SEMINARS I N NEUROLOGY-VOLUME

12, NO. 4 DECEMBER 1992

Herpes Zoster

ACUTE HERPES ZOSTER A herpesvirus confined to humans causes IWO disorders whose predominant clinical features are Whether during the period of viremia or via dermatologic-a vesicular rash-but whose most serious complications are neurologic. Varicella travel from the skin lesions along the sensory (chickenpox) is the primary infection, and herpes nerves, the virus reaches the dorsal root ganglia zcbster (shingles) occurs when the virus, which sur- (the trigeminal more often than any single thoracic7), vives indefinitely in the body, reactivates after a pe- where it resides in a latent state, presumably held riod of dormancy. Varicella usually occurs in child- in check by a cornbination of local host defenses hood, with the peak incidence between ages 5 and and systemic cell-mediated immunity. When these 7 years.' By age 20 years, about 80%, by age 40, falter, the reactivated virus migrates down the senabout 95%, and by age 60, virtually 100% of per- sory nerve to cause the skin lesions in its dermasons in the general population have been in- tome, known as herpes zoster. About 10 to 20% of fected.'~"ven in adults without a previous history the population develops this disorder, often withof' varicella, serologic tests indicate that most have out an apparent provoking factor. An important had the d i ~ e a s eThe . ~ infection is spread from per- aspect, however, is age: the risk of herpes zoster son to person by inhalation of aerosolized virus or rises from less than 1 case per 1000 person-years direct contact with the skin lesions of either vari- in children to about 5 in those over 75.4,8Impaired cella or zoster. 'l'hose with chickenpox are conta- cell-mediated immunity is also important; patients gious from about 2 days before the rash appears to with lymphoma, leukemia, immunosuppressive allout 5 days after, that is, about the time the le- therapy, organ transplantation, and infection with sions crust over. Secondary spread occurs in about the human immunodeficiency virus (HIV) are at 60 to 90% of susceptible household contact^.^.^ markedly increased risk. In those with an underUntil their lesions crust over, patients with herpes lying cancer, the malignancy is almost always adzoster are also infectious, but considerably less so: vanced, and an attack of' herpes zoster in an apsecondary cases develop in only about 15% of sus- parently healthy person does not warrant searching for an occult neoplasm or increasing ceptible children in the home.6 Once acquired, the virus replicates in the up- subsequent cancer surveillance without other per respiratory tract and disseminates hematoge- suggestive clinical abnormalities.9dtients at risk nously to cause varicella 10 to 2 1 (usually 14 to 17) for HIV infection, however, deserve a blood test to days after exposure. T h e rash typically appears detect that infection, since an attack of herpes zosfirst on the face and later involves the trunk and ter may be its first clinical manifestation.1° Trauma, extremities, producing about 200 to 500 mildly to such as recent surgery or previous radiation thermoderately pruritic lesions over 1 to 6 days in the apy, may also provoke an attack in the area of inaverage c h i l d . V h e y are initially papular, but jury." No convincing evidence, however, indicates quickly become clear vesicles on an erythematous that exposure to patients with active varicella or base, develop crusts over a few days, and then heal herpes zoster leads to an episode of herpes zoster. without scarring.

Seattle VA Medical Center, University o f Washington School of Medicine, Seattle, Washington Reprint requests: Dr. Hirschrnann, Medical Service (1 1 l ) , Seattle VA Medical Center, 1660 South Colurnbian Way, Seattle, WA 98108 Copyright O 1992 by Thieme Medical Publishers, lnc., 381 Park Avenue South, New York, NY 10016. All rights reserved.

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J. V. Hirschrnanr~,111.0.

Malaise, headache, fever, and nausea may precede the rash of herpes zoster by 1 to 3 days. A severe, burning superficial o r deep radicular pain lasting for a few days or, occasi'onally, for several weeksl%ay also antedate any dermatologic findings; when located in certain sites, it may mimic cardiac ischemia o r a severe intraabdominal process requiring surgery. T h e rash usually begins as erythematous macules o r papules in a unilateral area innervated through a single sensory nerve

Figure 1. Herpes zoster affecting midthoracic region. The lesions occur in clusters with uninvolved or less involved intervening areas.

root. Karely, it involves two dermatomes (zoster duplex), and a few scattered lesions occur distant from the original dermatome in about one third of immunocompetent hosts.'" T h e location is thoracic in about GO%, cranial (usually affecting the trigeminal nerve) in about 15%, cervical and lumbar in 10% each, and sacral in 5%; it is bilateral in less than 0.5%.X~"1 'The lesions appear in successive groups (crops) over several days (usually 2 to 4),14 transforming into clear vesicles on an erythematous base, but occasionally remaining papular throughout the course of disease. T h e vesicles may become pustular o r hemorrhagic, often with superficial necrosis (black discoloration), and then form crusts, which usually fall off in 2 to 3 weeks, commonly leaving scars and increased o r decreased pigmentation. Because the lesions occur in crops, they typically appear in small clusters, demonstrate different stages (for example, papules, vesicles, and pustules) at the same time, and have a nonuniform distribution within the dermatome, much of which may be uninvolved (Figs. 1 and 2). Their location in well-demarcated zones is responsible for the names of the disease; herpes, Greek for "to creep," refers to the spreading nature of the skin abnormalities and zoster, meaning a belt, to their bandlike distribution. Zoster translated into Latin became cingulus, into French, chingle, and into English, shingles. Aside from pigmentary changes and scarring, local cutaneous complications are uncommon, although superinfection with Staphylococcus aureus o r streptococci may occur, usually manifested by

Figure 2. Close-up of the patient in Figure 1 shows a cluster of lesions in various stages of evolution, including papules, vesicles, and crusts.

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HERPES ZOSI'ER-HIRSCHMANN

substantial spreading erythema (cellulitis) around the lesions. The disease may be prolonged in patients with impaired cell-mediated immunity, who seem at increased risk for recurrent herpes zoster, often in the same site, which also develops in about 5% of normal hosts.8 Occasionally, other dermatologic disorders, including sarcoidosis, granulonia annulare, and (in a HIV-infected patient) Kaposi's sarcoma,15 have appeared exclusively in dermatomes previously affected by herpes zoster. Cutaneous dissemination-variously arid arbitrarily defined, but perhaps most reasonably considered as more than about 25 lesions distant from the original and adjacent d e r r n a t o m e s curs alniost exclusively in patients with impaired cell-mediated immunity. It develops in about 12% of those with cancer,'V5% of those with lymphomas," and 35% of bone marrow transplant recipients,\' but very uricommonly in patients with HIV infection.18The attack of herpes zoster usually begins in a typical dermatomal distribution, but 4 to 11 days later numerous lesions appear over the entire skin surface. Even without treatment, these usually resolve over a few weeks, but occasionally persist for m o n t h ~ . ' ~ ~ ' "a~small i minority, visceral involvement also occurs, affecting the lungs, liver, brain, or eyes.

NEUROLOGIC COMPLICATIONS POSTHERPETZC NEURALGIA

'The most common neurologic complication of hcrpes zoster is postherpetic neuralgia, usually defined as pain in the affected dermatome lasting longer than 1 month.'"he overall rate is about 9'%.'.14 It occurs in fewer than 10% of those under 30 years, but progressively increases to more than 60% in patients over 60.2","It may also be more frequent in the immunocompromised. T h e pain gradually disappears in most, and, in a careful prospective study, was still present at 6 months in only 13% of those older than 60.20In some, however, it lasts for years. Typically, it is a steady discornf'ort, described as boring, aching, burning, tearing, or itching, superimposed on which may be paroxysmal stabbing or burning pains. Many patients have allodynia-pain provoked by non-noxious stimuli such as light contact with clothing. MOTOR NEUROPATHY

324

A motor ricuropathy occurs in about 5%) of cases, presumably frorri viral irlvasion of the anterior horn cell or rootlet, usually in the same spinal segment or cranial nerve whose dernlatome is involved by the rash." Lower motor neuron weak-

VOLUME 12, NUMBER 4 IIECEMHER 1992

ness typically appears within 2 weeks of the skin lesions. Most common are palsies of the cranial nerves, primarily VII. When loss of taste over the anterior two thirds of' the tongue, ear pain, and vesicles in the external auditory canal or pinna (herpes zoster oticus) accompany facial muscle weakness, the disorder is the Kamsay Hunt syndrome, which accounts for about 5 to 10% of cases of facial nerve Compared with patients with idiopathic facial nerve paralysis (Bell's palsy), those with the Rarrlsay Hunt syndrome have more severe muscle weakness and a higher incidence of corrlplcte denervation, pain, hyperacusis, hearing loss, and diminished tear^.'^ Total recovery occurs in about two thirds of patients with partial, but in only about 10% with complete, facial paralysis.'" Tinnitus, vertigo, and gait unsteadiness can also develop with herpes zoster oticus, reflecting damage to nerve VIII.22 Rarely, predominantly with involvement of the ophthalmic branch of the trigeminal ricrve (herpes zoster ophthalmicus), extraocular muscle palsies occur, representing injury to cranial nerves 111, IV, and VI, alone or in combination. With cervical or lumbosacral nerve damage, upper or lower extremity weakness may develop, sometimes involving two or more myotornes, usually simultaneously. When the thoracic segments are affected, the intercostal or abdominal muscles may weaken, although this complication is rarely detected clinically. In patients with limb involvement about 55% have conlplete recovery, 25% significantly improve, and the remainder have substantial residual disability, usually greater in the distal than proximal muscle^.^^^'^ ENCEPHALITIS

Encephalitis, presunlably arising from direct viral invasion of the brain, uncommonly complicates herpes zoster in any dermatorne, but, seerriingly, patients with cell-mediated immunodeficiency and cutaneous disseminatiorl have an increased risk. The neurologic features tend to develop a few days after the skin lesions appear, but nlay precede the111by up to 3 weeks or follow them by 6 weeks. Fever is corrirrion at the onset, which may be sudden. Abnormal mentation, ranging from confusion and delirium to stupor or coma, is usually present. Headache, nuchal rigidity, and ataxia are also frequent. Cranial nerve palsies or paralysis of upper or lower extremities occurs in about 2.5% of patients, sei~uresin about 10%. T h e cerebrospinal fluid (CSF) typically shows mononuclear pleocytosis (usually less than 20011rirn" and increased protein; the glucose is low in about 10%. Such spinal fluid changes occur in many patients

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SEMINARS I N NEUROLOGY

HERPES ZOSTER-HIRSCHMANN

CEREBRAL INFARCTION

Single or several cerebral infarctions may follow the onset of herpes zoster, usually in the ophthalmic branch of the trigeminal nerve, by an average of 7 weeks, but up to 6 months. The cerebral infiirctions are usually ipsilateral to the zoster, causing contralateral hemiparesis, hemisensory findings, or aphasia. Typically, examination of the CSF reveals mononuclear pleocyiosis, elevated protein, and normal glucose. Ar~giogramsusually reveal segmental constrictions or thrombosis, most con~monlyinvolving the rniddle cerebral artery, but also the anterior or posterior cerebral arteries and the internal carotid. A granulorriatous arteritis is characteristically present in the vessels, although some demonstrate only thrombosis with intimal fibromuscular proliferation. Sometimes, antigens of the varicella-zoster virus are detectable in the vessel wall.'" MYELITIS

Myelitis,"0 which occurs in less than 1%) of herpes zoster, can precede the rash, but usually follows it by about 2 weeks, with a range up to 10 weeks. I11 most reported cases the lcsioris have been in the thoracic tlerrnatomes. The neurologic findings, which typically evolve over 1 to 3 weeks, are usually unilateral initially or, if' bilateral, are asymmetrical. Ipsilateral leg weakness predominates early, but paraparesis or paraplegia eventuates in rrrost. Sensory loss, involving pair1 and temperature perception more than vibratory or proprioceptive, occurs in about 75% of patients. A sensory level to all modalities develops in about one third, impaired bowel or bladder function in about one half; a few have prominent back pain. T h e CSF examination usually discloses mononuclear pleocytosis, increased protein, and normal glucose. About one third of patients die from complications of the myelitis; the survivors usually show gradual i~llprovementover months, but. cornplete recovery

is uncommon. Neuropathologic findings, most severe at the segment of the spinal cord corresponding to the clinically involved dermatomes, include posterior horn necrosis and inflammation, wedgeshaped regions of deniyelination located near the root entry Lone, and vasculitis with necrosis around the involved areas of the cord and brainstem. These abnormalities suggest central spread of virus from dorsal root ganglia to cause myelitis. A few patients with herpes zoster, usually in the sacral dermatornes, develop urinary retention without other signs of' spinal cord disease. Presumably, the inflammatory reaction in the dorsal root ganglion spreads to the cord and impairs parasympathetic outflow to the bladder." Similarly, intestinal ileus may occur when herpes zoster affects the thoracic nerves.3y NEUROLOGIC COMPLICATIONS WITHOUT RASH

In some patients with acute inflammatory neurologic diseases-including aseptic meningitis, encephalitis, myelitis, cranial polyneuropathy, and acute polyneuritis (Guillain-BarrC syndrome)-significant rises in antibody to the varicella-zoster virus have occurred in the absence of cutaneous lesions."" In addition, some have applied the term "zoster sine herpete" to neurologic symptoms strongly suggesting herpes zoster, but without a rash, usually unilateral pain in a dermatome with or without corresponding muscle weakness." In some cases a significant rise in antibodies to the varicella-zoster virus has occurred.""

OCULAR COMPLICATIONS About 50% of patients with herpes zoster involving the ophthalmic division of the trigeminal nerve have ocular damage," especially when it affects the nasociliary branch of the nerve, which supplies sensation to the eyeball and the tip of the nose. Hutchinson's sign, vesicles or1 the end of'the nose, reflects involvenlent of this branch and suggests impending ocular disease, including corneal infection, which can lead to ulceration, diminished vision, decreased sensation, scarring, and even perforation. In fact, the most common cause of visual loss, occurring in about 30% of untreated patients, is corneal scarring or inflammati~n.~' Uveitis (anterior segment inflammation), another cornrrlorl complication, can cause photophobia, intense pain, and decreased vision. Irlflanimation can also afiect the sclera (scleritis) and episcer-a (episcleritis). In addition, scarring of the eyelids and damage to the lashes can complicate skin lesions on the lids.

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with herpes zoster but without any neurologic finding^,'^ suggesting that asymptonlatic inflammation somewhere in the central nervous system is common, even in uncomplicated cases. In some patients with encephalitis, virus has been grown from the CSF. Computed tomography of the brain is usually normal; most electroencephalograms show diffuse slow wave activity. The overall mortality rate is about 25%!, but the cause of death is commonly the underlying disease rather than the'encephalitis. In those who survive, the mental symptoms usually abate within I to 3 weeks, but the ataxia and cranial nerve palsies may take several weeks longer to r e s o l ~ e . ' ~ - ~ ~

VO1,UME 12, NUMBER 4 IIECEI~IBEK1992

An ur~usual, but dramatic, complication of' rus. When compared with placebo and instituted herpes zoster (and herpes simplex) is acute retinal no longer than 72 hours after the rash begins, acynecrosis, which is bilateral in about one third of'pa- clovir treatment in inlmurlocorripetent hosts causes tients.:" Most have mild to moderate ocular pain pain to subside a little rnore quickly, viral shedding or irritation and hazy vision. Eye findings include to cease earlier, and lesions to heal somewhat Unfortunately, it does not decrease the conjunctival injection with ciliary flush and anterior segment. inflammation with fine or gran- frequency of postherpetic neuralgia,"' and its exulomatous keratitic precipitates. Retinal examina- pense does not justify the minor clinical benefits. tion reveals narrowed and sheathed retinal arter- An exception is herpes zoster ophthalmicus: a plaies, representing vasculitis; retinal hemorrhages cebo-controlled clinical trial showed that acyclovir, corresponding to the course of the involved ves- especially when begun by 72 hours after the rash, sels; and confluent areas of retinal whitening, es- reduces the incidence of' the most common ocular pecially in the periphery, indicating necrosis. The complications-corneal ulceration, corneal inflamintlamed vitreous contains cells and debris, and in- rnation, and ~veitis.~"he oral dose is 600 to 800 flammation of the optic nerve causes a swollen disc mg five times a day for 10 days. In addition, it and impaired vision. Even without treatment, the seems reasonable to use acyclovir to treat acute retinflammatory changes subside, but many patients inal necrosis, encephalitis, myelitis, and cerebrodevelop retinal holes that can lead to retinal de- vascular disease due to herpes zoster, although no tachment, the commonest cause of serious visual controlled clinical trials exist for these circumstances. 'l'he appropriate intravenous (lose is 10 loss in this disorder. mglkg a7ery8 hours for 7 days.

DIAGNOSIS In most patients the diagnosis of herpes zoster is clinically obvious, and laboratory confirmation is unnecessary. A Tzarlck preparation-scrapings from the base of vesicles, pustules, or erosions smeared onto a slide and treated with any of' several stains, including Giemsa's or Wright's-will demonstrate multinucleated giant cells in about 90% of patients with varicella-zoster infection."" It cannot discriminate between herpes simplex and varicella-zoster, however, but can differentiate these viral diseases from other blistering disorders. Viral culture of the lesions is expensive and the growth of varicella-zoster is slow (usually 7 to 10 days), making it useful primarily for confusing or unusual situations. One such indication is to diagnose atypical herpes simplex, which occasionally causes a vesicular rash in a dermatomal distribution that mimics herpes zo~ter.~'Serologic tests, such as fluorescent antibody to membrane antigen, are most useful to determine whether a person has had varicella in the past, but a significant titer rise between acute and corivalescent blood specimens taken several weeks apart can help confirm an uncertain diagnosis, especially when suggestive neurologic features occur without a rash.

TREATMENT ZMMUNOCOMPETENT HOST

326

Oral and intravenous acyclovir in relatively high doses is active against the varicella-zoster vi-

ZMMUNOCOMPROMZSED HOSTS

Although herpes zoster resolves without cutaneous dissemination or visceral injury in most patients with severely impaired cell-mediated immunity, controlled trials indicate that acyclovir helps the cutaneous lesions resolve much more quickly and reduces the risk of' visceral involvement in those with either localized or disseminated herpes zoster.' With localized disease, oral acyclovir 800 mg five times a day for 7 to 10 days is reasonable; with disseminated disease, treatment is usually intravenous acyclovir 10 mglkg every 8 hours for 7 days or at least 2 days beyond the last for~nationof a new lesion, whichever is longer. Zostcr immune globulin, however, is ineffective in altering the course of' herpes Loster in immunocompromised

POSTHERPETZC NEURALGIA

'Two controlled trials of systemic corticosteroids (but without acyclovir) to treat elderly immunocompetent patients during acute herpes zoster have demonstrated a marked reduction in the . ~ corti~,~~ incidence of postherpetic n e ~ r a l ~ i a'The costeroid was begun an average of 5, but as late as 8, days after the rash began. A study using combined therapy with prednisolone and acyclovir compared with acyclovir alone discovered no difference in postherpetic neuralgia at 6 months, but there was a lower frequency of pain among prednisolone recipients until the 23rd week.4nThese investigations suggest that oral corticosteroids in doses of about 40 to 60 mg of prednisone for 1 week followed by a tapering schedule during the

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SEMINARS I N NEUROLOGY

TRANSMISSION OF DISEASE Because patients with herpes zoster infection can trarls~rlitthe virus uritil their skin lesions have crusted over, they should be careful to avoid contact with susceptible people (that is, those without previous varicella infection), especially those with risks of serious disease. These include patients with impaired cell-mediated immunity and women during pregnancy, in whom the infection threatens . ~ ~ varicella ocboth the fetus and t h e m ~ e l v e sWhen curs during the first trimester, in about 10% the congenital varicella syndrome develops, characterized by limb hypoplasia, cutaneous scars, microcephaly, cortical atrophy, chorioretinitis, cataracts, and other anomalies. When maternal infection is from 5 days before delivery to 2 days after, the risk is high for neonatal varicella, which is often associated with visceral involvement, particularly pneumonia, and a substantial mortality rate.54T h e incidence of varicella pneumonia, which can be severe and sometimes fatal, is as high as 10% in the

mother during the pregnancy. In addition, premature labor and deliver may occur.53 Developing varicella and subsequently transmitting the virus to patients is an occupational risk for health care personnel without previous varicella infection. Experts recommend that such people, when exposed to the virus, should be removed from contact with patients from days 10 to 21 after exposure. A serologic study of 241 health care personnel demonstrated that 36% ofthose without a history of varicella lacked protective antibody.55All susceptible people were 35 years of age or younger. Health care workers in that age group with a negative or uncertain history of varicella who lack antibodies on serologic testing rnight be candidates for the varicella vaccine (when it becomes available) to protect themselves and their patients.

REFERENCES I . Gordon JE. Chickenpox: a n epidemiological review. Am J Med Sci 1962;244:362-89 2. Heath RB, Kangro HO. Varicella zoster. In: Zuckernian AJ, Banatvala JE, Pattison JR, eds: Principles and practice of clinical virology. Chichestcr: John Nriley, 19YU:52 3. Gershon AA, Steinberg SJ. Antibody responses to varicella-zoster virus and the role of antibody in host dcPense. Am J Med Sci 1981;282:12-7 4. Hope-Si~ripsonRE. T h e nature of herpes zoster: a longterm study arid a new hypothesis. Proc R Soc Med 1965;58:Y-20 5. Ross AH. Modification of chickenpox in family contacts by administration of gamma globulin. N Engl J Med 1962;267:369-76 6. Seiler JE. A study of' herpes particularly in its relationship to chickenpox. J Hyg 1949;47:253-62 7. Mahalingham R, Wellish M, Wolf W, et al. Latent varicella-zoster viral DNA in human trigeminal and thoracic ganglia. N Engl J Med 1990;323:627-31 8. Ragozzino MW, Melton LJ, Kurland LT, et al. Population-based study of herpes zoster and its sequelae. Medicine (Baltimore) 1982;61:3 10-6 9. Ragozzino MW, Melton LJ, Kurland LT, et al. Risk of cancer after herpes zoster. A population-based study. N Engl Med 1982;307:393-7 10. Melbye M, Grossman RJ, Goedert JJ, e t al. Risk of AIDS aiter herpes zoster. Lancet 1987; 1 :728-3 1 11. Mazur M, Dolin K. Herpes zoster at the N I H : a 20 year experience. Am J Med 1978;65:738-43 12. Gilden DH, Dueland AN, Cohrs R, et al. Preherpetic neuralgia. Neurology 1991 ;4 1: 12 15-8 13. Ohert G , Svedmyr A. Varicelliform eruptions in herpes zoster-some clinical a n d serological observations. Scand J Infect Dis 1969;1:47-9 14. Burgoon CF, Burgoon JS, Baldridge GD. T h e natural history of herpes zoster. JAMA 1957;164:265-9 15. Langenherg A, Yen TSB, LeBoit PE. Granulomatous vasculitis occurring after cutaneous herpes zoster despite absencc of viral genome. J Am Acad Dern~atol1991; 24:429-33 16. Rusttioven JJ, Ahlgren P, Elhakim T, et al. Varicella-zoster infection in adult cancer patients. A population study. Arch Intern Med 1988; 148: 1.561-6 17. Locksley RM, Flourney N, Sullivan KM, Meyers JD. Infection with varicella-zoster virus after marrow tr-ansplantation. J Infect l)is 1985; 152: 1172-81

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next 2 weeks may be helpful in patients over 50 years of age with painful herpes zoster. No significant complications from the corticosteroids occurred in the trials. Patients have received many different local and systemic therapies for established postherpetic neuralgia, usually without any scientific support from controlled trials. The most impressive evidence, garnered from careful studies, is for tricyclic antidepressant agents. A double-blind, placebo-controlled, crossover trial of amitriptyline showed good to excellent response in 67% during treatnlerlt with the active agent compared with 4% with pla~ebo.~''l'he average effective daily dose was 75 mg (range; 25 to 137.5 mg). T h e medication was equally beneficial whether the patients were depressed or not, suggesting that pain relief was independent of the medication's antidepressant activity. In another double-blind, crossover study, amitriptyline, but not lorazepam, was effective in about one half of patients." A siniilar trial showed a good to excellent response in about 65% of patients receiving a nonsedating tricyclic antidepressant, desipramine, compared with 10% receiving placebo." The average daily dose was 167 mg. A double-blind, placebo-controlled investigation showed that topical capsaicin, a substance believed to diminish pain by depleting substance P (an excitatory peptide neurotransmitter), decreased postherpetic neuralgia in about one half of patients applying it three to four times a day.52In general, however, the pain relief was only modest.

18. Cohen PR, GI-ossman ME. Clinical fcaturcs of human imnrunodef'icierrcy virus-associated disseminated herpes zoster virus infection-a review of the literature. Clin Exp Derrrlatol 1989; 14:273-6 19. Watson CPN. Postherpetic neuralgia. Ncurol Clin 1989; 7:231-48 20. McKendrick MW, McGill J I , Wood MJ. Lack of effect ot' acyclovir on posthcrpctic ncuralgia. Br Med J 1989; 298:43 1 21. DeMoragas JM, Kicrland RR. T h c outcome of patients with herpes zoster. Arch Dermatol 1957;75: 193-6 22. Tbornas J E , Howard F M . Segrrlerltal zoster paresis-a disease profile. Neurology 1972;22:459-66 23. Devriese PP, Moesker WH. T h e natural history of t'acial paralysis in herpes zoster. Clin Otolaryngol 1988; 13: 289-98 24. Kobillard KB. Hilsingcr RI., Adour KK. Ramsay Hunt facial paralysis: clinical analyses of 185 patients. Otolaryngol Head Neck Surg 1986;95:292-7 25. Grant E D , Rowe CR. Motor paralysis of the extremities in herpes zoster. J Bone Joint Surg 1961;43A:885-96 26. Appelhaum E, Kreps SI, Sunshine A. Herpes zoster encephalitis. AIII J Med 1962;32:25-31 27. Jemsck J , Greenberg SB, Taber L, et al. Herpes zosterassociated encephalitis: clinicopathologic report of 12 cases a n d review of the literature. Medicine (Baltimore) 1983;62:81-97 28. Peterslund NA. Herpes zoster associated encephalitis: clinical findings and acyclovir treatmcnt. Scand J Int'ect Dis 1988;20:583-92 29. Reshef E, Greenberg SB, Jankovic J . Herpes zoster ophthalmicus followed by contralateral hemiparesis: report of two cases a n d review of the literature. J Neurol Neurosurg Psychiatry 1985;48: 122-7 30. Devinsky O , Cho ES, Petito CK, Price RW. Herpes zoster myelitis. Brain 1991;114:1181-96 3 1. Richmond W. 'l'he genito-urinary manifestations of herpes zoster. T h r e e case reports and a review of the literature. Br J Urol 1974;46: 193-200 32. Pai NB, Murthy KS, Kumar H.1', Gerst PH. Association of acute colonic pseudo-ohstruction (Ogilvie's syndrome) with herpes zoster. Am Surg 1990;56:691-4 33. Mayo DR, Boos J . Varicella zoster-associated neurologic disease without skin lesions. Arch Ncurol 1989;46: 3 13-5 34. Lewis GW. Zoster sine herpete. Br Med J 1958;2:418-21 3 5 . Easton HG. Zoster sine herpete causing acute trigeminal neuralgia. Lancet 1970;2: 1065-6 36. Liesegang TJ. Diagnosis a n d therapy of herpes zoster ophthalmicus. Ophthalmology 1991;98: 12 16-29 37. Womack LW, Liesegang .I'J. Complications of herpes zoster ophthalmicus. Arch Ophthalmol 1983;101:42-5 38. Duker JS, Blurnenkranz MS. Diagnosis and management of the acute retinal necrosis (ARN) syndrome. Surv Ophthalmol 1991;35:327-43

V O L U M E 12, NUMBER 4 DECEMBER 1992

39. Folkers E, Vreeswijk J , Orarrje AP, Duiverrvorden JN. Rapid diagnosis in varicella a n d herpes zoster: re-evali ~ a t i o nof direct smcar (Tzanck tcst) a n d clcctron microscopy in comparison with virus isolation. Br J Der~ n a t o l1989; 121 :28$-96 40. Kalman CM, Laskin 01.. Herpes zoster and zosteriform herpes simplex virus irlfectiorls in irnrnunocon~petent adults. Am J Med 1986;81:775-8 41. Peterslund NA. Seyer-IIansen K, Ipsen J , et al. Acyclovir in herpes zoster. Lancet 198 1;2:827-30 42. Wood h,fJ, Ogan PH, McKendrick MW, et al. Efficacy of oral acyclovir treatrrrerlt of acute herpes zoster. Am J Med 1988;85(suppl 2A):79-83 43. Coho LM, Goulks G N , Liesegang T, et al. Oral acyclovir in the treatment of acute herpcs zostcr ophthalmicus. Ophthalmology 1986;93:763-70 44. Ralfour H H , Bean B, 1.askin OI., et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med 1983;308:1448-53 45. Stevens D:2, Merigan TC. Zoster immune globulin prophylaxis of disseminated zoster in compromised hosts. A randomized trial. Arch Intern Med 1980;140:52-4 46. Eaglstein WH, Katz K. Brown J A . 'l'he effects of early cortic:osteroid therapy o n the skin eruption and pain of herpes zoster. JAMA 1970;211:1681-3 47. Keczkes K, Basheer AM. Do corticosteroids prevent postherpetic neuralgia? Br J Dermatol 1980;102:551-5 48. Esnlann B, Geil JP, Kroon S, et al. Prednisolone does not prevent post-herpetir neuralgia. Lancet 1987;2: 126-9 49. Watson CP, Evans RJ, Reed K, et al. Amitriptyline versus placcbo in postherpctic neuralgia. Neurology 1982;32: 671-3 50. Max MB, Schafer SC, Culnane M, et al. Amitriptyline, hut not lorazepam, relieves postherpetic neuralgia. Neurology 1988;38: 1427-32 51. Kishore-Kumar R, Max MB, Schafer SC, et al. Desipramine relieves postherpetic neuralgia. Clin Pharmacol T h c r 1990;47:305-12 52. Bernstein J E , Korman NJ, Bickers DR, et al. Topical capsaicin treatment of chronic postherpetic neuralgia. J Am Acad Dcrmatol 1989;2 1:265-70 53. Paryani SG, Arvin AM. Intrauterine infection with varirella-zoster virus after maternal varicella. N Engl J Med 1986;314: 1542-6 54. Straus SE, Ostrove J M , Inchauspe GT, et al. Varicellazoster virus infectio~ls.Biology, natural history, treatmcnt, and prevention. Ann Intern Med 1988;108:22137. 55. McKinney WP, Horowitz M M , Battiola RJ. Susceptibility of' hospital-based health care persorirlel to varicellazoster virus infcctions. Am J Infect Control 1989;17: 26-30

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SEMINARS I N NEUROLOGY

Herpes zoster.

SEMINARS I N NEUROLOGY-VOLUME 12, NO. 4 DECEMBER 1992 Herpes Zoster ACUTE HERPES ZOSTER A herpesvirus confined to humans causes IWO disorders whose...
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