Zooster-Neuralgia Post Herpes

Herpes Zoster and
Post-Herpetic Neuralgia
Carol Sue Carlson, MD

March 28, 2008
Zoster (AKA “Shingles”)
Case – MR
 53 yo ♂
 C5 Tetraplegic 2o to Spinal Cord Infarct
 PMHx: NonHodgkins Lymphoma s/p Chemo/RT
 on Decadron po
 c/o burning, achy pain in posterior neck

 ~36-48 hrs later  rash
 Dx: CN V3 Herpes Zoster

 Pain!!
 PCA, Acyclovir, Amitryptiline, Oxcarbazepine, Pregabalin, Duloxetine,
Capsaicin, Lidoderm 5% patch, Methadone, Hydrocortisone Cream,
Triamcinolone Cream
Case – MR
Overview
 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 Pathogenesis  Epidemiology
 Epidemiology  Risk Factors
 Natural History and  Clinical Manifestations
Infectivity  Pathogenesis
 Complications  Prevention
 Treatment  Treatment
 Prevention
 (3) EMG studies
Varicella-Zoster Virus
Varicella Zoster Virus
 Varicella Zoster Virus
 Varicella  “Chicken Pox”
 Zoster  “Shingles”
Varicella Zoster Virus – Pathogenesis
 Viral Latency
 Limited # of Proteins
Expressed
 Emergence from Latency

 Not Well-Understood
 Reactivation
 Spreads w/in Ganglion
 Multiple Sensory Neurons
 Infection of Skin
Varicella Zoster Virus – Pathogenesis
Acute Zoster Pathogenesis
 1st - Hemorrhagic
Inflammation
 Peripheral Nerve
 Dorsal Root
 DRG
 Spinal Cord
 Leptomeninges
 Nociceptor Activation
 Poorly Localized Pain
 “Pre-Herpetic Neuralgia”
 Nociceptor Sensitization
 Clinical Ramifications
Acute Zoster Pathogenesis
 2nd - Fibrosis
 DRG
 Nerve Root
 Peripheral Nerve
 Autopsy Results
 Similar +/- PHN
Zoster Pathogenesis
 Pain of Acute Herpetic

Neuralgia
 (1) Inflammation 2o to
Movement of Virus
 (2) Hyperexcitability of
Dorsal Horn Neurons
 Spontaneous Activity
 Exaggerated Responses
 Allodynia, Hyperalgesia
 Interneuron Spread
Intercostal Nerve Histology
Normal Post-Zoster
Zoster Pathogenesis – Reactivation
 DRG and Dorsal Horn

 Intense Inflammation
 Hemorrhagic Necrosis of Nerve Cells
 Neuronal Loss
 Fibrosis
Zoster Pathogenesis
 Neurotransmitters:
 Substance P
 Transmission
 Serotonin, NE
 Inhibition
 Therapeutic Implications
 Studies
 No Difference Side to Side
Zoster – Cell Mediated Immunity
 Cell-Mediated Immune Responses

 Control Viral Latency
 Limit Potential for Re-activation
 ↓ Skin Reactivity to VZV by 40 yo
 Severely ↓ by 60 yo
 ↑ Rates of Herpes Zoster In:

 Older Individuals
 Lymphoproliferative Malignancies
 BUT No ↑ Rates of Zoster or Protracted Varicella In:

 Children w/ Hypogammaglobulinemia
Overview

 Prevention
 (3) EMG studies
Zoster Epidemiology
 Cumulative Lifetime Incidence

 10-20% of Population
 Older Age Groups

 30% > 55 yo
 Incidence ↑ w/Age
 1 per 1000 in Pts < 20 yo
 5-10X Greater in Pts > 80 yo
 ***Highest Incidence after 6th decade***
 ♂=♀
Zoster Epidemiology
 Immunocompromised at ↑↑↑ Risk

 Age
 Disease
 Chemotherapy
 Several Times More Common in Pts w/ Ca, HIV,

Transplant Recipients
Zoster Epidemiology
Zoster Epidemiology
Overview

 Prevention
 (3) EMG studies
Zoster – Natural History and Infectivity
Zoster – Natural History
 75% have Prodromal Pain

 Grouped Vesicles or Bullae w/in 3-4 days
 Crusting in 7-10 Days
 No Longer Infectious
 Scarring, Hypo- or Hyperpigmentation

 Recurrence is Rare
Zoster Rash
Zoster – Natural History
 PAIN – Most Common Sx

 Deep, “Burning”, “Throbbing”, “Stabbing”
 Dermatomal
 Thoracic, CN V, Cervical – Most Common
 Zoster Keratitis, Zoster Ophthalmicus (CN V1)
 Systemic Sx – Rare (<20%)

 Most Cases – Self-Limited BUT:
 Can Interfere w/ Sleep, Appetite, Sexual Fnxn
 Psychosocial Dysfunction
Zoster Dermatomal Distribution
Zoster – Infectivity
 Immunocompetent Host Via:

 Direct Contact w/ Lesion
 Contact Precautions Recommended in Hosp. Pts

 Until Lesions Crust
 VZV Naïve Pts Exposed to Zoster

 At Risk to Develop 1o Varicella NOT Zoster
Zoster – Infectivity
 Immunocompromised Pt w/ Either:
 (1) Disseminated HZ
 (2) Local HZ in Pt at Risk for Dissemination

 Hospitalized, Strict Isolation
 Rx ~ Varicella (in which Airborne Spread is Possible)
Herpes Zoster
Herpes Zoster
Herpes Zoster
Overview

 Prevention
 (3) EMG studies
Zoster Complications
 POSTHERPETIC NEURALGIA
 ***Most Common*** (10-15%)
 Ocular
 Neurologic
 Motor Neuropathies – 2nd most common (2-3%)
 CN palsies
 Meningitis
 Myelitis
 Encephalitis
 Bacterial Superinfection
 Ramsey-Hunt Syndrome
Zoster Ophthalmicus
Zoster – Motor Paresis
Zoster – Bacterial Superinfection
Ramsey-Hunt Syndrome
Zoster Complications – Immunosuppressed
 Includes:
 HIV-infected pts
 Transplant Recipients
 Hematologic Malignancies
 ↑↑↑ Risk for Severe Complications

 Cutaneous Dissemination
 Visceral Involvement
 Pneumonitis, Hepatitis, Pancreatitis, Meningo-encephalitis
Overview

 Prevention
 (3) EMG studies
Uncomplicated Herpes Zoster Treatment
 Antiviral Therapy
 Goals:
 (1) Promote Rapid Healing
 (2) ↓ Severity and Duration of Pain
 (3) ↓ Incidence and Severity of PHN
 Prompt Use of Anti-Virals

 ↓ Duration of Pain by ½
 ↓ Overall Incidence of PHN

Acyclovir
 Oral Acyclovir 800 mg 5X/day

 Excellent Safety Profile
 Mainstay of Rx BUT:
 Poor Bioavailability
 Frequent Dosing
 Within 48-72 Hrs of Rash Onset

 Accelerates Resolution of Pain (Esp. in Pts > 50 yo)
 1 Meta-Analysis – Sig. ↓ in PHN at 6 months by 46%
Archives of Internal Medicine Vol 157 Apr 28, 1997, pp 909-911

Acyclovir with Corticosteroids
 Rx of Uncomplicated Acute HZ
 Study:
 ACV 800 mg po 5X/day X 21 days + Prednisone X 21 days
 ACV + Placebo
 Prednisone + Placebo
 2 Placebos
 ACV + Prednisone:
 Less Time to Crusting, Healing, Sleep, Return to Prior Activity
 Faster Resolution Acute Neuralgia
 Earlier D/C of Analgesics
 Drawbacks
Valacyclovir
 Valacyclovir 1000 mg po tid X 7-14 days vs. ACV

 Accelerated Resolution of Pain
 38 days vs. 51 days
 ↓ Duration of PHN
 Similar Adverse Events
Anti-Viral Recommendations
 Initiate w/in 72 hrs

 Esp. in Pts > 50 yo
 In Pts < 50 yo, Consider Risk Factors for Developing PHN
 Valacyclovir 1000 mg po tid X 7 days

 More Rapid Resolution Acute Neuritis
 Shorter Duration of PHN
 Lower Pill Burden  Improved Compliance
 BUT ↑ $$$
 Higher Cost than ACV
Anti-Viral Recommendations
 Steroids Have Only Been Studied w/ ACV

 Moderate Acceleration of Healing and Resolution of Pain
 No Effect on PHN
 ↑ Adverse Effects w/ Steroids
 May ↑ Risk of Bacterial Superinfection
 Recommend Prednisone 40 mg Taper over 7-10 days

 ONLY in Pts:
 (1) w/ Severe Sx at Onset
 (2) w/o Specific Contraindication
 Last Dose Should Coincide w/ End of Anti-Viral Rx

Overview

 Prevention
 (3) EMG studies
Zoster – Prevention
 Major Precipitant for Zoster Reactivation?

 Decline in Cell-Mediated Immunity!
 Elderly Population
 Immunosuppressed Pts
 Subclinical VZV Infection

 Enhanced VZV Cell-Mediated Immunity!
 Prevention in Immunosuppressed Hosts?

 ACV – ↓ Re-Activation in Hematopoietic Cell Transplant Recipients
Varicella Vaccine Concerns
 (1) ↑ Risk of Vaccine-Assoc. Zoster

 Esp. in Immunocompromised Children
 (2) ↑ Zoster in General Population

 ↓ Circulation Wild-Type Virus
 ↓ in Cell-Mediated Immunity
 Neither Concern Has Been Proven Correct

Varicella Vaccine in Older Adults
 2 Clinical Trials in Older Pts (55-87 yo)

 ↑ CMI to VZV after Immunization
 ↑ Freq. of VZV-Specific T-cells
 1 in 68,000  1 in 40,000
 Similar ratio to 35-40 yo!
Zoster Vaccine
 Randomized, Double-Blind Placebo-Controlled Trial

 38,546 Pts, 60 yo or Older
 Goal: Determine if Vaccine Would:
 ↓ Incidence and Severity of Zoster and PHN
 Results:
 (1) ↓ Incidence of Zoster by 51%
 (2) ↓ Incidence of PHN by 67%
 (3) Those Who Developed Zoster:

 Sig. Shorter Duration of Pain and Discomfort
New England Journal of Medicine June 2, 2005, Vol 352 No 22, pp 2271-2282
Zoster Vaccine
Zoster Vaccine
 Do Not Use In:

 Pregnant ♀
 Pts w/ hx/o Anaphylactic Rxn to Gelatin or Neomycin
 NOT Advised In:

 Pts w/ 1o or Acquired Immunodeficiencies
 AIDS
 Leukemia
 Lymphoma
 Malignancies of Bone Marrow or Lymphatic System
 Pts on Immunosuppressive Therapies
 NOT for Rx of Zoster or PHN

Overview

 Prevention
 (3) EMG studies
Post-Herpetic Neuralgia
 Acute Herpetic Neuralgia

 Pain Preceding or Accompanying Rash
 Up to 30 Days from Onset
 Subacute Herpetic Neuralgia

 Pain Persisting Beyond Healing of Rash
 Resolves w/in 4 mos of Onset
 Post-Herpetic Neuralgia
 Pain Persisting Beyond 4 mos from Initial Onset of Rash
Post-Herpetic Neuralgia – Epidemiology
 Incidence ↑ w/ Advanced Age

 Rare in Children
 Pts < 60 yo – Risk is < 2%

Overview

 Prevention
 (3) EMG studies
PHN Risk Factors
 Older Age
 Assoc w/ ↑ Severity and Persistence of Sx
 Greater Acute Pain

 Greater Rash Severity
 ♀ Sex
 Presence of a Prodrome
 Risk is NOT ↑ in Immunocompromised Individuals
Overview

 Prevention
 (3) EMG studies
PHN – Clinical Manifestations
 Pain
 Acute Zoster – Sharp, Stabbing
 PHN – Burning
 Allodynia
 > 90% of pts
 Anesthesia
 Deficits of Thermal, Tactile, Pinprick, Vibration
 Beyond Dermatomal Margins

PHN
 (1) Allodynia
 (2) Cutaneous Scarring
 (3) ↓ Sensation to Pinprick,

Cold, Touch
PHN
Overview

 Prevention
 (3) EMG studies
PHN – Pathogenesis Theories
 (1) Sensitized Nociceptors

 “ABC syndrome”
 (2) “Sensitization-like” Characteristics

 (3) Neuroma Formation
 (4) Central Hypersensitivity
 ~ “Trickle” Current
 (5) ABNL “Epileptiform” Activity in Spinal Neurons
 MULTIDETERMINATE!
 Therapeutic Implications
Overview

 Prevention
 (3) EMG studies
Prevention of PHN
 (1) Rx of Acute Zoster

 (2) Vaccine
 OR:
 Very Early Rx w/ Preventive Pain Medicines
 ie: TCAs, Anticonvulsants
 Epidural Steroid Injections w/ Anesthetics
 No Benefit
 Recommendation:
 Low-dose TCA w/in 2 days Rash Onset, X 90 days
 Gabapentin (If Limited By S/E)

Overview

 Prevention
 (3) EMG studies
Treatment of PHN
 Antidepressants
 Analgesics
 Capsaicin
 Topical Lidocaine
 Anticonvulsants
 Intrathecal Corticosteroids
 NMDA Receptor Antagonists
 Cryotherapy
 Surgery
PHN – Tricyclic Antidepressants
 Effective for PHN

 Mainstay of Rx
 Inhibit Re-uptake of NE and Serotonin
 ↑ Inhibition of Nociceptive Signals
 Study
 Amitriptyline vs. Lorazepam vs. Placebo
 Sig. More Effective for Moderate Pain Relief
 Sig. Correlation Btwn:

 Serum Amitriptyline levels & Degree of Pain Relief
PHN – Tricyclic Antidepressants
 Sig. Side Effects

 Esp. Sedation, Dry Mouth, Orthostatic Hypotension
 Nortriptyline vs. Amitriptyline

 Nortriptyline Better Tolerated but Similar Analgesic Action
 May be a Lag of Up To 3 Weeks
Neurology (51) October 1998 pp1166-1171

PHN – Analgesics
 ASA, NSAIDs – Limited Value

 Opioids
 Randomized, Double-Blind, Placebo-Controlled, Crossover
 Opioid vs. Tricyclic vs. Placebo – 8 weeks each
 Conclusions:
 Opioids and TCAs Better than Placebo
 Trend toward Opioids but Not Statistically Sig.
 No Appreciable Effect on Cognition Noted w/ Opioids
 Tramadol
 More Effective than Placebo
Neurology (59) October 2002, pp1015-1021; Pain 104 (2003) pp 323-331

PHN – Capsaicin
 Alkaloid Derivative from

Seeds of Plants
 (1) Enhances Substance

P Release from C-fibers
 (2) Prevents
Re-accumulation of
Substance P
PHN – Capsaicin
 Topical Application
 Burning, Stinging, Erythema
 Intolerable in ~ 1/3 of Pts
 Appears to be Effective for PHN

 Moderate Relief when Applied QID
 21% ↓ in Pain Score (vs. 6% w/ placebo)
 True Blinding is Impossible
Pain 33 (1988) pp 333-340

PHN – Topical Lidocaine
 Meta-analysis (2007)
 2 Small Trials
 Pain Relief Modestly
Greater than Placebo
 Recommendations:
 Insufficient Evidence to
Recommend as 1st Line
Agent
 May be Useful as
Adjunctive Rx
Cochrane Database for Systemic Reviews.

4,2007
PHN – Anticonvulsants
 Esp. Useful in Lancinating Component of Pain

 ie: CN V Neuralgia
 Commonly Used Anticonvulsants

 Phenytoin
 Carbamazepine
 Gabapentin
 Pregabalin
PHN – Gabapentin
 2 Studies
 1o Outcome
 Statistically Sig. ↓ in Pain
Score vs. Placebo
 2o Outcome
 ↓ Sleep Interference
 Improved Mood, QOL
 Side Effects
 Somnolence, Dizziness
 **Most Common**
 Peripheral Edema, Infection
Pain 94 (2001) pp 215-224; JAMA December 2,
1998 Vol 280, No 21, pp 1837-1842
PHN – Pregabalin
 Structural Analog of GABA (~Gabapentin)

 Results:
 Improvement in Sleep, ↓ in Pain
 150 mg to 600 mg po QD
 Side Effects
 Dizziness, Somnolence, Dry Mouth
 Peripheral Edema, Weight Gain
 Schedule V Controlled Substance – Euphoria

 If d/c  Taper Over 1 wk
 2o to Withdrawal Sx
Pain 109 (2004) pp 26-35; Neurology 60, April 2003, pp 1274-1283

PHN – Intrathecal Steroids
 Study of 277 pts w/ intractable PHN for 1 yr+

 Intrathecal Methylprednisolone + Lidocaine 1X/wk X 4 wks
 Intrathecal Lidocaine 1x/wk X 4 wks
 No Rx
Regional Anesthesia and Pain Medicine, Vol 24, No 4,

July-August 1999, pp 287-293
PHN – Intrathecal Steroids
 Results:
 (1) >90% of pts in Steroid Group Had:
 Good/Excellent Pain Relief at 4 wks, 1 yr, 2 yrs
 (vs. 6% in Lidocaine Group, 4% in No Rx Group)
 (2) Allodynia – ↓ by > 70% in Steroid Group
 (Lidocaine – ↓ by 25%)
 (3) ↓ Need for Diclofenac in Steroid Group
 Potential for Serious Neurologic Side Effects

 Adhesive Arachnoiditis
 Meningitis
Regional Anesthesia and Pain Medicine, Vol 24, No 4, July-August 1999, pp 287-293
PHN – NMDA Receptor Antagonists
 Animal Data
 Excitatory AA NTs – Role in Maintenance of Chronic Pain
 NMDA Antagonists Relieve Neuropathic Pain

 IV Ketamine
 Modest Pain Relief
 At Doses  Sedation, Dysphoria, Dissociative Episodes
 Dextromethorphan
 No Better than Placebo in PHN
 S/E – Ataxia, Sedation
Neurology 48, May 1997, pp1212-1218

PHN Treatment Recommendations
 Tricyclic Antidepressants  Topicals

 Amitriptyline  Lidocaine 5% Patch
 Nortriptyline  Capsaicin
 “Strong” Opioids  Intrathecal
 Methadone Methylprednisolone
 Morphine
 Tramadol
 Anticonvulsants
 Pregabalin
 Gabapentin
PHN Treatment
Limitations to Rx of PHN
Overview

 Prevention
 (3) EMG studies
Herpes Zoster of Head and Limbs
 158 Consecutive Cases, Head and Limbs

 Results:
 > ½  Sensory Axonal Neuropathy
 w/ NL or Only Slightly ↓ SNAP CV
 > 1/3  Motor Fiber Involvement
 19% Clinically – Segmental Motor Paresis
 17% Subclinical – by EMG
 55%  Improvement in Segmental Motor Paresis
 2.5%  Sensorimotor Axonal PN
 Severity of Peripheral Fiber Axonal Damage ↑ w/ Age
Archives of Physical Medicine and Rehabilitation, Vol 83, September 2002, pp. 1215-1220
Herpes Zoster of Head and Limbs
Electrophysiological Findings +/- PHN
 23 Pts w/ PHN, 64 Pts w/o PHN

 All Pts had ↓ SNAP Amplitude
 Assoc w/ NL or Only Slightly ↓ CV
 No Correlation Btwn Severity of Axonopathy & PHN

 So – PHN Not 2o to Damage of Lg Diameter Sensory Fibers
 10% had Segmental Paresis

 Additional 17% had EMG Evidence of Axonal Motor Damage
 No Sig. Diff. in EP Findings of Pts w/ or w/o PHN
Electroencephalography an Clinical Neurophysiology 101 (1996) pp 185-191

Electrophysiological Findings +/- PHN
Segmental Zoster Paresis of Limbs
 Report of 3 Cases and Literature Review

 (1) PSW and Fibs in 40-50% of Cutaneous Zoster
 Subclinical Motor Involvement – Not Uncommon
 (2) Weakness Commonly Occurs w/in 2 wks of Rash

 (3) Proximal Weakness More Common
 Older Age May Be a Risk Factor
 (4) Motor Paresis – ↑ Freq. of Assoc w/ Malignant Dz

 NCS: ↓ SNAP and CMAP Amplitudes
 Antiviral Rx May Be Assoc w/ ↓ Incidence of HZ Paresis
The Neurologist, Vol 13, Number 5, September 2007, pp 313-317

Effects of Acyclovir
 Goal: Eval. Efficacy of ACV in:

 ↓ Incidence of: PHN, Motor Paresis, Peripheral Nerve Damage
 No Difference in Incidence of PHN

 ACV Group:
 Sig. ↓ in Clinically Evident Motor Paresis & ABNL EMGs
 Un-Rx Group:
 More Freq. ABNL in SNCS, MNCS, H-Reflex, Blink Reflex
 ACV May Be Assoc w/:

 ↓ Sensory Axonopathy, ↓ Motor Paresis BUT No Effect on PHN
European Neurology, 1996;36:288-292

Motor Involvement in Acute HZ
 40 Pts w/ Acute HZ
 EMG ABNL in 53% – Fibs, PSWs

 In 62% EMG Findings were Subclinical
 Widespread ABNL
 Not Confined to Segment Invaded by Rash
 7 Pts had Motor Paresis
Muscle and Nerve, November 1997, pp 1433-1438

Conduction Block of VZV Neuropathy
 Case Report: 64 yo ♀ w/ CML

 Acute HZ in R C6-C7 Dermatome
 Weakness in RUE – Not Confined to C6-C7
 NCS:
 CB and CV Slowing in R Median Nerve in Forearm
 CB in R Radial Nerve Btwn Cubitus and Brachial Plexus
 EMG: Spontaneous Activity in R Triceps

 MRI: Extensive Lesions in Connective Tissue around FF Tendons & Muscles
Along Median Nerve
 Improvement in CBs & MMT of APB w/ Prednisone

Neurology, October 2003 (61) pp 1153-1154
Conduction Block of VZV Neuropathy
Conduction Block in Forearm
 29 yo ♂ w/ Left FA Numbness, Left Hand Weakness

 9 Days After Onset Severe 1o Attack Varicella
 PE: (+) Weakness Left APB, OP, 1st/2nd Lumb
 L MCN nerve – Sensory Branch Hypesthesia
 No Atrophy, DTRs +2
 MNCS: L Median (FA) – Partial CB (↓ CV, Absent F-wave)

 Elbow Mixed Median Nerve – ↓ on L (15.2 μV vs. 33.9 μV)
 SNCS: L Sensory Branch MCN – Absent, NL on R
 EMG: ↓ Interference Pattern L APB, (+) Fascics in APB

J Neurol Neurosurg Psychiatry 2005;76:1604-1605
Conduction Block in Forearm
 Explanation?
 (1) Median & Sensory MCN Share Cervical Roots → Lateral Cord
 (2) Close Anatomical Proximity in Arm 2o to Anatomical Variations

 Direct Spread of Virus Between Nerves
 (3) Indirect Spread from Purely Sensory MCN via Spinal Cord
J Neurol Neurosurg Psychiatry 2005;76:1604-1605

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Zooster-Neuralgia Post Herpes

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Herpes Zoster and

Carol Sue Carlson, MD

 c/o burning, achy pain in posterior neck

 Dx: CN V3 Herpes Zoster

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 Varicella Zoster Virus

 Varicella  “Chicken Pox”

 Emergence from Latency

 Pain of Acute Herpetic

 DRG and Dorsal Horn

 Hemorrhagic Necrosis of Nerve Cells

 Cell-Mediated Immune Responses

 Limit Potential for Re-activation

 ↓ Skin Reactivity to VZV by 40 yo

 ↑ Rates of Herpes Zoster In:

 BUT No ↑ Rates of Zoster or Protracted Varicella In:

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 Cumulative Lifetime Incidence

 Older Age Groups

 Immunocompromised at ↑↑↑ Risk

 Several Times More Common in Pts w/ Ca, HIV,

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 75% have Prodromal Pain

 Scarring, Hypo- or Hyperpigmentation

 PAIN – Most Common Sx

 Zoster Keratitis, Zoster Ophthalmicus (CN V1)

 Systemic Sx – Rare (<20%)

 Immunocompetent Host Via:

 Contact Precautions Recommended in Hosp. Pts

 VZV Naïve Pts Exposed to Zoster

 (2) Local HZ in Pt at Risk for Dissemination

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 ↑↑↑ Risk for Severe Complications

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 (2) ↓ Severity and Duration of Pain

 (3) ↓ Incidence and Severity of PHN

 Prompt Use of Anti-Virals

 ↓ Overall Incidence of PHN

 Oral Acyclovir 800 mg 5X/day

 Within 48-72 Hrs of Rash Onset

 1 Meta-Analysis – Sig. ↓ in PHN at 6 months by 46%

Archives of Internal Medicine Vol 157 Apr 28, 1997, pp 909-911

 Faster Resolution Acute Neuralgia

 Earlier D/C of Analgesics

 Valacyclovir 1000 mg po tid X 7-14 days vs. ACV

 Initiate w/in 72 hrs

 In Pts < 50 yo, Consider Risk Factors for Developing PHN

 Valacyclovir 1000 mg po tid X 7 days

 Shorter Duration of PHN

 Lower Pill Burden  Improved Compliance

 Steroids Have Only Been Studied w/ ACV

 ↑ Adverse Effects w/ Steroids

 May ↑ Risk of Bacterial Superinfection

 Recommend Prednisone 40 mg Taper over 7-10 days

 Last Dose Should Coincide w/ End of Anti-Viral Rx

 (1)Herpes Zoster  (2) PostHerpetic Neuralgia

 Major Precipitant for Zoster Reactivation?

 Subclinical VZV Infection

 Prevention in Immunosuppressed Hosts?

 (1) ↑ Risk of Vaccine-Assoc. Zoster

 (2) ↑ Zoster in General Population

 Neither Concern Has Been Proven Correct

 2 Clinical Trials in Older Pts (55-87 yo)

 Randomized, Double-Blind Placebo-Controlled Trial