What Is Herpes Zoster?
Herpes zoster, popularly known as "shingles," is the reactivation of the varicella-zoster virus (VZV) that remained latent in sensory nerve ganglia after primary infection (chickenpox). It manifests as a painful vesicular eruption following the distribution of a dermatome.
It affects approximately 1 in 3 people during their lifetime, with incidence rising significantly after age 50 and in immunosuppressed individuals. The main complication is postherpetic neuralgia (PHN) — persistent neuropathic pain after the cutaneous lesions resolve, which can last months to years.
Reactivation is triggered by the decline in cellular immunity specific against VZV, which occurs with aging, immunosuppression, severe physical or emotional stress, and certain diseases. The virus travels along the sensory nerve to the skin, causing neural inflammation and vesicles.
Ganglionic Latency
VZV remains latent in the dorsal root ganglia and cranial nerve ganglia for decades. Reactivation causes neural inflammation (ganglionitis) and neuropathy.
Postherpetic Neuralgia
In 10-20% of patients, pain persists after lesions heal. PHN is severe neuropathic pain from permanent damage to neural fibers.
Vaccine Prevention
The recombinant Shingrix vaccine demonstrated approximately 97% efficacy at ages 50-69 and 91% at ages 70 and older against herpes zoster in the pivotal studies (ZOE-50/ZOE-70); and 88-91% against PHN. Protection attenuates gradually over 4-7 years of follow-up. Recommended for adults aged 50 and older.
Pathophysiology
VZV remains latent in the dorsal root ganglia after chickenpox. With the decline of specific cellular immunity (T cells), the virus reactivates and replicates in ganglionic neurons, causing inflammatory ganglionitis. The virus then travels anterogradely along the sensory axon to the skin of the corresponding dermatome.
Neural inflammation causes damage to sensory fibers — destruction of myelinated fibers and demyelination. This neuropathy is responsible for acute pain and, when damage is extensive and permanent, for postherpetic neuralgia. PHN involves deafferentation (loss of afferent input), generating ectopic neuronal activity and central sensitization.
Postherpetic neuralgia results from both peripheral and central alterations: damaged C fibers generate spontaneous discharges, surviving A-beta fibers sprout and form aberrant connections with nociceptive pathways (allodynia), and dorsal horn neurons become hyperexcitable. Risk factors for PHN include age > 60 years, intense acute pain, extensive eruption, and ophthalmic involvement.
PHASES OF HERPES ZOSTER INFECTION
| PHASE | DURATION | MECHANISM | MANIFESTATION |
|---|---|---|---|
| Prodromal | 1-5 days | Viral replication in ganglion, ganglionitis | Pain, tingling, burning in dermatome (no lesions) |
| Acute eruptive | 7-10 days | Axonal transport, cutaneous infection | Grouped vesicles on erythematous base, intense pain |
| Resolution | 2-4 weeks | Immune response, healing | Crusts, gradual resolution, pain decreases |
| Postherpetic neuralgia | > 90 days | Permanent neural damage, sensitization | Chronic neuropathic pain, allodynia, hyperalgesia |
Symptoms
Herpes zoster has a characteristic clinical presentation: unilateral pain followed by vesicular eruption in a band, restricted to a dermatome. Pain frequently precedes lesions by 1-5 days, sometimes confused with other conditions (myocardial infarction, renal colic, appendicitis).
Clinical Manifestations
- 01
Unilateral neuropathic pain in a band
Acute, burning, or lancinating pain restricted to a dermatome. May be severe — many patients describe it as the worst pain ever experienced. Precedes cutaneous lesions by 48-72 hours.
- 02
Grouped vesicles on erythematous base
Characteristic eruption: clear-fluid vesicles on a red base, grouped in a unilateral band. Do not cross the midline. Evolve to pustules and crusts in 7-10 days.
- 03
Hyperesthesia and allodynia
Skin of the affected dermatome becomes hypersensitive to touch. Even light contact with clothing can cause intense pain (allodynia). Reflects neural-fiber sensitization.
- 04
Systemic symptoms
Low-grade fever, malaise, headache, and fatigue may accompany the eruption, especially in older adults and the immunosuppressed. Cutaneous dissemination > 2 dermatomes indicates immunosuppression.
- 05
Ophthalmic involvement (V1)
Ophthalmic herpes zoster (V1 trigeminal branch) affects 10-20% of cases. May cause keratitis, uveitis, and visual loss. Hutchinson sign (vesicles on the nose tip) indicates ocular involvement.
- 06
Postherpetic neuralgia
Pain persisting more than 90 days after the eruption. Manifests as constant burning pain, paroxysmal lancinating pain, and intense allodynia. May be disabling and resistant to treatment.
Diagnosis
The diagnosis of herpes zoster is predominantly clinical. The unilateral dermatomal distribution of vesicles is virtually pathognomonic. Laboratory tests are reserved for atypical presentations, immunosuppressed patients, and the prodromal phase (before lesions).
🏥Diagnosis of Herpes Zoster
Fonte: AAD and CDC Guidelines
Clinical Diagnosis
- 1.Unilateral pain preceding or accompanying dermatomal vesicular eruption
- 2.Grouped vesicles on an erythematous base, in a band, not crossing the midline
- 3.History of chickenpox or exposure to VZV
- 4.Temporal evolution: prodrome -> vesicles -> pustules -> crusts
Laboratory Confirmation (If Necessary)
- 1.PCR for VZV: gold standard, sensitivity > 95%, results in hours
- 2.Direct immunofluorescence: vesicle scraping, rapid result
- 3.Tzanck test: multinucleated giant cells, low specificity
- 4.Serology: limited utility in the acute phase
Differential Diagnosis
- 1.Zosteriform herpes simplex
- 2.Contact dermatitis in linear distribution
- 3.Zoster sine herpete (pain without lesions — difficult diagnosis)
- 4.Prodromal phase: myocardial infarction, renal colic, biliary colic
DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
Trigeminal Neuralgia (Zoster Sine Herpete)
- Pain in a dermatomal band without vesicles
- Zoster sine herpete (no eruption)
- Unilateral electric-shock trigeminal pain
- Follow-up without definitive diagnosis
Diagnostic Tests
- VZV PCR in saliva or blood
- VZV serology (acute IgM)
- Cranial MRI for trigeminal lesion
Acupuncture is effective for both trigeminal neuralgia and postherpetic neuralgia.
Contact Dermatitis
- Bilateral or non-dermatomal vesicles
- No prodromal pain
- Predominant pruritus
- Identifiable allergen exposure
Diagnostic Tests
- Distribution of lesions (non-dermatomal)
- Allergic patch test
- Response to topical corticosteroid
Bullous Impetigo
- Superficial bullae with yellow exudate
- More frequent in children
- No dermatomal distribution
- No intense pain
Diagnostic Tests
- Swab culture of lesions
- Gram-positive content
- Response to topical antibiotic
Cellulitis
- Diffuse erythema without vesicles
- Local warmth and edema
- Cutaneous portal of entry
- No dermatomal distribution
- Cellulitis in facial dermatome: rule out inadequately treated ophthalmic zoster
Diagnostic Tests
- Clinical: CBC and CRP
- Response to systemic antibiotic therapy
Erysipelas
- Erythema with raised, well-defined borders
- High fever
- Rapid progression
- More frequent in lower extremities
Diagnostic Tests
- Clinical
- CBC (leukocytosis)
- ASO and CRP
- Swab culture
Zoster Sine Herpete: Pain Without Eruption
Zoster sine herpete — herpes zoster without cutaneous eruption — is frequently underdiagnosed. The virus reactivates in ganglia and causes dermatomal neuropathic pain without visible vesicles. It can be confused with trigeminal neuralgia, intercostalgia, acute abdominal pain, or low back pain, depending on the affected dermatome. PCR for VZV in saliva or blood, plus serology with IgM, confirm the diagnosis.
Allergic contact dermatitis can mimic herpes zoster — especially after exposure to plants (Rhus) or metals — with linear vesicles. Non-dermatomal distribution, predominant pruritus, and absence of intense prodromal pain make the distinction. Patch testing confirms the allergen.
Ophthalmic Herpes Zoster: An Emergency Not to Be Missed
Vesicles on the nose (Hutchinson sign — involvement of the nasociliary branch of the ophthalmic nerve) indicate high risk of ocular involvement. Ophthalmic herpes zoster can cause keratitis, uveitis, and permanent visual loss. It requires urgent ophthalmologic referral and systemic antiviral at maximum dose. Acupuncture can serve as adjuvant to antiviral treatment for pain control and neuralgia prevention.
The main sequela of herpes zoster is postherpetic neuralgia (PHN) — dermatomal pain persisting more than 90 days after the eruption. It occurs in 10-20% of patients, with risk rising significantly after age 60. Studies suggest acupuncture can contribute to pain control in PHN as adjuvant to pharmacologic treatment, though the available literature is still of limited methodologic quality.
Treatment
Treatment of herpes zoster has two objectives: controlling the acute infection and preventing postherpetic neuralgia. Early initiation of antiviral therapy (ideally within 72 hours) is fundamental for both objectives.
Oral Antiviral
Start ≤ 72h — 7 days of treatmentValacyclovir 1000 mg three times daily or famciclovir 500 mg three times daily for 7 days. Acyclovir 800 mg five times daily is an alternative. Reduces lesion duration, acute-pain intensity, and PHN risk. Indicated in patients > 50 years, intense pain, extensive or facial involvement.
Acute Phase Analgesia
From the onset of symptomsAcetaminophen and NSAIDs for mild pain. Tramadol or weak opioids for moderate pain. Early gabapentin/pregabalin can reduce PHN risk. Regional nerve block in refractory pain. Adequate analgesia in the acute phase is protective against PHN.
Treatment of Postherpetic Neuralgia
If pain persists > 90 daysGabapentin (1200-3600 mg/day) or pregabalin (150-600 mg/day): first line. Tricyclic antidepressants (amitriptyline, nortriptyline). Topical lidocaine 5% patch. Topical capsaicin 8% (patch). Opioids in refractory cases.
Prevention — Vaccination
Adults ≥ 50 yearsShingrix (recombinant adjuvanted vaccine): 2 doses, 2-6 months apart. Efficacy > 90% in preventing herpes zoster and > 85% against PHN. Indicated even for those who have had herpes zoster. Also indicated in immunosuppressed individuals.
Acupuncture as Treatment
Acupuncture has solid evidence in both the acute phase of herpes zoster and in postherpetic neuralgia. In the acute phase, it acts on the modulation of nociceptive and neuropathic pain and can reduce neurogenic inflammation. In PHN, it modulates central sensitization and ectopic neural activity.
Needling around the lesions ("circling the dragon") is traditionally used in the acute phase, combined with distal points such as LI-4, LR-3, and local points along the meridian of the affected dermatome. Electroacupuncture at the corresponding paravertebral points modulates afferent input at the segmental level.
In PHN, acupuncture promotes release of endogenous opioids (enkephalins, dynorphins) that modulate altered nociceptive pathways. Electroacupuncture at alternating frequencies (2/100 Hz) activates different opioid-receptor subtypes, optimizing analgesia. Neuroimaging studies confirm modulation of pain-processing brain áreas.
Prognosis
Acute herpes zoster resolves in 2-4 weeks in most immunocompetent patients. PHN is the most feared complication: it affects 10-20% of patients, with increased risk in older adults (> 50% of patients > 85 years not treated early).
PHN can be disabling and resistant to treatment, but most cases improve gradually over months to years. Early antiviral therapy, adequate analgesia in the acute phase, and early acupuncture are the best strategies to prevent chronicity.
Myths and Facts
Myth vs. Fact
Herpes zoster is contagious like chickenpox.
Herpes zoster is not transmitted as zoster. However, vesicle fluid contains virus and can cause chickenpox in people who have never had chickenpox or been vaccinated. Contagion requires direct contact with open lesions.
Myth vs. Fact
If zoster 'closes the circuit' around the body, it is fatal.
This is a popular myth without medical basis. Unilateral herpes zoster is the rule. Bilateral or generalized dissemination is rare and occurs in severe immunosuppression, but is not more lethal because it 'closes the circuit' — it indicates that immunity is compromised and requires intensive treatment.
Myth vs. Fact
Anyone who has had zoster does not need the vaccine.
Herpes-zoster recurrence occurs in 5-10% of cases. The Shingrix vaccine is recommended even for those who have had herpes zoster, since it significantly reduces the risk of recurrence and of PHN in a future episode.
When to Seek Help
Frequently Asked Questions about Herpes Zoster
The virus can be transmitted to people without chickenpox immunity (unvaccinated or who never had chickenpox) through contact with vesicle fluid — causing chickenpox, not zoster. It is not airborne. People with active zoster should avoid contact with susceptible pregnant women, newborns, and the immunosuppressed.
It is the most common complication of herpes zoster — dermatomal pain persisting more than 90 days after the cutaneous eruption. It affects 10-20% of patients, with risk rising dramatically after age 60 (up to 40% in those over 70). Patients frequently describe the pain as constant burning, electric shocks, or allodynia. Acupuncture is an option as adjuvant in multimodal pain management, though the evidence remains heterogeneous and does not replace first-line pharmacologic treatment.
Shingrix is recommended for all adults from age 50, regardless of prior zoster, and for the immunosuppressed from age 18. It is the most effective vaccine against zoster (efficacy 90%+) and against postherpetic neuralgia. Availability and coverage vary by country.
Antivirals (acyclovir, valacyclovir, famciclovir) are most effective when started within the first 72 hours of vesicle onset. They reduce eruption duration, acute-pain severity, and, primarily, postherpetic-neuralgia risk. After 72 hours, they may still benefit severe cases or at-risk dermatomes (eye, ear).
As an adjuvant to standard antiviral treatment, acupuncture can contribute to acute-phase pain relief and is an option in postherpetic-neuralgia management. The evidence is heterogeneous — part of the literature is Asian in origin with methodologic limitations — and acupuncture does not replace early antiviral (≤72h) or first-line drugs for PHN. The decision should be individualized with the physician.
Yes. Ophthalmic zoster (V1 trigeminal branch) affects 10-25% of head-zoster cases. It can cause keratitis, uveitis, and, without treatment, permanent visual loss. The Hutchinson sign (vesicle on the nose tip) indicates nasociliary-branch involvement and high ocular risk. Seek an ophthalmologist urgently.
Yes, though uncommon. Herpes-zoster recurrence (in the same or a different dermatome) occurs in 1-6% of patients, especially the immunosuppressed. Each episode can be treated with antiviral. Shingrix vaccination is recommended even for those who have had zoster — it reduces recurrence risk.
Both are herpesviruses, but different. Herpes simplex (HSV-1 and HSV-2) causes recurrent lesions on lips (HSV-1) or genitals (HSV-2). Herpes zoster (VZV) causes a unilateral dermatomal-band eruption, generally on the trunk, with intense pain — and occurs in people who have previously had chickenpox.
Yes. Patients with HIV, hematologic malignancies, transplant recipients, or those on immunosuppressants have an increased risk of disseminated zoster, VZV encephalitis, severe ophthalmic zoster, and severe postherpetic neuralgia. In these patients, antiviral should be started with a lower threshold of suspicion and may be indicated intravenously.
Acupuncture in the acute phase of zoster modulates the inflammatory response in the dorsal ganglion, reduces central and peripheral sensitization, and stimulates regeneration of injured nerve fibers. Some observational studies and trials of heterogeneous quality suggest that adjuvant acupuncture in the first 72 hours may reduce acute-pain intensity; the preventive effect on PHN specifically remains uncertain and unconfirmed in high-quality trials.
Related Reading
Deepen your knowledge with related articles