Postherpetic Neuralgia Medication

  • Author: W Alvin McElveen, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: Jan 19, 2012
 

Medication Summary

The goal of therapy for postherpetic neuralgia (PHN) is to reduce morbidity through the use of tricyclic antidepressants, anticonvulsants, anesthetics, analgesics, corticosteroids, and antiviral agents. A recently approved vaccine is also effective for preventing herpes zoster (HZ) outbreaks and PHN. A recent trial demonstrated that the combination of gabapentin and nortriptyline was more efficacious than either drug as monotherapy for neuropathic pain.[13] Another study found that a single 60-minute treatment with the high-concentration capsaicin patch NGX-4010 reduced PHN for up to 12 weeks regardless of concomitant systemic neuropathic pain medication use.[14]

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Tricyclic antidepressants

Class Summary

Complex group of drugs that have central and peripheral anticholinergic effects as well as sedative effects. They have central effects on pain transmission. They block the active reuptake of norepinephrine and serotonin.

Amitriptyline (Elavil)

 

By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS. Useful as analgesic for certain types of chronic and neuropathic pain.

Nortriptyline (Pamelor, Aventyl HCl)

 

Has demonstrated effectiveness in treatment of chronic pain; by inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS; pharmacodynamic effects such as desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play role in its mechanisms of action.

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Analgesics

Class Summary

Pain control is essential to quality patient care; it ensures patient comfort and promotes pulmonary toilet. Most analgesics have sedating properties, which are beneficial for patients who experience pain.

Capsaicin topical (Dolorac, Capsin, Zostrix)

 

Natural chemical derived from plants of Solanaceae family. By depleting and preventing reaccumulation of substance P in peripheral sensory neurons, may render skin and joints insensitive to pain. Substance P thought to be chemomediator of pain transmission from periphery to CNS.

Capsaicin 8% transdermal patch (Qutenza)

 

Transient receptor potential vanilloid-1 (TRPV1) agonist indicated for neuropathic pain associated with postherpetic neuralgia. TRPV1 is an ion channel–receptor complex expressed on nociceptive skin nerve fibers. Topical capsaicin causes initial TRPV1 stimulation that may cause pain, followed by pain relief by reduction in TRPV1-expressing nociceptive nerve endings. Neuropathic pain may gradually recur over several months (thought to be caused by TRPV1 nerve fiber reinnervation of treated area).

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's immune response to diverse stimuli.

Dexamethasone (Decadron, Alba-Dex, Dalalone L.A.)

 

Used to treat various allergic and inflammatory diseases. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and by reversing increased capillary permeability.

Prednisone (Deltasone, Orasone, Sterapred)

 

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and by reversing increased capillary permeability.

Methylprednisolone (Solu-Medrol, Adlone, Duralone)

 

Decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability.

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Antiviral agents

Class Summary

The goal of antivirals is to shorten the clinical course, prevent complications, prevent the development of latency and/or subsequent recurrences, decrease transmission, and eliminate established latency.

Famciclovir (Famvir)

 

Pro-drug that, when biotransformed into active metabolite penciclovir, may inhibit viral DNA synthesis/replication.

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Anesthetics

Class Summary

These agents stabilize the neuronal membrane so the neuron is less permeable to ions. This prevents the initiation and transmission of nerve impulses, thereby producing the local anesthetic action.

Lidocaine anesthetic (DermaFlex gel, Lidoderm 5% patch)

 

Several recent studies have advocated topical administration of lidocaine as treatment of PHN. Lidocaine gel (5%) in placebo-controlled study showed significant relief in 23 patients studied. Lidocaine tape also decreases severity of pain.

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Anticonvulsants

Class Summary

These agents are used to manage severe muscle spasms and provide sedation in neuralgia. They have central effects on pain modulation.

Pregabalin (Lyrica)

 

Approved by FDA for use in PHN. Freynhagen et al describe a statistically significant reduction in mean pain score and in pain-related sleep interference compared with placebo. Pregabalin binds with high affinity to alpha2-delta subunit of voltage-gaited calcium channels, thereby reducing excitatory neurotransmitters. Has half-life of approximately 6 h and is eliminated by renal excretion. Decrease in creatinine clearance results in decrease elimination and, therefore, increase in plasma concentration. Peak plasma concentration occurs at one and one half hours after oral intake. Bioavailability is 90%. Following repeated dosing, steady state concentration is achieved at 24-48 h. Can be taken with or without food.

Gabapentin (Neurontin)

 

This medication has been approved by the FDA for the treatment of PHN. Has properties common to other anticonvulsants and antineuralgic effects. Exact mechanism of action is not known. Structurally, gabapentin is related to GABA, but it does not interact with GABA receptors. Believed to have a binding site at the alpha 2-delta protein, an auxiliary subunit of voltage-gaited calcium channels. In the rat brain, binding is localized on neuronal dendritic areas. Relevance of these observations to treatment of PHN is not known.

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Vaccines

Class Summary

Used for prevention of HZ outbreak.

Zoster vaccine live (Zostavax)

 

A randomized, double-blind, placebo-controlled trial included 38,560 patients age 60 years and older for 3.1-year median surveillance; 95% completed the trial. HZ development decreased 51.3% (P < 0.001) and PHN decreased 66.5% (P < 0.001). In the ZEST trial, the vaccine significantly reduced the risk by 70% in individuals aged 50-59 years.

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Contributor Information and Disclosures
Author

W Alvin McElveen, MD  Director, Stroke Unit, Lakewood Ranch Medical Center; Neurologist, Manatee Memorial Hospital

W Alvin McElveen, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, American Stroke Association, and Southern Clinical Neurological Society

Disclosure: Nothing to disclose.

Coauthor(s)

Ralph F Gonzalez, MD  Private Practice, Bradenton Neurology, Inc; Consulting Staff, Department of Neurology, Blake Hospital, Lakewood Ranch Medical Center, Manatee Memorial Hospital

Ralph F Gonzalez, MD is a member of the following medical societies: American Academy of Neurology and Florida Medical Association

Disclosure: Nothing to disclose.

Douglas Sinclair, DO  Consulting Staff, Department of Neurology, Blake Medical Center and Bradenton Neurology, Inc

Disclosure: Nothing to disclose.

Specialty Editor Board

Joseph Carcione Jr, DO, MBA  Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans

Joseph Carcione Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James H Halsey, MD  Professor, Department of Neurology, University of Alabama Medical Center

James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

References
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