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Herpes zoster (shingles) and PHN are caused by the same virus as
chicken pox1,2



Chicken pox is the primary risk factor for shingles and subsequent postherpetic neuralgia (PHN) pain1,2

  • 95% of Americans have had chicken pox1
  • Approximately 1 million new cases of herpes zoster (HZ; shingles) in the United States each year1,2
  • HZ can occur at any age
  • Incidence increases with age3
  • Approximately 120,000 to 200,000 PHN cases annually in the United States1

PHN develops in more than 50% of patients 50 years and older who have had shingles1

  • Risk of PHN is 80% in patients 80 years and older1
  • Risk factors include: presence of a prodrome, severe acute pain, severe HZ rash within 3 days of HZ infection2,4

PHN pain presents with multiple pain qualities, making it difficult to diagnose5,6

  • 80% of PHN patients are misdiagnosed7
  • Clinical features of PHN pain include: burning, stabbing, shooting, abnormal sensations, sensory loss, allodynia, hyperalgesia5,6
  • PHN can severely impact patients’ lives2,8

PHN can occur anywhere on the body, and sometimes in more than one place9

  • Most commonly occurs on the torso (chest and back), waistline, or upper arm

Shingles

Shingles, or herpes zoster, is a disease caused by reactivation of the varicella zoster virus (VZV) that has remained dormant in the dorsal root ganglia following a prior systemic VZV infection, such as chicken pox10.

Upon reactivation of the latent herpes zoster virus by advancing age or immunosuppression, a severe inflammatory response is initiated within the dorsal root ganglion10. Reactivated viral particles multiply and spread along sensory axons to the skin's surface, producing the characteristic, and usually painful, vesicular rash of acute herpes zoster in the distribution of the affected dermatome11.

As the virus spreads, inflammation occurs and usually leads to complications such as demyelination and sclerosis. Peripheral afferent nerves, as well as the dorsal root ganglia and central nervous system, may be irreversibly damaged10.

The rash does not cross the midline and is generally confined to the area of skin innervated by a single sensory ganglion (i.e., a single dermatome). Skin lesions typically resolve within approximately 4 weeks after rash onset12.

Over one million Americans are afflicted with shingles each year, and roughly 20 percent of those diagnosed with shingles develop postherpetic neuralgia (PHN)1, the most common and debilitating sequela of shingles11.

Postherpetic Neuralgia (PHN)

There are varying opinions as to how much time must elapse following acute zoster outbreaks before pain is definitively termed postherpetic neuralgia (PHN); however PHN is commonly defined as pain that persists or occurs at least one month after acute herpes zoster10,11.

In damaged peripheral nerve axons, as in the case of PHN, there is an increase in the number of sodium channels which function abnormally at the sites of peripheral nerve injury. These abnormally functioning sodium channels are thought to result in foci of ectopic impulses and the spontaneous transmission of pain signals13.

Over time, excessive firing of injured peripheral nerves can lead to central sensitization and increased excitability of the second order neuron14,15.

Patients with PHN may present with one or more of the following10:

  • A constant burning, throbbing, or deep aching pain
  • An intense, intermittent pain with a lancinating or jabbing quality (may be spontaneous)
  • A dysesthetic pain, known as allodynia, that is evoked by normally innocuous stimuli such as light touch or exposure to heat or cold 1,12

Sensory abnormalities such as numbness, itching, altered sensation, and sensory deficits are often present in the affected region, as are areas of skin pigmentation change and/or scarring from the zoster rash10.

While the pain of PHN resides in the area of the prior herpes zoster rash, the size of the affected region can vary considerably, from small, discrete regions within the involved dermatome, to larger areas that extend beyond the margins of the initial skin rash and involve other dermatomes10.

It is believed that this extended hypersensitivity may reflect dynamic changes within the central nervous system associated with peripheral nerve damage10.

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Important Safety Information

LIDODERM® (lidocaine patch 5%) is indicated for relief of pain associated with post-herpetic neuralgia. Apply only to intact skin.

LIDODERM is contraindicated in patients with a history of sensitivity to local anesthetics (amide type) or any product component.

Even a used LIDODERM patch contains a large amount of lidocaine (at least 665 mg). The potential exists for a small child or pet to suffer serious adverse effects from chewing or ingesting a new or used LIDODERM patch, although the risk with this formulation has not been evaluated. It is important for patients to store and dispose of LIDODERM out of reach of children, pets, and others.

Excessive dosing, such as applying LIDODERM to larger areas or for longer than the recommended wearing time, could result in increased absorption of lidocaine and high blood concentrations leading to serious adverse effects.

Avoid contact of LIDODERM with the eye. If contact occurs, immediately wash the eye with water or saline and protect it until sensation returns. Avoid the use of external heat sources as this has not been evaluated and may increase plasma lidocaine levels.

Patients with severe hepatic disease are at greater risk of developing toxic blood concentrations of lidocaine, because of their inability to metabolize lidocaine normally. LIDODERM should be used with caution in patients receiving Class I antiarrhythmic drugs (such as tocainide and mexiletine) since the toxic effects are additive and potentially synergistic. LIDODERM should also be used with caution in pregnant (including labor and delivery) or nursing mothers.

Allergic reactions, although rare, can occur.

During or immediately after LIDODERM treatment, the skin at the site of application may develop blisters, bruising, burning sensation, depigmentation, dermatitis, discoloration, edema, erythema, exfoliation, irritation, papules, petechia, pruritus, vesicles, or may be the locus of abnormal sensation. These reactions are generally mild and transient, resolving spontaneously within a few minutes to hours. Other reactions may include dizziness, headache and nausea.

When LIDODERM is used concomitantly with local anesthetic products, the amount absorbed from all formulations must be considered.

Immediately discard used patches or remaining unused portions of cut patches in household trash in a manner that prevents accidental application or ingestion by children, pets, or others.

Before prescribing LIDODERM, please refer to the full Prescribing Information.

References

  1. Cluff RS, Rowbotham MC. Pain Caused by Herpes Zoster Infection. Neurol Clin. 1998;16(4):813-832.
  2. Weaver BA. The burden of herpes zoster and postherpetic neuralgia in the United States. J Am Osteopath Assoc.
  3. Insinga RP, Itzler RF, Pellissier JM, Saddier P, Nikas AA. The incidence of herpes zoster in a United States administrative database. J Gen Intern Med. 2005;20:748-753.
  4. Jung BF, Johnson RW, Griffin DR, Dworkin RH. Risk factors for postherpetic neuralgia in patients with herpes zoster. Neurology. 2004;62(9):1545-1551.
  5. Galer BS. Neuropathic pain of peripheral origin: advances in pharmacologic treatment. Neurology. 1995;45(suppl 9):S17-S25.
  6. Panlilio LM, Christo PJ, Raja SN. Current Management of Postherpetic Neuralgia. Neurologist. 2002;8:339-350.
  7. Dworkin RH, White R, O'Connor AB, Baser O, Hawkins K. J Am Geriatr Soc. 2007;55(8):1168-1175.
  8. Rowbotham MC. Postherpetic neuralgia. Semin Neurol. 1994;14(3):247-254. 2007;107(suppl 1):S2-S7.
  9. Shingles: hope through research. National Institute of Neurological Disorders and Stroke. National Institutes of Health Web site. http://www.ninds.nih.gov/disorders/shingles/detail_shingles.htm?css=print. Accessed October 12, 2007.
  10. Kost RG, Straus SE. Postherpetic Neuralgia – Pathogenesis, Treatment, and Prevention. N Engl J Med. 1996;335:32-42.
  11. Rowbotham MC, Davies PS, Fields HL. Topical lidocaine gel relieves postherpetic neuralgia. Ann Neurol. 1995;37:246-253.
  12. Wallace MS, Oxman MN. Anesthesiol Clin N Am. 1997;15.
  13. Fields HL, Rowbotham MC, Baron R. Postherpetic neuralgia: irritable nociceptors and deafferentation. Neurobiol Dis. 1998;5(4):209-227.
  14. Galer BS, Advances in the treatment of postherpetic neuralgia: the topical lidocaine patch. Today's Therapeutic Trends. 2000;18:1-20.
  15. Woolf CJ, Mannion RJ. Neuropathic pain: aetiology, symptoms, mechanisms, and management. Lancet. 1999;353:1959-1964.