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Shingles nerve patterns: Nerve Paths That Shingles Follow: Dermatomes Map

Nerve Paths That Shingles Follow: Dermatomes Map

Content
  • Overview
  • What are shingles?
  • How are shingles transmitted?
  • What are the risk factors for shingles?
  • Are there common shingles nerve pathways maps?
  • What are the symptoms of shingles?
  • What are the complications of shingles?
  • Treating nerve damage from dermatomes shingles
  • The lowdown

You probably received a vaccine against shingles when you were a child. It is a common childhood disease. In later years, you may experience a reactivation of the varicella-zoster virus, which causes this condition and manifests as a shingles rash.

Let’s go over what shingles are and the nerve paths it follows. This post will also explain the dermatomes map, how it helps manage vesicular rashes, and the risk of shingles complications.

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Shingle is a disease caused by the varicella-zoster virus, the same virus that causes chickenpox. Chickenpox is a common illness in children and is generally mild, with symptoms that include a fever and a rash that eventually goes away. The virus lies inactive in your nerve cells after the chickenpox infection subsides.

Herpes zoster, or shingles, is a skin rash with severe pain caused by the varicella-zoster virus reactivating as your immunity declines with age. The virus travels along the nerve paths to your skin, causing a painful, itchy rash that lasts 3–5 weeks. The rash can also lead to blisters that may leave scars.

Shingles most often occur in people over 50, but it can occur at any age. It is more common in women than men. The shingles rash is more likely to occur in immunocompromised patients, like those with cancer or HIV/AIDS, and those taking certain medications such as steroids or chemotherapy.

The varicella-zoster virus is spread through direct contact with the rash or, more rarely, through the air when an infected person coughs or sneezes. You can also get shingles by coming into contact with the fluid from a shingles blister.

A child with chickenpox could increase an older adult’s risk of contracting this painful rash because the varicella-zoster virus manifests as shingles in people over 50.

However, an older adult with this viral infection does not pose a risk to children because the chickenpox immunity generally acquired during childhood would protect them.

How are shingles diagnosed?

Shingles are typically diagnosed based on the appearance of the rash and painful areas. A skin biopsy or viral culture may be necessary to confirm the diagnosis. Another way to test for the virus is through a blood test.

Shingle is a condition that everyone should try to prevent. The virus is already within you waiting to be reactivated, or you could get it from kids with chickenpox. How well you take care of yourself determines how fast you age and how healthy you will be in your older years.

However, time takes a toll on everyone eventually. Did you know that your odds of dealing with shingles increase as you age, and 33% of people have shingles at some point in their lives? Most people who get shingles are over 50 years old.¹

How does immunity affect shingles?

Your immune system protects you from infection by overcoming harmful bacteria, viruses, and other invaders. However, some complications weaken your immunity, making it easier for you to get sick. 

Immunocompromised patients often:

  • Have cancer

  • Suffer chronic stress

  • Take certain medications (such as corticosteroids and chemotherapy drugs)

  • Have HIV/AIDS

  • Are malnourished

  • Are submitted to radiation therapy

It is of paramount importance to keep your immunity levels up to avoid getting sick in the first place. A healthy, balanced diet coupled with an active lifestyle helps you maintain a strong immune system.

Is there a shingles vaccine?

Yes, there is a shingles vaccine that can help prevent the virus from reactivating. The shingles vaccine is most effective in people over 50 years of age.

What is a shingles nerve pathways map (dermatome map)?

Shingles nerve pathways maps are diagrams that show the path that nerves take as they innervate the skin. These maps can help understand how herpes zoster virus travels along nerve pathways and can help to explain why the rash of shingles typically occurs in a band-like or stripe pattern.

The cranial nerves exit directly from the brain. On the other hand, the spinal nerves exit from the spinal cord. Everyone has 31 pairs of spinal nerves and 12 pairs of cranial nerves. Each skin area (dermatome) is innervated by one of these nerves.  

The most common nerve path that shingles follow is the thoracic dermatome. The thoracic dermatome is a band of skin supplied by sensory nerves exiting from the spine in the thoracic region. 

The rash associated with shingles typically starts as a band of raised red bumps on one side of the neck and chest and often wraps around the side to the back.

A shingles rash can also occur along the path of other sensory nerves, such as cranial and cervical. The rash associated with shingles on these nerve paths is typically less severe than the thoracic dermatome rash.

What are the cranial nerve paths that shingles follow?

The varicella-zoster virus travels along these nerve paths to your skin:

The trigeminal nerve, the 5th cranial nerve

This nerve innervates the face, scalp, teeth, and mucous membranes of the mouth and nose. The chickenpox virus travels along this nerve to cause herpes zoster ophthalmicus, which causes a rash around the eye.

The facial nerve

It’s the 7th cranial nerve and serves the muscles of facial expression and the lacrimal and salivary glands. The chickenpox virus can travel along this nerve to cause a rash around the ear.

The 9th cranial nerve

Also called the glossopharyngeal nerve, it supplies the tongue, pharynx, and larynx. The chickenpox virus can travel along this nerve to cause a rash in the throat.

The vagus nerve

It’s the 10th cranial nerve and innervates the heart, lungs, and digestive organs. No other cranial nerve is longer or more complex than the vagus nerve. The chickenpox virus can travel along this nerve to cause a rash on the chest or abdomen.

The dorsal root ganglia 

These are clusters of nerves located along the spinal column. The varicella-zoster virus travels along these nerves to cause a rash on the trunk, back, or buttocks.

The most common symptom of shingles is a painful, itchy rash that can appear anywhere on your body but most often appears as a stripe of blisters wrapping around one side of your torso. Other symptoms of shingles include:

The symptoms of shingles can be mild to severe. Some people with shingles only have a rash, while others may experience more severe symptoms such as fever and headaches.

What is the difference between shingles and chickenpox?

Herpes zoster and chickenpox, though caused by the same virus, are different diseases. Chickenpox is a mild, contagious childhood disease characterized by a rash of itchy blisters.

Shingles are a reactivation of the chickenpox virus that manifests as a painful, itchy rash in older individuals.

The most common complication of shingles is postherpetic neuralgia. It is a condition that causes persistent burning pain after the rash has healed. Other complications of shingles include:

Pneumonia

The varicella-zoster virus can cause pneumonia, a severe lung infection in people with weakened immunity.

Cranial nerve damage

Ramsay Hunt syndrome is a rare complication of shingles that can cause paralysis of the facial muscles and hearing loss. Blisters around your ears can also lead to Bell’s palsy, further complicating your facial muscles.²

Labyrinthitis

Labyrinthitis is an inflammation of the inner ear that can cause vertigo or a spinning sensation. This condition often goes away alone, but it can be severe and require medication to treat.

Encephalitis

The varicella-zoster virus can also cause encephalitis, an inflammation of the brain, as it travels along the nerve paths to your brain. Encephalitis can be deadly.³

Motor nerve damage

Up to 5% of people who suffer from shingles develop segmental zoster paresis, which results in muscle weakness or paralysis on one side of the body.⁴

Shingles can also cause post-zoster opsoclonus, characterized by rapid, uncontrolled eye movements.

Myocarditis

Myocarditis is an inflammation of the heart muscle. Rarely, the varicella-zoster virus causes myocarditis, but it is possible. Myocarditis can also be fatal.

Vision loss

Clusters of water-filled blistering rashes on or around your eye can cause vision loss if left untreated. Shingles manifesting around your eye is called herpes zoster ophthalmicus and can blind you in that eye if not treated quickly and aggressively.

Medical experts are likely to start by drawing a dermatome map to determine the source and severity of the nerve pain. It helps to rule out other possible causes of the pain, such as a herniated disc or arthritis.

A shingles outbreak may manifest in one or two dermatomes. The most common site for a shingles outbreak is on the torso, but it can also appear on the face, neck, and legs.

The rash and pain of shingles can be so severe that it interferes with your daily activities.

There are a few ways to ease the pain and help your nerve damage heal:

Antibiotics

Antibiotics may be prescribed if the person has a bacterial infection that develops as a secondary infection along with the herpes zoster virus.

Antiviral treatment

These drugs can help shorten the duration of the virus and lessen the severity of symptoms from the incidence of zoster.

Corticosteroids

These drugs can help reduce inflammation and pain.

Pain medication

Over-the-counter or prescription pain relievers can help ease the pain of shingles.

Shingles can be painful and debilitating, but treatments are available to help ease the symptoms. It helps to see a doctor as soon as possible if you think you may have shingles so that you can begin treatment and prevent further complications.

Nerve Paths That Shingles Follows, Their Impact on the Condition

Shingles, also called herpes zoster, is a disease caused by a reactivation of the varicella-zoster virus that leads to chickenpox. The virus can remain dormant in your nerve cells for decades without presenting any symptoms.

Shingles most commonly occurs in people over the age of 50. About 1 in 3 people in the United States will develop it in their life. The main symptom of shingles is a painful rash on one side of your body that usually goes away after 2 to 4 weeks.

The rash can appear on any part of your body, but it typically appears on one side of your trunk or torso. The location of a shingles rash depends on which nerve in your body the virus spreads from. Usually, the rash is contained in one or two areas of your skin called dermatomes.

Keep reading as we take a look at how and why shingles follows along nerve paths.

Shingles is caused by a reactivation of the virus that causes chickenpox. Only people who’ve had chickenpox or chickenpox vaccines can develop shingles. Having a chickenpox vaccine can lead to shingles because the vaccine contains the virus that causes chickenpox.

Shingles isn’t contagious, but people who have not had chickenpox can develop chickenpox if they come in contact with open blisters of somebody with shingles.

After your body fights off a chickenpox infection, the herpes zoster virus remains dormant in your cranial nerves and spinal ganglia until it becomes reactivated. Spinal ganglia are nerve cells that connect your spinal cord to nerves in your body and limbs.

The virus reactivates when your immune system is no longer able to suppress it. Reactivation most commonly occurs in older adults because the immune system tends to get weaker with age, as well as in people with suppressed immune systems.

Once the virus is active, it usually spreads down sensory nerve fibers that lead from your spinal cord to your skin. These nerves carry sensory information like feelings of pain, itchiness, or pressure from your skin to your spinal cord and brain.

Once the virus gets to the end of these sensory nerves, it reaches your skin and usually leads to a rash. This rash often shows up in one or two nearby areas of skin called dermatomes.

You have 31 spinal nerves on each side of your body that help send information between your body and spine. Each of these nerves is associated with a dermatome except for the C1 spinal nerve in your neck.

A dermatome is an area of your skin where the sensation is supplied by one spinal nerve.

For example, the C5 spinal nerve found on the right side of your body is responsible for delivering sensory information from your right collarbone and upper shoulder to your spinal cord and brain. All the skin in this region is one dermatome.

Shingles rashes tend to form along one or two dermatomes on one side of your body. Their location depends on which nerve the virus spreads from. The rash doesn’t cross the midline of your body because each spinal nerve supplies sensory information only for the left or right side of your body.

As the herpes zoster virus travels along your sensory nerves, it can cause damage and inflammation that leads to pain, even after your rash disappears.

Postherpetic neuralgia

The most common long-term complication of shingles is a condition called postherpetic neuralgia.

Postherpetic neuralgia refers to pain or intense itchiness that lasts after a shingles rash heals. It’s estimated that 10 to 18 percent of people with shingles develop postherpetic neuralgia.

Most people recover from postherpetic neuralgia within a year, but in some cases, it can be permanent.

Motor nerve damage

The herpes zoster virus can also infect the nerves that help you move your muscles. It’s thought that about 0.5 to 5 percent of people with shingles develop a condition called segmental zoster paresis. This condition leads to weakness in the muscles around the shingles rash.

Cranial nerve damage

In some cases, the herpes zoster virus affects one of the major nerves in your head called cranial nerves. Less than 1 percent of shingles cases affect cranial nerve VII (facial nerve) and lead to a condition called Ramsay Hunt syndrome.

This syndrome can cause symptoms such as:

  • facial paralysis on one side
  • ear pain
  • blisters in your ear
  • changes in taste in the front two-thirds of your tongue
  • dry eyes
  • hearing loss
  • vertigo
  • tinnitus

Damaged sensory nerves can lead to a condition called postherpetic neuralgia, in which pain persists after your rash disappears.

Four types of medications are used to treat pain from postherpetic neuralgia. Sometimes, a combination of medications is used.

Anticonvulsants

Anticonvulsants, such as gabapentin and pregabalin, are approved by the Food and Drug Administration (FDA) to treat postherpetic neuralgia. These drugs bind to calcium channels and influence neurotransmitter release to relieve pain.

Antidepressants

A wide range of antidepressants may be used at low dosages to help manage pain. One group of antidepressants commonly used for this purpose is tricyclic antidepressants. These drugs inhibit the reuptake of serotonin and norepinephrine.

Opioids

Opioid medications are effective at treating nerve pain, but doctors are often reluctant to prescribe them unless other options fail. Opioids are often the last resort because of their potential to lead to dependence or overdose. Prescription opioids include:

  • hydrocodone
  • oxymorphone
  • morphine
  • codeine
  • fentanyl

Topical local anesthetics

Two types of creams are commonly used to help manage nerve pain. Lidocaine is FDA-approved specifically for treating postherpetic neuralgia. Capsaicin cream is available over the counter and has been found to be somewhat effective, but many people experience burning pain while putting it on.

Postherpetic neuralgia can be very painful, but here are some things you can do at home to lessen your discomfort:

  • wear comfortable clothing made from cotton or silk to reduce irritation
  • apply an ice pack wrapped in a towel to the sore area
  • eat a balanced diet
  • get plenty of rest
  • minimize stress
  • exercise regularly

The same virus that causes chickenpox can also cause shingles. The virus can remain dormant in your nerves for decades after chickenpox infection before becoming active again.

Once reactivated, the virus spreads to your skin by traveling down your nerves. The area that your rash appears on depends on which nerve the virus travels from.

Shingles is thought to appear when your immune system is no longer able to suppress the virus. Keeping your immune system healthy by eating a balanced diet, exercising regularly, and minimizing stress may help reduce your chance of developing shingles. You can also get one of two FDA-approved shingles vaccines.

Postherpetic neuralgia – causes, symptoms, diagnosis and treatment

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    Chicken pox

    Herpes

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    Postherpetic neuralgia: causes, symptoms, diagnosis and treatment.

    Definition

    Postherpetic neuralgia is pain or abnormal sensory sensations associated with damage to the nervous system by the varicella zoster virus.

    Causes of postherpetic neuralgia

    After suffering chicken pox (chickenpox), the human herpes virus type 3 – Varicella zoster virus ( Varicella zoster ) – from rashes on the skin and mucous membranes, it can move to sensitive ganglia (nodes consisting of clusters of neurons) of the spinal nerves of the thoracic, lumbar levels or the trigeminal nerve. There, the virus can remain in a latent (inactive) state for decades. With a decrease in immunity (for example, against the background of viral diseases, chemotherapy, oncological diseases, therapy with glucocorticosteroid hormones for systemic connective tissue diseases (rheumatic diseases)) the virus can become activated and cause the development of herpes zoster (shingles, Herpes zoster ) or trigeminal neuralgia.

    The disease begins with unilateral pain, burning sensation, increased skin sensitivity, after which, sometimes after 1-2 weeks, redness appears, and then blistering rashes on the skin. In 50% of patients, rashes are localized on the trunk (as a rule, along the intercostal spaces at the level of the thoracic spine, sometimes in the lumbar region, sacrum), in 20% – on the head (with damage to the trigeminal nerve, damage to the eyes, ears is possible), in 15% – on the hands, and 15% – on the legs. In most cases, over time, the pain goes away on its own – recovery occurs after 2-3 weeks, but sometimes (in about 20% of patients) a complication of herpes zoster develops – postherpetic neuralgia.

    Postherpetic neuralgia is rarely seen in children and young adults, but its frequency increases significantly in old age.

    The real prevalence of postherpetic neuralgia is unknown, since there is no single point of view on the time interval between rashes, the onset of pain, and the duration of the pain syndrome.

    Classification of postherpetic neuralgia

    0029 Herpes zoster .

    1. Acute herpetic neuralgia in which the pain lasts up to 30 days from the onset of the rash.
    2. Subacute herpetic neuralgia lasting 30-120 days after onset of rash.
    3. Postherpetic neuralgia in which pain persists for more than 120 days after the onset of the rash.

    Most patients recover completely within one year of the onset of pain, but some patients experience pain for years.

    Symptoms of postherpetic neuralgia

    The main complaint of patients is pain. It is characterized by varying intensity and frequency – from mild to extremely painful, from short-term to permanent. With herpes zoster, pain can spread beyond the localization of the rash. In the clinical picture of postherpetic neuralgia, the following types of pain can be distinguished:

    • constant pain that patients describe as dull, pressing or burning;
    • paroxysmal (paroxysmal) pain that comes on suddenly, sharp, shooting, stabbing;
    • allodynia – pain that occurs in response to even very weak stimuli that under normal circumstances do not cause pain – for example, to a light touch with a cold hand.

    Often patients note constant fatigue, lack of appetite, decreased mood, sleep disturbances.

    Some patients complain of intense itching, which is localized, as a rule, in the head and neck.

    Diagnosis of postherpetic neuralgia

    At the onset of herpes zoster, when patients are only concerned about pain, the doctor may suspect heart disease, intercostal neuralgia, osteochondrosis. However, with the appearance of rashes, the diagnosis becomes obvious.

    The persistence of the pain syndrome after resolution of the rash indicates postherpetic neuralgia.

    Instrumental and laboratory diagnostics, as a rule, are not carried out.

    In atypical cases, a serological test 256 may be prescribed in combination with test No. 257 (IgM antibodies) for the diagnosis of chickenpox. In addition, these studies may be required to assess immunity to the virus.

    Antibodies of the IgG class to the Varicella-Zoster virus (Varicella-Zoster Virus IgG, anti-VZV IgG, antibodies of the IgG class to the varicella-zoster virus and shingles)

    Synonyms: Blood test for antibodies to the chickenpox virus; Chicken pox; Human herpes virus type 3; HBV-3 type; varicellae-zoster virus; Herpes zoster.

    chickenpox; Human h…

    Up to 4 business days

    Available with house call

    RUB 965

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    Antibodies of the IgM class to the Varicella-Zoster virus (Varicella-Zoster Virus IgM, anti-VZV IgM, antibodies of the IgM class to the varicella-zoster virus and herpes zoster)

    Synonyms: Blood test for antibodies to the chickenpox virus; Chicken pox; Human herpes virus type 3; HBV-3 type; varicellae-zoster virus; Herpes zoster.

    chickenpox; Human herp…

    Up to 1 working day

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    1 050 RUB

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    Which doctors to contact

    Management of patients with postherpetic neuralgia is carried out

    neurologists

    ,

    internists

    , general practitioners, rarely infectious disease specialists.

    Treatment of postherpetic neuralgia

    Early antiviral therapy, especially in the first days after the onset of rashes, can reduce the severity or even prevent the development of postherpetic neuralgia.
    In the treatment of herpes zoster, various painkillers are also used. Note that the more severe the period of rashes, the greater the likelihood of chronic pain.

    Effective pain relief can positively influence the further course of postherpetic neuralgia.

    Strictly under the supervision of a doctor! In addition to traditional analgesics, anticonvulsants (anticonvulsants), tricyclic antidepressants are used to relieve pain at the stage of herpes zoster and postherpetic neuralgia.
    To restore the functions of the affected nerve, neurotropic vitamin preparations of group B are prescribed.

    Complications

    Like any chronic pain syndrome, the course of postherpetic neuralgia is complicated by a significant decrease in the quality of life of patients. Most of them note depressed mood, irritability, disturbed night sleep, general weakness.

    Prevention of postherpetic neuralgia

    Vaccination may be recommended for the prevention of herpes zoster and postherpetic neuralgia in people over 50 years of age, especially those at risk of developing the disease. Vaccines against Herpes zoster are not included in the National Immunization Schedule, and the decision on the advisability of their use in each individual patient is made by the doctor. In some cases, vaccination may be recommended for persons under 50 years of age.

    Sources:

    1. Federal clinical guidelines for the management of patients with herpes zoster. Russian Society of Dermatovenerologists and Cosmetologists. 2015.
    2. Mendelevich E.G., Mendelevich S.V. Postherpetic neuralgia: therapeutic and prophylactic aspects and therapy with pregabalin // Neurology, neuropsychiatry, psychosomatics. 2014(2). pp. 57-61. DOI.

    IMPORTANT!

    The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.
    For a correct assessment of the results of your analyzes in dynamics, it is preferable to do studies in the same laboratory, since different laboratories may use different research methods and units of measurement to perform the same analyzes.

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    Postherpetic trigeminal neuralgia – prevention and treatment options | Kamchatnov P.

    R., Evzelman M.A., Chugunov A.V.

    Herpetic ganglionitis of the gasser ganglion (synonyms: “shingles”, “herpes zoster”) is a fairly common infectious disease, manifested by the occurrence of serous rashes in the region of innervation of individual branches of the trigeminal nerve. It is caused by the Varicella zoster virus from the group of herpes viruses. According to the results of epidemiological studies, the information obtained from the analysis of statistical data on outpatient medical care visits shows that approximately 500,000 cases of the disease are registered in the United States annually [2]. The incidence is about 2–3 cases per 1000 people per year [3]. It has been convincingly proven that the incidence of herpes zoster increases with age. Thus, in a population older than 80 years, its frequency is already 10 per 100 people per year [5].

    The disease is based on the reactivation of the Varicella zoster virus, which is capable of persisting in the ganglia of the posterior horn for a long period of time. Accordingly, in relation to the trigeminal nerve, the area of ​​\u200b\u200btheir location is the Gasser node. In the event of certain conditions favorable for the activation of the virus, a disease develops. It is believed that risk factors for its reactivation are advanced age or, conversely, infection in childhood (up to 18 months), a state of immunosuppression of various origins (acquired immunodeficiency, oncological diseases, immunosuppressive therapy), intrauterine contact with the varicella-zoster virus. The disease is realized in conditions of reduced cellular immunity due to various reasons.

    The herpes virus can be transmitted from person to person, in particular, in cases where the individual did not tolerate chicken pox or was not promptly vaccinated for this infection. The disease is not prone to recurrence. It is believed that relapses occur in about 6% of patients, and the period from the first episode to relapse can be several decades [5]. Clinical experience suggests that a relapse may be due to a disease that has arisen in a patient, the presence of which negatively affects the state and nature of the immune response.

    Clinical manifestations

    The development of the disease is preceded by a prodromal period, which is characterized by fever, nausea, diffuse headache, which, growing, can be observed for several days. Characteristic is the increase in local pain, which is neuropathic in nature, as well as an unpleasant burning, stabbing tint of itching, which can be accompanied by allodynia, hyperesthesia and hyperpathia. As a rule, this kind of pain is localized in the area of ​​subsequent rashes and is limited to the zone of one or more corresponding dermatomes. In the vast majority of cases, these manifestations are unilateral, although in some patients they can spread to the opposite half of the body [8]. The pain can be extremely intense, which often simulates a number of somatic diseases, in particular pleurisy, acute myocardial infarction, renal colic. The defeat of the gasser node can cause difficulties in differential diagnosis with dental diseases, damage to the paranasal sinuses.

    Against the background of these symptoms, hyperemia and multiple maculopapular rashes appear, which subsequently become vesicular. Vesicles are filled with transparent colorless serous contents. In cases of a favorable course of the disease, rashes can be localized only in a separate part of the dermatome. The appearance of new rashes is possible for 5-7 days. A few days after the appearance of the first rashes, their contents become cloudy (the so-called pustulation stage). Subsequently, in the absence of complications, dry crusts form at the site of the existing rashes, which fall off after 2-3 weeks. In these areas, cicatricial changes or areas of altered pigmentation may remain. The disease, as a rule, has a favorable prognosis, is characterized by a monophasic course and has a slight tendency to recurrence.

    Diagnosis can be difficult until characteristic lesions appear. After their occurrence, the correct diagnosis is usually not difficult. Confirmation of the diagnosis is possible by conducting a polymerase chain reaction, which makes it possible to detect DTCs of the Varicella zoster virus in the contents of existing rashes.

    Complications

    Among the possible complications, it should be noted local infectious lesions caused by infection of the damaged skin with streptococcus or staphylococcus, up to the development of cellulitis. When the ophthalmic branch of the trigeminal nerve is involved in the pathological process, keratitis may develop, which can lead to serious consequences in the form of corneal damage, up to monocular blindness. Rarely, there are lesions of a herpetic infection of the brain tissue (with the development of encephalitis) or its membranes with the occurrence of serous meningitis.

    One of the most frequent and rather severe complications of gasser ganglionitis caused by herpetic infection is postherpetic neuralgia. The pathogenesis of this condition is quite complex and includes at least two main mechanisms [5]. First, an increase in the excitability of primary afferents due to damage to peripheral neurons takes part in its development. As a result, there is an excessive excitability of nociceptors and, as a consequence, the formation of central sensitization. Clinically, such a combination of pathophysiological processes is manifested by the occurrence of pain and the development of allodynia. Secondly, due to the degeneration of nociceptive neurons, deafferentation of the upstream sensory systems occurs, causing their hyperactivity. As a result of this, the formation of pain is observed, which, however, is not accompanied by allodynia. According to the authors, in one patient, a combination of both mechanisms is possible, which is the reason for the peculiarity of the pain syndrome and differences in the effectiveness of the therapy.

    This pathological condition is characterized by all clinical characteristics typical for neuropathic pain syndrome. Establishing a diagnosis is possible if the pain persists for at least 30 days after the onset of complete healing of existing rashes.

    Risk factors for the development of postherpetic trigeminal neuralgia are age over 60 years, female gender, the presence of a prodromal period, multiple rashes, and a high intensity of pain at the onset of the disease [6]. According to the authors of the study, pain syndrome of moderate intensity, not accompanied by subsequent development of postherpetic neuralgia, is observed in younger patients and is probably associated with extensive local tissue damage and inflammation in the presence of multiple lesions. The importance of the age factor as an important predictor of the development of pain syndrome should be emphasized in patients who had herpes zoster at the age of 9 years.0 years, postherpetic neuralgia occurs in about half of cases [5]. An unfavorable prognostic factor for the development of pain syndrome is the detection of the Varicella zoster virus in the blood.

    As with the vast majority of chronic neuropathic pain syndromes, a combination of psychosocial factors plays an extremely important role in the development of postherpetic neuralgia. The presence of previous depressive and anxiety disorders, insufficient social adaptation of the patient, violation of social ties, living outside the family, etc. may increase the likelihood of developing a pain syndrome.

    The course of postherpetic neuralgia can be different. In some patients, there is a significant regression or complete disappearance of the existing pain syndrome over a period of about six months. Unfortunately, a less benign course is possible, when the pain syndrome becomes chronic and leads to disability of the patient and a sharp decrease in his quality of life [10]. The risk of severe pain syndrome increases with age, so, in more than 5% of elderly patients, intense pain persists for more than 12 months. [5]. The features of the course of the disease may be associated with differences in the pathogenesis of the pain syndrome, the direction and intensity of compensatory reactions of the body, as well as the effectiveness and adequacy of the therapy, in particular, its timely start.

    Quite often, along with the development of postherpetic neuralgia, patients experience motor disorders in the form of peripheral paresis of the cranial nerves (most often, the facial nerve) [1]. This form of herpes infection is known as Ramsay Hunt syndrome. There are no convincing data on the prognostic significance of motor disorders in relation to the frequency and duration of the pain syndrome.

    Treatment

    The most effective treatment for patients with herpes zoster is the use of antiviral drugs. At present, the high efficacy of valaciclovir (Virdel, the pharmaceutical company “Stada”) has been convincingly demonstrated in the treatment of patients with herpes zoster, the recommendation to apply the 50-50-50 rule is of interest [8]. It has been shown that the maximum effectiveness of antiviral therapy is observed when it is started no later than 50 hours after the onset of rashes, in patients over the age of 50 years and in the presence of at least 50 elements of rashes. Subject to this rule, it is possible to reduce the healing time for existing skin lesions, as well as reduce the risk of developing postherpetic neuralgia [9]. The authors of this study demonstrated that in this situation, all the applied criteria for assessing the effectiveness of therapy (the likelihood of developing pain syndrome, the timing of its onset, pain intensity) testified to the undoubted advantage of timely initiation of valaciclovir therapy and an adequate choice of indications for its implementation. A later start of antiviral therapy (more than 72 hours after the appearance of rashes) provides a slight reduction in the healing time [11]. The use of antiviral drugs in the case of a small number of rashes (less than 50) is also not associated with a significant decrease in the likelihood of developing neuropathic pain syndrome.

    Probably, non-compliance with this rule led to the fact that the results of a systematic review on the study of the results of antiviral therapy could not confirm its effectiveness in preventing the development of neuralgia after 4 and 6 months. after the appearance of rashes [7]. These data indicate the need for proper selection of patients to achieve the desired effect and timely initiation of treatment.

    To achieve a therapeutic effect in the form of reducing the risk of developing postherpetic neuralgia, it is necessary to use valaciclovir (Virdel) at a daily dose of 1000 mg 3 times for 7 days. It is possible to use local dosage forms of antiviral drugs, but the achievement of a therapeutic effect is possible only with their systemic administration in adequate daily dosages and a sufficient duration of treatment. The drug Virdel is well tolerated, its simultaneous use with other drugs is possible.

    As a means of potentiating the therapeutic effects of valaciclovir, the simultaneous administration of glucocorticoids is proposed. There is evidence that combination therapy can reduce the intensity of pain in the acute stage of the disease [12]. Less convincing information about the ability of glucocorticoids to reduce the risk of postherpetic neuralgia. The authors of studies conducted in this direction point out that the use of glucocorticoids is associated with an increased risk of developing undesirable side effects, in particular, exacerbation of gastric ulcer, hyperglycemia, accession of a local infectious process, and the frequency of such complications increases with age. Undoubtedly, combination therapy requires a comprehensive consideration of its possible positive effect and the risk of adverse reactions associated with treatment, due to the condition of a particular patient.

    In the event that the patient has persistent postherpetic neuralgia, which is observed in the long-term period after the healing of the rash, the treatment of the patient requires other approaches. In this situation, representatives of tricyclic antidepressants (amitriptyline, nortriptyline) can be used, which have a fairly high efficiency. However, despite the good analgesic effect, the widespread use of these drugs is limited by the frequent occurrence of unwanted side reactions, especially when they are prescribed in high dosages. Achieving an analgesic effect while reducing the risk of side effects is possible by prescribing antidepressants that have the ability to inhibit the reuptake of both serotonin and norepinephrine. It should be noted that the analgesic effect of antidepressants in postherpetic neuralgia, as in other neuropathic pain syndromes, is not associated only with their antidepressant effect.

    Antiepileptic drugs, in particular carbamazepine, are widely used to treat patients with traditional postherpetic neuralgia. Currently, new drugs have become widespread, the pharmacological effects of which are realized due to interaction with gamma-aminobutyric acid receptors, the main inhibitory mediator in the central nervous system (gabapentin, pregabalin). Their better tolerability is noted in comparison with antiepileptic drugs of previous generations. In a number of countries, weak or even strong opioids are used for postherpetic neuralgia.

    Of interest is the possibility of using local forms of drugs. Thus, it has been shown that the local use of lidocaine preparations may be appropriate in the presence of a pain syndrome accompanied by allodynia. There is also evidence of the possible effectiveness of capsaicin in patients with postherpetic neuralgia. It should be noted that its widespread use is limited by not always satisfactory tolerability of therapy.

    Thus, the available data on the effectiveness of the use of valaciclovir (Virdel) in patients with herpes zoster allow us to recommend its widespread use in this group of patients. Timely initiation of treatment, the correct selection of patients for prescribing the drug can increase the effectiveness of the therapy, prevent the development of postherpetic neuralgia.