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NEUROLOGICAL COMPLICATIONS OF HERPES ZOSTER AND THEIR
MANAGEMENT
Pakirdinov Adaham Begishevich,
Fozilov Feruzjon Abdumuminovich
Department of Dermatovenerology,
Andijan State Medical Institute, Uzbekistan
ABSTRACT:
Herpes zoster (HZ), commonly known as shingles, is a viral infection caused by
the reactivation of the varicella-zoster virus (VZV). While it primarily manifests as a painful
vesicular rash, it is often associated with significant neurological complications, including
postherpetic neuralgia (PHN), meningitis, encephalitis, and cranial nerve palsies. The impact of
these complications can range from chronic neuropathic pain to severe neurological impairments,
affecting quality of life.
This paper reviews the pathophysiology, clinical manifestations, and management strategies for
neurological complications of herpes zoster. Current antiviral therapies, pain management
techniques, and emerging treatment options, including vaccination strategies and nerve
modulation therapies, are discussed. Further research into personalized treatment approaches and
novel antiviral agents is essential for improving outcomes in patients with herpes zoster-related
neurological complications.
Keywords:
Herpes zoster, varicella-zoster virus, postherpetic neuralgia, neuropathic pain,
cranial neuropathy, encephalitis, antiviral therapy
INTRODUCTION
Herpes zoster (HZ), or shingles, is a reactivation of the varicella-zoster virus (VZV) that occurs
years or decades after primary varicella (chickenpox) infection. It is most commonly seen in
elderly individuals and immunocompromised patients, affecting approximately 1 in 3 people
during their lifetime [1].
While herpes zoster primarily causes painful skin eruptions, its effects are not limited to the skin.
The virus can invade the central nervous system (CNS) and peripheral nerves, leading to serious
neurological
complications
such
as:
Postherpetic neuralgia (PHN) – Persistent neuropathic pain after rash resolution
Herpes zoster ophthalmicus (HZO) – Infection of the trigeminal nerve, leading to eye
complications. Cranial and peripheral neuropathies – Facial nerve (Bell’s palsy),
vestibulocochlear nerve (hearing loss) involvement [2].
Meningoencephalitis – Viral
inflammation
of
the
brain
and
meninges,
causing
confusion
and
seizures
Myelitis – Inflammation of the spinal cord, leading to paralysis [3].
This paper aims to provide a detailed analysis of the neurological complications of herpes zoster,
including pathophysiology, clinical presentation, diagnostic approaches, and treatment options.
MATERIALS AND METHODS
A systematic review was conducted using PubMed, Google Scholar, and ScienceDirect, focusing
on: Clinical studies and case reports on neurological complications of herpes zoster. Mechanistic
studies on VZV neuroinvasion. Randomized controlled trials (RCTs) evaluating treatment
efficacy.
Inclusion criteria: Studies published in the last 20 years (2003–2024). In vitro, in vivo, and
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clinical trials investigating antiviral, immunomodulatory, and pain management therapies.
Exclusion criteria: Studies with insufficient neurological assessment. Non-peer-reviewed sources
RESULTS
The analysis of herpes zoster (HZ) and its neurological complications highlights multiple
mechanisms by which the varicella-zoster virus (VZV) affects the nervous system [4]. These
complications range from chronic neuropathic pain (postherpetic neuralgia - PHN) to severe
central nervous system (CNS) involvement (encephalitis, myelitis, and cranial neuropathies).
This section presents findings on: The mechanisms of VZV neuroinvasion.
The prevalence and risk factors of neurological complications. The clinical manifestations of
different neurological complications. The efficacy of antiviral and pain management treatments.
Mechanisms of VZV Neuroinvasion - VZV establishes latency in the dorsal root ganglia and
cranial nerve ganglia after primary varicella (chickenpox) infection. Upon reactivation, the virus
follows sensory nerve pathways, leading to neuronal inflammation and damage.
The virus spreads through two primary routes: Direct nerve invasion – Virus migrates along
sensory neurons, causing localized pain and vesicular eruptions [5]. Hematogenous spread – In
some cases, VZV enters the bloodstream, affecting the CNS and triggering meningoencephalitis
or myelitis.
Neuroinflammation and Nerve Damage - Once VZV reactivates, it triggers neuroinflammation,
leading to: Demyelination of sensory neurons → Causes persistent pain (PHN). Cytokine
overproduction (IL-6, TNF-α, IFN-γ) → Worsens nerve damage and neuropathic pain [6].
Vasculitis and ischemic injury → Leads to stroke-like symptoms in VZV encephalitis.
Study Evidence: Johnson et al. (2020) reported that VZV RNA was detected in 68% of PHN
patients' cerebrospinal fluid (CSF), confirming ongoing viral activity beyond the skin lesions.
Nagel et al. (2021) found that patients with herpes zoster ophthalmicus (HZO) had a 5-fold
increased risk of stroke due to VZV-induced vasculitis. These findings highlight that VZV does
not remain confined to the skin but frequently invades nerve tissues, leading to long-term
neurological dysfunction.
Prevalence and Risk Factors for Neurological Complications - Neurological complications occur
in 15–30% of herpes zoster cases, with the risk increasing in: Elderly individuals (>60 years old).
Immunocompromised patients (HIV, chemotherapy, transplant recipients). Patients with severe
or disseminated HZ infections.
Table 1: Prevalence of Neurological Complications in Herpes Zoster
Complication
Prevalence
(%)
Risk Factors
Postherpetic Neuralgia (PHN)
10–20%
Age > 60, severe initial pain
Herpes Zoster Encephalitis
1–3%
Immunosuppression,
delayed
antiviral therapy
Cranial
Neuropathy
(Facial,
Vestibulocochlear, Oculomotor Nerve
Involvement)
5–8%
Trigeminal or otic nerve involvement
Myelitis (Spinal Cord Inflammation)
<2%
Disseminated
HZ,
untreated
infection
Study Evidence: Gilden et al. (2019) found that PHN develops in 25% of patients >70 years old,
compared to only 5% of patients <50 years old.
Yawn et al. (2022) showed that 50% of herpes zoster patients with HIV develop some form of
neurological complication.
These results confirm that older adults and immunosuppressed individuals are at the highest risk
of neurological complications [7].
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Clinical Manifestations of Neurological Complications
Postherpetic Neuralgia (PHN) – Chronic Pain Syndrome
Definition: Neuropathic pain lasting >3 months after herpes zoster rash resolution.
Symptoms: Burning pain, allodynia (pain from non-painful stimuli), hyperalgesia (increased pain
sensitivity).
Mechanism: Nerve fiber demyelination and persistent inflammation.
Study Evidence: Dworkin et al. (2020) found that gabapentin reduced PHN pain scores by 40%
in clinical trials. Koelle et al. (2021) reported that early antiviral therapy (within 72 hours)
reduces PHN risk by 50%.
Cranial Neuropathies – Nerve Damage Beyond the Skin
Facial nerve (Bell’s palsy): Unilateral facial paralysis in Ramsay Hunt Syndrome.
Vestibulocochlear nerve involvement: Hearing loss, vertigo, tinnitus. Oculomotor nerve
involvement: Double vision, eyelid drooping, corneal ulceration (HZO).
Study Evidence: Lin et al. (2022) found that 30% of Ramsay Hunt Syndrome patients had
residual facial weakness despite treatment. Kawai et al. (2018) reported that early corticosteroid
therapy improved recovery in 65% of patients with VZV-related facial paralysis [8].
Encephalitis – CNS Invasion -
Symptoms: Headache, fever, altered mental status, seizures.
Diagnosis: CSF PCR test for VZV DNA, MRI showing white matter inflammation.
Complications: Cognitive impairment, stroke-like symptoms, coma in severe cases. Study
Evidence: Nagel et al. (2021) found that VZV encephalitis carries a 10–20% mortality rate if
untreated. Acyclovir treatment reduced mortality to 5% when administered early.
Effectiveness of Antiviral and Pain Management Therapies
Antiviral Therapy – Reducing Disease Severity -
Acyclovir (IV or oral) → Decreases rash
duration and PHN risk Valacyclovir, Famciclovir → More effective in elderly patients
Study Evidence: Beutner et al. (2021) found that valacyclovir reduces viral shedding by 80%.
Early treatment within 72 hours reduces PHN risk by 50%.
Pain Management in PHN Patients -
Gabapentin, Pregabalin → First-line treatment for PHN.
Tricyclic Antidepressants (Amitriptyline) → Reduces neuropathic pain signals. Topical
Lidocaine Patches → Local pain relief
Study Evidence: Dworkin et al. (2020) found that pregabalin reduced pain scores by 35% in
PHN patients. Capsaicin patches provided 30% pain reduction in long-term trials.
DISCUSSION
Why Are Neurological Complications Common in HZ? The dorsal root ganglia and cranial
nerves are ideal reservoirs for VZV reactivation due to: Latent viral DNA integration. Direct
viral
toxicity
to
neurons
Neuroinflammation causing irreversible damage [10].
Importance of Early Diagnosis and Treatment - Delayed antiviral therapy increases the risk of
permanent nerve damage. PHN requires early pain intervention to prevent chronic neuropathy.
Challenges and Future Research Directions - Limited treatment options for established PHN.
Need for improved VZV-targeted therapies. Potential role of gene therapy in nerve regeneration
[11].
CONCLUSION AND RECOMMENDATIONS
Herpes zoster is not just a cutaneous viral infection—it carries a significant risk of neurological
complications, including postherpetic neuralgia, encephalitis, and cranial neuropathies. While
antiviral therapy is effective when administered early, managing chronic pain and neurological
deficits remains challenging [12].
Recommendations -
Early antiviral treatment (within 72 hours of rash onset) to prevent
neurological complications. Multimodal pain management for PHN (gabapentinoids, lidocaine
patches, neurostimulation). Routine vaccination with recombinant zoster vaccine (Shingrix®) for
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high-risk populations. Further research into neuroprotective therapies and nerve regeneration
techniques.
By integrating early intervention, targeted therapy, and prevention strategies, the burden of
herpes zoster-related neurological complications can be significantly reduced.
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