Varicella-Zoster Virus Myelitis:

MRI Diagnosis, CT Imaging Findings, Differential Diagnosis, and Emergency Radiology Interpretation

Introduction

A 74-year-old woman arrives at the emergency department with an unusual complaint. Over the past two weeks, she has experienced progressively worsening numbness in both lower extremities. She has metastatic breast cancer but has remained neurologically stable until recently. During the physical examination, clinicians notice something that immediately changes the diagnostic direction—a painful, linear vesicular rash extending from the right buttock to the foot.

Could this be spinal metastasis?

Acute spinal cord infarction?

Multiple sclerosis?

Or something much rarer?

The answer lies in one of the most fascinating yet easily overlooked neurological complications of Varicella-Zoster Virus (VZV)—Varicella-Zoster Virus Myelitis.

Although herpes zoster ("shingles") is common worldwide, spinal cord involvement occurs in only a tiny fraction of patients. Because symptoms often resemble spinal tumors, ischemia, autoimmune disease, or demyelinating disorders, diagnosis is frequently delayed. In emergency medicine, such delays can result in irreversible neurological deficits.

For radiologists, neurologists, emergency physicians, and medical imaging specialists, recognizing the subtle MRI appearance of VZV myelitis is critical. While MRI is the gold standard, CT imaging still plays an important complementary role by excluding compressive lesions, fractures, hemorrhage, and metastatic disease during the initial emergency workup.

This article presents an in-depth review of VZV myelitis through the lens of diagnostic radiology, using a real clinical case and integrating the latest evidence from neuroradiology, infectious disease, and spinal imaging literature. It is designed for healthcare professionals while remaining accessible to medical students and informed readers.

A Real Clinical Story: When a Skin Rash Revealed a Hidden Spinal Cord Disease

The patient was a 74-year-old woman with metastatic breast cancer who presented with two weeks of progressive lower-extremity sensory loss. Neurological symptoms had gradually worsened, raising concern for metastatic spinal cord compression.

However, physical examination revealed an important clue: a linear vesicular eruption on a hemorrhagic base extending from the right buttock to the foot, corresponding to a dermatomal distribution.

This seemingly dermatologic finding dramatically shifted the diagnostic pathway toward a viral etiology.

Subsequent MRI demonstrated characteristic abnormalities involving the right dorsal spinal cord, ultimately leading to the diagnosis of Varicella-Zoster Virus myelitis.

This case highlights one of the most important principles in radiology:

Imaging findings are most powerful when interpreted in the context of clinical information.

A spinal MRI without knowledge of the dermatomal rash might easily be mistaken for inflammatory demyelination, ischemia, or even metastatic disease.

What Is Varicella-Zoster Virus Myelitis?

Varicella-Zoster Virus (VZV) belongs to the alpha-herpesvirus family and infects only humans.

Primary infection causes chickenpox (varicella), which usually occurs during childhood.

Following recovery, the virus does not disappear.

Instead, it establishes lifelong latency inside:

dorsal root ganglia
cranial nerve ganglia
autonomic ganglia
enteric nervous system

Years—or even decades—later, declining cell-mediated immunity allows viral reactivation.

The most familiar manifestation is herpes zoster (shingles).

However, in rare situations, viral spread extends beyond peripheral nerves into the central nervous system, producing:

meningitis
encephalitis
vasculopathy
cerebellitis
retinal necrosis
transverse myelitis

Among these complications, VZV myelitis is exceptionally uncommon but potentially devastating.

Why Does the Virus Attack the Spinal Cord?

Researchers now believe VZV myelitis develops through multiple overlapping mechanisms.

Rather than a single disease process, it represents a combination of:

1. Direct Viral Infection

The virus may spread from the dorsal root ganglion directly into the spinal cord.

Because the dorsal sensory roots serve as the point of entry, dorsal column involvement is commonly observed.

This explains why many patients initially experience:

sensory abnormalities
neuropathic pain
proprioceptive dysfunction

before motor weakness develops.

2. Immune-Mediated Inflammation

In some patients, viral antigens trigger an exaggerated immune response.

Inflammatory cytokines lead to:

demyelination
edema
axonal injury
secondary neuronal dysfunction

This mechanism resembles autoimmune transverse myelitis and contributes to the variability of MRI findings.

3. Viral Vasculopathy

Perhaps the most intriguing mechanism involves vascular injury.

VZV is well known for infecting arterial walls.

The resulting vasculitis can produce:

ischemia
infarction
hemorrhage
spinal cord hypoperfusion

Some patients demonstrate diffusion restriction on MRI, strongly suggesting ischemic injury rather than purely inflammatory disease.

This vascular hypothesis explains why imaging appearances differ dramatically among reported cases.

Epidemiology

Although shingles affects millions of individuals worldwide every year, spinal cord involvement remains remarkably rare.

Published studies estimate that transverse myelitis develops in only approximately 0.3% of herpes zoster cases.

The condition is predominantly observed in:

adults over 60 years
cancer patients
transplant recipients
HIV-positive individuals
patients receiving chemotherapy
chronic corticosteroid users
individuals with impaired T-cell immunity

Interestingly, VZV myelitis has also been reported in otherwise healthy adults, indicating that immunocompetence does not eliminate risk.

Risk Factors Every Clinician Should Recognize

Several clinical features substantially increase suspicion.

Advanced age

Cell-mediated immunity naturally declines with aging.

Malignancy

Patients with hematologic or solid-organ cancers frequently experience viral reactivation.

The presented patient had metastatic breast cancer, representing a classic high-risk profile.

Immunosuppressive Therapy

Examples include:

chemotherapy
biologic agents
anti-TNF medications
corticosteroids
post-transplant immunosuppression

Organ Transplantation

Solid organ transplant recipients have a markedly increased risk of disseminated VZV infection.

HIV Infection

Reduced CD4 counts correlate strongly with neurological complications.

Clinical Presentation

Unlike ordinary shingles, VZV myelitis extends beyond the skin.

Patients often present with a combination of dermatologic and neurological symptoms.

Typical manifestations include:

Pain

Neuropathic pain usually precedes neurological deficits.

Pain often follows a dermatomal distribution.

Vesicular Rash

The classic shingles eruption remains one of the strongest diagnostic clues.

However, approximately 10% of patients may develop neurological disease without obvious skin lesions (zoster sine herpete), making diagnosis much more challenging.

Sensory Dysfunction

Common symptoms include:

numbness
tingling
proprioceptive loss
impaired vibration sensation

Because dorsal columns are frequently affected, patients often complain that they "cannot feel where their legs are."

Weakness

Motor deficits range from mild weakness to complete paraplegia.

Bladder Dysfunction

Urinary retention may occur in severe transverse myelitis.

Gait Instability

Loss of dorsal column function causes sensory ataxia, particularly in dark environments when visual compensation is unavailable.

Why Early Recognition Matters

The interval between symptom onset and antiviral treatment strongly influences neurological recovery.

Delayed diagnosis increases the risk of:

irreversible axonal injury
spinal cord infarction
chronic neuropathic pain
permanent disability

Therefore, emergency physicians should maintain a high index of suspicion whenever the following triad is present:

shingles rash
acute myelopathy
abnormal spinal MRI

Even when MRI findings appear subtle, the combination of clinical history and imaging should prompt urgent cerebrospinal fluid analysis and initiation of intravenous antiviral therapy rather than waiting for confirmatory laboratory results.

Key Takeaways

Varicella-Zoster Virus myelitis is a rare but serious neurological complication of herpes zoster.
Older adults, cancer patients, and immunocompromised individuals are at highest risk.
Dermatomal vesicular rash combined with progressive myelopathy is a crucial diagnostic clue.
MRI is the imaging modality of choice, while CT primarily helps exclude compressive or osseous pathology in emergency settings.
Early diagnosis and prompt antiviral treatment significantly improve neurological outcomes.

MRI Diagnosis of Varicella-Zoster Virus Myelitis

The Radiologist's Perspective

One of the greatest challenges in diagnosing Varicella-Zoster Virus (VZV) myelitis is that its imaging appearance is highly variable. Unlike classic demyelinating diseases, which often exhibit predictable lesion patterns, VZV myelitis can mimic inflammatory, ischemic, infectious, neoplastic, and vascular disorders.

For this reason, radiologists should never interpret spinal MRI findings in isolation. The combination of clinical history, dermatologic examination, laboratory testing, and imaging remains the cornerstone of accurate diagnosis.

Fortunately, several MRI characteristics can substantially increase diagnostic confidence.

Why MRI Is the Gold Standard

Among all imaging modalities, magnetic resonance imaging (MRI) provides the highest sensitivity for evaluating intrinsic spinal cord disease.

MRI offers several advantages:

Excellent soft-tissue contrast
Detection of cord edema
Identification of inflammatory lesions
Evaluation of enhancement patterns
Assessment of diffusion restriction
Visualization of longitudinal lesion extent

In contrast, CT has limited sensitivity for intramedullary abnormalities because of poor spinal cord soft-tissue contrast.

Therefore:

MRI answers the question "What is happening inside the spinal cord?" whereas CT primarily answers "Is something compressing the spinal cord?"

MRI Sequences Every Radiologist Should Review

A comprehensive spinal MRI protocol should include:

Sequence	Diagnostic Value
Sagittal T1-weighted	Cord anatomy, hemorrhage, chronic change
Sagittal T2-weighted	Cord edema, inflammation
Axial T2-weighted	Lesion localization
STIR	Cord edema
Post-contrast T1	Blood-spinal cord barrier disruption
Diffusion-weighted imaging (if available)	Ischemia and infarction

Among these, T2-weighted imaging remains the most sensitive sequence for detecting VZV myelitis.

Figure 1. Sagittal T1-Weighted MRI

Radiologic Interpretation

The lesion demonstrates:

focal T1 hypointensity
no evidence of hemorrhage
preserved overall spinal alignment
no epidural mass
no vertebral metastatic compression

The absence of abnormal enhancement suggests that active disruption of the blood-spinal cord barrier is minimal at this stage. The imaging appearance favors inflammatory myelitis rather than metastatic disease.

Why This Figure Matters

In elderly oncology patients, spinal metastasis is often the leading diagnostic concern.

This image immediately helps exclude:

metastatic epidural compression
vertebral collapse
epidural abscess
large intramedullary tumor

Instead, it points toward an intrinsic spinal cord abnormality.

Figure 2. Sagittal T2-Weighted MRI

This sequence contains the most important diagnostic information.

The lesion appears as:

longitudinal T2 hyperintensity
dorsal cord predominance
discontinuous ("moth-eaten") appearance
intervening normal spinal cord
absence of significant cord expansion

This "moth-eaten" morphology has been described as one of the characteristic MRI appearances of VZV myelitis.

The "Moth-Eaten" Appearance

Perhaps the most fascinating imaging feature of VZV myelitis is the so-called moth-eaten appearance.

Rather than forming one continuous lesion, multiple focal abnormalities are scattered longitudinally within the dorsal spinal cord.

Normal spinal cord tissue remains between lesions.

This differs substantially from:

neuromyelitis optica
spinal infarction
multiple sclerosis

where lesions usually demonstrate more continuous involvement.

The moth-eaten pattern reflects multifocal viral injury involving:

dorsal root entry zones
inflammatory spread
vascular injury

Figure 3. Axial T2-Weighted MRI

Axial imaging reveals one of the most diagnostically valuable observations.

Instead of involving the entire spinal cord, the lesion remains confined to the:

right dorsal column
posterior sensory pathways

Importantly:

anterior horn cells remain intact
ventral cord remains preserved
lateral corticospinal tracts are largely spared

These findings correlate closely with the patient's predominant sensory symptoms.

The unilateral dorsal distribution also explains the patient's impaired proprioception and sensory loss rather than profound motor paralysis.

MRI Signal Characteristics

The reported MRI spectrum of VZV myelitis includes:

T2-weighted imaging

Typical finding:

hyperintense lesion

Represents:

edema
inflammation
demyelination

T1-weighted imaging

Usually demonstrates:

hypointensity
preserved cord contour

Contrast Enhancement

Highly variable.

Possible appearances include:

no enhancement
punctate enhancement
patchy enhancement
ring enhancement
diffuse enhancement

A normal post-contrast study does not exclude VZV myelitis.

Diffusion Restriction

Occasionally present.

When observed, diffusion restriction suggests:

ischemia
viral vasculopathy
spinal cord infarction

This supports the vascular hypothesis of VZV-related neurological injury.

Brain MRI Findings

Interestingly, this patient also demonstrated:

FLAIR hyperintensity
diffusion restriction
right dorsal medullary involvement

These findings indicate that viral spread extended beyond the spinal cord into the lower brainstem, emphasizing the importance of imaging the neuraxis when neurological deficits extend beyond a single spinal level.

What About CT?

Because many emergency departments perform CT before MRI, clinicians frequently ask:

Can CT diagnose Varicella-Zoster Virus myelitis?

The answer is generally no.

CT has poor sensitivity for detecting intramedullary spinal cord inflammation.

However, CT remains extremely valuable in the emergency diagnostic pathway.

Important Roles of CT

CT is useful for excluding:

vertebral fracture
spinal metastasis
epidural hematoma
calcified disc herniation
severe cervical spondylosis
destructive bone lesions
spinal instability

Therefore, although CT rarely visualizes VZV myelitis directly, it narrows the differential diagnosis and identifies conditions requiring urgent surgical intervention.

CT Limitations

CT cannot reliably demonstrate:

cord edema
demyelination
viral inflammation
dorsal column lesions
diffusion restriction
subtle intramedullary abnormalities

Consequently, a normal CT should never reassure clinicians when clinical suspicion for myelitis is high.

Urgent MRI remains mandatory.

Imaging Pearls for Radiologists

When reviewing spinal MRI, several clues should immediately raise suspicion for VZV myelitis:

✓ Elderly or immunocompromised patient

✓ Dermatomal vesicular rash

✓ Sensory symptoms predominating over motor deficits

✓ Dorsal spinal cord lesions

✓ Longitudinal discontinuous T2 hyperintensity

✓ Minimal or absent enhancement

✓ Associated dorsal medullary lesion

✓ Positive cerebrospinal fluid VZV PCR

No single feature is diagnostic, but together they form a highly suggestive imaging pattern.

Differential Diagnosis

The dorsal spinal cord pattern has a broad differential diagnosis. Correlation with the clinical presentation, laboratory studies, and MRI characteristics is essential.

Disease	Typical MRI Findings	Distinguishing Features
Varicella-Zoster Virus myelitis	Dorsal T2 hyperintensity, moth-eaten lesions	Dermatomal rash, VZV PCR positive
Vitamin B12 deficiency	Symmetric posterior column involvement	Macrocytic anemia, chronic course
Multiple sclerosis	Small peripheral plaques	Younger adults with brain lesions
Neuromyelitis optica	Longitudinally extensive lesions	Aquaporin-4 antibody positive
Tabes dorsalis	Posterior column atrophy	Positive syphilis serology
Cervical spondylotic myelopathy	Compression with cord signal change	Degenerative stenosis
HIV vacuolar myelopathy	Symmetric posterior column lesions	Advanced HIV infection
Spinal cord infarction	Diffusion restriction, anterior cord	Sudden onset
Intramedullary metastasis	Expansile enhancing lesion	Known systemic malignancy

The uploaded case specifically lists several important differentials, including vitamin B12 deficiency, multiple sclerosis, tabes dorsalis, cervical spondylotic myelopathy, HIV-related myelopathy, Friedreich ataxia, and external compression.

Radiology Reporting Example

A structured report for this case could read:

Findings: Longitudinal multifocal T2 hyperintense, T1 hypointense, non-enhancing lesions involving the right dorsal spinal cord with intervening normal cord, producing a moth-eaten appearance. No significant cord expansion or epidural compression. Additional FLAIR hyperintense lesion with diffusion restriction within the right dorsal medulla.

Impression: Imaging findings are highly suggestive of infectious myelitis. Given the associated dermatomal vesicular rash, Varicella-Zoster Virus myelitis is strongly favored. Recommend cerebrospinal fluid analysis including VZV PCR and intrathecal antibody testing, with prompt initiation of antiviral therapy if clinically appropriate.

Key Takeaways

MRI is the gold-standard imaging modality for VZV myelitis.
Characteristic findings include T2-hyperintense, T1-hypointense dorsal cord lesions with a discontinuous "moth-eaten" appearance.
CT has limited sensitivity for intramedullary disease but is valuable for excluding compressive, traumatic, and osseous pathology in emergency settings.
Correlation with the patient's dermatomal rash and neurological deficits is essential to avoid misdiagnosis.
A structured radiology report can expedite confirmatory CSF testing and early antiviral treatment.

Diagnostic Workflow for Varicella-Zoster Virus Myelitis

From Emergency Department to Definitive Diagnosis

Early diagnosis is the single most important factor influencing neurological recovery in Varicella-Zoster Virus (VZV) myelitis. Because the disease is uncommon and often mimics other causes of acute myelopathy, clinicians must adopt a systematic diagnostic approach that integrates clinical findings, radiologic evaluation, and laboratory confirmation.

A practical workflow is outlined below.

Step 1. Clinical Suspicion

Diagnosis begins with recognizing the characteristic clinical constellation.

Clinicians should suspect VZV myelitis when an adult—particularly an elderly or immunocompromised patient—presents with:

Progressive sensory deficits
Limb weakness
Acute or subacute myelopathy
Dermatomal neuropathic pain
Vesicular rash suggestive of herpes zoster
Bladder or bowel dysfunction

Although the vesicular eruption is an important clue, clinicians must remember that zoster sine herpete (VZV reactivation without a rash) can occur, making the diagnosis considerably more challenging.

Step 2. Emergency Imaging

The first imaging study in many emergency departments is CT.

Emergency CT

CT is valuable for rapidly excluding conditions requiring immediate surgical intervention:

Vertebral fracture
Epidural hematoma
Metastatic compression
Severe cervical spondylosis
Disc extrusion
Epidural abscess

However, CT cannot reliably demonstrate spinal cord inflammation.

Therefore, a normal CT should never delay MRI when clinical suspicion remains high.

MRI

MRI should be obtained as soon as possible.

Typical findings include:

T2 hyperintense spinal cord lesions
T1 hypointense lesions
Dorsal cord predominance
Longitudinal multifocal involvement
Variable enhancement
Possible diffusion restriction
Occasionally associated brainstem abnormalities

The imaging findings in the uploaded case closely match these classic features, with multifocal non-enhancing lesions in the right dorsal spinal cord and an additional dorsal medullary lesion.

Step 3. Cerebrospinal Fluid Examination

Lumbar puncture remains an essential component of the diagnostic workup.

Recommended CSF studies include:

Routine Analysis

White blood cell count
Protein concentration
Glucose
Opening pressure

Typical findings:

Mild lymphocytic pleocytosis
Elevated protein
Normal glucose

Polymerase Chain Reaction (PCR)

PCR for VZV DNA is considered the most specific laboratory test during the early phase of disease.

Advantages include:

Rapid confirmation
High specificity
Useful before antibody production

However, sensitivity decreases later in the disease course.

Intrathecal Antibody Testing

Measurement of:

VZV IgM
VZV IgG

can improve diagnostic sensitivity, particularly when PCR becomes negative.

Combining PCR with antibody testing provides the highest diagnostic yield.

Step 4. Laboratory Evaluation

Routine blood investigations should include:

Complete blood count
Electrolytes
Liver function tests
Renal function
Vitamin B12
HIV testing
Syphilis serology
Autoimmune markers (when indicated)

These studies help exclude alternative causes of transverse myelopathy.

Diagnostic Algorithm

Treatment

Because neurological injury may become irreversible, treatment should begin as soon as VZV myelitis is suspected, even before laboratory confirmation in highly suggestive cases.

Antiviral Therapy

The cornerstone of treatment is intravenous Acyclovir.

Standard regimen

10–15 mg/kg IV every 8 hours
Duration: 10–14 days
Dose adjustment for renal impairment

Acyclovir inhibits viral DNA polymerase, limiting viral replication and reducing further spinal cord injury.

After clinical improvement, some patients transition to oral antiviral agents such as Valacyclovir to complete therapy.

Corticosteroids

The role of corticosteroids remains controversial.

Potential benefits include:

Reduced inflammation
Decreased spinal cord edema
Faster neurological recovery

However, evidence from randomized controlled trials is lacking.

Current practice varies among institutions.

Steroids are often administered after antiviral therapy has been initiated to avoid exacerbating viral replication.

Pain Management

Neuropathic pain may persist long after viral replication has ceased.

Common medications include:

Gabapentin
Pregabalin
Duloxetine
Tricyclic antidepressants

Adequate pain control is important for quality of life and rehabilitation.

Rehabilitation

Many patients require prolonged rehabilitation.

Management may include:

Physical therapy
Occupational therapy
Balance training
Gait rehabilitation
Bladder management
Psychological support

Early rehabilitation improves long-term functional outcomes.

Clinical Pearls for Treatment

✔ Never delay acyclovir while awaiting PCR results when clinical suspicion is high.

✔ MRI abnormalities may persist despite clinical recovery.

✔ Neurological improvement often continues for months after treatment.

✔ Early intervention is associated with better outcomes.

Prognosis

The prognosis of VZV myelitis is highly variable.

Several factors influence recovery.

Favorable Prognostic Factors

Early diagnosis
Prompt antiviral therapy
Immunocompetent status
Mild neurological deficits
Limited MRI involvement
Absence of extensive cord edema

Poor Prognostic Factors

Delayed treatment
Disseminated VZV infection
Severe immunosuppression
Extensive longitudinal spinal cord lesions
Diffusion restriction indicating infarction
Respiratory involvement
Advanced age with significant comorbidities

Expected Clinical Outcomes

Published studies describe a broad spectrum of outcomes.

Complete Recovery

Some patients regain nearly normal neurological function within several months.

Partial Recovery

The most common outcome.

Residual symptoms may include:

Mild sensory loss
Neuropathic pain
Fatigue
Gait imbalance

Severe Disability

A minority develops:

Persistent paraparesis
Neurogenic bladder
Chronic pain
Permanent disability

Mortality

Death is uncommon but may occur in severely immunocompromised individuals with disseminated infection and central nervous system involvement. The uploaded case discussion emphasizes that outcomes range from full recovery in immunocompetent patients to severe complications or death in immunocompromised patients.

Potential Complications

Clinicians should monitor for:

Chronic neuropathic pain
Persistent sensory ataxia
Muscle weakness
Bladder dysfunction
Pressure injuries in immobile patients
Secondary infections
Depression and reduced quality of life

Long-term multidisciplinary follow-up is recommended.

Clinical Practice Pearls

For Radiologists

Carefully evaluate the dorsal spinal cord in patients with sensory-predominant symptoms.
A moth-eaten pattern of discontinuous T2 hyperintensity should raise suspicion for VZV myelitis.
Mention VZV in the differential diagnosis when appropriate, especially if a dermatomal rash is present.

For Emergency Physicians

Do not rely on a normal CT scan to exclude myelitis.
Request an urgent MRI when clinical findings suggest spinal cord involvement.
Initiate empirical antiviral therapy when suspicion is high.

For Neurologists

Combine MRI findings with CSF PCR and intrathecal antibody testing.
Consider VZV even in patients without a visible rash.
Coordinate early rehabilitation to maximize neurological recovery.

Clinical Summary Table

Category	Key Points
Etiology	Reactivation of latent Varicella-Zoster Virus
High-Risk Patients	Older adults, cancer, transplant recipients, immunocompromised
Hallmark MRI Finding	T2 hyperintense dorsal cord lesions with a "moth-eaten" appearance
Role of CT	Excludes compressive and osseous pathology; limited for intramedullary disease
Laboratory Confirmation	CSF VZV PCR and intrathecal IgM/IgG
First-Line Treatment	Intravenous Acyclovir
Adjunct Therapy	Corticosteroids (selected patients), rehabilitation
Outcome	Highly dependent on early diagnosis and treatment

Key Takeaways

Maintain a high index of suspicion for VZV myelitis in older or immunocompromised patients with acute myelopathy and a dermatomal rash.
MRI is essential for diagnosis, while CT serves primarily to exclude compressive pathology.
CSF VZV PCR and antibody testing provide laboratory confirmation and should be obtained promptly.
Early intravenous acyclovir is the cornerstone of treatment and should not be delayed when clinical suspicion is strong.
Long-term outcomes depend on timely diagnosis, immune status, and the extent of spinal cord involvement.

Frequently Asked Questions (FAQ)

1. What is Varicella-Zoster Virus (VZV) myelitis?

Varicella-Zoster Virus (VZV) myelitis is a rare neurological complication of herpes zoster (shingles) in which reactivated VZV infects the spinal cord, leading to inflammation, demyelination, and occasionally ischemic injury. It typically presents with sensory deficits, weakness, neuropathic pain, and bladder dysfunction. Although uncommon, it is considered a neurological emergency because delayed treatment can result in permanent disability.

2. Can CT diagnose VZV myelitis?

No. Conventional CT has very limited sensitivity for detecting intramedullary spinal cord inflammation.

However, CT remains extremely useful in emergency settings because it rapidly excludes:

Vertebral fracture
Epidural hematoma
Metastatic compression
Disc herniation
Severe spinal stenosis

MRI remains the gold standard for evaluating VZV myelitis.

3. Why is MRI superior to CT?

MRI provides excellent soft tissue contrast, allowing visualization of:

Cord edema
Demyelination
Inflammatory lesions
Diffusion restriction
Enhancement patterns

These abnormalities are usually invisible on CT.

4. What is the hallmark MRI appearance?

Although imaging findings vary, one characteristic pattern is the "moth-eaten appearance," characterized by multiple discontinuous T2-hyperintense lesions in the dorsal spinal cord, with normal cord tissue between lesions. This distinctive pattern was demonstrated in the uploaded case.

5. What laboratory tests confirm the diagnosis?

The preferred confirmatory studies include:

Cerebrospinal fluid VZV PCR
Intrathecal VZV IgM
Intrathecal VZV IgG

These should be interpreted together with MRI findings and clinical presentation.

6. What is the first-line treatment?

The standard treatment is:

Intravenous Acyclovir
Early initiation
Supportive care
Rehabilitation

Corticosteroids may be considered in selected patients after antiviral therapy has been started.

7. Is recovery possible?

Yes.

Many immunocompetent patients recover well if treatment begins early.

However, delayed diagnosis or severe immunosuppression may result in:

Persistent weakness
Chronic neuropathic pain
Bladder dysfunction
Permanent disability

Clinical Imaging Pearls

✓ Always inspect the dorsal spinal cord carefully.

✓ A dermatomal vesicular rash should immediately raise suspicion for VZV.

✓ Normal CT does not exclude spinal cord disease.

✓ MRI abnormalities may precede laboratory confirmation.

✓ Do not delay antiviral therapy while awaiting PCR results when clinical suspicion is high.

✓ Always evaluate the brainstem when neurological findings extend beyond one spinal level.

Quiz

Question 1. A 74-year-old woman presents with progressive lower-extremity numbness and a painful vesicular rash involving the right leg. MRI demonstrates multifocal dorsal spinal cord T2 hyperintensity with intervening normal cord. Which diagnosis is most likely?

A. Multiple sclerosis

B. Cervical spondylotic myelopathy

C. Varicella-Zoster Virus myelitis

D. Spinal metastasis

E. Vitamin B12 deficiency

Correct Answer: C. Varicella-Zoster Virus myelitis. Explanation: The dermatomal rash strongly suggests herpes zoster. Combined with the characteristic dorsal cord MRI findings and sensory-predominant neurological deficits, VZV myelitis is the most likely diagnosis.

Question 2. Which imaging modality is considered the gold standard for diagnosing VZV myelitis?

A. Plain radiography

B. CT

C. Ultrasound

D. MRI

E. PET/CT

Correct Answer: D. MRI. Explanation: MRI provides superior visualization of spinal cord inflammation, edema, demyelination, and enhancement. CT primarily excludes compressive osseous pathology but is insensitive to intramedullary disease.

Question 3. Which treatment should be initiated promptly when VZV myelitis is strongly suspected?

A. Broad-spectrum antibiotics

B. Intravenous Acyclovir

C. Aspirin

D. High-dose methotrexate

E. Surgical decompression

Correct Answer: B. Intravenous Acyclovir. Explanation: Early antiviral therapy with intravenous acyclovir is the cornerstone of management and is associated with improved neurological outcomes. Treatment should not be delayed while awaiting laboratory confirmation when the clinical suspicion is high.

Key Takeaways

Clinical

VZV myelitis is a rare but potentially devastating complication of herpes zoster.
Elderly and immunocompromised patients are at greatest risk.
A dermatomal rash is an invaluable diagnostic clue.

Radiology

MRI is the imaging modality of choice.
Dorsal spinal cord T2 hyperintensity is the hallmark finding.
The "moth-eaten" pattern is highly suggestive.
CT is useful for excluding compressive pathology but cannot reliably detect spinal cord inflammation.

Treatment

Early intravenous acyclovir significantly improves prognosis.
Corticosteroids may be considered in selected patients.
Rehabilitation plays an important role in functional recovery.

Final Summary

Varicella-Zoster Virus myelitis is an uncommon but clinically significant cause of acute myelopathy. The diagnosis depends on integrating clinical findings—especially a dermatomal vesicular rash—with characteristic MRI features such as dorsal cord T2 hyperintensity and the distinctive "moth-eaten" appearance. While CT remains valuable for excluding compressive spinal pathology, MRI is indispensable for detecting intramedullary disease. Prompt recognition, cerebrospinal fluid confirmation, and early intravenous acyclovir therapy are essential to optimize neurological recovery and minimize long-term disability.

References

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[4] B. C. Ari et al., "Transverse myelitis caused by Varicella-Zoster Virus," Infectious Disease in Clinical Practice, vol. 27, no. 4, pp. 231–233, 2019.

[5] J. E. Lee et al., "A case of transverse myelitis caused by Varicella-Zoster Virus in an immunocompetent older patient," Infection & Chemotherapy, vol. 48, no. 4, pp. 334–337, 2016. doi: 10.3947/ic.2016.48.4.334

[6] A. P. Sebastian et al., "Transverse myelitis caused by Varicella-Zoster," BMJ Case Reports, vol. 14, e238078, 2021. doi: 10.1136/bcr-2020-238078

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[8] Y. Tajima and Y. Mito, "Longitudinally disseminated spinal cord lesions (moth-eaten appearance) in Varicella-Zoster myelitis," Internal Medicine, vol. 50, no. 18, pp. 2059–2060, 2011.

[9] M. D. Maher et al., "Clinical and neuroradiologic characteristics in Varicella-Zoster Virus reactivation with central nervous system involvement," Journal of the Neurological Sciences, vol. 437, 120262, 2022.