The best ways to treat herpes zoster in humans

Postherpetic neuralgia is a condition that is accompanied by pain and usually follows an episode of herpes zoster. The term itself refers to the condition (pain after herpes).

Shingles (herpes zoster) - the cause is the reactivation of the varicella zoster virus, which is latent in the human body and for unknown reasons is activated and causes an episode of herpes zoster. The exact reasons for the activation of the virus are not yet known.

The reactivated virus spreads along the nerves, causing pain and rashes or small blisters on the skin. Typically, shingles rash and pain usually occur on one side of the torso or head. Most often, rashes occur in the chest area. The disease usually lasts for several weeks and goes away without leaving a trace. But sometimes the virus damages nerve fibers, which results in pain and other symptoms after the rash disappears. This is postherpetic neuralgia

Symptoms of postherpetic neuralgia vary (depending on the individual characteristics of the individual) and may include severe pain, numbness, tingling, and paresthesia in the area affected by the viral infection. Postherpetic neuralgia can have a negative impact on both daily life and ability to work. But, at present, there are quite effective ways to treat this condition (physiotherapy, drug treatment).

Risk factors

Only those who have had chickenpox can get shingles. But there are certain groups that are more susceptible to postherpetic neuralgia:

• Age – the chance of postherpetic neuralgia is higher in the older age group. (30% of people over 60 years of age who have had herpes zoster subsequently develop postherpetic neuralgia) and only 10% of the younger group develop postherpetic neuralgia.
• Localization of rashes - symptoms of neuralgia are more pronounced if the rashes were in the forehead or eyes.
• Concomitant pathology – The presence of a suppressed immune system (after chemotherapy or taking immunosuppressants) or diseases such as AIDS.

Early treatment of herpes zoster is important. Treatment started within 2-3 days after the rash appears can help reduce symptoms and avoid the risk of postherpetic neuralgia.

Complex treatment of herpetic lesions of the peripheral nervous system

The incidence of herpes zoster varies from 0.4 to 1.6 cases per 1000 people under the age of 20 years and from 4.5 to 11.8 cases per 1000 people in the older age group. Men and women get sick with the same frequency. Important risk factors for the development of herpes zoster include stress, hypothermia and physical trauma. Complications of the disease are more likely in old age, in the presence of concomitant autoimmune, oncological and hematological pathologies, diabetes mellitus, and taking immunosuppressive drugs (corticosteroids, cytostatics). HIV infection adversely affects both the risk of development and the severity of dermatosis. Thus, the incidence of herpes zoster between the ages of 20 and 50 years in HIV-infected people is almost 8 times higher than that in immunocompetent individuals. Relapses of the disease occur in less than 5% of those who have recovered [14, 45]. A distinctive feature of the causative agent of chickenpox and herpes zoster – Varicella zoster virus (VZV) of the subfamily Alphaherpesvirinae of the Herpesviridae family – is the ability to persist for a long time in the sensory ganglia of the nervous system and to be reactivated under the influence of any unfavorable endogenous and (or) exogenous factors. In fact, we are talking about two clinical forms of the disease caused by the same etiotropic agent. Dermatosis manifests with a primary infection - chickenpox, then goes into a latent phase with localization in the ganglia of the dorsal roots of the spinal cord and the ganglia of the cranial nerves, subsequently relapsing with herpes zoster [10, 12, 14]. The mode of transmission of Varicella zoster virus is airborne. After viral replication on the mucous membranes of the respiratory tract, they migrate to the lymph nodes and CD4+ lymphocytes, as well as to epithelial cells. Infection of sensory nerve endings is mediated by an extracellular virus present in large quantities in vesicles on the skin. Further spread of VZV in the macroorganism can occur by hematogenous, lymphogenous and neurogenic (along the axons of sensory nerves) routes. The virus infects the sensory ganglia of the nervous system, which ensures its lifelong persistence in the human body. Activation products of a number of virus genes lead to blockade of interferon and a decrease in the expression of a number of receptors on immunocompetent cells, as a result of which VZV acquires the ability to “escape” the protective mechanisms of the human immune system. A decrease in the intensity of cellular reactions leads to reactivation of the virus, which is accompanied by damage not only to the skin, but also to nerve endings. Histologically, when the virus is reactivated in the ganglia, hemorrhages, edema and lymphocytic infiltration are revealed throughout the sensory nerve. The nature of these changes determines the presence and severity of pain. Most dermatovenerologists propose to distinguish the following clinical forms of herpes zoster: vesicular, without rash (zoster sine herpete), generalized, disseminated, mucous membranes, ophthalmic herpes, Hunt syndrome, as well as atypical (bullous, hemorrhagic, ulcerative necrotic, gangrenous, abortive) [14 ]. By localization, lesions of the trigeminal (Gasserian) and geniculate ganglia, cervical, thoracic and lumbosacral ganglia are distinguished. According to most experts, the skin areas innervated by the spinal and trigeminal nerves are most often affected, and the thoracic dermatomes are most often involved in the pathological process. According to a number of other authors, herpetic lesions of the gasserian ganglion are more common than spinal ganglionitis [17]. The disease usually manifests itself as pain. About 70–80% of patients with herpes zoster in the prodromal period complain of pain in the affected dermatome, in the area of ​​which skin rashes subsequently appear. In the prodromal period, pain can be constant or paroxysmal. The pain is most often described as burning, shooting, stabbing or throbbing. Some patients feel pain only when touched. In other patients, the leading clinical symptom is severe skin itching. The prodromal period usually lasts 2–3 days, but sometimes reaches a week. Paresthesia in the affected areas is common. The intensity of the pain syndrome is determined by the degree of involvement of peripheral nerves in the pathological process. After 2–7 days, the typical shingles rash begins to appear on the skin. In the case of the classic course, herpes zoster is ephemeral erythema, swelling, then multiple papules, quickly transforming into vesicles within 2-3 days. Efflorescences tend to group and merge with each other. Due to the addition of a secondary pyococcal infection, pustulization is observed in the lesions. Severe general infectious manifestations (fever, cephalgia, myalgia, fatigue, general malaise), as well as enlargement of regional lymph nodes, are observed in less than 20% of patients. According to a number of authors, when examining the cerebrospinal fluid in herpes zoster, lymphocytic pleocytosis is determined [36]. After 3–5 days, erosions appear at the site of the vesicles and crusts form, disappearing by 3–4 weeks. At the site of resolved rashes, hypo- or hyperpigmentation usually persists for a long time. If the period of appearance of new vesicles lasts more than 1 week, this indicates a high probability that the patient has an immunodeficiency state. Instead of crusts, shallow erosions form on the mucous membranes. Rashes on the mucous membranes may go unnoticed altogether. It is important that with herpes zoster, the spread of the pathological process corresponds to a specific dermatome on one side of the body (left or right) and does not cross the anatomical midline of the body, with the exception of zones of mixed innervation. In immunocompetent patients, one dermatome is usually affected, but due to individual variability in innervation, adjacent dermatomes may also be involved. The rash is usually accompanied by the same pain as in the prodromal period. However, in some cases, pain may appear only in the acute period of the disease. In the abortive form of herpes zoster, skin rashes are limited to erythema and papules, without transformation into cavitary elements. In the hemorrhagic form of herpes zoster, the contents of the vesicles are mostly hemorrhagic, the pathological process involves not only the epidermis, but also the dermis, and after the rash resolves, scar formation is possible. The most severe types of herpes zoster include necrotic and disseminated forms of herpes zoster [14]. The pain during the entire period of the rash, as a rule, is of an intense burning nature, the zone of its distribution corresponds to the roots of the affected ganglion. Usually the pain intensifies at night and when exposed to various stimuli (tactile, temperature, etc.). An objective examination may reveal sensitivity disorders in the form of hyperesthesia, hypoesthesia or anesthesia, including anesthesia dolorosa, and others. Sensitivity disorders are usually limited to the area of ​​the rash, but are very variable in form and intensity. The severity of pain does not always correlate with the severity of skin manifestations. In a number of patients, despite the severe gangrenous form of skin lesions, the pain remains insignificant and short-lived. At the same time, other patients experience prolonged intense pain with minimal skin manifestations. With Gasserian ganglionitis, excruciating pain, sensory disturbances and rashes are observed in the area of ​​innervation of one (I, II or III), two or (rarely) all branches of the trigeminal nerve. With ophthalmoherpes, keratitis, episcleritis, iridocyclitis are possible, in rare cases - damage to the retina of the eye, optic neuritis resulting in optic nerve atrophy, as well as glaucoma. Damage to the III, IV, VI cranial nerves is possible, which is manifested by oculomotor disorders and ptosis. Infection with VZV and the herpes simplex virus (HSV) is the most common cause of Bell's palsy; cutaneous manifestations may be absent, and the etiological role of VZV or HSV can be determined using laboratory tests. Often, herpetic lesions of the VII cranial nerve are manifested not only by peripheral prosoparesis, but also, when the geniculate ganglion is affected, by hyperacusis and hypogeusia (Hunt syndrome) [31]. Damage to the VIII cranial nerve usually presents with tinnitus. Hypoacusis can occur not only when the auditory nerve is damaged, but also when the middle ear apparatus is involved. Vestibulatory disorders usually develop slowly and range from mild dizziness to severe vestibular ataxia. When the rash is localized in the area of ​​innervation of the IX cranial nerve, pain and impaired sensitivity are observed in the area of ​​the soft palate, palatine arch, tongue, and posterior pharyngeal wall. Due to the development of herpetic radiculitis and neuritis, movement disorders are sometimes observed, usually corresponding to the area of ​​sensory impairment. Damage to the cervical nodes is accompanied by rashes on the skin of the neck and scalp. With ganglionitis of the lower cervical and upper thoracic localization, Steinbrocker syndrome can be observed (pain in the hand is accompanied by swelling of the hand, trophic disorders in the form of cyanosis and thinning of the skin, hyperhidrosis, brittle nails) [10]. Thoracic ganglionitis often simulates the clinical picture of angina pectoris or myocardial infarction, which leads to diagnostic errors. With herpetic lesions of the ganglia of the lumbosacral region, pain occurs that simulates pancreatitis, cholecystitis, renal colic, and appendicitis. In connection with the development of ganglioradiculitis, the symptoms of Neri, Lassegue, Matskevich, and Wasserman are caused. A neurogenic bladder with peripheral urinary disorders may be associated with herpes zoster of the sacral dermatomes S2–S4. Acute and chronic herpetic encephalitis and myelitis are serious complications, often leading to death or disability [10, 33, 36]. Pain syndrome is the most painful manifestation of herpes zoster when the peripheral nervous system is affected. In some patients, the rash and pain have a relatively short duration; in 10–20% of patients, postherpetic neuralgia occurs, which can last for months or even years. Significantly reducing the quality of life, it can lead to long-term temporary disability and is accompanied by significant financial costs. This is why effective treatment of pain associated with herpes zoster is an important clinical goal. According to modern concepts, the pain syndrome in herpes zoster has three phases: acute, subacute and chronic [32]. Acute herpetic neuralgia occurs, as a rule, in the prodromal period and lasts up to 30 days. In most patients, the appearance of pain and rash is preceded by a burning or itching sensation in a specific dermatome. The pain can be stabbing, throbbing, shooting, paroxysmal or constant. In a number of patients, the pain syndrome is accompanied by general systemic inflammatory manifestations: fever, malaise, myalgia, headache. Determining the cause of pain at this stage is extremely difficult. Depending on its location, differential diagnosis should be made with angina pectoris, myocardial infarction, acute attack of cholecystitis, pancreatitis, appendicitis, pleurisy, intestinal colic, vertebrogenic radiculopathy and other conditions. The cause of the pain usually becomes obvious after the appearance of characteristic rashes. The immediate cause of prodromal pain is subclinical reactivation and replication of VZV in neural tissue. The presence of severe pain in the prodromal period increases the risk of more severe acute herpetic neuralgia during the rash period and the likelihood of subsequently developing postherpetic neuralgia. In the majority (60–90%) of immunocompetent patients, the appearance of skin rashes is accompanied by acute, severe pain. The severity of acute pain increases with age. A characteristic feature of acute herpetic neuralgia is allodynia - pain caused by exposure to a non-painful stimulus, such as the touch of clothing. It is believed that allodynia in the acute phase is a predictor of the occurrence of postherpetic neuralgia. The subacute phase of herpetic neuralgia begins at the end of the acute phase (after 30 days from the beginning of the prodromal period). With adequate treatment, it can be stopped or continue for more than 120 days, turning into postherpetic neuralgia. Factors predisposing to the persistence of pain include: old age, female gender, the presence of a long prodromal period, massive skin rashes, localization of rashes in the area of ​​innervation of the trigeminal nerve (especially the eye area) or brachial plexus, severe acute pain, the presence of immunodeficiency. With postherpetic neuralgia, patients describe three types of pain: 1) constant, deep, dull, pressing or burning pain; 2) spontaneous, periodic, stabbing, shooting pain, similar to an electric shock; 3) pain when dressing or lightly touching (in 90% of patients). According to the International Herpes Treatment Forum, postherpetic neuralgia is defined as pain that lasts more than 4 months. (120 days) after the onset of the prodromal period of herpes zoster [33–35]. Pain syndrome is usually accompanied by sleep disturbances, loss of appetite and weight loss, chronic fatigue, and depression, which leads to social maladaptation of patients. If in the acute phase the pain syndrome is mixed (inflammatory and neuropathic) in nature, then in the chronic phase it is typical neuropathic pain. Each of the listed phases has its own treatment features, based on the pathogenetic mechanisms of pain and confirmed by controlled clinical studies. Treatment of herpes zoster is currently a pressing interdisciplinary problem, in which not only dermatovenerologists and neurologists, but also infectious disease specialists, ophthalmologists, otorhinolaryngologists, and doctors of other specialties take part. The drugs of choice for etiotropic therapy for herpes zoster currently remain synthetic acyclic nucleosides (acyclovir and its analogues - famciclovir and valciclovir). The most well studied drug at present is acyclovir. The mechanism of action of acyclovir is based on the interaction of synthetic nucleosides with the replication enzymes of herpes viruses. Thymidine kinase of herpes viruses binds to acyclovir much faster than cellular ones, as a result of which the drug accumulates mainly in infected cells. Acyclovirs line up in a chain of DNA being built for the “daughter” viral particles, ending the pathological process and stopping the reproduction of the virus. Valacyclovir is characterized by high bioavailability, which allows you to significantly reduce the dose and frequency of administration of the drug. Famciclovir, due to the higher affinity of herpesvirus thymidine kinase for it than for acyclovir, has more pronounced effectiveness in the treatment of herpes zoster. The main regimens for antiviral therapy for herpes zoster in adult patients are: valacyclovir 1000 mg 3 times a day. orally for 7 days or famciclovir 500 mg 3 times a day. orally for 7 days, or acyclovir 800 mg 5 times a day. orally for 7–10 days. It should be remembered that acyclic nucleosides should be prescribed as early as possible - in the first 72 hours from the onset of skin rashes. As noted above, pathogenetic treatment in different phases of the disease has its own characteristics. In the prodromal and acute phases, it is advisable to prescribe anti-inflammatory drugs (NSAIDs), decongestant, and desensitizing therapy. As is known, the “gold standard” for the effectiveness of NSAIDs, the standard for studying the therapeutic potential and safety of new and “old” drugs in this group is diclofenac sodium. Diclofenac has been tested in all areas of clinical use of NSAIDs, its effectiveness has been proven in randomized clinical trials both in urgent conditions and in chronic pain. Moreover, numerous studies have shown that none of the existing NSAIDs is superior to diclofenac in effectiveness, while the latter may be inferior to some of them in safety. According to a number of authors, diclofenac remains the most popular NSAID in the Russian Federation, which is primarily due to the financial availability of generics of this drug. According to a survey of 3 thousand patients in Moscow and other 6 regions of Russia who regularly receive NSAIDs, this drug was used by 72% of respondents [8]. However, it was cheap generics that were not subjected to large clinical research for their effectiveness and safety [9], which cannot be said about the original drug Diclofenac and its analogues. The positive qualities of Diclofenac are primarily due to the optimal physical, chemical and structural characteristics of the drug, its ability to penetrate and accumulate in the foci of inflammation, as well as good compatibility with many other drugs. The anti-inflammatory effect of diclofenac is due to inhibition of the activity of cyclooxygenase 1 and 2 (COO-1 and COO-2). TsOG-1 is considered structural, and TSOG-2 is considered an induced form of the key enzyme of the metabolism of arachidonic acid. COX-1 ensures the synthesis of prostaglandins (PGs) involved in the secretion of gastric mucus and has bronchodilator properties. Prostacyclin has vasodilating and disagreement properties, improving microcirculation in the kidneys, lungs and liver. COX-2 ensures the synthesis of PGs involved in the inflammatory process and is found only at the site of inflammation. The anti -inflammatory activity of NSAIDs is due to oppression precisely the TSOG -2. Most non-election NSAIDs are more inhibited by the COO-1 than the COO-2. Diclofenac inhibits both isoenzyme to be approximately equally, therefore, it is less common to defeat the gastrointestinal tract (gastrointestinal tract). The drug disrupts the metabolism of arachidonic acid and reduces the amount of PG both in the focus of inflammation and in healthy tissues, suppresses the exudative and proliferative phases of inflammation. The greatest efficiency of its action is noted with inflammatory pain, which is important in the treatment of acute herpetic neuralgia [13]. Like all NSAIDs, Diclofenac has anti -aggregate activity. However, it does not compete with acetylsalicylic acid for binding with the active center of the COO-1 and does not affect its antitromobocytic effect. Diclofenac reduces the permeability of capillaries, stabilizes lysosomal membranes, reduces the production of ATP in oxidative phosphorylation processes, inhibits the synthesis of inflammation mediators (PG, histamine, bradykinins, lymphkinines, complement factors and others). The drug blocks the interaction of bradykinin with tissue receptors, restores impaired microcirculation and reduces pain in the focus of inflammation. The analgesic effect is due to a decrease in the concentration of biogenic amins with algogenic properties, and an increase in the threshold of pain sensitivity of the receptor apparatus. With prolonged use, a desensitizing effect can have. As for the risk of serious complications, the safety of the diclofenac in relation to the gastrointestinal tract is generally higher than other non -election NSAIDs, and in patients with a relatively low risk of complications, it is comparable to selective NSAIDs [19]. However, the total frequency of complications by the digestive tract, primarily dyspepsia against the background of diclofenac, is significantly higher than when using ethricoxib, celloxib, nimesulide and meloxicam. The use of diclofenac is associated with an increase in the risk of destabilization of arterial hypertension and heart failure, as well as the development of cardiovascular disasters. Diclofenac is able to cause serious hepatotoxic complications, although the clinically pronounced liver pathology is rare. Nevertheless, according to many researchers, taking into account the ratio of efficiency, tolerance and low cost, Diclofenac can be considered the drug of choice for the treatment of acute and chronic pain in patients who do not have serious risk factors for the development of NSAID gastropathy who do not suffer from cardiovascular and hepatobiliary diseases systems. With moderate risk - in the elderly without serious comorbid pathology or patients with ulcerative history (without serious complications) - diclofenac can be used in combination with gastroprotectors, but in the absence of cardiovascular pathology or its effective drug correction. In postherpetic neuralgia, which is chronic neuropathic pain, drugs are the forefront in the treatment of patients that suppress the peripheral and central sensitization and activate the antinociceptive system. Such drugs include antidepressants (preference is given to selective inhibitors of the reverse capture of serotonin and norepinephrine) and anticonvulsants [1, 3, 22]. The purpose of neuroprotective drugs is shown. In complex treatment, both acute and chronic pain use B vitamins [7]. The metabolic and neurotrophic effect of vitamin B1 (thiamine) is described - the most important component of the physiological system for conducting nerve impulses. It was established that vitamins B6 and B12 (pyridoxine and cyanocobalamin) play an important role in the processes of myelinization of nerve fibers. Pyridoxine is involved in the synthesis of mediators not only of the peripheral, but also of the central nervous system [2, 5, 26, 40]. A number of works emphasize that both the combination and the separate use of vitamins B1, B6, B12 have an analgesic effect [20, 24, 27–29, 38, 41, 42]. It is proved that the combination of vitamins B in pain inhibits nociceptive answers that do not change after the introduction of Noxson [24], enhances the effect of norepinephrine and serotonin - the main “antinocyceptive” neurotransmitters [29]. A number of experimental studies revealed a distinct antinociceptive effect of individual vitamins and their complexes with neuropathic pain [15, 21, 25, 44]. When treating a group of vitamins of group in for 3 weeks. 1149 patients with pain syndromes and parestheses caused by polyneuropathies, neuralgia, radiculopathies, mononeuropathy, a significant decrease in the intensity of pain and paresthesia in 69% of cases was noted [23]. In a review of works on the study of the antinocyceptive action of a complex of vitamins into I. Jurna in 1998, having analyzed the experimental and clinical studies that had existed by that time, it came to the conclusion that their use can reduce both skeletal and radicular back pain [back. 28]. There is data from a synergistic effect in a decrease in tactile allodinia while using vitamin B12, B1 and anti -vocalsant of carbamazepine or gabapentin [37, 41], which seems important for the implementation of the mechanisms of action of drugs when they are simultaneously used in patients with neuropathic pain. One of the drugs containing a complex of B vitamins is neuromultivitis, the treatment of which is continued at a dose of 1-3 tablets per day for 1-2 months. Depending on the effectiveness of therapy. The inclusion of neuromultivitis in the complex therapy of pain allows you to achieve a more pronounced effect while using NSAIDs, reduce the duration of the pain episode and the duration of therapy, and reduce the frequency of relapse. A neurodiclite that contains in 1 capsule with a modified release of 50 mg of sodium diclofenac, 50 mg of hydrochloride thiamine, 50 mg of pyridoxine hydrochloride and 250 μg cyanocobalamin deserves special attention. The drug is prescribed at a dose of 1-3 capsules per day for 1-2 weeks. The use of a combination of vitamins B1, B6, B12 and diclofenac allows you to achieve a more pronounced analgesic effect, while the duration of therapy can be reduced, which is confirmed by a number of clinical studies [7, 18, 18, 30, 43], including multicenter -centered double blind randomized studies [ 37]. With combined therapy, the acuity of pain according to the subjective sensation of patients is reliably reduced earlier than with monotherapy of NSAIDs. With a combination of NSAIDs with B vitamins, a dose of NSAIDs can be reduced [4, 6, 18, 30, 43]. In several clinical studies using a complex of vitamins B as adjuvant therapy when prescribing diclofenac [37, 39, 43], the analgesic effect was confirmed not only by a decrease in the intensity of pain on the visual and analysis scale, but also by normalization of patients with night sleep and improvement of the quality of life. 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Causes

Postherpetic neuralgia has a specific pathogenesis. Nerves in their structure are similar to electrical wires that run throughout the body and conduct impulses from the central nervous system and back, with information about the state of organs and tissues. Sensory nerves transmit pain, temperature, and tactile sensations.

Postherpetic neuralgia occurs when the shingles virus damages sensory nerves. Damaged nerves begin to function poorly and send pain impulses to the central nervous system. This leads to chronic pain or sensory disturbances in certain areas of the body.

Symptoms

Symptoms of postherpetic neuralgia typically occur only in the area of ​​the body affected by shingles and include:

• Pain (can be sharp, cutting, throbbing, burning),
• Numbness, tingling, itching
• Headaches if shingles is localized to the head or face
• Rarely, muscle weakness or paralysis if the nerve supplying a particular muscle is damaged.

Sometimes patients experience allodynia. Allodynia is a reaction that is not proportionate to the stimulus (that is, the patient reacts to minor stimuli such as a slight change in temperature or the touch of clothing with severe pain).

Complications of genital herpes

Complications of genital herpes include dryness and the formation of painful bleeding cracks on the mucous membranes of the external genitalia, which occurs due to mechanical stress (for example, during sexual intercourse).

A special place among other complications is occupied by pain syndrome caused by specific herpetic neuralgia of the pelvic nerve plexus. In this case, women complain of periodically occurring nagging pain in the lower abdomen, in the area of ​​​​the projection of the ovaries, radiating to the lumbar region and rectum, pain in the perineum. Pain with recurrent herpes can occur regardless of the presence of skin rashes, which greatly complicates diagnosis. Recurrent genital herpes, disrupting the normal sex life of patients, often causes neuropsychiatric disorders and leads to conflicts in the family.

Genital herpes in some women causes miscarriage and infertility.

Diagnosis

If pain occurs after an episode of rashes or sensory disturbances, you should consult a doctor. Diagnosis is based on medical history, examination and laboratory tests (necessary to exclude other diseases). Instrumental diagnostic methods (CT, MRI, EMG, ultrasound) are prescribed only if there is a need for differential diagnosis.

Forecast

Exercise therapy, physiotherapy and drug treatment in most cases help reduce symptoms and restore quality of life. Especially if treatment is carried out in a timely manner.

Treatment

Drug treatment:

• Analgesics such as acetaminophen (Tylenol, Panadol, Tempra), and nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, naproxen, and Celebrex.
• Opioids – Your doctor may prescribe opioid analgesics for severe pain that is not controlled by regular analgesics, but these medications should be used with caution due to the risk of serious side effects. For example: This group includes tramadol or oxycodone. Some studies suggest that oxycodone may also help reduce allodynia.
• Antidepressants – These medications are effective in treating depression. In addition, they improve sleep (for example, amitriptyline, Cymbalta, etc.).
• Anticonvulsants – Drugs in this group are intended mainly for the prevention of convulsive conditions. But sometimes they are quite effective for postherpetic neuralgia (Neurontin, Lyrica, Topamax, carbamazepine).
• Blocks - Injections of corticosteroid into paravertebral points sometimes lead to a significant reduction in pain.
• Local painkillers - ointments, gels containing analgesics or anesthetics (lidocaine). Helps temporarily reduce symptoms.

Treatment of herpes zoster in adults

It is necessary to start fighting herpes zoster as quickly as possible - already when the first signs of the disease appear. The doctor will always prescribe a comprehensive treatment that will relieve the patient of the unpleasant symptoms of the disease, reduce the risk of complications, and also support the immune system.

Diagnostics

Usually the diagnosis is made based on examination of the clinical picture. When the patient has already developed a rash, it becomes obvious. But at the very beginning of the disease it can be confused with pleurisy, trigeminal neuralgia, appendicitis, angina pectoris, pulmonary infarction, and renal colic. It is also important for the doctor to distinguish lichen from ordinary herpes, chickenpox, and acute eczema.

To make a correct diagnosis or clarify it, doctors resort to various methods of laboratory diagnostics:

• PCR analysis - it detects pathogen DNA in vesicular fluid, blood, saliva;
• enzyme-linked immunosorbent assay (ELISA) - helps to detect antibodies to the virus and understand the primary infection;
• immunofluorescence analysis - allows you to find antigens;
• HIV/AIDS test – may be prescribed if a generalized form develops.

The patient may also be given directions for a general and biochemical blood test, and a general urinalysis.

Modern methods of treatment

Shingles is treated mainly on an outpatient basis. But with gangrenous, generalized, ophthalmic and ear forms, patients are admitted to the hospital.

There is a wide range of medications that are used to treat this infection:

Local antiviral agents. These include ointments Acyclovir, Zovirax, Panavir. They help to cope with rashes faster.

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Antiviral agents for oral administration. Tablets Acyclovir, Valtrex, Famvir, Valacyclovir help fight the virus more effectively.

Painkillers . Non-steroidal antiviral drugs (Nimesil, Meloxicam, Naproxen) not only eliminate pain, but also treat inflammation. Lidocaine-based ointments also help cope with pain.

Antihistamines. Tavegil, Suprastin and other similar medications help get rid of itching.

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Vitamins. B vitamins (tablets or even injections) are needed to prevent tissues from actively deteriorating.

Antibiotics. If a bacterial infection is associated with shingles, the doctor will prescribe Gentamicin, Tetracycline, Oxacillin, etc.

Often the patient is prescribed physiotherapeutic procedures - UHF, electrophoresis, ultrasound, ultraviolet irradiation. With proper treatment and compliance with all specialist recommendations, the prognosis is favorable.

Prevention

Certain antiviral medications may help prevent or reduce the effects of shingles, thereby reducing the risk of postherpetic neuralgia:

• Chickenpox vaccine – The varicella zoster virus vaccine (Varivax) is now a routine childhood vaccine, but may also be recommended for older children and adults who have never had chickenpox. This vaccine does not guarantee that a person will not get chickenpox or shingles, but it may reduce the duration and severity of symptoms and the risk of complications such as postherpetic neuralgia.
• Shingles vaccine - (Zostavax) can be given to people over 60 years of age (who have had chickenpox but not shingles). Zostavax is not recommended for use in certain groups of people (for example, those undergoing cancer treatment or those who are immunocompromised).
• Antiviral medications – Antiviral medications such as acyclovir, valocyclovir, famciclovir, when taken within the first 72 hours after the shingles rash appears, can help shorten the duration of shingles and reduce the chance of developing postherpetic neuralgia.

Physiotherapy helps reduce pain and relieve inflammation. Various techniques are used (including transcutaneous electrical stimulation).

Exercise therapy helps restore the elasticity of ligaments and muscles. Exercises can be carried out both on simulators and in the form of gymnastics.

Acupuncture. This method is quite effective in restoring conductivity and reducing pain.