future rashes. Rashes appear along the course of individual sensory nerves in the form of indistinct pinkish spots (3-5 cm), against which, after 18-24 hours, groups of painful vesicles are formed (unlike other herpetic skin lesions, they are limited by a clear demarcation zone). Most often, the lesions are localized on the chest, but can also be located along any sensory nerve and, as a rule, on one side.The lesions disappear within 2–4 weeks, and pain may persist for weeks or months.
• Eye mold . A particularly severe course is characteristic, accompanied by a lesion of the trigeminal (Gasser) node. The rashes are localized along the branches of the trigeminal nerve – on the mucous membranes of the eye, nose, on the skin of the face; often the eyeball is involved.
• Hunt’s Syndrome (damage to the ears), due to the defeat of the geniculate ganglion. It is extremely rare that lesions are observed in children under 10 years of age, the incidence increases in proportion to age (up to 20% of people who have reached 90 years of age get sick).
• Gangrenous (necrotic) form of shingles is manifested by deep skin lesions with the formation of scars.
• Meningoencephalitic form (rarely observed) is characterized by a severe course and high mortality (over 60%), begins with ganglionic manifestations. Later (within 2-3 weeks) symptoms of meningoencephalitis appear.
• Any form of may be accompanied by damage to the autonomic ganglia with the development of symptoms unusual for herpes zoster (vasomotor disorders, Horner’s syndrome, urinary retention, constipation or diarrhea).
• Shingles may be one of the earliest symptoms of HIV infection. In this case, damage to several neighboring dermatomes is observed. Often, such patients develop shingles with disseminated skin lesions, clinically resembling chickenpox.

Research methods (rarely necessary) • Microscopy of the discharge (including bronchoalveolar fluid in patients with pneumonia) to detect Tzank cells • Isolation of the pathogen is carried out on cell cultures in cases that are difficult to diagnose, or with generalized lesions • Possible setting ELISA with biopsy material (in rare cases) or the detection of increasing AT titers (in paired sera) in RPHA or a neutralization reaction.

Differential diagnosis • Contact dermatitis • Superficial pyoderma • Erysipelas • Eczema • For pain (especially in the intercostal spaces) – cholecystitis, pleurisy, MI.

TREATMENT
Drug therapy • Antiviral agents, when used within 48 hours after the onset of the rash, accelerate its resolution and eliminate the symptoms of the disease, in the acute phase they reduce postherpetic neuralgia, absolutely indicated for concomitant severe diseases and eye damage •• Acyclovir 800 mg 5 r / day every 4 hours (except for the night) for 7-10 days or •• Famciclovir 500-750 mg 3 r / day orally for 7 days • Paracetamol, codeine, NSAIDs – for pain • Silver sulfadiazine – topically for the second an infected rash.
Alternative drugs • Vidarabine • Idoxuridine – eye drops.

Complications • Postherpetic neuralgia • Involvement of eye structures in case of facial herpesvirus infection • Meningoencephalitis • Spread over the skin • Superinfection through skin lesions • Hepatitis • Pneumonia • Muscular weakness with lesions of the peripheral nerves • Segmental nerve lesions • Segmental nerves and facial (Ramsey Hunt syndrome) • Ulceration of the cornea • Guillain-Barré syndrome.

Course and prognosis • Resolution of rash within 14–21 days • Postherpetic neuralgia – defined as pain that persists for at least a month after the rash disappears. The incidence of postherpetic neuralgia increases dramatically with age (4% at the age of 30-50 and 50% at the age of over 80).

ICD-10 • B02 Herpes zoster

Note. Tzanka test – detection of giant multinucleated (acantholytic) cells with intracellular inclusions in scrapings taken at the base of the vesicle; indicates chickenpox, herpes zoster, or herpes simplex infection.

Test for IgG antibodies to the varicella-zoster virus (herpes type 3) to hand over in Rubtsovsk

Method of determination
Immunoassay.

Study material
Blood serum

An indicator of the humoral immune response to infection or vaccination.

The Varicella-Zoster virus belongs to the herpesvirus family – human virus type 3.The primary infection is in the form of chickenpox (varicella, chickenpox). Like other herpes viruses, it can become a latent infection. When the virus reactivates, shingles (herpes zoster) occurs.

Chickenpox is a highly contagious infection spread throughout the world. Children are most susceptible to it. It is transmitted by air and in contact with the elements of the rash. The incubation period of chickenpox lasts about 14 days. Multiplying and getting into the skin, the virus causes a characteristic vesicular rash – on the face, trunk, scalp, then throughout the body, accompanied by severe itching.The humoral and cellular (basic) immune response quickly suppresses the infection. The disease is mild and goes away without treatment. But with insufficient cellular immunity (lymphomas, lymphogranulomatosis, bone marrow and organ transplant recipients, AIDS), there is a threat of disseminated life-threatening infection. The infectious period with chickenpox begins two days before the onset of the rash and lasts until all the elements of the rash are covered with crusts (normally after 5 days).Chickenpox in a person who has been ill does not reappear, but the virus is not completely removed from the body, remaining in a latent state in the ganglia of the nervous system.

Any immunodeficiency states (not only AIDS!) Threaten the reactivation of the virus with the development of the second form of clinical manifestation of the infection – shingles, often with severe postherpetic neuralgia. This is a recurrent disease. The likelihood of its occurrence increases with age (more often after 50 years), which is due to a decrease in specific immunity.The incidence increases during the cold season. When the body is weakened under the influence of any diseases, intoxication, taking immunosuppressants, stress, the virus reactivates, multiplies and spreads along the nerves into the skin, usually affecting 1 or 2 adjacent dermatomes on one side of the body. First, red spots appear, in the place of which groups of vesicles appear. The appearance of a rash may be preceded by pain and paresthesia. Chest pain due to acute neuritis is sometimes mistaken for an attack of angina pectoris.The prognosis of the disease is usually good. But with severe immunodeficiency, shingles can be severe and cause complications such as myocarditis, pneumonia, hepatitis, Guillain-Barré syndrome, myelitis, meningoencephalitis, granulomatous arteritis.

Contact with patients with shingles of children who do not have specific immunity can cause them to develop chickenpox. Pregnant women rarely get chickenpox. But with infection in the first half of pregnancy, intrauterine damage to the fetus and the occurrence of malformations are possible.In case of chickenpox disease immediately before childbirth (4 days or less), a severe form of chickenpox may develop in a newborn, since he does not have transplacental maternal antibodies. In case of chickenpox disease more than 4 days before delivery, maternal antibodies formed and passed through the placenta, although they do not protect the child from infection, prevent its severe course. Shingles in the mother does not pose a risk of fetal injury.

Laboratory diagnostics.Chickenpox and shingles are usually diagnosed clinically. In atypical cases, laboratory methods of confirming the diagnosis are used – serological tests. In INVITRO No. 256 and No. 257 – determination of specific antibodies of the IgG and IgM classes. Specific antibodies to the Varicella-Zoster virus appear within 4 to 5 days from the onset of the chickenpox rash. Seroconversion (the appearance of IgG antibodies in the dynamics of observation in their initial absence) confirms the infection with Varicella-Zoster.Antibodies of the IgG class after a previous illness usually persist for life. Chickenpox does not recur, but the immune system is not sterile. The virus remains in the body in a latent form, and the presence of IgG antibodies does not guarantee against reactivation of the infection in the form of shingles. This is due to a decrease in the body’s defense systems. Therefore, the determination of IgG is used in a comprehensive assessment of the state of the immune status and susceptibility to infection with the Varicella-Zoster virus. In the blood of newborns in the first months after birth, maternal IgG antibodies may be present, which have the ability to pass through the placenta.

Limits of definition.
3 IU / L – 5000 IU / L

90,000 Applications: Latest news from Russia and the world – Kommersant Healthcare (110482)

A significant part of the Russian population suffers from a pain syndrome called neuropathic pain. For a long time, sometimes months, a person may experience incessant pain, which often becomes the cause of depression, constant discomfort. In this case, there is no need to talk about any level of quality of life that a person deserves.In recent years, more and more patients with this diagnosis, which, among other things, are difficult to treat. Andrey Danilov, MD, DSc, Professor, Department of Nervous Diseases, Institute of Postgraduate Education, P.M. IM Sechenov, I am sure that with a correct diagnosis and competent treatment, everyone has good chances of successfully getting rid of this type of pain.

Neuropathic pain today occurs in 6-7% of patients, and at neurological appointments, patients with neuropathic pain account for 18%.If we associate this type of pain with diseases, then up to 30-40% of cancer patients suffer from it, every fourth patient with diabetes mellitus, every tenth patient who has had a stroke, and a significant percentage of patients with chronic back pain – from 10% to 37% of all suffering from this disease. In Russia, according to a large-scale epidemiological study carried out in 19 cities, every fifth patient who goes to a polyclinic to consult a neurologist suffers from neuropathic pain.

– Recently, experts have increasingly talked about neuropathic pain as a serious social problem. What is neuropathic pain and how is it dangerous?

– Neuropathic pain is a separate type of pain that is not treated with conventional pain relievers such as NSAIDs (non-steroidal anti-inflammatory drugs) or analgesics. Previously, there was practically no division of pain by type. The need for a new approach to an old problem has arisen due to the fact that pain syndromes are differently sensitive to different forms of drug therapy.Therefore, they were divided into two groups – nociceptive and neuropathic. It has been determined that pain syndromes that are effectively treated with NSAIDs and analgesics are pain arising from irritation of pain receptors – nociceptors, which are located in the skin, muscles, ligaments and internal organs. A person feels this type of pain when tissue is damaged: burns, trauma, inflammation, stretching. But the second category of pain syndromes is not treated with either NSAIDs or simple analgesics. This type of pain occurs when the nervous system is affected, both peripheral and central.It is called neuropathic.

Unfortunately, this is indeed a very big social problem. Despite the development of medical science, scientists still do not fully understand how a person feels pain. Pain sensitivity depends on many factors, including psychological ones. When a person is in pain, of course, he needs help. It would seem that there are a lot of painkillers. But sometimes these funds are powerless. And the constant feeling of pain reduces the quality of life of people, their social adaptation, and ability to work.

– Is it true in this case that neuropathic pain is a signal for a person to pay more attention to their health?

– The fact is that this type of pain is associated with damage to the nerve structures involved in pain control. And this can happen with various diseases: in patients with diabetes mellitus, after herpes zoster on the skin, with radiculitis, after operations, after injuries. At the same time, reflexes are often reduced, numbness and dryness of the skin appear, persistent, persistent, burning, intense pains that follow the patient day and night and do not respond to any analgesics.Neuropathic pain can occur with spinal cord injury, multiple sclerosis, syringomyelia, tumors, after cerebral strokes (post-stroke central pain). This is a very painful condition that destroys normal life. The peculiarity of this pain is that its causes and mechanisms are not located in the place where it hurts. Therefore, it is difficult enough for diagnosis and for the patients themselves to understand that, perhaps, it hurts in one place, and the cause of the pain and its mechanisms in another.That is why conventional pain relievers that act locally are ineffective in this case. In terms of mechanisms, neuropathic pain is a consequence of a malfunction of the systems responsible for pain control due to their damage in various diseases of the nervous system.

– If people suffer from this type of pain syndrome for a long time, then the state in which they live can already be called a disease. How difficult is it to diagnose?

– Specialists identify it.These are mainly those who deal with nervous diseases, that is, neurologists. But this can be done by other doctors who know about the main symptoms. The main characteristics of this pain are a burning sensation, numbness, tingling sensation, lumbago, sharp pain with non-painful touch. When such characteristics sound, we immediately start thinking about neuropathic pain. For the diagnosis of neuropathic pain, there is a very convenient and simple approach proposed by the International Association for the Study of Pain – the 3C rule: “Listen”, “Watch”, “Relate”.

The physician should carefully listen to how the patient describes his pain, and find, hear characteristic verbal characteristics, such as electric shocks, tingling. Further, the specialist must check whether the patient has local sensory disturbances, and must correlate what the patient said to him with what he sees himself.

Questionnaire methods that allow the doctor to make a diagnosis as objectively as possible have recently become a serious help for the diagnosis of neuropathic pain.After filling out such a questionnaire, points are calculated, and if their sum turns out to be equal to or higher than a certain level, with a high degree of probability we can talk about the presence of neuropathic pain in the patient. Although I believe that none of these questionnaires can replace a detailed clinical examination of the patient by a doctor.

– What is the situation with the diagnosis of neuropathic pain in Russia today?

– Fortunately, basic methods for diagnosing neuropathic pain, such as questionnaires, clinical examination, do not require special expensive equipment and are available to every doctor in most medical institutions in the country.Of course, in some cases, additional examination methods may be required to clarify the level of damage to the nervous system. Nevertheless, in recent years, the situation with the diagnosis of neuropathic pain in our country has improved. Recently, a study was conducted among outpatient doctors who answered questions about the diagnosis and treatment of neuropathic pain. It was shown that the main group of applicants was patients with radicular syndrome with back pain and diabetic polyneuropathy.The good news is that doctors quite often began to use special drugs for the treatment of this type of pain, as well as comprehensive approaches to treatment and other symptoms that bother the patient.

– That is, neuropathic pain is successfully treated, and thus the patient who seeks the doctor has the opportunity to get rid of the pain syndrome that has followed him for a long time?

– The main method of treatment is pharmacotherapy. In addition to special groups of drugs for the treatment of this type of pain, international and Russian recommendations have been developed, which describe both priority proven methods of treatment and secondary possibilities.Antidepressants, anticonvulsants, analgesics, and local anesthetics may also be used.

In most Russian and international recommendations, the key place in the first line of therapy is occupied by modern anticonvulsants, which were originally created for the treatment of epilepsy, but have a special indication for the treatment of all types of neuropathic pain. Their mechanism of action is very subtle: the drug “chooses” malfunctioning “overexcited” cells in the central nervous system as a target and normalizes their work.As a result, the drugs allow not only to cope with pain, but also to reduce the severity of other unpleasant symptoms, for example, sleep disturbance, level of anxiety. All this has a positive effect on the whole complex of treatment. If we are talking about drugs that effectively help such patients, then they are. They are included in international recommendations. These are drugs that have already been tested by international studies and have proven to be effective and safe means. They are used all over the world, and so are ours.But these medicines must be prescribed by a doctor. Each patient should be selected the program that he needs.

Along with drugs, simple non-drug methods also make a significant contribution. For example, a person can listen to their favorite music, be creative, walk in a picturesque park, and exercise regularly. It sounds trite, but today, neuroscience studies at the molecular level are proving the amazing effectiveness of these exercises in combating pain.It has been proven that even simple communication with beautiful, pleasant people can reduce pain by acting on the mechanisms of its regulation in the brain. It relieves everything that gives you joy, pleasure, aesthetic pleasure. Attention, approval, respect, love. Science has confirmed this with numerous studies. Today, the approach to treating any chronic pain involves many components. This is not only a medicine: there is psychological support, social support, physiotherapy methods, and stimulation methods.A lot of them. All this in modern medicine is included in the concept of a biopsychosocial approach, which is recognized throughout the world for working with patients suffering from chronic pain. Taking into account the individual characteristics of the patient, the doctor draws up an individual treatment program, including those medications and those recommendations that are needed for this particular patient. There can be no standard here.

– What is particularly important to consider when treating patients diagnosed with neuropathic pain?

– It is very important that the patient and the doctor set realistic goals together.Because, in my opinion, the most difficult situation is that the patient comes to the appointment with pain and expects that he will take pills and tomorrow or the day after tomorrow the pain will go away. Unfortunately, neuropathic pain does not go away quickly. And you need to understand, together with the doctor, in what time frame it will be possible to cope with the pain. You can reduce pain, in parallel with this – improve sleep, you can convince the patient to move more, start communicating more. That is, to change your life. Therefore, in recent years, we do not say “fight pain” in the sense of removing it in any way.We are trying to restore human life.

In parallel with the fact that we remove pain, we try to improve the patient’s life. There is a huge amount of research that shows that if a person is supported morally, psychologically, socially, he is not abandoned, but, on the contrary, to reach out to him, then the intensity of pain is dulled. Because the perception of pain is not in the back or in the hand. The perception of pain also depends on what happens in the head.

Therefore, of course, if the doctor, the patient and his family are set for success together, carefully consider the steps on the patient’s path to recovery and use competently available modern methods of treatment, then neuropathic pain is not a sentence.And the patient can definitely return to a fulfilling life without pain. Everyone has a good chance of successful treatment.

Recorded by Konstantin Anokhin

90,000 Herpes zoster epidemiology, treatment and prevention: a comprehensive review

Introduction

Herpes zoster or herpes zoster occurs due to reactivation of the varicella-zoster virus. Adults over the age of 50 are at increased risk of developing herpes zoster, probably due to age-related immunochemical aging, but it can occur in people of all ages, especially people with suppressed cell-mediated immunity due to a disease or medication …With herpes zoster, complications associated with the involvement of the ocular, adrenal, cerebral and motor nerves are noted. However, the most common complication is postherpetic neuralgia. The mainstay of prevention of herpes zoster infection is vaccination against the herpes zoster virus. Many treatments have been developed for the treatment of herpes zoster as well as for postherpetic neuralgia. However, approximately 22% of herpes zoster patients still suffer from postherpetic neuralgia.With an increase in life expectancy and an increase in the prevalence of the modern epidemic human immunodeficiency virus (HIV), an increase in the incidence of herpes zoster and postherpetic neuralgia is expected. Increased use of varicella-zoster vaccination leads to a decrease in the prevalence of varicella, which leads to a decrease in the likelihood of periodic re-exposure to chickenpox. This, in turn, can reduce the natural boost in immunity and lead to an increased incidence of herpes zoster.The main goal of our study is to determine the incidence, risk and complications of herpes zoster in healthy and immunocompromised patients and to improve patient care through accurate diagnosis, early treatment initiation, and methods for preventing herpes zoster and its recurrence.

Etiopathogenesis

The varicella-zoster virus is one of eight herpes viruses that are pathogenic only to humans. It causes a primary infection called chickenpox, most commonly in children, which is highly contagious.Most often, it is transmitted by air from person to person or through direct contact with a lesion. During primary infection, the virus spreads through the bloodstream to the skin, oral mucosa, and lymph nodes, causing a generalized chickenpox rash. After primary infection or vaccination, the varicella-zoster virus remains dormant in the cells of the spinal cord sensory root ganglia. Resolution of the primary infection induces the induction of memory T cells specific to the varicella-zoster virus.Memory T cell immunity declines over time. A decrease below the theoretical ‘herpes zoster threshold’ is correlated with an increased risk of herpes zoster infection. Memory immunity to varicella-zoster virus can be increased by exogenous enhancement (by exposure to chickenpox) or endogenous enhancement (subclinical reactivation due to latency). The average duration of immunity against chickenpox after infection is 20 years. Age, stress, immunocompromised conditions, and immunosuppressive drugs are known factors in the reactivation of the virus.Those who develop shingles are advised to determine their HIV status. Once the virus is reactivated, it travels along the affected sensory nerve, causes neuronal damage, reaches the corresponding dermatomes, and forms a vesicular shingles rash. Herpes zoster is usually characterized by a unilateral, painful vesicular rash that is limited to a single dermatome. Studies have shown that more than 95% of adults are infected with the varicella-zoster virus and are therefore at risk of developing herpes zoster.After contracting herpes zoster, there is a high likelihood of damage to the peripheral and central nervous systems, which leads to postherpetic neuralgia. The two main factors that play a role in the development of postherpetic neuralgia are sensitization and deafferentiation. The frequency of involvement of localizations in descending order is as follows: thoracic, lumbar and cervical, sacral. An increased spread of the herpes zoster virus beyond the isolated ganglion nerve dermatome is observed in patients with T-lymphocyte deficiency and macrophage immune defense.Involvement of the lungs, central nervous system (CNS), mucous membranes, liver, cardiovascular system (CVS), bladder, skeletal system, blood vessels, and gastrointestinal tract can be observed in patients with disseminated disease. Involvement of the lungs, liver and central nervous system can be fatal. Shingles does not occur after exposure to the varicella-zoster virus. However, people with herpes zoster can transmit the varicella-zoster virus to seronegative contacts who develop chickenpox rather than shingles.Individuals exposed to herpes zoster have a lower risk (16%) of developing varicella-zoster infection compared to individuals exposed to varicella-zoster virus (61-100%). Transmission of varicella zoster virus from cases of shingles is more common through direct contact with lesions than by air. Vaccination against varicella-zoster virus in children has been shown to result in a long-term reduction in the risk of developing herpes zoster in vaccinated people.However, a study by Brisson et al. showed that mass childhood immunization against chickenpox virus caused an increase in the incidence of herpes zoster during the first 30-50 years of life. The pathogenesis of varicella-zoster virus reactivation is unknown. But any factor that affects cellular immunity can play a role in the reactivation of the varicella-zoster virus.

Epidemiology

A systematic review published in 2014 reported that the average incidence of herpes zoster in North America, Europe and the Asia-Pacific region is 3-5 cases, at the age of 60 years – 6 – 8 people, at the age of 80 years – 8- 12 cases per 1000 people per year.Three studies carried out in Italy in 1999, 2004 and 2010 showed an incidence of 4.14 / 1000 people per year, 1.59 / 1000 people per year and 6.31 / 1000 people per year, respectively, showing that the incidence of herpes zoster varies from year to year. 10-20% of patients with herpes zoster develop ophthalmic herpes with a risk of life in 1%.

Age distribution

The incidence of herpes zoster increases with age, which was confirmed by a population study conducted in Korea, which reported incidence rates ranged from 2.0 / 1000 persons per year in the children’s group to 21.8 / 1000 persons per year at the age of 70– 79 years old.The peak incidence of herpes zoster is documented in the 60–69 age group, and a low incidence is noted over the age of 80. Legami et al. Reported an increased rate of hospitalization for herpes zoster among patients> 72 years of age (0.46 / 1000 persons per year) compared with patients aged 15–44 years (0.03 / 1000 persons per year) , suggesting that advanced age is a risk factor for herpes zoster and requires hospitalization. According to a study conducted in the United States with data from the medstat marketcan, there was an increase in hospital admissions, cost burden, complications, outpatient visits, and prescriptions for analgesics among older adults compared to younger adults.Postherpetic neuralgia, bacterial infections, ocular involvement, neurologic involvement, and widespread shingles have been reported as frequent complications requiring hospitalization for herpes zoster. The median length of hospital stay for the primary diagnosis of herpes zoster in patients aged 50 and over in the study by Stein et al. was 6.8 days. However, the same study found that the average hospital stay was 15.5 days for patients with a minor diagnosis [rehabilitation, chronic obstructive pulmonary disease (COPD), pneumonia, etc.)herpes zoster. In a study by Ghaznawi et al., Comparing patients by age at the onset of herpes zoster ophthalmicus (<60 years and ≥60 years), there was a peak number of cases of herpes zoster ophthalmosis among people aged 50-59 years, which may be a consequence of mandatory vaccination against chickenpox in children, leading to a higher incidence of herpes zoster virus infection among younger people. Many recommend vaccination against herpes zoster for people over 60 years of age, but some others suggest that it is better to vaccinate immunocompetent patients under the age of 60, given the severity and chronicity of the disease in young people.

Gender distribution

Many studies show that gender plays a major role in the incidence of herpes zoster. Kim Y.J. et al. showed that the incidence of herpes zoster among women was high compared to men (12.6 per 1000 people per year versus 8.3 per 1000 people per year). In another study, the incidence was 6.05 / 1000 and 4.75 / 1000 people per year for women compared to men (4.30 / 1000 and 3.82 / 1000 people per year). A retrospective cohort study conducted in China showed that the incidence of women and men was 3.95 / 1000 people per year and 2.89 / 1000 people per year, respectively.According to these studies, differences in immune response to latent viral infection may be responsible for the higher incidence among women. Some studies have shown no statistical difference in the incidence of disease among men and women. However, some studies show a predominance of men, as supported by studies from India, Nepal and Pakistan, in which the ratio of men to women is 1.74: 1, 2.16: 1. and 2: 1, respectively. This disparity in gender incidence across studies may be due to differences in sample collection or a lower chance for men to seek medical attention.Our review shows that shingles is not a gender-specific disease. However, further research on gender distribution is needed to determine any sexual propensity for herpes zoster.

Seasonal and local distribution

Seasonal variability for herpes zoster has been noted in several studies showing a high probability of infection in early summer. However, other studies have not documented significant seasonal variation for herpes zoster and postherpetic neuralgia.An increase in the incidence of herpes zoster was shown in urban areas (7.65 / 1000 people per year) compared to rural areas (2.06 / 1000 people per year) in a study conducted in China. Likewise, a study from the Netherlands found an increased impact of the degree of urbanization compared to the countryside. However, there are other studies that show no difference in incidence between rural and urban areas. This indicates that more research is needed to confirm seasonal and regional differences in the incidence of herpes zoster.Several previous studies have shown that the incidence of herpes zoster is high among immunocompromised people compared to the healthy population. Into Chen’s study. there was a higher incidence of herpes zoster among bone marrow or stem cell recipients (43.03 / 1000 people per year) than among solid organ recipients (17.04 / 1000 people per year). HIV, systemic lupus erythematosus, rheumatoid arthritis, cancer, inflammatory bowel disease, multiple sclerosis, and psoriasis increase a patient’s risk of developing herpes zoster.An earlier study in San Francisco reported an incidence of herpes zoster of 29.4 per 1000 people per year among HIV seropositive people versus HIV seronegative people (2.0 per 1000 people per year) and others. controls. Cellular immunity plays a role in the inactivation of the herpes zoster virus. HIV patients experience a decrease in the CD4 + cell count and an increase in the CD8 + cell count, resulting in an increased incidence of herpes zoster.Insinga et al. Reported 10.3 cases of herpes zoster per 1000 people per year among patients of all age groups with cancer, HIV infection, or transplantation compared to the general population (3.0 per 1000 people per year). Another study in cancer patients, Yenikomshian et al. Showed that the incidence of herpes zoster was low in those with prostate cancer (12.3 per 1000 people per year), and high in those with Hodgkin’s lymphoma (47.8 per 1000 person per year). The same study reported a higher incidence of herpes zoster in hematologic cancer (31.0 / 1000 people per year) compared to solid organ cancer (14.9 / 1000 people per year).In addition, a higher incidence was noted among those receiving immunosuppressive drugs or chemotherapeutic agents. Although those receiving immunosuppressive drugs are at high risk of developing herpes zoster, the study by Megna et al. Reported that biologics for psoriasis were not associated with any significant increase in the risk of developing herpes zoster. Two different studies in Japan and Israel have shown an increased incidence of herpes zoster infection in diabetic patients.Herpes zoster is also more common among patients with COPD, hypertension, Sjogren’s syndrome, mental illness, osteoskeletal disease, eye disease, and kidney failure.

Risk of postherpetic neuralgia

The incidence of postherpetic neuralgia after herpes zoster is high. Gaultier reported that 19.5% of patients with herpes zoster develop pain that persists for at least 1 month and in 13.7% that persists for at least 3 months after the onset of the rash.Similarly, an Italian study found 9.4% and 7.2%, respectively, among immunocompetent herpes zoster patients. The incidence of postherpetic neuralgia increases with age, and this observation was supported by Stein et al. They showed an increased incidence of postherpetic neuralgia at age ≥80 years (3.16 cases per 1000 people per year) compared with people aged 50-59 years (0 , 73 per 1000 people per year) and under 50 (0.08 per 1000 people per year). Postherpetic neuralgia tends to affect women more than men.Postherpetic neuralgia has a longer duration than herpes zoster infection, and therefore the pain load affects the patient’s quality of life.

Clinical features

Herpes zoster infection usually begins with prodromal symptoms such as pain, fever, malaise, headache, pruritus, and paresthesias that precede the rash by several hours to several days in most patients. Frequent itching or pain that occurs before the rash appears, the diagnosis may be delayed.After the prodromal phase, the active phase begins, when patients show characteristic skin lesions such as erythema, papules, which progress into vesicles after 12-24 hours, and into pustules after 1-7 days and eventually crust over after 14-21 day. (resolution phase). The chronic phase of the disease is associated with the development of postherpetic neuralgia, damage to the cranial nerves and damage to internal organs. Postherpetic neuralgia is defined as herpes zoster pain that persists for more than 3-6 months after the rash appears, or pain that persists even after the rash has completely healed.In most patients, postherpetic neuralgia is characterized by severe, persistent or intermittent pain or burning pain with allodynia. Damage to the fifth cranial nerve (trigeminal nerve) leads to Ramsey-Hunt syndrome and ophthalmic herpes. If the hearing aid is affected, severe otalgia and an erythematous vesicular rash in the external auditory canal and auricle are observed. A condition associated with ipsilateral facial palsy is known as Ramsey-Hunt syndrome. The facial and auditory nerves are infected with the varicella-zoster virus, which leads to herpetic inflammation of the ganglion.A common symptom of herpes zoster includes pain in and around the ear accompanied by dizziness, hearing loss, tinnitus, nausea, and vomiting. Most dizziness patients experience hearing loss. However, hearing loss does not develop in patients without vertigo. Although Ramsay Hunt syndrome is a rare manifestation of herpes zoster in childhood, it is known to be the second most common cause of facial palsy in children after Bell’s palsy. Reactivation of the virus in the ophthalmic (V1) section of the trigeminal nerve leads to herpes zoster ophthalmicus.If vesicles are present on the side and tip of the nose (Hutchinson’s sign), it affects the outer division of the naso-filial branch, indicating the likelihood of eye damage (about 76% of cases). Complications associated with herpes zoster ophthalmicus initially affect the skin and anterior segments of the eye, and then affect the optic nerve, retina and central nervous system. The risks and complications associated with herpes zoster are more common in older adults and immunocompromised patients.

Complications

Complications of herpes zoster are more common in the elderly and immunocompromised patients.Shingles and its complications can affect a patient’s quality of life. Most patients experience sleep and social disruption. Postherpetic neuralgia is the most common complication of herpes zoster. Other complications noted after postherpetic neuralgia include secondary bacterial infections, ophthalmic complications, cranial and peripheral nerve palsy, and segmental paresis. Severe postherpetic neuralgia can lead to sleep disturbances, depression, weight loss, chronic fatigue, and an inability to carry out daily activities.Pain can extend beyond the involved dermatome. The severity of postherpetic neuralgia usually depends on the presence of pain before the rash, the severity of the rash, inflammation, old age, and an immunocompromised condition. Treatment of postherpetic neuralgia is often difficult due to the lack of a definitive treatment algorithm for this disease. Secondary bacterial infections such as cellulitis, septicemia, herpes zoster, and necrotizing fasciitis caused by Staphylococcus aureus and Streptococcus pyogenes are the most common complications seen after postherpetic neuralgia.The elderly and immunocompromised patients are more susceptible to bacterial infections. Cellulite can lead to necrosis and scarring. Necrotizing fasciitis is a serious condition that can be complicated by streptococcal toxic shock-like syndrome. A rare but serious complication of ocular herpes zoster is granulomatous arteritis. The condition is characterized by headache and hemiplegia on the contralateral side of the lesion secondary to stroke.Other complications associated with herpes zoster ophthalmicus include blepharitis, conjunctivitis, epithelial keratitis, stromal keratitis, neurotrophic keratopathy, uveitis, episcleritis, scleritis, acute retinal necrosis and progressive retinal necrosis syndrome and acute retinus. The syndrome of progressive retinal necrosis leads to retinal detachment. Compared with acute retinal necrosis, PORN syndrome is more severe with a poor prognosis and is more common in patients with progressive AIDS or in patients with other immunosuppressed diseases.According to a report by Tran et al., The recurrence rates for herpes zoster at ages 1, 3, 5, and 6 years were 8%, 17%, 25% and 31%. respectively. This proves that ocular complications can sometimes recur after a long period of up to 10 years after an episode of shingles. Myelitis from herpes zoster is a rare acute-onset neurological complication that most commonly affects immunocompromised patients. This occurs shortly after the onset of the rash, with the development of sensory, motor, and autonomic dysfunction.Ong et al. reported that the neurological progression caused by myelitis in herpes zoster can be prevented by oral antiviral therapy even after a delay in diagnosis. Segmental zoster paresis is a neurological complication following herpes zoster infection and is characterized by focal asymmetric motor weakness affecting the myotome, corresponding to the distribution of the rash dermatome. In the case of segmented herpes zoster paresis of the abdominal cavity, this can lead to weakness of the abdominal wall.It most often affects middle-aged and elderly people. Weakness in the abdomen often results in a lateral bulge, which can be misdiagnosed as a hernia of the abdominal wall. The condition is usually self-limiting with a good prognosis. Teo et al. Reported a case of segmented herpes zoster paresis with lower limb involvement in a patient with multidermatoma herpes zoster infection with a good prognosis and complete recovery of limb strength and resolution of the rash.Facial nerve involvement can lead to Bell’s palsy. Segmented paresis in half of the cases involves the thoracic dermatome, and can develop in the facial, cervical, and lumbosacral dermatomes. However, a high incidence of motor complications is observed with lesions of the face and limbs. Acute urinary retention is a complication seen in elderly and young immunocompromised patients with herpes zoster due to damage to the spinal cord, sensory ganglia of the spine, or sacral nerve roots.Herpes zoster patients are more likely to develop urinary or intestinal dysfunction. In most cases, patients experience bladder dysfunction as soon as the rash appears or within a few days after the rash appears. Rothrock et al. reported a case of herpes zoster with neurogenic bladder when the onset of rash was delayed up to six weeks after the onset of urinary retention.

Diagnostics

The diagnosis of herpes zoster can be made clinically as soon as the rash appears.Tzank’s smear and electron microscope can detect the presence of the herpes virus in the vesicles. However, these methods cannot distinguish between herpes simplex virus and varicella-zoster virus. Polymerase chain reaction (PCR), direct immunofluorescence analysis, skin biopsy and viral culture are laboratory diagnostic tests for atypical herpes zoster. PCR can detect chickenpox virus DNA in the vesicular fluid and is therefore considered the most sensitive and specific diagnostic test for shingles.PCR can be performed with fluid from the lesion, blood, plasma, cerebrospinal fluid, and bronchoalveolar secretions. Direct immunofluorescence assay can be used as an alternative to PCR. It is preferred over viral culture due to its high sensitivity, low cost and processing time compared to viral culture. In patients with herpes zoster myelitis, viral isolation cannot be done from blood or cerebrospinal fluid. Therefore, the diagnosis of myelitis in herpes zoster can be made only by the clinical manifestation of a rash on a specific dermatome with clinical signs of transverse myelitis and magnetic resonance imaging (MRI) of the spine.In the case of segmental herpes zoster paresis, the diagnosis may be confirmed by a painful skin rash with muscle weakness. Electromyography can reveal acute denervation of the affected area.

Treatment

The main goals of treatment for herpes zoster are to reduce pain, induce quick healing, and avoid complications. Antiviral therapy is used to treat herpes zoster once diagnosed and reduces the risk of developing postherpetic neuralgia.Corticosteroids can help control pain and breakouts. Other components of therapy include isolation of the patient and topical treatment of skin lesions. Isolation of the patient is essential to prevent nosocomial infections.

Antiviral drugs

Antiviral drugs such as acyclovir, famciclovir, and valacyclovir are used to relieve acute herpes zoster. These drugs help relieve pain, promote faster healing, and prevent postherpetic neuralgia.Antiviral treatment should be started within 72 hours of the onset of the rash. Famciclovir has been shown to be superior to valacyclovir in reducing acute pain in herpes zoster, which was confirmed in a Japanese study by Ono et al. They observed earlier pain relief within 3-4 days with a 7-day course of treatment with famciclovir. A retrospective study by Lam et al. showed that oral acyclovir and valacyclovir were not associated with a higher risk of acute kidney injury compared with famciclovir.The use of intravenous acyclovir is associated with acute kidney damage. The drug leads to sedimentation and crystallization in the tubules, which causes obstruction and cell necrosis. Therefore, IV acyclovir is an absolute contraindication for patients with renal insufficiency. A short course of acyclovir therapy (800 mg five times daily for 4 days) has shown similar efficacy in patients with rash durations of no more than 72 hours and for less than 72 hours. Acyclovir plus ultraviolet B (UVB) has been shown to reduce the incidence of subacute herpetic neuralgia (41.67%) and postherpetic neuralgia (16.67%) compared to those taking acyclovir alone (61.54% vs. 46.15%) ).Among patients receiving UV-B radiation, adverse effects such as erythema and first-degree burns were observed. However, the patients recovered after lowering the dose. Oral acyclovir given within 72 hours of the onset of the rash can reduce the frequency and severity of cold sores, reducing pain and other long-term complications. A study by Aylward et al. have not shown a positive effect of oral acyclovir on ocular complications of herpes zoster. This may be due to late initiation of initial treatment.Topical acyclovir has no prophylactic effect in the treatment of herpes zoster. 830 nm light-emitting diode (LED) therapy + famciclovir showed faster wound healing and reduced pain in patients with ophthalmic herpes compared with famciclovir alone. Visual impairment and blindness are often reported as complications of herpes zoster. Therefore, early initiation of antiviral treatment in a primary care center is essential before referring a patient to a superior ophthalmologic center.In a survey conducted among corneal specialists and ophthalmologists regarding their opinion on the management of recurrent and chronic ophthalmic herpes, 56% of respondents preferred acyclovir for prevention of ophthalmic herpes, 63% preferred oral antiviral drug + topical steroid for patients with signs of recurrent ophthalmic herpes in the effectiveness of the use of anti-herpes vaccine for adults in order to reduce the frequency of recurrence of ocular herpes zoster.Ganciclovir gel has shown a rapid healing effect in patients with persistent or recurrent ocular herpes zoster. The drug acts only on infected cells and, therefore, has good efficacy and is less toxic. For acute retinal necrosis / PORN syndrome, intravenous acyclovir 1500 mg / m2 / day divided into three doses for 7-10 days is recommended, followed by 800 mg of acyclovir orally five times a day for 14 weeks.

Systemic corticosteroids

Corticosteroid therapy is recommended for special situations such as acute pain in herpes zoster, Ramsey-Hunt syndrome and ocular complications.Corticosteroid therapy is more useful when combined with an antiviral agent. Early use of acyclovir + steroid has shown good improvement in adults and children in the treatment of otherpes / Ramsey Hunt syndrome. Hearing recovery also increases with early therapy. The prognosis for Ramsay-Hunt syndrome is good for younger patients and those on antiviral + steroid combination therapy within 72 hours of rash onset. Combination therapy of acyclovir and a steroid in Ramsey Hunt syndrome improved facial nerve function.Murakami et al. showed the effectiveness of a combination of acyclovir and steroids for the treatment of Ramsey-Hunt syndrome with acyclovir 250 mg IV three times a day / oral acyclovir 800 mg five times a day for 7 days along with iv / prednisone 1 mg / kg / day twice a day for 5 days with a decrease in the steroid dose until complete withdrawal within the next 10 days. Coulson et al. For Ramsay-Hunt syndrome, oral acyclovir 200 mg 5 times a day for 21 days was prescribed together with oral prednisolone 1 mg / kg for 14 days with a decrease to 10 mg / day and complete cancellation.Dosage, route of administration and treatment period varied from study to study. It has been shown that the combined treatment with acyclovir and prednisolone for herpes zoster in patients over 50 years of age improves the quality of life. Acyclovir + prednisolone may clear up rashes and reduce acute herpes zoster disease, but long-term effects in preventing postherpetic neuralgia are not known. A study comparing ACTH and prednisone showed that neither of the two agents was effective in preventing postherpetic neuralgia.Two early studies by Eaglstein et al. and Elliot et al. showed a reduction in postherpetic neuralgia with early oral corticosteroid therapy. However, both studies were limited by their small sample size. Intravenous acyclovir 10-15 mg / kg three times daily for 7 days and prednisolone 60-80 mg three times daily for 5 days is recommended for the treatment of granulomatous arteritis, but the risk of irreversible cerebral infarction is often observed by the time of diagnosis.The effectiveness of corticosteroids in treating herpes zoster and preventing postherpetic neuralgia remains unclear.

Acyclovir-resistant herpes zoster

Resistance to acyclovir is usually observed in patients with severely weakened immunity receiving long-term therapy with acyclovir for varicella-zoster virus and herpes zoster virus. Resistance to acyclovir arises from a mutation in viral thymidine kinase that suppresses enzymatic activity.A study from Turkey showed that early detection of resistance and the use of foscarnet and cidofovir can reduce mortality in immunocompromised patients. The recommended dose of foscarnet for acyclovir-resistant varicella-zoster virus infection is 120 mg / kg / day (40 mg / kg thrice daily or 60 mg / kg twice daily). Breton et al. their study used a higher dose of foscarnet (200 mg / kg / day) for acyclovir-resistant herpes, and 10 out of 13 patients responded well to this therapy.The study suggested increasing the dose of foscarnet from 120 to 200 mg / kg / day for acyclovir-resistant herpes zoster. A mutation in viral DNA polymerase sometimes causes an inability to identify acyclovir triphosphate, resulting in cross-resistance to foscarnet. A study by Blot et al. found that cidofovir can be used as a rescue therapy for patients with severe herpes simplex virus (HSV) infection resistant to acyclovir and foscarnet. Cidofovir is a monophosphate nucleotide analogue that is converted to its active form cidofovir diphosphate regardless of any viral involvement.Therefore, a viral mutation causing altered phosphorylase activity does not result in resistance to cidofovir. Ross et al. suggested using combination therapy with intralesional interferon alfa-2b and 1% trifluorothymidine ophthalmic solution as a third-line therapy for acyclovir-resistant herpes zoster when other treatments fail.

Treatment of herpes zoster during pregnancy

Acyclovir or valacyclovir can be used to treat herpes zoster during pregnancy.Acyclovir is considered the drug of choice in early pregnancy without an increased risk of malformations or premature birth. A woman who was 28 weeks pregnant and treated with acyclovir + acetaminophen for herpes neuralgia Zoster responded well to the drugs and gave birth to a healthy baby after 2 months. A 17-week-old pregnant woman who received valacyclovir for herpes zoster responded well to the drug. According to the Centers for Disease Control and Disease Prevention Advisory Committee (CDC ACIP) guidelines for chickenpox prevention, chickenpox immunoglobulin is highly recommended for susceptible pregnant women exposed to chickenpox to prevent complications associated with chickenpox during pregnancy, as well as for immunocompromised children for passive immunization after significant exposure to varicella-zoster virus or herpes virus.Newborns whose mothers have chickenpox or herpes zoster within 5 days before and 2 days after birth are advised to take varicella-zoster immunoglobulin regardless of maternal history of varicella-zoster immunoglobulin. Varicella-zoster immunoglobulin should not be given to healthy newborns whose mothers have had chickenpox for more than 5 days before delivery because the baby is already protected from chickenpox by acquired transplacental maternal antibodies.Premature babies who have postpartum exposure to chickenpox or herpes zoster are advised to be given varicella-zoster immunoglobulin because of their weakened immune systems and are less likely to acquire transplacental maternal antibodies.

Treatment of shingles in children

Shingles is rare in children and, if present, is usually benign. If the child continues to develop new lesions even after 3 weeks of infection, possible immunodeficiency should be considered.In children, acyclovir oral suspension may be used. However, it is not usually used to treat young children as it is not approved for these age groups. Treatment with acyclovir is recommended for young children if they have eye damage, an immunocompromised condition, or malignant neoplasms. Otherwise, no specific treatment is available for this age group. Four children aged 4-11 months with infantile herpes zoster received oral (three cases) and parenteral (one case) acyclovir and recovered completely without complications.All four children had previous experience with chickenpox virus. Shingles in infants and newborns can be caused by a mother’s chickenpox virus infection during pregnancy. Children experience shingles in the first decade of life due to a chickenpox viral infection before the age of 2 months. Likewise, children can develop shingles in the first two decades of life due to infection with the varicella-zoster virus before 12 months of age. According to the US Advisory Committee on Immunization Practice (CDC ACIP) guidelines for chickenpox prevention, the chickenpox vaccine is only recommended for children 1 year of age and older, and the vaccine is not indicated for the prevention of herpes zoster.Likewise, the CDC ACIP does not recommend herpes zoster vaccines for the prevention of herpes zoster in any patient under 60 years of age. There is no vaccine for children that can prevent contracting herpes zoster after contracting chickenpox during the first year of life. Shingles in newborns is very rare, with an estimated incidence of 0.74 cases / year. But if it does, it is usually not treated because of its benign nature, which is characteristic of children under adolescence, unless severe infection or eye damage caused by herpes zoster is noticed.

Treatment of herpes zoster in immunocompromised people

Acyclovir has a known prophylactic effect against herpes zoster in immunocompromised patients. A study in Africa among HIV-infected patients with CD4 + T cell counts> 250 cells / μL showed that prophylaxis with acyclovir (400 mg twice daily) reduced the risk of herpes zoster by 62%. Localized herpes zoster in immunocompromised patients was well treated with topical acyclovir.The ointment was applied four times a day for 10 days. Local therapy can help shorten the hospital stay required for intravenous drug administration and reduce the side effects associated with intravenous treatment. For herpes zoster in patients with underlying malignant diseases, oral brivudine was as effective as intravenous acyclovir. A 5-day oral dose of 125 mg every 6 hours is recommended and can be administered on an outpatient basis. Outpatient therapy with valacyclovir 1–2 g three times daily has been shown to be cost effective for herpes zoster in immunocompromised patients compared with patients receiving intravenous acyclovir as inpatients.In a study by Tyring et al. compared the efficacy of famciclovir and acyclovir for herpes zoster in 149 immunocompromised patients. Famciclovir was well tolerated and recommended as an alternative to acyclovir. An HIV patient treated with valacyclovir did not respond well to the drug. However, later the patient achieved a favorable outcome with intravenous acyclovir. Further large clinical trials are needed to investigate the effectiveness of valacyclovir. In patients taking bortezomib for multiple myeloma, acyclovir has been used with a prophylactic agent to prevent herpes zoster.

Treatment of postherpetic neuralgia

Antiviral drugs are the main treatment for herpes zoster and reduce the risk of postherpetic neuralgia, however, this does not prevent postherpetic neuralgia. Several analgesics are used to reduce pain associated with herpes zoster, such as acetaminophen, NSAIDs, opioids, tricyclic antidepressants, anticonvulsants, and topical medications.

Topical therapy

Topical 8% capsaicin patch is useful for postherpetic trigeminal neuralgia.The mechanism of pain relief with capsaicin is unknown. The main side effect of topical application of capsaicin cream is a burning sensation at the site of application. It should be applied 3-5 times a day. Topical 5% lidocaine patches (≤3 patches / day for 12 hours / day) have been shown to be of great benefit in postherpetic neuralgia patients, especially in the elderly, due to reduced side effects compared to other systemic agents. Lidocaine drug patches relieve pain through the action of absorbed lidocaine on the sodium channels of sensitized afferents in the affected skin and through a barrier effect that protects allodynic skin from mechanical irritants.

Systemic therapy

Tricyclic antidepressants have previously been used as the first line of treatment for postherpetic neuralgia. However, later, because of their increased side effects, including anticholinergic effects, gabapentin began to be preferred. Carbamazepine, a first-generation anticonvulsant, is effective in the treatment of chronic neuropathic pain, but several cases of carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis have been reported and is therefore not recommended.Gabapentin has been shown to have a good effect on patients’ sleep and quality of life. A single daily dose of 600 mg gastro-pretentive gabapentin was associated with a rapid reduction in pain on day 2 with a decrease in the incidence of side effects. Pregabalin is often recommended as the first line of treatment for postherpetic neuralgia. However, the study by Perez et al. showed no significant difference in efficacy between gabapentin and pregabalin. Gabapentin acts by binding to the α2δ-1-subunit of the voltage-controlled calcium ion channel, decreasing their effect on the dorsal root ganglion, inhibiting membrane transfer (from the cytoplasm to the plasma membrane) and anterograde transfer (axoplasmic transport).Gabapentin also exhibits acute analgesic effects by decreasing the release of neurotransmitters such as substance P. Gabapentin and pregabalin should be used with caution in patients with renal impairment. Combination therapy with pregabalin and oxycodone has been shown to reduce pain intensity and improve quality of life. Another study comparing the efficacy of amitriptyline 25 mg and pregabalin 75 mg in the treatment of postherpetic neuralgia showed better efficacy of pregabalin with good improvement at the end of 8 weeks.4-week study by Xu et al. found cobalamin to be effective in treating pain and discomfort in patients with acute herpetic neuralgia. Local subcutaneous injection of mecobalamin (MeB12) is safer and more effective in older patients than systemic therapy. Intravenous vitamin C has also been shown to be effective in treating pain associated with herpes zoster. Early diagnosis and treatment of herpes zoster can reduce the duration of herpes zoster and the risk of postherpetic neuralgia

Interventional therapy

Intrathecal and epidural injections

The potent anti-inflammatory effect of corticosteroids can reduce nerve damage, thereby preventing pain after herpetic neuralgia.Studies comparing intrathecal midazolam and epidural methylprednisolone have shown a prolonged analgesic effect on postherpetic neuralgia of the lumbosacral dermatome. This effect may be associated with the antinociceptive effect of these drugs on the roots of the spinal cord. A study in 598 patients over 50 years of age with acute herpes zoster showed that a single epidural injection of methylprednisolone and bupivacaine reduced acute zoster-associated pain for 1 month.The study did not show long-term prevention of postherpetic neuralgia with these drugs. According to Pasqualucci et al., Epidural administration of methylprednisolone and a local anesthetic (bupivacaine) prevents postherpetic neuralgia at 12 months, with only 1.6% of patients experiencing pain in the epidural + steroid group and 22.2% in the acyclovir + steroid group. However, a meta-analysis comparing 5 clinical trials showed that corticosteroids are useful in relieving pain associated with herpes zoster during the acute phase of infection and have no effect on preventing postherpetic neuralgia.Epidural anesthetics and steroids have been shown to reduce acute pain associated with herpes zoster, but more research is needed to clearly understand the effect of corticosteroids in preventing postherpetic neuralgia.

Cryoanalgesia / Cryotherapy of intercostal nerves

Cryotherapy of the intercostal nerve is an old technique, but it is still in clinical practice for the treatment of severe chest pain caused by thoracotomy, rib fractures, post-thoracotomy syndrome, intercostal and postherpetic neuralgia.Cryotherapy provides pain relief by freezing the intercostal nerves at -60 ° C with carbon dioxide or nitrous oxide for 30 to 45 seconds using a cryoprobe, which destroys the myelin sheath and thereby blocks nerve conduction. The nerve axon remains unharmed, therefore, after the regeneration of the myelin sheath, functional restoration of the nerves occurs. In a retrospective study of 70 patients with chronic intercostal pain, the outcome for patients with postherpetic neuralgia was poor.The author did not prefer intercostal nerve cryotherapy for postherpetic neuralgia. Calandria et al. reported a new non-freezing technique (NFT) by applying a liquid nitrogen (LN) spray to the skin of the affected dermatome, forming a cloud of nitrogen, preventing the area from freezing. An excellent result was observed in 75% of patients. This technique was adopted because it did not freeze the skin or cause erythema or burning at the site of application. The long-term reduction in chronic chest pain caused by postherpetic neuralgia by cryoanalgesia is unclear.For a better understanding, more research is needed on cryoanalgesia for the treatment of postherpetic neuralgia.

Spinal cord stimulation

The spinal cord stimulator stimulates sensitized neurons in the dorsal horn, restoring impaired excitatory and inhibitory functions. The technique only works if there is no complete deafferentation or intraspinal neuronal death due to postherpetic neuralgia. A cure rate of 27–82% was seen with spinal cord stimulation, increasing the cost to $ 52,091.US per patient for 24 months. Several studies have shown that spinal cord stimulation is a useful option for treating postherpetic neuralgia. Temporary spinal cord stimulation has also been helpful in reducing subacute herpes pain and preventing its progression to chronic herpes pain. Another study from Japan showed a good effect of temporary spinal cord stimulation in reducing persistent pain after herpes zoster and preventing the transition to postherpetic neuralgia.Temporary spinal cord stimulation is less costly and less invasive than conventional spinal cord stimulation. It is more convenient to use because there is no need for MRI. Microsurgical lesion of the dorsal root zone during spinal cord stimulation is also an effective treatment for postherpetic neuralgia. Spinal cord stimulation given to chronic kidney disease patients with postherpetic neuralgia has also helped to manage pain. Deep brain stimulation of the contralateral periventricular gray area (PVG) and ventral posterior lateral thalamic nucleus (VPL) was effective for the control of postherpetic neuralgia in a 30-year-old patient with a 10-year history of right-sided facial distortion of the face after herpes zoster at age 20.The pain score at the last follow-up after 6 months was 0/10. More research is needed to confirm the effectiveness of thalamic stimulation in postherpetic neuralgia. According to Kolšek et al. Transcutaneous electrical nerve stimulation provided pain relief and resolution of skin lesions with minimal complications in herpes zoster compared to antiviral agents, and has been considered a good adjunct or even alternative to antiviral drugs in the treatment of acute herpes zoster and in reducing the incidence of postherpetic neuralgia.Transcutaneous electrical nerve stimulation + topical methylcobalamin have also shown good analgesic effects in postherpetic neuralgia.

Prevention

Zostavax, a live attenuated varicella-zoster virus vaccine, has been shown to reduce the incidence of herpes zoster and postherpetic neuralgia in immunocompetent people over 60 years of age worldwide. The vaccine enhances cell-mediated immunity to varicella-zoster virus, thereby controlling the reactivation or replication of latent varicella-zoster virus and preventing or decreasing herpes zoster infection.Both the chickenpox vaccine and the herpes vaccine are derived from a strain of the varicella-zoster virus. However, the herpes vaccine is 14 times more effective than the varicella-zoster virus vaccine. This live attenuated vaccine is not recommended for pregnant women, children, or immunocompromised patients. People who have had herpes zoster in the past may be vaccinated to prevent further episodes of the herpes vaccine. Herpes vaccine is contraindicated in patients receiving biologics such as adalimumab, infliximab, and etanercept.However, the US Immunization Practices Advisory Committee (CDC ACIP) allows the herpes vaccine to be administered to these patients either 14 days before starting immunosuppressive therapy or one month after stopping these drugs. The vaccine should not be given if the patient is on antiviral therapy because the antiviral agent can prevent the vaccine virus from multiplying, resulting in vaccine failure. Therefore, patients on chronic antiviral therapy should stop taking medication at least 24 hours before vaccination and should not take medication for 14 days after vaccination.The Canadian National Advisory Committee on Immunization has advised that patients receiving low-dose immunosuppressive therapy may receive a herpes zoster vaccine after consultation with an immunodeficiency specialist, depending on the patient’s case. In a randomized, placebo-controlled study by Lal et al., The herpes zoster vaccine (HZ / Su) reduced the risk of herpes zoster in people aged 50 and over with an overall vaccine efficacy of 97.2%.However, the study reported several vaccine-related side effects in 4 participants. A study by Domingo et al. Showed that intravenous administration of Zostavax vaccine was well tolerated and had a similar immune response to that of subcutaneous administration. However, in the group receiving the vaccine intramuscularly, fewer reactions and side effects were observed at the injection site than in the subcutaneous group. The preferred route of administration of the vaccine in some European countries is intramuscularly.The route of administration of the vaccine differs between countries and health systems. A large prevention study by Oxman and Levin reported a 61.1% reduction in the incidence of herpes zoster after using the herpes zoster vaccine. Similarly, the incidence of herpes zoster and postherpetic neuralgia also decreased by 51.3% and 66.5%, respectively. Research has shown that the herpes zoster vaccine reduces the incidence of herpes zoster and postherpetic neuralgia in the elderly.Only mild reactions at the injection site were noted. Routine vaccination is recommended for all patients over 60 years of age, with the exception of patients with severe immunodeficiency and allergy to any form of vaccine. As the cost of treating herpes zoster and postherpetic neuralgia has become a burden for most patients, it has been found that vaccination against herpes zoster in older adults will provide a cost-effective solution to improve their quality of life. The general population should be aware of the risks and complications of herpes zoster infection in order to independently determine the need for seeking medical attention and vaccinations.

Immunoglobulin Zoster

Zoster immunoglobulin is a plasma gamma globulin fraction obtained from a patient recovering from herpes zoster. It is widely used and effective in immunocompromised children to provide passive immunization against varicella-zoster virus. It should be administered within 72 hours of exposure to chickenpox. Normally susceptible children exposed to chickenpox have also been shown to benefit from the administration of Zoster immunoglobulin.The study of immunoglobulin zoster and immunoglobulin from normal serum did not reveal differences in their effectiveness in patients with disseminated herpes zoster against a background of immunodeficiency. Administration of pooled gamma globulin showed a reduction in shingles infection. Immunoglobulin Zoster has provided effective post-exposure prophylaxis for varicella-zoster virus infection. However, its effect on the herpes zoster virus is unclear.

Conclusions

Herpes zoster can affect any age group with a higher incidence in elderly and immunocompromised patients.The need for hospitalization and complications associated with herpes zoster increase with age. More research is needed to confirm gender, seasonal variation and regional distribution of herpes zoster. Treatment with antiviral drugs within 72 hours of the onset of the rash showed a reduction in herpes zoster and its complications. Found that famciclovir is superior to valacyclovir. Oral acyclovir and valacyclovir are preferred over famciclovir for patients with acute kidney injury.Pregnant women, children, and immunocompromised patients respond well to acyclovir. Pregabalin and gabapentin, together with oxycodone, vitamin C infusion, and mecobalamin (MeB12) infusion, have shown significant effect in the treatment of postherpetic neuralgia. Spinal cord stimulation is effective in reducing and preventing postherpetic neuralgia, but at a higher cost. Acute girdle pain can be reduced with epidural anesthetics and steroids. More research is needed on the effectiveness of intercostal nerve cryotherapy and thalamic stimulation in the prevention of postherpetic neuralgia.Vaccination against herpes zoster for people 60 years of age and older reduces the incidence, disease burden and morbidity associated with herpes zoster and postherpetic neuralgia. Post-exposure prophylaxis with zoster immunoglobulin for herpes zoster is unclear. Despite several treatments for herpes zoster and its complications, treatment remains a challenge.

Herpes zoster is … What is herpes zoster?

Shingles (Herpes zoster) (syn.- herpes zoster) is an acute infectious disease caused by the varicella-zoster virus, which affects the nervous system and skin.

Epidemiology

Persons who have previously had chickenpox fall ill. Mostly elderly and senile persons get sick. The incidence of the disease varies from 5 to 10 per 1000 people aged 60-80 years. In some patients (about 2% among patients with normal immunity and in 10% of patients with immunodeficiency), the disease occurs again.If previously unhealthy children come into contact with patients with shingles, they may develop typical chickenpox.

Pathogenesis

Shingles often occurs in individuals who are exposed to various influences that weaken the immune system (patients with leukemia, lymphogranulomatosis, neoplasms, receiving chemotherapy, long-term corticosteroids and immunosuppressants, especially often the infection develops in patients with acquired immunodeficiency syndrome). Persons of old age get sick due to age-related decrease in immune defense.As a result, a latent infection with the varicella-zoster virus is activated, which has remained in the body for several decades without causing any clinical manifestations. An obligatory component of the activation of the infection is a kind of viral ganglioneuritis with damage to the intervertebral ganglia (or ganglia of the cranial nerves) and damage to the posterior roots. The virus can involve autonomic ganglia in the process and cause meningoencephalitis. Internal organs can also be affected. Thus, in the picture of shingles, in contrast to chickenpox, it is not so much the epitheliotropic as the neurotropic properties of the virus that come to the fore.

Symptoms

With herpes zoster, the process is localized along the nerve trunks, more often intercostal, and branches of the trigeminal nerve; a characteristic sign is the one-sidedness of the lesion. Skin manifestations are usually preceded by general malaise, fever, slight itching, tingling sensation, neuralgic pain at the site of future rashes. Then pink edematous spots appear, against the background of which, within 3-4 days, groups of erythematous papules are formed, which quickly turn into vesicles with transparent contents; there is an increase in local lymph nodes and an increase in pain.After 6-8 days, the bubbles dry up, forming yellow-brown crusts, which then fall off, leaving little pigmentation. Unpleasant sensations at the site of the lesion may persist.

Complications

Transverse myelitis, accompanied by motor paralysis. Shingles in HIV-infected and with other immunodeficiencies is more severe. The duration of the period of onset of the rash increases to 1 week, the crusts covering the vesicles dry out no earlier than the 3rd week of the disease.Patients with lymphogranulomatosis or lymphoma are at greatest risk of developing progressive herpes zoster; about 40% of them may have a rash that spreads over the entire surface of the skin. 5-10% of people with disseminated cutaneous manifestations develop viral pneumonia, meningoencephalitis, hepatitis and other serious complications.

Diagnosis and differential diagnosis

With a detailed clinical picture of the ganglionic forms of herpes zoster, the diagnosis is not difficult.Errors often occur in the initial period of the disease, when there are symptoms of intoxication, fever and severe pain. In these cases, they mistakenly diagnose angina pectoris, pleurisy, pulmonary infarction, renal colic, acute appendicitis, etc. Differentiate from herpes simplex, erysipelas, acute eczema; the generalized form of herpes zoster – from chickenpox. For laboratory confirmation of the diagnosis, detection of the virus by microscopy or using the immunofluorescence method, isolation of the virus on tissue cultures, and serological methods are used.

Atypical shingles

There are atypical forms of herpes zoster: abortifacient (without blistering eruptions), blistering (rashes in the form of large blisters), hemorrhagic (blisters and blisters filled with bloody contents) and gangrenous tissue with subsequent formation of tissue necrosis …

Course of the disease

The course of uncomplicated shingles is 3-4 weeks.The pain sometimes persists for several months.

Treatment

Pumpkin seed oil (pumpkinol): lubricate the rash 4 times a day, drink Echinacea tincture and 200 mg acyclovir tablets, 4 tablets 3 times a day, drink a week and everything will pass. For severe pain, drink anesthetic (pentalgin). During illness, you cannot wash and take a bath! Add cereals and vitamins to the diet. In severe forms, immunoglobulin.

Forecast

Favorable, except for the encephalitic form.Preventive measures are not carried out in the outbreak.

References

Literature

• Khebif T. P. Skin diseases: diagnosis and treatment. – M .: MEDpress-inform, 2007 .– 2nd ed. S. 218-223. ISBN 5-98322-290-2

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2010.

What drugs are used? – Medaboutme.ru

In most patients, herpes zoster clears up fairly quickly even without active treatment, and many people can cope with pain and discomfort in the area of ​​the rash with pain relievers.However, it is important to see a doctor within three days so that a specialist can decide on a treatment plan, including taking antiviral drugs that suppress the activity of the herpes virus. People with advanced age or those with immune system problems should call a doctor immediately, as shingles can pose a greater risk to their overall health, causing neuralgia, eye damage and other complications.

Pain relief: what is acceptable?

Shingles is characterized by pain along the damaged areas of the skin, as well as discomfort and itching in the area of ​​the rash.Paracetamol or an over-the-counter nonsteroidal anti-inflammatory medication such as ibuprofen can be effective in relieving mild pain. For more severe pain in elderly or debilitated patients, prescription NSAIDs or narcotic analgesics are used.

In some cases, oral corticosteroids (prednisone) can be given to relieve the discomfort, inflammation, pain, redness, and itching associated with a rash with an exacerbation of herpes zoster. Common side effects of prednisone include high blood pressure, high blood sugar, muscle weakness, and mood changes.Oral antihistamines can also help relieve pain and itching, but may cause drowsiness.

Suppression of herpes virus activity

Antiviral drugs that suppress the activity of the herpes virus can also be helpful in treating herpes zoster relapse. To reduce pain, limit the duration of symptoms, and prevent complications of herpes, antiviral drugs should be started within 72 hours of the first sign of illness.These herpes suppressants are taken by mouth and include acyclovir, valacyclovir, and famciclovir. The standard course of treatment lasts one week. These medicines are very well tolerated with little or no side effects. Antiviral drugs that suppress cold sores can help reduce the risk of eye complications if the infection affects the face.

Herpes zoster usually does not appear more than once in adults with a normally functioning immune system. Fewer than 5% of people will suffer from recurrent shingles and will need the most active treatment.

Treatment of eye lesions: complication of shingles

The infection can travel along nerve fibers in the head and neck, possibly involving the eyes, wings of the nose, cheeks, and forehead. In about 40% of patients with shingles in this area, the virus infects the cornea. Pain, numbness, and pressure in the eye are typical symptoms of a condition called ophthalmic (ocular) herpes, and this can lead to severe corneal damage or scarring.

Doctors often prescribe oral antiviral medications to reduce the risk of the virus in deep tissue in the cornea, which can cause inflammation and scarring, leading to decreased vision. The disease can also cause a decrease in the sensitivity of the cornea, due to which foreign substances (trapped eyelash, sand, foreign bodies) in the eyes are not felt so sharply and injure the mucous membranes. For many, this reduced sensitivity becomes permanent.It is important that patients who develop shingles on their face get an eye exam because corneal problems can occur several months after the flare has subsided.

Ramsey-Hunt syndrome drug use

Ramsay Hunt type I syndrome, also known as herpes zoster oticus, is a complication of an illness caused by the spread of the virus to the facial nerve area. The syndrome is characterized by intense ear pain, rashes around the ear, mouth, face, neck and head, and paralysis of the facial nerves.Additionally, symptoms may include hearing loss, dizziness, and tinnitus. Loss of taste on the tongue, dry mouth and eyes may also occur.

Individual cases of Ramsay Hunt syndrome do not require treatment with any specific medications; standard therapy is used. When therapy is needed, special medications, such as antiviral drugs or corticosteroids, may be prescribed. Vertigo can be treated with diazepam.

In general, the prognosis for Ramsay Hunt syndrome is favorable.But in some patients, irreversible hearing loss is possible. Dizziness can last for days or weeks. Facial paralysis can be temporary or permanent.

Postherpetic neuralgia: how is it treated?

Postherpetic neuralgia is a severe, chronic condition that sometimes develops after herpes zoster. When the rash has healed and the skin is cleared, neuralgia pain is still felt in areas that were previously damaged. If postherpetic neuralgia develops, severe pain persists for longer, even three to four months after the onset of the rash.Such neuralgia is typical for the elderly or patients whose immune system has been suppressed due to various influences. It is unclear why the pain persists after the skin heals, but scientists believe it could be caused by the varicella-zoster virus, which leaves scarring or other damage in the cells of the plexus and associated nerves.

Although postherpetic neuralgia is extremely painful, it is not dangerous. Even in severe cases, sensory disturbances and pain usually subside over time.Treatment with antiviral drugs at the first sign of a rash, within the first 72 hours, is thought to reduce the risk of postherpetic neuralgia and may speed up the healing process.

In the treatment of post-herpetic neuralgia, powerful narcotic pain relievers provide marked relief, but because they can have serious side effects, doctors often prescribe safer pain relievers.

Lidocaine patches have an anesthetic effect, penetrating the upper layers of the skin and reducing pain in the area of ​​damaged nerves.Research has also shown that some of the anticonvulsants used to treat epilepsy, such as carbamazepine, are sometimes effective for neuralgia, as are antidepressants. Some doctors use alternative pain relief methods such as acupuncture and electrical nerve stimulation.

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