About all

Does Shingles Cross the Midline: A Comprehensive Clinical Overview of Herpes Zoster

by alexxlab

What is shingles? Does shingles cross the midline? Learn about the causes, clinical features, complications, and epidemiology of herpes zoster (shingles) in this comprehensive guide.

Causes of Herpes Zoster (Shingles)

Herpes zoster, also known as shingles, is caused by the reactivation of the varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox). After a person has had varicella, the virus remains latent in the dorsal root ganglia. VZV can then reactivate later in a person’s life and cause the painful maculopapular and vesicular rash associated with herpes zoster.

Clinical Features of Herpes Zoster

People with herpes zoster typically experience a rash in one or two adjacent dermatomes, most commonly on the trunk along a thoracic dermatome or on the face. Importantly, the rash usually does not cross the body’s midline. In the days before the rash appears, a person may experience symptoms such as headache, photophobia (sensitivity to bright light), and malaise.

The rash develops into clusters of vesicles, with new vesicles continuing to form over 3 to 5 days. The rash then progressively dries and scabs over, usually healing within 2 to 4 weeks. Permanent skin discoloration and scarring can occur.

Complications of Herpes Zoster

Postherpetic Neuralgia (PHN)

The most common complication of herpes zoster is postherpetic neuralgia (PHN), which is pain that persists in the area where the rash was located for more than 90 days after the rash onset. PHN can last for months or even years, and the risk increases with age. Approximately 10% to 18% of people with herpes zoster will develop PHN, which is rare in those younger than 40 years old.

Herpes Zoster Ophthalmicus

Herpes zoster that affects the ophthalmic division of the trigeminal nerve, known as herpes zoster ophthalmicus, can result in acute or chronic ocular sequelae, including vision loss.

Disseminated Zoster

Disseminated zoster can include generalized skin eruptions where the lesions occur outside of the primary or adjacent dermatomes, making it difficult to distinguish from varicella. Visceral involvement of the central nervous system, lungs, and liver can also occur. Disseminated zoster generally occurs in people with compromised or suppressed immune systems.

Vaccination and Transmission

The recombinant zoster vaccine (RZV, Shingrix) is the recommended vaccine to prevent shingles and related complications. People with active herpes zoster lesions can spread VZV, which can cause varicella in people who have never had the disease or received the varicella vaccine. Active herpes zoster lesions are infectious through direct contact with vesicular fluid or through breathing in virus particles from the blisters until they dry and scab over.

Epidemiology and Risk Factors

Approximately 1 in 3 people in the United States will develop herpes zoster during their lifetime, with most people having only one episode. However, herpes zoster can recur.

A person’s risk for herpes zoster and related complications sharply increases after 50 years of age. This is because a person’s VZV-specific cell-mediated immunity declines with increasing age and certain medical conditions or medications that suppress the immune system. People with conditions like bone marrow or solid organ transplants, cancer, HIV, and those taking immunosuppressive medications have an increased risk of developing herpes zoster.

Key Takeaways

  • Herpes zoster (shingles) is caused by the reactivation of the varicella-zoster virus, which remains latent in the body after a person has had chickenpox.
  • The rash associated with herpes zoster typically appears on one or two adjacent dermatomes and does not cross the body’s midline.
  • The most common complication of herpes zoster is postherpetic neuralgia (PHN), which is persistent pain in the area where the rash was located.
  • People with compromised or suppressed immune systems are at higher risk for severe, long-lasting rashes and more serious complications from herpes zoster.
  • The recombinant zoster vaccine (Shingrix) is the recommended vaccine to prevent shingles and related complications.
  • Active herpes zoster lesions can spread the varicella-zoster virus, causing chickenpox in susceptible individuals.

Clinical Overview of Herpes Zoster (Shingles)

Cause

Herpes zoster, also known as shingles, is caused by reactivation of varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox).

Primary infection with VZV causes varicella. After a person has varicella, the virus remains latent in the dorsal root ganglia. VZV can reactivate later in a person’s life and cause herpes zoster, a painful maculopapular and then vesicular rash.

Clinical Features

People with herpes zoster most commonly have a rash in one or two adjacent dermatomes. The rash most commonly appears on the trunk along a thoracic dermatome or on the face and it usually does not cross the body’s midline.

The rash is usually painful, itchy, or tingly. A person can experience the following symptoms several days before the rash appears:

  • Headache
  • Photophobia (sensitivity to bright light)
  • Malaise

The rash develops into clusters of vesicles. New vesicles continue to form over 3 to 5 days, and the rash progressively dries and scabs over. The rash usually heals in 2 to 4 weeks. Permanent skin discoloration and scarring can occur.

Complications

Postherpetic neuralgia (PHN)

PHN is the most common complication of herpes zoster. PHN is pain that persists in the area where the rash once was located and continues more than 90 days after rash onset. PHN can last for months or even years.

A person’s risk of having PHN after herpes zoster increases with age. Older adults are more likely to have longer lasting, more severe pain. Approximately 10% to 18% of people with herpes zoster will have PHN. PHN is rare in people younger than 40 years old. The likelihood of PHN is also higher in people who experience more pain with the rash or have a large rash.

Herpes zoster ophthalmicus

Herpes zoster that affects the ophthalmic division of the trigeminal nerve is called herpes zoster ophthalmicus. This can result in acute or chronic ocular sequelae, including vision loss.

Disseminated zoster

Disseminated zoster can include generalized skin eruptions where the lesions occur outside of the primary or adjacent dermatomes. It can be difficult to distinguish from varicella. Visceral involvement of the central nervous system (meningoencephalitis), lungs (pneumonitis), and liver (hepatitis) can also occur. Disseminated zoster generally occurs in people with compromised or suppressed immune systems.

People with compromised or suppressed immune systems are more likely to have a severe, long-lasting rash and experience more severe complications from herpes zoster.

Vaccination

Recombinant zoster vaccine (RZV, Shingrix) is the recommended vaccine to prevent shingles and related complications. For information about vaccination recommendations see Shingles Vaccination.

Transmission

People with active herpes zoster lesions can spread VZV , which causes varicella in people who never had varicella or never received varicella vaccine. Once varicella resolves, these people would be at risk for herpes zoster.

Active herpes zoster lesions are infectious through direct contact with vesicular fluid or through breathing in virus particles from the blisters until they dry and scab over. People with active herpes zoster lesions should cover their lesions and avoid contact with susceptible people in their household and in occupational settings until their lesions are dry and scabbed.

Also see Managing People at High Risk for Severe Varicella and Preventing VZV Transmission from Herpes Zoster in Healthcare Settings

 Top of Page

Epidemiology

Risk Factors

Anyone who had varicella can develop herpes zoster. Approximately 99.5% of people born before 1980 in the United States were infected with wild-type VZV. Children who receive varicella vaccine have a lower risk of herpes zoster compared with children who were infected with wild-type VZV.

Approximately 1 in 3 people in the United States will develop herpes zoster during their lifetime. Most people have only one episode; however, herpes zoster can recur.

A person’s risk for herpes zoster and related complications sharply increases after 50 years of age. The reasons why VZV reactivates and causes herpes zoster are not well understood. However, a person’s risk for herpes zoster increases as their VZV-specific cell-mediated immunity declines. This decline in immunity can result from increasing age and medical conditions or medications that suppress a person’s immune system. People with the following conditions that compromise or suppress their immune system have an increased risk for herpes zoster:

  • Bone marrow or solid organ (renal, cardiac, liver, and lung) transplant recipients
  • Cancer, especially leukemia and lymphoma
  • Human immunodeficiency virus (HIV)
  • Taking immunosuppressive medications, including steroids, such as for treatment of autoimmune diseases and other immune system deficiencies

Other potential risk factors for herpes zoster have been identified, but the findings are either inconsistent or unexplained. For example:

  • More women than men develop herpes zoster.
  • Herpes zoster is less common in Blacks than in Whites.

Disease Rates

An estimated one million cases of herpes zoster occur annually in the United States.

  • The incidence of herpes zoster varies by age and is approximately 2–9 cases per 1,000 US population annually.

The precise incidence of recurrence is not known.

Complications

  • Approximately 10% to 18% of people with herpes zoster will have PHN.
  • Approximately 1% to 4% of people with herpes zoster are hospitalized for complications.
  • Older adults and people with compromised or suppressed immune systems are more likely to be hospitalized. About 30% of people hospitalized with herpes zoster have compromised or suppressed immune systems.

Deaths

One study estimated 96 deaths occur each year where herpes zoster was the underlying cause (0.28 to 0.69 per 1 million population). Almost all the deaths occurred in older adults or those with compromised or suppressed immune systems.

Trends

Herpes zoster rates among adults in the United States gradually increased over a long period of time. We do not know the reason for this increase. However, the rates across age groups have recently plateaued or declined.

CDC studies have found that herpes zoster rates started increasing before varicella vaccine was introduced in the U.S. and did not accelerate after the routine varicella vaccination program started.

Herpes Zoster in People Who Received Varicella Vaccine

Varicella vaccines contain live attenuated VZV, which results in latent infection. Although herpes zoster has always been uncommon among children, the rate of herpes zoster in U.S. children has declined since the routine varicella vaccination program started in 1996.

  • Children (healthy and immunocompromised) vaccinated against varicella have lower rates of herpes zoster compared to children who had natural infection with varicella.
    • Vaccinated children are less likely to become infected with wild-type VZV.
    • The risk of reactivation of vaccine-strain VZV in children is lower compared with reactivation of wild-type VZV.
  • Few older adults have received the varicella vaccine since it was licensed in 1995. There is very little information on the risk of herpes zoster in people who got varicella vaccine as adults.

CDC continues to monitor the impacts of the U.S. varicella and herpes zoster vaccination programs among adults and children.

References

  1. CDC. Use of Recombinant Zoster Vaccine in Immunocompromised Adults Aged ≥19 Years: Recommendations of the Advisory Committee on Immunization Practices — United States, 2022. MMWR Recomm Rep. 2022;71(3):80-84.
  2. Leung et al. The Impact of Universal Varicella Vaccination on Herpes Zoster Incidence in the United States: Comparison of Birth Cohorts Preceding and Following Varicella Vaccination Program Launch. Journal of Infection Diseases. 2022.
  3. Harpaz and Leung. The Epidemiology of Herpes Zoster in the United States During the Era of Varicella and Herpes Zoster Vaccines: Changing Patterns Among Older Adults. Clin Infect Dis.2019;69(2):341-344.
  4. CDC. Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP) Recommendations for use of Herpes Zoster Vaccines. MMWR Recomm Rep. 2018;67(03):103-108.
  5. Thomas SL, Hall AJ. What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis. 2004;4(1):26-33.
  6. Tseng HF, Smith N, Harpaz R, et al. Herpes zoster vaccine in older adults and the risk of subsequent herpes zoster disease. JAMA. 2011;305(2):160-6.
  7. Mahamud A, Marin M, Nickell SP, et al. Herpes zoster-related deaths in the United States: validity of death certificates and mortality rates, 1979-2007. Clin Infect Dis.2012;55(7):960-6.
  8. Leung J, Harpaz R, Molinari NA, et al. Herpes zoster incidence among insured persons in the United States, 1993-2006: evaluation of impact of varicella vaccination. Clinical Infectious Diseases. 2011;52(3):332-340.
  9. Yih W, Brooks D, Lett S, et al. The Incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage. BMC Public Health. 2005;5(68).
  10. Jumaan AO, Yu O, Jackson LA, et al. Incidence of herpes zoster, before and after varicella vaccination-associated decreases in the incidence of varicella. Journal of Infectious Diseases. 2005;191:2002-7.
  11. Hales CM, Harpaz R, Joesoef MR, Bialek SR. Examination of links between herpes zoster incidence and childhood varicella vaccination. Annals of Internal Medicine. 2013;159(11):739-45.
  12. Russell ML, Dover DC, Simmonds KA, Svenson LW. Shingles in Alberta: before and after publicly funded varicella vaccination. Vaccine. 2014;32(47):6319-24.
  13. Weinmann S, Chun C, Schmid DS, et al. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, 2005–2009. Journal of Infection Diseases. 2013;208(11):1859-68.
  14. Hardy I, Gershon AA, Steinberg SP, LaRussa P. The incidence of zoster after immunization with live attenuated varicella vaccine. A study in children with leukemia. Varicella Vaccine Collaborative Study Group. N Engl J Med. 1991;325(22):1545-50.

 Top of Page

Disseminated shingles: Transmission, symptoms, and treatment

Disseminated shingles is a widespread form of shingles that covers more areas of the body.

Shingles, or herpes zoster, is a skin rash that causes blisters across one side of the body. The same virus that causes chickenpox, the varicella-zoster virus, causes shingles.

Disseminated shingles occurs when the rash covers a wider area of the body than localized shingles, in which a rash is contained within a certain area.

This article looks at what disseminated shingles is, who it may affect, symptoms, possible complications, and treatment.

Disseminated shingles is a complication of shingles where the rash covers a wider area of the body.

A dermatome is an area of skin that a spinal nerve supplies. Spinal nerves, called nerve roots, branch off the spinal cord at different points along the spine.

There are 31 pairs of different spinal nerves. Each dermatome in the body corresponds to a pair of spinal nerves and uses the nerves to communicate with the brain.

According to a 2019 article, shingles usually occurs in one or two dermatomes on the face or chest area and does not spread across the midline of the body.

Shingles appears as a cluster of bumps or fluid-filled blisters. People may have a few lesions outside the main cluster, but if there are more than 20 lesions outside the main rash, this is disseminated shingles.

Disseminated shingles may affect three or more dermatomes.

Learn more about shingles here.

It is possible for anyone who has had chickenpox to get shingles. This is because the virus that causes both conditions remains dormant in nerve cells in the body after people recover from chickenpox.

If the virus activates again, it causes shingles. There is no clear reason why the virus becomes active, but risk factors include older age and having a weakened immune system.

According to the National Institute on Aging, around 50% of shingles cases affect people who are 60 years old or above, and the risk of shingles becomes greater at 70 years or above. If the immune system is less capable of fighting off an infection, it puts people at a higher risk of shingles.

Factors that can weaken the immune system include:

  • older age
  • HIV
  • cancer and cancer treatments
  • excess sun exposure
  • organ transplant drugs

Stress or a cold can also weaken the immune system temporarily.

Disseminated shingles affects around 2% of the general population. It affects people with compromised immune systems in around 15–30% of cases.

Learn about the link between shingles and HIV here.

The varicella-zoster virus causes shingles and chickenpox. The virus can pass easily from a person with chickenpox to someone who has never had chickenpox or has not had a vaccination against chickenpox.

Once people have had chickenpox, the varicella-zoster virus remains dormant in the body. If the virus reactivates, it causes shingles.

It is also possible for people with shingles to pass on the varicella-zoster virus to people who have not previously had chickenpox or the chickenpox vaccine.

The virus can pass on through close contact with a person with shingles, such as direct contact with the blisters or breathing in virus particles from the blisters.

It is not possible to get shingles from a person with shingles. If people come into contact with the infection, it will cause chickenpox. However, they may develop shingles later in life.

Disseminated shingles may appear similar to chickenpox, and it may be difficult to tell the difference between the conditions.

Symptoms of disseminated shingles include:

  • a painful rash, which may itch or tingle
  • itching, tingling, or pain several days before a rash appears, as well as a general feeling of being unwell
  • headache
  • sensitivity to bright light

Shingles usually occurs as a single stripe of blisters around one side of the body or on one side of the face. Disseminated shingles may cover a wider area than this and may cross the midline of the body.

Treatment for disseminated shingles may involve antiviral medications. People with a weakened immune system may require treatment in hospital.

Treatment in a hospital can involve intravenous antiviral medication, such as acyclovir. Doctors may also give people pain relief medication, such as morphine.

If symptoms are improving, people may then switch to taking acyclovir orally and be able to continue their recovery at home.

The Centers for Disease Control and Prevention (CDC) recommends that people have the recombinant zoster vaccine to prevent shingles and any complications.

According to the CDC, two doses of the vaccine Shingrix offers over 90% protection against herpes zoster and postherpetic neuralgia (PHN), which is long lasting, persistent pain following shingles. People will have around 85% or more protection for a least 4 years following vaccination.

Learn more about the Shingrix vaccine for shingles and chickenpox.

The most common complication of disseminated shingles is PHN. PHN is persistent pain in the area where a shingles rash was that continues for over 90 days after the rash appeared.

Disseminated shingles may also cause a nerve disorder called plexopathy, which can cause weakness in the limbs.

Other possible complications can affect the liver, lungs, or brain and may cause encephalitis or pneumonitis.

Learn more about some aftereffects of shingles.

People need to contact a doctor right away if they think they have shingles or disseminated shingles, particularly if they have a weakened immune system.

Antiviral medications to treat shingles are most effective when people take them as soon as possible after the rash first appears.

Disseminated shingles is rare and most often affects people with severely compromised immune systems.

Prompt treatment is essential in managing the condition and preventing serious complications such as encephalitis or pneumonitis.

A person’s outlook may depend on their age, the status of their immune system, the severity of their symptoms, and other health conditions.

Early diagnosis and treatment along with high quality care may help provide good outcomes for people with disseminated shingles.

Shingles is a painful, itchy rash that causes blisters to form on one side of the body or face. Disseminated shingles covers a wider area and may cross the midline of the body.

Disseminated shingles is rare but can be more serious than localized shingles. Older adults and people with a weakened immune system may be at higher risk of developing disseminated shingles.

Prompt treatment with antiviral medication can help treat disseminated shingles and prevent complications.

Postherpetic neuralgia

INTRODUCTION and CAUSES OF POSTHERPETIC NEuralGIA

Postherpetic neuralgia (PHN) is a chronic neuropathic pain syndrome, one of the serious complications after infection – herpes zoster, also known as herpes zoster [1, 2, 3]

Symptoms of herpes disappear after a few weeks, but pain caused by damage to nerve structures persists in the affected area for several months and is known as postherpetic neuralgia [6].

Our doctors wrote a very complete and detailed article on the topic of postherpetic neuralgia, described all the methods of treatment existing in the world and how we treat at Smart Clinic. Read the article to the end to get the most out of this issue. In the end, we will also tell you that will definitely not help with PHN so that you do not waste money and time!

The cause of PHN is a herpes virus, the same one that causes herpes on the lips and chicken pox (chickenpox), which are familiar to us.

Herpes itself manifests itself as a rash (erythematous maculo-papular) followed by the formation of transparent vesicles, pustules and, finally, crusts and scabs [6, 9, 11]. Herpes lesions do not cross the midline ; it is unilateral and in most cases affects one dermatome [3, 11]. The patient complains of itching, tingling, and mild to severe pain associated with the rash. Skin lesions heal within 2-4 weeks. It looks like this.

Postherpetic neuralgia is the most common complication of herpes. It is described as pain persisting for 3 months or more after the onset of a rash in the same affected dermatome. In most cases, the pain gradually decreases; only in 1–2% pain persists for years [9, 11, 12].

PHN pain is classified into three types:

1) constant pain (often described as continuous burning, aching, throbbing),

2) paroxysmal pain (often described as stabbing, shooting, electric shock-like pain),

3) pain from irritation – pain caused by a painless stimulus, such as a light touch of clothing or something else. [3, 6, 12].

TREATMENT

The classic treatment for postherpetic neuralgia is medication. All drugs for treatment are prescription drugs. Their doctor appoints a neurologist at the reception.

Make an appointment

1. Anticonvulsants

Since the 1960s, antiepileptic drugs (also known as anticonvulsants) have been used to treat pain, although their use is mainly limited to neuropathic pain [15, 16]. Anticonvulsants such as gabapentin and pregabalin are recommended and approved as first line treatment for PHN [2, 14]. The duration of taking the drugs is individual, most often while it hurts and usually ranges from 3 months.

2. Antidepressants

Many antidepressants have been used to treat neuropathic pain due to PHN since the early 1980s at lower doses that provide only pain relief and no relief of depression [2, 14].

Once again – antidepressants are just the name of a group of drugs that have analgesic effect !

Tricyclic antidepressants (TCAs) such as amitriptyline, nortriptyline and desipramine have been studied and are widely used as a treatment for patients with PHN. Further, more modern drugs were developed with better tolerance, but a slightly less pronounced analgesic effect: venlafaxine and duloxetine. The term of admission is from 3 months.

3. Topical lidocaine

Lidocaine is a local anesthetic and can provide superficial pain relief when applied topically [14]. To facilitate transport through intact skin, lidocaine is formulated as a patch for the treatment of chronic pain such as PHN [29]. The Versatis drug patch is a 10 cm × 14 cm hydrogel adhesive containing 700 mg of 5% lidocaine attached to a non-woven backing [30]. It is applied to the skin, it works on average 12 hours, it is safe, it is used while there is pain.

4. Topical capsaicin

Capsaicin is an irritant found in hot chili peppers of the genus Capsicum. This drug can be said to “burn out” the cells responsible for pain for a long period. In Russia, this is the Kutenz patch (At the time of this writing, it is not available for purchase). The application is made once, after anesthesia of the skin. The duration of the effect is usually 1-3 months, after which the procedure can be repeated.

5. Tramadol and Opiates.

May have an effect, but are practically unavailable in Russia.

7. Botulinum toxin A

Botulinum toxin A (BTX-A), a toxin secreted by Clostridium botulinum, has been used clinically for decades to treat a variety of conditions. Recent studies have demonstrated the use of botulinum toxin A (BT-A) in the treatment of neuropathic pain, including PHN [14, 42].

The mechanism of the analgesic action of BTX-A is not fully understood; however, there are several theories regarding its mechanism. It mainly acts by inhibiting the release of pain mediators from nerve endings and dorsal root ganglia, reducing inflammation around nerve endings, deactivating sodium channels, and exhibiting axonal transport [43].

Botulinum toxin diluted before injection.

One study examined the effects of BTX-A in 58 patients who suffered from PHN symptoms for 4–15 months. In this study, BTX-A was effective in reducing pain in 18 (31%) cases and showed significant results in 27 (46.6%) cases. However, in the remaining 13 (22.4%) patients, it was ineffective [44]. Pain intensity, frequency of seizures, duration of seizures decreased significantly after treatment. Those. on average, botulinum toxin (botox) for the treatment of postherpetic neuralgia is effective in 8-9cases out of 10.

How is it done in our clinic?

The injection of botulinum toxin is carried out with a thin insulin syringe subcutaneously or intradermally in the area of ​​pain. The number of units needed is individual and depends on the size of the diseased area. The procedure is performed by a neurologist with specialized training in botulinum therapy.

8. Nerve block

Various studies support the efficacy and safety of sympathetic nerve blocks for the prevention and treatment of PHN [14]. A recent systematic review from Korea concluded that early nerve block could not only relieve the acute pain of herpes, but could also prevent its sequelae, i.e., PHN [45]. In this study, the authors concluded that among the various nerve blocks, stellate ganglion blocks had a lesser effect in reducing the incidence of PHN. However, somatic blocks, including repeated or continuous epidural and paravertebral blocks, prevented PHN and reduced its frequency [45].

The risk of developing hemodynamic changes after nerve blocks is most often observed in the elderly. There are many studies reporting long-term pain relief in PHN with nerve blocks, but the quality of the evidence is limited [10].

In order for the blockade to be sure to be effective and to hit exactly the affected nerve, it must be performed by a trained specialist under image-guided ultrasound (ultrasound) or X-ray. An injection of a local anesthetic just like that “by eye” is not a proven method of treatment! It is these blockades that we perform in our clinic.

9. Neuromodulation

Another treatment option that has recently been used for chronic pain conditions after failure of conservative treatment is neuromodulation. Neuromodulation with various modalities, including transcutaneous electrical nerve stimulation (TENS) [46], peripheral nerve stimulation (PNS) [47], spinal cord stimulation (SCS), and radiofrequency, combined with conservative treatment, contributed to the prevention of PHN [48, 49, 50]. At the moment, there is not much data on these treatments and they should be considered as a last resort when other more proven ones are not effective.

10. What could potentially work?

There is evidence that reflexology, high-intensity magnetic therapy and other methods of physiotherapy can be effective within the framework of complex therapy. This issue also requires further study.

What exactly does not work and how not to treat postherpetic neuralgia

1. Droppers with vascular preparations, hormonal agents (dexamethasone, etc.).

2. Old Soviet physiotherapy, portable devices such as Almag and others.

3. Common painkillers/anti-inflammatory drugs that are most commonly prescribed for these patients.

Correct diagnosis is essential! If it is incorrect (for example, osteochondrosis), then the treatment will be incorrect!

CONNECTIONS

Postherpetic neuralgia is a complex and debilitating neuropathic pain that affects a person’s daily activities and quality of life. The doctors of our clinic have extensive experience in treating postherpetic neuralgia with a combination of the most effective methods. We use prescribing drugs, botulinum toxin therapy, targeted blockades. Due to the competent combination of methods and the experience of doctors, it is almost always possible to alleviate the patient’s condition and relieve the pain that torments him.

1. Gan E.Yu., Tian E.A., Tei H.L. Treatment of herpes zoster and postherpetic neuralgia. Am J Clin Dermatol. 2013; 14:77–85. [PubMed] [Google Academy]

2. Massengill J.S., Kittredge J.L. Practical considerations in the pharmacological treatment of postherpetic neuralgia for the primary care physician. Jay Pain Res. 2014; 7:125–132. [PMC Free Article] [PubMed] [Google Scholar]

3. Mullick-Searle T, Snodgrass B, Brant JM. Postherpetic neuralgia: epidemiology, pathophysiology and pharmacology of analgesia. J Multidiscip Healthc. 2016; 9:447–454. [PMC Free Article] [PubMed] [Google Scholar]

4. Nalamachu S, Morley-Forster P. Diagnosis and treatment of postherpetic neuralgia. Drugs Aging. 2012; 29:863–869. [PMC Free Article] [PubMed] [Google Scholar]

5. Khadem T, Stevens W. Therapeutic options for postherpetic neuralgia: a systematic review. J Pain Paliat Care Pharmacist. 2013; 27:268–283. [PubMed] [Google Academy]

Postherpetic neuralgia: a review. Curr Pain Headache Rep. 2016; 20:17. [PubMed] [Google Scholar]

7. Kawai K., Gebremeskel B.G., Acosta S.J. A systematic review of the incidence and complications of herpes zoster: towards a global perspective. Open BMJ. 2014; 4 :e004833 [PMC Free Article] [PubMed] [Google Scholar]

Looking back to move forward: a twenty-year audit of herpes zoster in the Asia-Pacific region. BMC Infect Dis. 2017; 17:213. [Free PMC Article] [PubMed] [Google Scholar]

9. Werner R.N., Nickels A.F., Marinovich B., Shefer M., Charnechka-Operach M., Agius A.M. et al. European consensus (S2k) guidelines for the treatment of herpes zoster led by the European Dermatological Forum (EDF) in collaboration with the European Academy of Dermatology and Venereology (EADV), Part 1: Diagnosis. J Eur Acad Dermatol Venereol. 2017; 31:9–19. [PubMed] [Google Academy]

10. Jung Yu.H. Herpes zoster and postherpetic neuralgia: practical considerations for prevention and treatment. Korean Jay Payne. 2015; 28:177–184. [Free PMC Article] [PubMed] [Google Scholar]

11. Bader M.S. Herpes zoster: diagnostic, therapeutic and preventive approaches. postgraduate med. 2013; 125:78–91. [PubMed] [Google Academy]

12. Johnson R.W., Rice A.S. Postherpetic neuralgia. N Engl J Med. 2014; 371: 1526–1533. [PubMed] [Google Academy]

13. Schmader K. Herpes zoster. Klin Geriatr Med. 2016; 32:539–553. [PubMed] [Google Academy]

14. Khaanpaa M., Rice A.S., Rowbotham M.S. Treatment of herpes zoster and postherpetic neuralgia. Pain Clin Updates. 2015; 23:1–8. Available at https://s3.amazonaws.com/rdcmsiasp/files/productio… . [ Google Scholar ]

15. Blom S. Trigeminal neuralgia: its treatment with a new anticonvulsant drug (G-32883) Lancet. 1962; 1:839–840. [PubMed] [Google Academy]

16. Moore RA, Straube S, Wiffen PJ, Derry S, McQuay HJ. Pregabalin for acute and chronic pain in adults. Cochrane Database System, eds. 2009: CD007076. [Free PMC article] [PubMed] [Google Scholar]

17. Pfizer. Neurontin 2017 [Internet] New York, NY: A division of Pfizer Inc.; 2017. [cited 17 October 2017]. Available at http://labeling.pfizer.com/ShowLabeling.aspx?id=63… . [ Google Scholar ]

18. Meng FY, Zhang LC, Liu Y, Pan LH, Zhu M, Li CL, et al. Efficacy and safety of gabapentin for the treatment of postherpetic neuralgia: a meta-analysis of randomized controlled trials. Minerva Anesthesiol. 2014; 80: 556–567. [PubMed] [Google Academy]

19. Depomed. Gralise 2012 [Internet] Newark, NJ: Depomed, Inc.; 2012. [cited October 17, 2017]. Available at https://www.gralise.com/sites/default/files/GRALIS… . [ Google Scholar ]

20. Sang SN, Sathyanarayana R, Sweeney M. DM-1796 Study Investigators. Gabapentin Gastroretentive (G-GR) Reduces Pain Associated with Postherpetic Neuralgia (PHN) Clin J Pain. 2013; 29:281–288. [PubMed] [Google Academy]

21. Gazebo. Horizant 2016 [Internet] Atlanta, GA: Arobor Pharmaceuticals, LLC; 2016. [cited October 17, 2017]. Available at https://www.horizant.com/assets/docs/Horizant_Pres… . [ Google Scholar ]

22. Lal R., Sukbunterng J., Luo W., Towera J., Lassose M. L., Kandi K. S. Population pharmacokinetics and pharmacodynamics of gabapentin after administration of gabapentin enacarbil. J. Clean Pharmacol. 2013; 53:29–40. [PubMed] [Google Academy]

23. Pfizer. Lyrica 2016 [Web] New York, NY: A division of Pfizer Inc.; 2016. [cited October 17, 2017]. Available at http://labeling.pfizer.com/showlabeling.aspx?id=56… . [Google Academy]

24. Ifuku M, Iseki M, Hidaka I, Morita Y, Komatus S, Inada E. Replacement of gabapentin with pregabalin in the treatment of postherpetic neuralgia. Pain Med. 2011; 12:1112–1116. [PubMed] [Google Scholar]

25. Zilliox L.A. neuropathic pain. Continuum (Minneap Minn) 2017; 23:512–532. [PubMed] [Google Academy]

Analgesic therapy for postherpetic neuralgia: a quantitative systematic review. PLOS Med. 2005; 2:e164. [PMC Free Article] [PubMed] [Google Scholar]

27. Enamandram M, Rathmell JP, Kimball AB. Treatment of chronic pain in dermatology: a guide to evaluation and non-opioid pharmacotherapy. J Am Acad Dermatol. 2015; 73: 563–573. [PubMed] [Google Scholar]

28. Harden R.N., Kay A.D., Kintanar T., Argoff K.E. Evidence-based guidelines for the management of postherpetic neuralgia in the primary care setting. postgraduate med. 2013; 125:191–202. [PubMed] [Google Academy]

29. Derry S, Wiffen PJ, Moore RA, Quinlan J. Topical lidocaine for neuropathic pain in adults. Cochrane Database System, eds. 2014: CD010958. [Free PMC Article] [PubMed] [Google Scholar]

30. Gruntal. Versatis 2015 [Internet] Buckinghamshire: Grunenthal Ltd.; 2015. [cited October 17, 2017]. Available at http://www.medicines.org.uk/emc/medicine/19291/SPC… [Google Scholar].

31. Krumova EK, Zeller M., Westermann A., Mayer S. Lidocaine patch (5%) produces a selective but incomplete blockade of Aδ and C fibers. Pain. 2012; 153: 273–280. [PubMed] [Google Academy]

32. Campbell BJ, Rowbotham M, Davis PS, Jacob P, 3rd, Benowitz NL. Systemic absorption of topical lidocaine in healthy volunteers, patients with postherpetic neuralgia, and patients with acute herpes zoster. J. Pharm. 2002; 91: 1343–1350. [PubMed] [Google Scholar]

33. Navez ML, Monella C, Bösl I, Sommer D, Delorme C. Lidocaine 5% medicated patch for the treatment of postherpetic neuralgia: a review of clinical safety and tolerability. Pain Ter. 2015; 4:1–15. [PMC Free Article] [PubMed] [Google Scholar]

34. Baron R, Mayoral V, Leijon G, Binder A, Steigerwald I, Serpell M. Lidocaine 5% medicated patch versus pregabalin for postherpetic neuralgia and diabetic polyneuropathy : an open two-stage RCT with no less efficiency. Curr Med Res Opin. 2009G.; 25: 1663–1676 [PubMed] [Google Academy]

35. Baranidharan G, Das S, Bhaskar A. A review of a highly concentrated capsaicin patch and experience with its use in neuropathic pain. Therapy for nervous breakdown. 2013; 6: 287–297. [PMC Free Article] [PubMed] [Google Scholar]

et al. A multicenter, randomized, double-blind, controlled trial of NGX-4010, a high concentration capsaicin patch, for the treatment of postherpetic neuralgia. Pain Med. 2011; 12:99–109. [PubMed] [Google Academy]

37. Accord. Qutenza 2013 [Internet] Ardsley, New York: Acorda Therapeutics, Inc.; 2013. [cited October 17, 2017]. Available at http://www.qutenza.com/_docs/qutenza_full_PI_.pdf. [Google Scholar]

38. Derry S., Rice A.C., Cole P., Tan T., Moore R.A. Topical capsaicin (high concentration) for chronic neuropathic pain in adults. Cochrane Database System, eds. 2017: CD007393. [Free PMC Article] [PubMed] [Google Scholar]

39. Burness S.B., McCormack P.L. Capsaicin patch 8%: a review of peripheral neuropathic pain. Drugs. 2016; 76:123–134. [PubMed] [Google Academy]

40. Raja S.N., Heitornthveit J.A., Pappagallo M., Clarke M.R., Travison T.G., Sabin S. et al. Opioids versus antidepressants in postherpetic neuralgia: a randomized, placebo-controlled trial. Neurology. 2002; 59:1015–1021. [PubMed] [Google Academy]

41. Boureau F, Legallicier P, Kabir-Ahmadi M. Tramadol for postherpetic neuralgia: a randomized, double-blind, placebo-controlled trial. Pain. 2003; 104: 323–331. [PubMed] [Google Scholar]

42. Shackleton T, Ram S, Black M, Ryder J, Clark GT, Enciso R. Efficacy of botulinum toxin for the treatment of trigeminal neuralgia and postherpetic neuralgia: a systematic review with meta-analysis. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016; 122:61–71. [PubMed] [Google Scholar]

43. Park Jay, Park HJ. Botulinum toxin for the treatment of neuropathic pain. Toxins (Basel) 2017; 9 :pii:E260. [Google Scholar]

44. Ding SD, Zhong J, Liu YP, Chen H.S. Botulinum as a toxin for the treatment of postherpetic neuralgia. Iran J Public health. 2017; 46: 608–611. [Free PMC Article] [PubMed] [Google Scholar]

45. Kim HJ, Ahn HS, Lee JY, Choi SS, Cheong YS, Kwon K, et al. Effects of nerve blocks in the prevention of postherpetic neuralgia in patients with acute herpes zoster: a systematic review and meta-analysis. Korean Jay Payne. 2017; 30:3–17. [PMC Free Article] [PubMed] [Google Scholar]

46. Ing MR, Helreich PD, Johnson DW, Chen JJ. Transcutaneous electrical nerve stimulation in chronic postherpetic neuralgia. Int J Dermatol. 2015; 54: 476–480. [PubMed] [Google Scholar]

47. Lerman I.R., Chen J.L., Hiller D., Soyuzdalnitsky D., Shian G., Wallace M. et al. A novel high-frequency peripheral nerve stimulator for the treatment of refractory postherpetic neuralgia: a brief technical note. Neuromodulation. 2015; 18: 487–493. [PubMed] [Google Academy]

48. Kim K, Joe D, Kim E. Pulsed radiofrequency to the dorsal root ganglion in acute herpes zoster and postherpetic neuralgia. Pain doctor. 2017; 20: E411–E418. [PubMed] [Google Scholar]

49. Kim ED, Lee Yi, Park HJ. Comparison of the effectiveness of continuous epidural blockade and pulsed dorsal root ganglion radiofrequency for the treatment of pain persisting after the acute phase of herpes zoster. PLOS One. 2017; 12: e0183559. [PMC Free Article] [PubMed] [Google Scholar]

50. Shi Y, Wu W. Treatment of neuropathic pain with pulsed radiofrequency: a meta-analysis. Pain doctor. 2016; 19:429–444. [PubMed] [Google Academy]

51. Yanamoto F, Murakawa K. Effect of temporary spinal cord stimulation (or spinal cord stimulation) on the treatment of early postherpetic neuralgia one to six months after onset. Neuromodulation. 2012; 15:151–154. [PubMed] [Google Scholar]

52. Ko Yu.K., Li H.I., Li V.Yu. Clinical experience of the impact of scrambler therapy on patients with postherpetic neuralgia. Korean Jay Payne. 2013; 26:98–101. [PMC Free Article] [PubMed] [Google Scholar]

53. Marineo G, Yorno V, Gandini S, Moschini V, Smith TJ. Scrambler therapy may relieve chronic neuropathic pain more effectively than recommended drug treatment: results from a pilot randomized controlled trial. J Management of pain symptoms. 2012; 43:87–95. [PubMed] [Google Academy]

54. Harpaz R, Ortega-Sanchez IR, Seward JF Advisory Committee on Immunization Practices (ACIP) Centers for Disease Control and Prevention (CDC) Herpes zoster prevention: recommendations from the Advisory Committee on Immunization Practices (ACIP) MMWR Recomm Rep. 2008; 57:1–30. [PubMed] [Google Scholar]

55. Merck. Zostavax 2017 [Internet] Kenilworth: Merck Sharp & Dohme Corp.; 2017. [cited 17 October 2017]. Available at http://www.merck.com/product/usa/pi_circulars/z/zo… . [ Google Scholar ]

56. Kang D.H., Kim S.I., Kim H.G., Pak J.H., Kim T.K., Kim K.H. Early treatment increases the chances of completely getting rid of postherpetic neuralgia. Korean Jay Payne. 2017; 30:214–219. [Free PMC article] [PubMed] [Google Scholar]

Herpes zoster – Sibnews

Herpes zoster .

Etiology and pathogenesis

The causative agent of herpes zoster – the virus Varicella zoster – is also the causative agent of chicken pox. The development of shingles is the result of the reactivation of a latent virus after chickenpox suffered in childhood. Age, immunosuppressive drugs, lymphoma, fatigue, emotional disorders, and radiotherapy play a role in virus reactivation. Older people are at greater risk of developing neuralgia, which can last for months after skin lesions have healed. Pain may mimic pleurisy, myocardial infarction, abdominal disease, or migraine and can be a difficult diagnostic problem until a characteristic rash appears. Symptoms of headache, photophobia, and malaise may precede the rash by several days. Fever is not typical. A shingles attack does not confer long-term immunity, so it is not unusual for a person to have 2 or 3 episodes of the disease in a lifetime. Regional lymphadenopathy may be noted. Herpes zoster, including its recurrent course, may be the earliest clinical sign of the development of AIDS in individuals at high risk.

Clinical picture

The incubation period has not been established. The disease often begins with prodromal symptoms in the form of malaise, fever, weakness, headache, nausea, and unilateral neuralgia of a certain zone of innervation. Then, in the zone of occurrence of neuralgia on hyperemic and edematous skin, grouped vesicles appear, located along the affected nerve and its branches, as a rule, unilaterally (more often along the intercostal nerves, along the facial, trigeminal nerves). The contents of the vesicles soon become cloudy, pustules are formed, upon opening of which erosions are formed, covered with crusts. In severe cases, ulcerative and ulcerative-necrotic lesions occur with dense hemorrhagic crusts. The duration of the disease is from 1 to 3 weeks. In 2-4% of cases, there may be a generalized form of the lesion with an increase in lymph nodes and rashes spread over the skin without severe pain. This form occurs in persons with severe concomitant diseases (lymphoma, leukemia, cancer of the internal organs), in patients receiving long-term immunosuppressants, cytostatics, corticosteroids. The most severe form is gangrenous, which develops in debilitated and elderly people suffering from diabetes mellitus, stomach ulcers. At the same time, the formed gangrenous ulcers do not heal for a long time and leave scars behind. The pain syndrome is due to the neurotropism of the virus, pain can remain for a long time after the resolution of the rash. They are blunt, shooting, burning. With lesions in the eye area, rashes can damage the cornea, conjunctiva, sclera, and iris. The virus can enter the subarachnoid space and cause severe and prolonged meningoencephalitis.

Ocular form of herpes zoster (ophthalmic herpes) – rash rubs from the level of the eyes to the top of the head, but does not cross the midline. Alar vesicles are associated with the most serious ocular complications. Among patients with ophthalmic herpes who have not received antiviral therapy, complications develop (keratopathy, episcleritis, iritis). Systemic antiviral therapy leads to a decrease in late ocular complications. Patients with ophthalmic herpes need to consult an ophthalmologist.

Postherpetic neuralgia is pain that persists for 30 days after the rash has disappeared. The presence and duration of this pain change with age. The pain may persist for months or years after the disappearance of the foci. The pain is often severe, persistent, exhausting. Patients protect zones of hyperesthesia to avoid the slightest pressure, which causes a new wave of pain.

Diagnosis

The diagnosis of herpes is based on the clinical picture. There are laboratory methods for detecting the virus Varicella zoster , which are rarely used – usually a fairly characteristic clinical picture of the disease.

Treatment

Systemic antiherpetic drugs reduce acute pain, inflammation, and vesicle formation. Treatment is most effective if started within the first 48 hours. In the treatment of herpes zoster, more often Famvir 500 mg 3 times a day for 7 days, or Valtrex 1 g 3 times a day for 7 days, or Zovirax 800 mg 5 times a day for 7-10 days, or Panavir 5 ml intravenously 5 injections at intervals of 48 hours.