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Shingles and Interventional Pain Treatment
Acute shingles patients rarely come to the attention of the pain physician; instead, it is
only after the lesions have healed that patients are referred to pain management.
Unfortunately, by that time there is very little that can be done. Aggressive education is
necessary to convince family doctors and patients that early interventional treatment by a
pain physician can provide excellent pain relief as well as decrease the risk of
postherpetic neuralgia – the leading cause of suicide in pain patients over 70 years old.
Key words:

Shingles and post herpetic neuralgia (PHN) are becoming a larger health issue as our
population ages, influencing health care dollars and quality of life. Patients and health
care providers have been told that the condition is untreatable, but that the pain usually
goes away in time. Unfortunately, post herpetic neuralgia (the nerve pain after shingles),
is a debilitating pain that may last up to a year in 50% of patients, and may even last up to
a lifetime. The good news is that aggressive interventional pain management is both cost
effective and efficacious in treating shingles and preventing PHN.
Herpes zoster, or shingles, has been plaguing man since ancient times. In his book,
Shingles And PHN, Thomas Carl Thomsen (1) references an essay in the History of
Medicine, which stated that " 'Job was afflicted with a general eruption of sores, causing
great itching, severe pain, and discoloration of skin, and tending to cause swelling of the
eyelids and closure of the eyes.' A pretty good description of.shingles affecting the

The family of herpes viruses gets its name from the Greek herpetum for “creeping skin
disease.” Varicella is a Latin word meaning "little pox" to distinguish the chickenpox
virus from smallpox, the highly contagious and often fatal scourge that disfigured or
killed millions of people. Zoster is the Greek word for "girdle"; shingles often produces a
girdle of blisters or lesions around the waist. Shingles derives its name from the Latin
cingulum, which also means girdle or belt. In Italy, shingles is called St. Anthony's fire.
Herpes varicella and herpes zoster were initially felt to be two different diseases, but as
early as 1909 a German scientist suspected that the viruses causing chickenpox and
shingles were one and the same. In the 1920's and 1930's the case was strengthened by an
experiment where children were inoculated with fluid from the lesions of patients with
shingles. Within 2 weeks about half the children came down with chickenpox. Finally, in
1958, detailed analyses of the viruses taken from patients with either chickenpox or
shingles confirmed that the viruses were identical. The virus is now often called herpes
varicella-zoster or HVZ.
The primary infection with HVZ causes chickenpox. It has been estimated that 90% of
US children have contracted chickenpox by the age of 15. Approximately 1 in 10
individuals who have had chickenpox will develop shingles. Shingles strikes an estimated
200,000 (2) to 800,000 U.S. patients each year, mostly among the elderly or
immunosuppressed (3). The incidence of herpes zoster infection is estimated to be as high
as 4.8 cases per 1000 persons each year (2). The disease is rare in young healthy adults,
but occurs in 5.1 of each 1,000 patients over age 50 and in 10.1 per 1,000 patients in their
Incidence of Shingles
The incidence increases with age and is higher in immunosuppressed patients or patients with cancer (4). Shingles also may be an early signal of HIV infection, especially when it occurs in a younger person (5). The incidence of herpes zoster has increased over the past several decades (6), and population studies project that 22% of Americans will be 65 or older by the year 2030 with the number of people over the age of 85 soaring to 8 million. The lifetime incidence of shingles may be 10% to 20% in the general population, and up to 50% in a cohort surviving to age 85.
HVZ is a human alpha herpes virus and looks as though a mathematician designed it. It is
a microscopic sphere encasing a 20-sided geometric figure called an icosahedron. Inside
the icosahedron is the genetic material of the virus, deoxyribonucleic acid (DNA). When
activated, the virus reproduces inside the nucleus of an infected cell. It acquires its
spherical wrapping as it buds through the nuclear membrane.
The clinical infection of chickenpox has a usual course of about two weeks. After the
infection, nerve terminals each receive an aliquot of defective virus particles, which cause
no injury to the sensory nerves up which they travel to become latent in the first nucleate
cells they encounter. Therefore, the latent virus is found in the neurons and supporting
cells of the sensory ganglia, where they exist for the remainder of the host’s life. For
whatever reason (senility of the body’s antibodies, infection that distracts the body’s
immune system, immunocompromise, stress), the virus can “break out of prison”, “raping
and pillaging” along the path of the nerve in which it was living. Strauss (7) has likened
this eruption to "varicella within a single dermatome." The body’s response (like any
good general) appears to be to cut off the “supply lines”, which in this case is the blood
flow to the nerve itself. Ischemia of the nerve leads to death of the large myelinated or
modulator nerves, leaving the small unmyelinated pain nerves unopposed. This has been
confirmed by biopsy and autopsy studies (8).
Clinical course:
Sub clinical presentations of herpes zoster have been reported where herpes zoster had
migrated to the CNS in immunocompetent patients without symptoms of CNS infection.
However, for most patients, the initial presentation is of pain in a dermatomal pattern. At
this time, rising titers of virus can begin to be detected. The body’s response to this
invader is the initiation of the sympathetic system response, with ischemia of the nerve.
Forty percent of patients experience pain more than 4 days prior to the skin eruption and
35% experience it less than 48 hours prior to the development of the rash (9). In some
cases, the pain starts more than 100 days before the rash and is referred to as "preherpetic
neuralgia" (10). Pruritus, paresthesias, fever, malaise and myalgia may accompany the
pain of preherpetic neuralgia. In the prelesion phase, the differential diagnosis for the
pain may be quite long. Trigeminal distribution might mimic subarachnoid hemorrhage
or migraine headache, upper extremity lesions may look like a cervical disc pathology,
while thoracic ischemia may be mistaken for cardiac pathology, costochondritis, pleurisy,
or rib fracture. Abdominal pain can lead to workup for cholecystectomy, appendicitis, or
peritonitis, while lower extremity shingles can look like a sciatica, or radiculitis before
the lesions appear. When the rash appears, initially there may be erythema and then
papules, vesicles, blebs, pustules, and then crusting. In severe cases, the lesions may
coalesce to cover the entire dermatome. The crusts usually fall off by the 5th week,
leaving pink scars that become hypoesthetic and hypopigmented.
The most common dermatome affected is the thoracic (55% of cases), followed by the
cranial (trigeminal; 15% of cases), the lumbar (14% of cases), and sacral (3% of cases)
(11). While a few patients do not report pain with shingles, they are the exception. Most
patients describe the pain as debilitating.

There is a condition known as zoster sine herpete, which is a dermatomal pain without a
visual rash due to reactivation of the varicella zoster virus. This condition can be
associated with segmental pain and motor deficits, and is diagnosed by viral analysis.
However, since the varicella zoster virus can affect all levels of the nervous system in the
absence of skin lesions, reactivation of the virus without rash encompasses a much
broader syndrome complex than localised pain, and may be much harder to diagnose.
Although the virus is presumed to hide in the nervous system between bouts of
chickenpox and shingles, it has never been recovered from nerve cells at autopsies unless
the patient had shingles at the time of death. In contrast, herpes simplex, which causes
recurrent infections of cold sores and fever blisters, has been identified in spinal nerve
cells during its latent periods.
Neurologic sequelae:
Motor deficits can occur in the intercostal and abdominal muscles. Trigeminal nerve
involvement may result in ptosis, and the Hunt-Ramsey syndrome (involvement of the
ear) may cause facial nerve paralysis. Occasionally, the rash will appear as a single spot
or cluster of spots on the tip of the nose, called Hutchinson's sign. This may herald
involvement of the ophthalmic nerve, which may lead to temporary or permanent
blindness. Central nervous system complications include meningitis, encephalitis,
mellitus and cerebral angiitis (12).
Postherpetic Neuralgia
20 to 30% of shingles patients continue to have pain after the shingles lesions have
healed, which is called post herpetic neuralgia (PHN). The risk increases with age,
approaching 75% of patients over 70 years old. Although the mechanism of pain is not
clear, ischemia of the nerve would explain the prelesion pain and the subsequent
hypoesthesias. Nerve biopsies of post herpetic nerves show a loss of large myelinated
“modulator” nerves, and a proliferation of unmeylinated pain nerves. It is important to
note that the elderly are at higher risk for this ischemia due to peripheral vascular
deterioration and fewer large fibers to begin with, and therefore would be expected to be
more susceptible to the pain of post herpetic neuralgia. The natural history of PHN is not
clear, but 50% of patients with PHN may continue to have pain after three months, and
although 80% have resolution within 5 years, 2% have pain for more than 5 years (13).
Many of these patients are refractory to treatment, and may get worse instead of better
over time. In addition, some patients have pain-free intervals of weeks to months, only to
have the pain reoccur (14). PHN may profoundly affect a patient’s life and functional
status, leading to anorexia, depression, and interference with activities of daily living
such as bathing and mobility (15). It has been described as one of the most common
causes of pain in the elderly and the leading cause of suicide in chronic pain patients over
the age of 70 (16). Watson estimates that "despite all . . . measures, at least 30% of
patients with PHN remain either completely refractory or unsatisfactorily relieved by the
best we have to offer, and new approaches to this vexing problem are sorely needed."
Treatment approach for shingles:
The goal of treatment is to treat the pain of the acute disease and prevent the occurrence
of post herpetic neuralgia. The earlier a patient is treated, the less likely the condition will
progress to PHN. Some physicians only send the patient for treatment after the lesions have healed. This is a great disservice to the patients, allowing needless pain and suffering. Because it is impossible to accurately predict which patients will progress to PHN, it is our suggestion that all patients be considered for treatment. The incidence of PHN goes up dramatically with age, and the length of time with pain also goes up. Up to 50% of patients over 70 year old with shingles will still have pain after more than one year. Antivirals have been advocated since the late 1970’s, initially with encouraging results. If begun within 72 hours after the appearance of the rash, famciclovir, valacyclovir or acyclovir reduce acute pain in immunocompetent patients with zoster. However, the long-term results have been less impressive, and a survey of the incidence of PHN in 1992 was not significantly changed since the 1940’s, suggesting that the antivirals did not change the risk of subsequent PHN (18). Systemic corticosteroids before zoster and treatment of zoster with acyclovir or corticosteroids do not significantly affect the prevalence of PHN (19). In a study of 600 adults over the age of 50 with early shingles (less than 7 days after the rash occurred) patients were randomized to receive either IV acyclovir with prednisone or epidural local anesthetic and steroids. At one year, 22% of the acyclovir patients still had pain, while only 1% of the epidural patients still had pain (20). The interventional approach to the treatment of shingles can be traced to as early as 1969,
when Colding described the use of regional sympathetic blocks (21) for zoster treatment.
Sympathetic blocks can be used to prevent the vasoconstriction thought to cause the pain
and nerve damage. Winnie (22) described that the incidence of success is a function of
the rapidity of treatment. Virtually 100% success was obtained if the injections were done
within 1-2 weeks after the onset of the lesions. After 4-6 weeks, the success rate falls to
20%, and continues to fall with time (23). Bonica felt so strongly about the effectiveness
of interventional treatment that he said "I am so convinced of the efficacy of the
procedure that I have had neural blockade as the sole treatment for my own case of
HZ and for that of my wife and one of my siblings." (24)

Case histories
A 55 year-old male presented to our clinic with complaints of left shoulder pain and rash
for a week. Pain was gradually getting worse despite oxycodone, prednisone, and
acyclovir. He was noted to have a vesicular rash along a T11 dermatome. Patient had a
history of atrial fibrillation and was on coumadin. He was treated with one paravertebral
nerve block and topical ketoprofen/lidocaine. One week later he returned and noted 100%
pain relief
A 70 year old male presented to the ER with a history of a severe vertex headache for
several days. He was diagnosed as having a “migraine” (despite a negative history of
similar headaches in the past) and was given oxycodone. Two days later, skin lesions
appeared over his right eyebrow and forehead. He went to his internist who also gave
him narcotics. Eight weeks later when he saw his dermatologist for an unrelated problem,
and he was referred to our office. He was then treated with Gabapentin 900mg/day and
three supraorbital nerve blocks over a ten-day period. At his last visit, he stated he had
about 75% relief. It is important to note that the total time elapsed from the initial onset
of pain to appropriate treatment was eight weeks.
A 75 year old male presented to our pain clinic complaining of a constant pain in his left
eye. The patient described the pain as a “red-hot poker being stuck in the eye”. Fourteen
months previously he had been diagnosed with Shingles. During that period, he had been
treated with the following medications: antivirals; anticonvulsants; antidepressants; non-
steroidal anti-inflammatories; narcotics and topical creams. Since coming to the pain
center, he has undergone six interventional procedures including cryotherapy of the left
supraorbital nerve. Despite these many procedures, the patient noted no significant relief
and continues to complain of significant pain as described above.
Case IV
A 35 year old male presented to our pain clinic with a six month history of intractable
chest well pain. He had experienced a minor case of shingles 6 months earlier, initially
associated with minimal pain. However, over the next few weeks, the pain became
progressively worse, to the point that he could no longer keep a shirt on despite
oxycodone 40 mg BID. He eventually required 300 mg of methadone and 6 grams of
Keppra to be able to return to work. He has had no relief with multiple injections, and he
is considering a spinal cord stimulator.
Outcome data
A review of records billed with the ICD-9 code 035.9 (shingles or postherpetic neuralgia)
for a 6 month period revealed 15 patients.
Patient Age length Location Pain degree # of inj
Patient 6 was an HMO patient who was approved for the initial treatment (which gave
good relief) but was not approved for follow-up treatment when her lesions reoccurred 2
weeks later. Subsequent treatment was delayed for more than eight weeks, and she has
required cryoneuroablation of the intercostal nerves.
Patients presenting to our office with supraorbital lesions are offered supraorbital nerve
blocks with deposteroid and local anesthetic (1/2cc total volume). Cervical paravertebral
nerve blocks and occasionally cervical epidural steroids are used for upper extremity
lesions. Thoracic shingles patients are offered a paravertebral nerve block, followed by a
thoracic epidural if complete relief is not obtained. Lumbosacral lesions are treated with
lumbar or caudal epidural steroids. In addition to the injection, patients are started on a
topical ketoprofen-lidocaine compounded salve as well as samples and a prescription for
oral gabapentin (Neurontin®). Most have already been started on antivirals before they
reach our office, but if not, they may be given antivirals as well.
It has been extremely gratifying to treat the active shingles patients, especially those in
extreme pain. Within moments after the injection the pain is gone, and for most patients
pain never returns or returns at a much decreased level. The erythema and swelling are
markedly decreased by the second visit 2 to 3 days later, and the lesions are usually
drying up within that timeframe as well. If there is not complete relief, the patient is
offered a second (and rarely, a third or fourth) injection.
As the US population ages, the incidence of shingles (and therefore post herpetic
neuralgia) would be expected to increase. The economic impact of lost wages is hard to
quantify, especially in a retired population. However, the expected increased utilization
of medical resources can be significant, both initially and long term. Early interventional
treatment is effective and provides rapid and often complete relief. Extensive workups
before the lesions appear, analgesics for the acute pain, and then expensive treatments
such as spinal cord stimulation for the post herpetic neuralgia all represent avoidable
costs if the herpes zoster infection is aggressively recognized and treated. Because of the
time issues, it is critical that patients and physicians be educated in the importance of
rapid and aggressive treatment. Too often, patients are told that “nothing can be done”
and that “the rash will go away on its own”. Unfortunately, pain physicians are usually
used to seeing chronic pain patients, where onset of treatment is not an issue. It is not
uncommon for many pain practices to have 4 to 6 week waiting times for an appointment,
clearly too long to wait with this condition. Community doctors have to be educated
the pain practitioners themselves regarding the acute interventional treatment of
shingles. The entire office staff needs to be sensitized to the time critical nature of this
patient population. In our practice, we lecture frequently to the family doctors in my area,
explaining to them the “code word” – “active shingles” which will get their patient into
my office that day or the next morning. Our staff is trained to tell patients on the phone to
immediately come into the office. We have written several small articles for the local
newspaper on the topic, and have even convinced one of the most difficult local HMOs to
give carte blanche approval for immediate treatment of their shingles patients. Despite
these efforts, we are still referred patients with untreated pain weeks, months, and years
after the lesions have healed.
Rapid interventional treatment of acute shingles can dramatically decrease the pain of
active shingles and potentially decrease the risk of post herpetic neuralgia. Although
there have never been any controlled studies of interventional therapy to treat acute
shingles pain or to prevent postherpetic neuralgia, injections (especially peripheral nerve
blocks) are safe and reasonable in experienced hands (25). Pain management has always
been the treatment of last resort, and as a result, patients suffer needlessly, and costs
escalate. Treatment options for PHN are very limited, ineffective, and cost prohibitive, so
early, aggressive treatment of shingles is critical.
Where can I get more general information about shingles?
Tel: 800-352-9424 American Chronic Pain Association (ACPA) Email: [email protected] Tel: 916-632-0922 Fax: 916-632-3208 National Chronic Pain Outreach Association (NCPOA) Email: [email protected] VZV Research Foundation [For Research on Varicella Zoster] [email protected] Tel: 212-472- 3181 Tel Toll free: 800-472-VIRUS (8478) Fax: 212-861-7033 National Foundation for the Treatment of Pain [email protected] 1. Thomsen TC. Shingles and PHN, Cross River Press, 2003. 2. Gilden DH. Herpes zoster with postherpetic neuralgia -- persisting pain and frustration. N Engl J Med. 1994;330:932-934. 3. Schmader KE. Herpes zoster in older adults. Clin Infect Dis 2001;32:1481-1486 4. Kost RG, Straus SE. Drug therapy: Post-herpetic neuralgias - Pathogenesis, treatment and prevention. N Engl J Med 1996; 335: 32-42. 5. Beutner KR. Clinical management of herpes zoster in the elderly patient. Compr 6. Hanumanthu S. The great impostor. J Tenn Med Assoc. 1996; 89:47-48. 7. Strauss SE. Overview: the biology of varicella-zoster virus infection. Ann Neurol 8. Watson CPN, Morshead C, Van de Kooy D, Deck J, Evans RJ. Postherpetic neuralgia: postmortem analysis of a case. Pain. 1988;34:129-138. 9. Wood MJ. How to measure and reduce the burden of zoster-associated pain. Scand J Inf Dis 1996;100(suppl):55-58. 10. Lycka BAS, Williamson D, Sibbald RG. Dermatologic aspects of herpes zoster. Herpes Zoster and Post Herpetic Neuralgia 22nd edition Elsevier 001 11. Mamdani FS. Pharmacologic management of herpes zoster and postherpetic neuralgia. Can Fam Physician. 1994;40:321-326, 329-332. 12. Haanpää M. Neurologic complications of herpetic zoster. (Watson CPN and Gershon AA editors) Herpes Zoster and Post Herpetic Neuralgia 2nd edition Elsevier 2001 13. Mohamed SA, Carr DB. Pain during herpes zoster (shingles) and long after. Pain 14. Watson PN, Evans RJ. Postherpetic neuralgia: A review. Arch Neurol 15. Mauskopf J Austin R, Dix L, Berzon R. The Nottingham Health Profile as a measure of quality of life in zoster patients: convergent and discriminant validity. Qual Life Res 1994;3:431-435. 16. Winnie AP: Panel on Herpes Zoster. American Society of Regional Anesthesia 8th Annual Meeting, Orlando, FL, March, 1983 17. Watson CPN. Herpes Zoster and Postherpetic Neuralgia, Pain Research and 18. Edmunds WJ, Brisson M, Rose JD. The epidemiology of herpes zoster and potential cost-effectiveness of vaccination in England and Wales. Vaccine 2001:19:3076-3090 19. Choo PW. Risk factors for postherpetic neuralgia. Arch Intern Med 1997 Jun 20. Pasqualucci A, Pasqualucci V, Galla F, De Angelis V, et al. Prevention of post- herpetic neuralgia: acyclovir and prednisone versus epidural local anesthetic and methylprednisolone. Acta Anaesth Scand 44(8):910 Sept 2000 21. Colding A: The effect of regional sympathetic blocks in the treatment of herpes zoster. Acta Anaesth Scand 13:133-141, 1969 22. Winnie AP: The patient with herpetic neuralgia. In Moya F, Gion H (eds.): Postgraduate Seminar in Anesthesiology, program syllabus. Miami Beach, 1983, p.165-170 23. Winnie AP, Hartwell PW: Relationship between time of treatment of acute herpes zoster with sympathetic blockade and prevention of post-herpetic neuralgia: Clinical support for a new theory of the mechanism by which sympathetic blockade provides therapeutic benefit. Reg Anesth 18:277-282, 1993. 24. Bonica JJ. The Management of Pain, 2nd edition. Lea & Febiger, 1990:257–263, 25. Watson CPN, Oaklander AL. Postherpetic neuralgia. Pain Practice. 2002;2(4):


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