Herpes Zoster Vertigo Treatment

Chorioretinits and neuritis of the optic nerve are more frequently observed in AIDS patients. Also, herpetic retinal necroses due to VZV infection with the risk of bilateral blindness were reported in HIV positive patients.

Other neurologic complications comprise zoster meningitis, motor neuropathies and paralysis, Guillain-Barre syndrome, granulomatous arteritis and affection of cranial nerves (Malin, 1996). The most frequent and important complication of zoster affecting the nervous system, is acute and chronic pain also known as PHN. PHN is defined as pain that persists for longer than 4 weeks or that occurs 4 weeks after a pain-free interval. Approximately 10-20% of zoster patients of all ages are affected by PHN. Chronic zoster pain in children is extremely rare (Malin, 1996).

The manifestation rate of PHN shows a clear age-dependence. In zoster patients over 55, 60 and 70 years it is 27, 47 and 73%, respectively. In women and patients with zoster ophthalmicus, PHN seems to occur more frequently. Immunodeficiency seems to be no risk for the development of chronic pain (Hope-Simpson, 1975; Guess et al., 1985; Gross, 1997).

Best documented complications are postzosteric neuropathies and paralysis such as phrenoplegias, abdominal hernias, bladder dysfunction and cystitis. In some cases these symptoms may be misinterpreted (Malin, 1996). Another neurologic complication is segmental paralysis which has a good outcome, since in every second case complete regression occurs.

8. Zoster in Immunodeficient Patients

Zoster may present atypically in patients with pathologic or iatrogenic immunodeficiency. The rash may occur mitigated with few symptoms. However, in most cases, distinct inflammation, partly with hemorrhages and occasionally with necroses, is found. In some cases, more than one dermatome is involved and the rash may persist for a longer period than in immunocom-petent patients.

Disseminated zoster with varicella-like skin involvement and involvement of inner organs is observed more frequently in immunodeficient patients (Cohen et al., 1998; Rustoven et al., 1998). Zoster is regarded as an early marker for HIV infection (Melbye et al., 1978; Friedmann-Kiein et al., 1986; Schofer, 1991). Therefore, HIV infection should always be excluded serologically in zoster patients younger than 50.

With reduced cellular immunity, the zoster rash may be associated with atypic varicelliform or even verrucous or ecthymiform lesions (Galagher and Merigan, 1979; Hoppenjans et al., 1990; Schofer, 1991; Schofer et al., 1998).

9. Diagnosis

Zoster is usually diagnosed by inspection with an asymmetrical dermatomal rash and grouped vesicles. Further evidence is found with the rash limited by the midline, its dermatomal arrangement and, especially, prodromal and zoster-associated segmental pain. Diagnostic problems may occur particularly in the prodromal or early phase of zoster when only erythematous skin lesions exist.

9.1. Laboratory Diagnosis

The differentiation of the VZV infection from herpes simplex and bullous dermatoses is an important indication for virological diagnosis. Also, VZV infections of pregnant women and of newborn infants, atypical infections of immunodeficient patients and suspected VZV infection of the central nervous system must be confirmed by laboratory diagnosis.

Today, the VZV polymerase chain reaction (PCR) as well as the direct detection of virus in cell cultures and the detection of specific antibodies to VZV in special circumstances are recommended.

The enzyme-linked immunosorbent assay and the immunofluorescence technique are especially suited for the detection of VZV-specific immunoglobulins of classes IgG, IgM and IgA. VZV-IgG rises may occur spontaneously and in recurrent HSV-infections due to cross reactivity of epitopes. However, additional detection of IgM and high-titered IgA anti-VZV antibodies usually indicates a reactivated VZV-infection regardless whether lesions are visible or not. Generally the patient consults a physician 1-3 days after the occurrence of symptoms. Thus clinical diagnosis is mostly supported by serologic findings (Doerr et al., 1987; Wutzler and Doerr, 1995; Doerr and Rabenau, 1996). Serological diagnosis is particularly efficient and helpful in immunodeficient patients suffering from VZV reactivation (Wutzler and Doerr, 1995).

In very early zoster (erythematous stage), detection of VZV infection in tissue by the VZV-specific PCR may occasionally be helpful (Lilie and Wassilew, 1999). Additionally, VZV infection can be detected using the immunofluorescence test. Another indirect but less sensitive detection procedure is the so-called Tzanck test that examines the cytopathic effect of VZV in the epidermis with characteristics multinucleate giant cells and intranuclear inclusions (Barr et al., 1977; Solomon et al., 1986; Gross and Doerr, 1997). Unfortunately, this cytopathic effect is not VZV-specific since it is also seen in cutaneous HSV-infections.

Electron microscopy allows the morphological detection of herpes viruses in vesicular fluids or smears. However, this again does not allow dif ferentiation of the herpes viruses VZV, HSV-1 and HSV-2 (Barr et al., 1977; Gross and Doerr, 1997). Furthermore electron microscopy cannot be used routinely.

9.2. Differential Diagnosis

The major differential diagnoses of zoster are the zosteriform herpes simplex and the different forms of erysipelas, such as hemorrhagic and bullous erysipelos.

Further differential diagnoses are contact dermatitis, insect bites, bullous dermatoses such as the bullous pemphigoid and pemphigus vulgaris. Phlegmones and panniculitis pose less frequently differential diagnosis problems. In cases where the clinical presentation is atypical, particularly if no symptoms exist, viral detection should be done by PCR, or viral culture as well as by serology and also by the Tzanck test (Gross and Doerr, 1997; Lilie and Wassilew, 1999).

If chronic pain persists after the zoster lesions have healed diagnosis can be confirmed retrospectively by serologic tests. Viral detection is not possible in this phase.

10. Therapy

The aim of zoster treatment is to relieve pain in the acute phase, to limit the spread and duration of zosteric skin lesions and to prevent or alleviate PHN and other acute and chronic complications (Table 1). It is of utmost importance that ophthalmological complications should be referred for specialist ophthalmic management as soon as possible. Complications related to zoster of other cranial nerves such as zoster oticus always require consulting a specialist.

10.1. Symptomatic Therapy of Zoster

Depending on the stage of the rash, treatment will be done locally either through drying and antisepsis, e.g. with wet dressings, with lotio alba, vioform zinc mixture or later by crust removal. A satisfactory local therapy with proven antiviral efficacy does not exist. Local zoster therapy with antiviral substances has shown to be ineffective and is not recommended (Gross, 1997).

Painlessness should be achieved by appropriately-dosed analgesics (e.g. tramadol), often in combination with a neuroactive agent, (e.g. amitriptylin) (Malin, 1996). However, it is unknown as to whether systemic analgesia prevents the development of PHN in the early stage of zoster.

Table 2. Indications for systemic antiviral therapy of zoster

Urgent indications

Zoster of any localization in patients beyond the age of 50 Zoster in the head/neck area of patients at any age Severe zoster on the trunk/on the extremities Zoster in immunodeficient patients

Zoster in patients with severe atopic dermatitis and severe eczemas Relative indications

Zoster on the trunk/on the extremities in patients younger than 50 years

10.2. Indications for Antiviral Chemotherapy

Zoster is a self-limiting disease affecting skin and nervous system.

Even without specific antiviral treatment, the circumscribed zoster on the trunk and on the extremities of young individuals without risk factors usually heals without complications.

Antiviral treatment shortens the healing process and is especially important when a complicated clinical course is expected (Table 2).

Systemic antiviral therapy is urgently indicated in patients beyond the age of 50, in immunodeficient patients, in patients with malignant primary disease as well as in patients with involvement of cranial nerves, especially with affection of the first branch of trigeminal nerve (zoster ophthalmicus) but also with zoster oticus. Furthermore, urgent indications for systemic antiviral treatment are severe dermatitis atopica and other severe eczemas. It is noteworthy that zoster ophthalmicus and zoster oticus as well as an age beyond 50 are also major risks for the development of PHN.

Furthermore, antiviral therapy should always be initiated if vesicles develop on more than one skin segment. Patients with hemorrhagic lesions and/or patients with mucosal affection should also always receive systemic antiviral treatment (Table 2). The Zoster Study Group of the Dermatological Research Cooperative Group (ADF) of the German Dermatology Society and of the Paul-Ehrlich-Society developed a zoster score (Meister et al., 1998a, b) which can be used as decision aid for the initiation of systemic antiviral therapy. This score takes into account the following risk factors.

Age beyond 50, dermatomal pain, female gender, more than 50 efflorescences, hemorrhagic efflorescences, involvement of cranial or sacral der-matomes. The practicability of this zoster score system in clinic routine has been demonstrated at the Department of Dermatology and Venereology of the University of Rostock (Schlecht et al., in preparation).

10.3. When to Start Systemic Antiviral Therapy

The success of each antiviral treatment is dependent on the starting point of therapy. Systemic virostatic therapy must be initiated as soon as possible, i.e. if possible within 48 to a maximum of 72 h after onset of skin symptoms. The effect level of the antiviral drug must be achieved rapidly and maintained for an optimum therapeutical success. In the following situations, systemic antiviral therapy can also be started even at a later date (after 72 h).

Disseminated zoster with evidence of immuno-deficiency and affection of inner organs, persisting zoster ophthalmicus and zoster oticus. Furthermore, even after 72 h, antiviral treatment of zoster is urgently indicated in all patients with known immunodeficiency. Some more recent data suggest that valacy-clovir, the prodrug of acyclovir, continues to be beneficial in preventing PHN even if given 72 h after onset of symptoms.

10.4. Antiviral Therapy of Zoster

A total of 4 different systemic antiviral substances for treatment of zoster have become available in Germany: acyclovir, valacyclovir, famciclovir and brivudin, which very recently has been approved (illustration), whereas in the United States only three drugs - acyclovir, valacyclovir and famciclovir - are in use (Gnann and Whitley, 2002).

All of these substances can be given orally (Gross and Laskowski, 2001). Only acyclovir can be administered both enterally and parenterally. Up to now, valacyclovir and famciclovir have been the world-wide most commonly used antiviral drugs for the oral treatment of uncomplicated zoster. Better pharma-cokinetics, better bioavailability and easier application make them superior to oral acyclovir. A recent double-blind randomised study showed valacyclovir and famciclovir to have similar effects on zoster-associated pain and on PHN in immunocompetent patients (Tyring et al., 2000). Valacyclovir and famciclovir have to be administered orally 3 times daily for 7 days, whereas oral acyclovir must be given in a dose of 800 mg, 5 times daily. Brivudin has the great advantage of requiring only once daily dosing. In VZV infections, brivudin has a markedly higher antiviral potency than acyclovir, valacyclovir and famciclovir (De Clercq et al., 1979). Brivudin, when given once daily (1 X 125 mg for 7 days), is therefore well effective and superior to oral acy-clovir treatment (5 times daily dosing) (Table 3).

This is especially true for patients beyond the age of 50 who are at a higher risk of developing PHN. Patients treated with brivudin had significantly faster stop of viral replication compared to patients treated by oral

Table 3. Current antiviral therapy for zoster

Valacyclovir oral

1000 mg

3 X daily

7 days

Acyclovir oral

800 mg

5 X daily

7 days

Acyclovir intravenous

5-7.5 mg

3 X daily

7 days

Acyclovir intravenous3

8-10 mg

3 X daily

7-10 days

Famciclovir oral

250 mg

3 X daily

7 days

Brivudin oral

125 mg

1 X daily

7 days

aZoster in immunodeficient patients.

aZoster in immunodeficient patients.

acyclovir (5 X 800mg per day) (Wutzler et al., 2001). Already in 1995, Wutzler et al. were able to show that oral administration of brivudin, 125 mg 4 times daily, is as effective as intravenous acyclovir, 10 mg per kg body weight with regard to acute zoster symptoms in immunodeficient patients (Wutzler et al., 1995).

Recently, a randomised observation study showed an 11% lower PHN rate in the patient group treated with brivudin (32.7%) than in the acyclovir group (43.5%) (P = 0.006). As with all observation studies this study carried certain drawbacks and the observation needs further evaluation (Wassilew et al., 2001a). A restriction applies to immunosuppressed patients, children and pregnant or lactating women who cannot be treated with brivudin. Furthermore, brivudin must not be used in combination with 5-fluorouracil or with other drugs containing 5-fluoropyrimidines. In the last year, brivudin has been approved in Germany for oral treatment of zoster, due to the markedly more convenient administration, brivudin (125 mg once daily) seems to be superior, especially in the elderly, to the oral antiviral drugs valacyclovir (1000 mg,

3 times daily) and famciclovir (250 mg, 3 times daily).

A large multicenter, prospective, double-blind, randomised study in 2027 patients showed brivudin (125 mg, once daily) to be at least as effective as the antiviral famciclovir (250 mg, 3 times daily) for prevention of PHN. Both PHN duration as well as zoster-associated pain were influenced by once daily brivudin in the same way as with the triple dosed famciclovir (Wassilew et al., 2001b). Currently recommended antiviral therapy in Germany is shown in Table 3.

10.5. Intravenous Antiviral Therapy

Parenteral therapy with acyclovir (5-10 mg per kg body weight, 3 times per day) is the standard treatment for zoster in immunodeficient patients.

However, in contrast to studies comparing intravenous acyclovir versus oral Brivudin (Wutzler et al., 1995), no controlled studies comparing intravenous acyclovir with oral treatment of acyclovir, valacyclovir or famciclovir have been performed for this patient group so far.

The doses of intravenous acyclovir, oral acyclovir, oral valacyclovir and oral famciclovir have to be adapted for patients with reduced renal function. In contrast, even with reduced creatinine clearance, it is not necessary to change the dosage of oral brivudin.

10.6. Treatment of Zoster Affecting Cranial Nerves

There are no controlled studies comparing intravenous acyclovir in zoster ophthalmicus and zoster oticus with oral antiviral treatments such as acyclovir, valacyclovir, brivudin or famciclovir. The maintenance of a sufficient virostatic plasma level is of utmost importance especially for the treatment of zoster of these locations. Therefore, in most cases, intravenous acyclovir therapy under stationary conditions has to be preferred to oral antiviral therapy.

10.6.1. Ophthalmological Complications

Systemic intravenous or oral antiviral treatment of zoster ophthalmicus must be done as soon as possible. For oral treatment, acyclovir 800 mg 5 times a day for at least 7 days and valacyclovir 1000 mg 3 times a day, also for 7 days are recommended. Colin et al. showed that the latter valaclovir dose has the same efficacy as acyclovir (5 times 800 mg per day) in the prophylaxis of ocular complications of zoster such as conjunctivitis, keratitis and pain (Colin et al., 2000). Longer treatment may occasionally be needed. However, controlled studies showed no significantly better clinical efficacy when acyclovir was given for 14 or 21 days (Hoang-Xuan et al., 1992; Beutner et al., 1995).

Viral epithelial keratitis must be treated with local virostatic agents (e.g. acyclovir eye ointment). It is recommended to refrain completely from steroid therapy, except in endothelitis and trabeculitis. In this case, systemic combination therapy consisting of acyclovir and prednisolone is recommended. The steroids dose should be carefully considered to balance between the antiviral effect and the tissue-damaging immune reaction (Sundmacher, 1996).

10.6.2. Zoster Oticus

Zoster oticus results from an infection of ganglial cells of the VII and VIII cranial nerves. Clinically, it is characterised in most cases by severe earache, loss of hearing (conductive deafness), vertigo and/or facial paresis. After ENT consultation and specific otological diagnosis, the following therapy is usually indicated: high dose antiviral therapy (intravenously preferred) in combination with glucocorticoids, infusion treatment with rheologics or physiological saline solution with vasoactive substances. Analgesics and, in cases with strong vertigo, anti-vertigo agents are additionally indicated.

10.7. Corticosteroid Therapy

The additive zoster therapy with high dose steroids shortens the duration of acute zoster pain, but has no essential effect on chronic pain (PHN). This is the result of 2 large prospective studies (Wood et al., 1994; Whitley et al., 1996). The use of corticosteroids must be carefully considered, especially in view of possible side effects.

It is not recommended to use corticosteroids without systemic antiviral therapy. Study results are available only for a combination therapy of prednisolone (40 and 60 mg per day, dose reduction over ~ 10-14 days to 5 mg per day) and acyclovir. However, nothing speaks against possible combination of prednisolone with valacyclovir, brivudin or famciclovir.

10.8. Therapy of Neuralgia: Step-by-Step Scheme

Patient-specific aspects and side effects are important considerations in pain therapy. Early presentation to a pain therapist or a pain outpatient clinic may be required.

1) Step 1: non-steroidal analgesics (e.g. paracetamol 1.5-5 g per day)

2) Step 2: additional low-potency opioid analgesics (e.g. tramadol 200-400 mg per day, codeine 120 mg per day), if necessary, combined preparations.

3) Step 3: in addition to a 'peripheral' analgesic, administration of a high-potency central opioid (e.g. buprenorphine 1.5-1.6 mg per day; oral morphine 30-360 mg per day) is indicated. This refers to patients who fail to respond the more measured treatment approaches.

In severe neuralgic pain, step 1 or 2 in combination with an anti-convulsant (carbamazepine 400-1200 mg per day). Anti-convulsants (carbamazepine) can reduce the lancinating pain, but are not effective for continuous pain. Another option is gabapentine (900-2400 mg per day). Also, anti-depressants, amitryp-tilin 10-75 mg) and neuroleptics (levomepromazin 20-150 mg per day) may be efficient, especially in elderly patients (Malin, 1996; Wassilew, 2000).

Further treatment possibilities consist in local therapy with capsaicin, local anesthetic blocking of sympathetic nerve, transcutaneous electric nerve stimulation, if necessary, neurosurgery (e.g. thermocoagulation of substantial gelatinosa Rolandi) in exceptional cases.

10.9. Therapy of Other Neurologic Complications of Zoster

Zoster meningitis, zoster encephalitis and zoster myelitis should be treated with parenteral acyclovir in a dose of 10 mg per kg body weight, 3 times daily. Also in severe zoster ophthalmicus and zoster oticus, intravenous acyclovir should be preferred to enteral therapy.

10.10. Therapy of Zoster in Children and Adolescents

Zoster in childhood is usually not a strict indication for systemic antiviral therapy. An exception is zoster affecting cranial nerves. Also, children with hereditary or acquired immunodeficiency as well as atopic children might benefit from antiviral therapy. As long as there are no controlled treatment studies in children with immunodeficiency and zoster available, one can only speculate whether antivirals, given early, might prevent viral spread, reduce the severity of inflammation and prevent secondary immunosuppression. It is likely, but not yet proven, that severe tissue destruction, secondary bacterial infections and scar formation, might be reduced by an early antiviral therapy. In analogy of the sometimes severe, but individually not predictable course of zoster in patients with HIV infection we suggest to treat immunodeficient and atopic children with acyclovir intravenously.

10.11. Therapy of Zoster in Immunodeficient Patients

Only acyclovir has been approved so far for the treatment of zoster in severely immunocompromized patients. Other oral virostatic agents such as brivudin, valacyclovir and famciclovir showed positive results in case reports especially in HIV-infected patients, but are not officially approved. In a given case, the responsible physician may use these drugs after careful consideration of the risks involved.

It has been shown that the therapeutical regimen of acyclovir is dependent on the severity of immunodeficiency and clinical findings. If the CD4 cells are roughly within limits of normal (>400 cells per |xl), segmental zoster may be treated with a standard dose of acyclovir intravenous (5-7.5 mg per kg body weight every 8 h). In severe immunodeficiency with extended skin lesions, especially when neurologic symptoms are present, treatment with high dose intravenous acyclovir (10 mg per kg every 8h) and continuous monitoring of renal function is required. In severe immunodeficiency with extended skin lesions, especially when neurologic symptoms are present, treatment with high dose intravenous acyclovir (10 mg per kg every 8h) is required. As acyclovir has some nephrotoxic properties and cumulates in patients with impaired renal function, serum creatinine clearance must be tested with the first given dose of acyclovir. In case of reduced serum creati-nine clearance the interval to the following acyclovir infusions must be prolonged from 8 to 12 or even 24 h (according to the nomograms or tables provided by the producers of acyclovir).

Acyclovir resistance has to be assumed if the clinical findings improve only slowly or not at all. In such cases, another treatment option would be intravenous foscarnet which, however, is highly nephrotoxic (Breton et al., 1998).

Apart from the constant number of HIV patients in Germany (~ 1500— 1700 new infections in 2000), especially the prophylaxis and therapy of other immunodeficient patients such as organ transplant recipients, patients under immunosuppressive agents and tumor patients strongly require therapeutics that can be used if acyclovir resistance has developed. Also, zoster patients with renal damage (contraindications for acyclovir and foscarnet) require new non-nephrotoxic virostatic agents.

10.12. Therapy of Zoster in Pregnancy

Unlike varicella, maternal zoster is hardly considered a risk for the unborn. Normally, there is no viremia that could pose a risk to the development of the unborn. Antiviral therapy of the mother with intravenous acyclovir (3 times 5-10 mg per kg body weight for 7 days) is indicated only in exceptional cases. If possible, zoster during pregnancy should be treated locally and symptomati-cally. Topical acyclovir is definitely not recommended. The treatment of a pregnant zoster patient in a gynaecologic practice should be in such a way that non-pregnant women without immune protection are not put at risk of varicella.

11. Resistance of Varicella Zoster Virus to Antivirals

VZV can become resistant to nucleoside analogues such as acyclovir, vala-cyclovir, famciclovir and brivudin, probably due to mutations in the thymidin kinase (TK) gene or mutations in the polymerase gene. Viral strains with mutations in the TK gene are usually resistant to acyclovir, famciclovir and also to ganciclovir. Such virus strains have been isolated from several HIV infected patients who had been suffering from chronic VZV infections and who had been treated with acyclovir for longer periods. Acyclovir-resistant VZV strains have no TK or no proper TK due to their altered substrate specificity. Usually, this mechanism cannot be by-passed by increasing the dose. In such cases, treatment of choice is intravenous foscarnet, 3 times 40 mg or 2 X 50 mg per kg body weight per day (Breton et al., 1998). However, foscarnet may also be ineffective in polymerase gene mutations. The only alternative would then be treatment with intravenous cidofovir (Safrin et al., 1997).

Appendix A: Illustration







Systemic antiviral substances for zoster therapy approved in Germany.


Balfour HH. Varicella zoster virus infections in immunocompromised hosts. Am J Med 1988;85:68-73.

Barr RJ, Hertens J, Graham JH. Rapid method for Tzanck preparation. J Am Med Ass 1977;237: 1119-20.

Beutner KR, Friedman DJ, Forszpaniak C, et al. Valacyclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother 1995;39: 1546-53.

Bloss G, Ebisch MA, Kunz M, Gross G. Bilateraler asymmetrischer Zoster im Jugendalter. Hautarzt 2001;4:335-8.

Breton G, Fillet AM, Katlama C, et al. Acyclovir-resistant herpes zoster in human immunodeficiency virus-infected patients: results of foscarnet therapy. Clin Infect Dis 1998;27:1525-7.

Cohen RR, Beltraini VP, Grossman ME. Disseminated herpes zoster in patients with human immunodeficiency virus infection. Am J Med 1998;84:1076-80.

Colin J, Prisant O, Cochener B, et al. Comparison of the efficacy and safety of valacyclovir and acyclovir for the treatment of herpes zoster ophthalmicus. Ophthalmology 2000;107:1507-11.

De Clereq E, Descamps J, De Somer P, et al. (E)-5-(2 Bromovinyl)-2'-deoxyuridine: a potent and reactive anti-herpes agent. Proc Natl Acad Sci USA 1979;76:2947-51.

Doerr HW, Rabenau H. Dermatotrope Herpesviren, Infektionsbiologie, Epidemiologie und Diagnostik. Chemotherapie J 1996;1:1-8.

Doerr HW, Rentschler M, Schleifler G. Serologic detection of active infections with human herpes viruses (CMV, EBV, HSV, VZV): diagnostic potential of IgA class and IgG subclass-specific antibodies. Infection 1987;15:93-8.

Dworkin RH, Carrington D, Cunningham A, et al. Assessment of pain in herpes zoster: lessons learned from antiviral trials. Antivir Res 1997;33:73-85.

Feldman S, Hughes WT, Kim HY. Herpes zoster in children with cancer. Am J Dis Child 1973;126: 178-84.

Friedmann-Kiein AE, Lafleur FL, Gendler E, et al. Herpes zoster: a possible early sign for development of acquired immunodeficiency syndrome in high-risk individuals. J Am Acad Dermatol 1986;14: 1023-8.

Galagher JG, Merigan TC. Prolonged herpes zoster infection associated with immunosuppressive therapy. Am Intern Med 1979;91:842-6.

Glynn C, Crockford G, Garaghan D, et al. Epidemiology of shingles. J R Soc Med 1990;83:617-9.

Gnann JW, Whitley RJ. Herpes zoster. N Engl J Med 2002;347:340-6.

Gross G. Zoster. Dtsch med Wschr 1997;122:132-9.

Gross G, Doerr HW. Labordiagnose dermatotroper Virusinfektionen: Erregerisolierung. In: Korting HC, Sterry W, editors. Diagnostische Verfahren in der Dermatologie. Berlin, Wien: Blackwell Wissenschaftsverlag; 1997, p. 197-202.

Gross G, Laskowski J, Virustatika. In: Korting HC, Sterry W, editors. Therapeutische Verfahren in der Dermatologie, Berlin, Wien: Blackwell Wissenschaftsverlag; 2001, p. 647-54.

Guess HA, Broughton DD, Melton LJ, Kurland LJ, III. Epidemiology of herpes zoster in children and adolescents: a population-based study. Pediatrics 1985;76:512-7.

Hoang-Xuan T, Büchi R, Herbort CP, et al. Oral acyclovir for herpes zoster ophthalmicus. Ophthalmology 1992;99:1062-70.

Hope-Simpson RE. The nature of herpes zoster: a long term study and new hypothesis. Proc R Soc Med 1965;58:9-20.

Hope-Simpson RE. Postherpetic neuralgia. J R Coll Gen Practit 1975;25:571-5.

Hoppnjans WB, Bibler MR, Orne RL, et al. Prolonged cutaneous herpes zoster in acquired immunodeficiency syndrome. Arch Dermatol 1990;126:1048-50.

Kost RG, Strauss SE. Postherpetic neuralgia - pathogenesis, treatment and prevention. N Engl J Med 1996;335:23-42.

Liesegang TJ. Diagnosis and therapy of herpes zoster ophthalmicus. Ophthalmology 1991;98:1216-29.

Lilie HM, Wassilew SW. Shingles (Zoster). In: Wolff MH, Schünemann S, Schmidt A, editors, Varicella-zoster-virus. Molecular biology pathogenesis and clinical aspects, vol. 3. Contrib Microbiol Basel Karger, 1999;111-27.

Locksley RM, Flournoy N, Sullivan KM, et al. Infection with varicella-zoster virus after marrow transplantation. J Infect Dis 1985;152:1172-81.

Malin JP. Zoster und Nervensystem. Dtsch med Wschr 1996;121:635-8.

Meier JL, Strauss SE. Comparative biology of latent varicella-zoster virus and herpes simplex virus infections. J Inf Dis 1992;166(Suppl):S13-23.

Meister W, Neiss A, Gross G, et al. Demography, symptomatology and course of disease in ambulatory zoster patients. Intervirology 1998a;41:272-7.

Meister W, Neiss A, Gross G, et al. A prognostic score for postherpetic neuralgia in ambulatory patients. Infection 1998b;26(6):359-63.

Melbye M, Grossman RJ, Goebert JJ, et al. Risk of AIDS after herpes zoster. Lancet 1978;1:728-30.

Ragozzino MW, Melton LJ, Kurland TL, et al. Population based study of herpes zoster and its sequelae. Medicine (Baltimore) 1982;61:310-6.

Rudra T. Zoster sine herpete. Brit J Clin Pract 1990;44:284.

Rustoven JJ, Ahlgren P, Elhakim T, et al. Varizella zoster infection in adult cancer patients: a population study. Arch Intern Med 1998;148:1561-6.

Safrin S. Cherrington J, Jaffe HS. Clinical uses of cidofovir. Rev Med Virol 1997;7:145-56.

Solomon AR, Rasmussen JE, Weiss JS. A comparison of Tzanck smear and virus isolation in varizella and herpes zoster. Arch Dermatol 1986;122:282-5.

Sundmacher R. Therapie der Viruserkrankungen des vorderen Augenabschnittes. In: Kampik A, editors. Das äußere Auge: Hauptreferate der XXXI—Essener Fortbildung für Augenärzte, Bücherei des Augenarztes; 1996, Vol. 137, p. 121-5.

Schlecht K, Laskowski J, Gross G. Zoster-Scoresystem zur Risikoabschätzung bezüglich der Entwicklung einer post-zosterischen Neuralgie-Erste Anwendungen in der Praxis. In preparation.

Schöfer H. Frühsymptome der HIV-Erkrankung an Haut- und Schleimhäuten. AIDS-Forschung (AIFO) 1991;6:633-48.

Schöfer H, Baur S, Gregel C, et al. Hyperkeratotic varicella zoster virus infection in a HIV-infected patient. Successful treatment of persistent lesions with cryosurgery. Br J Dermatol 1998;138:714-5.

Tyring SK, Beutner KR, Tucker BA, et al. Antiviral therapy for herpes zoster. Randomized, controlled clinical trial of valacyclovir, and famciclovir therapy in immunocompetent patients of 50 years and older. Arch Fam Med 2000;9:863-9.

Veenstra J, Krool A, van Praag RM, et al. Herpes zoster, immunological deterioration and disease progression in HIV-1 infection. AIDS 1995;9:1153-8.

Vu AQ, Radonich MA, Heald PW. Herpes zoster in seven disparate dermatomes (zoster multiplex): report of a case and review of the literature. J Am Acad Dermatol 1999;40:868-9.

Wassilew SW. Differentialtherapie der Herpesvirusinfektionen. In: Plettenberg A, Meigel WN, Moll I, editors. Dermatologie an der Schwelle zum neuen Jahrtausend: Springer-Verlag; 2000, p. 315-8.

Wassilew SW, Schumacher K, Städtler G, et al. A randomised double-blind survey on the effect of brivudin in the prevention of postherpetic pain in comparison with acyclovir. Fourth International Conference on Varicella, Herpes Zoster, Postherpetic Neuralgia. La Jolla, USA; 2001, March, p. 3-5.

Wassilew SW, Schumacher K, Macher K, Städtler G, et al. Brivudin compared to famciclovir in the prevention of postherpetic neuralgia: a randomised double-blind multi-center trial. Fourth International Conference on Varicella, Herpes Zoster, Postherpetic Neuralgia. La Jolla, USA; 2001, March, p. 3-5.

Weller TH. Varicella and herpes zoster: changing concepts of the natural history, control and importance of a not-so-benign virus. N Engl Med 1983;309:1362-8.

Weller TH. Varcella and herpes zoster. A perspective and overview. J Infect Dis 1992;166(Suppl 1):1—6.

Whitley RJ, Weiss H, Gnann IW, et al. Acyclovir with and without prednisone for the treatment of herpes zoster. A randomised placebo-controlled trial. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. Ann Intern Med 1996;125:376-83.

Wood MJ, Johnson RW, Mc Kendrick MW, et al. A randomised trial of acyclovir for 7 days or 21 days with and without prednisolon for treatment of acute herpes zoster. N Engl J Med 1994;330:896-900.

Wutzler P, Doerr HW. Der Herpes zoster-ein Morbus herpes non simplex. Dtsch med Wschr 1995;120: 1133-8.

Wutzler P, de Clercq E, Wutke K, Färber I. Oral brivudin vs. intravenous acyclovir in the treatment of herpes zoster in immunocompromised patients: a randomised double-blind trial. J Med Virol 1995;46:252-7.

Wutzler P. Stubinski BM, Koch I, et al. Brivudin compared to acyclovir in the treatment of acute herpes zoster: a randomised, double-blind, multicenter trial. Fourth International Conference on Varicella, Herpes Zoster, Postherpetic Neuralgia. La Jolla, USA; 2001, March, p. 3-5.

Gerd Gross, MD

Professor of Dermatology and Venereology, Director Department of Dermatology and Venereology University of Rostock Augustenstrasse 80-84 DE-18055 Rostock (Germany)

Tel. +49 381 4949701, Fax +49 381 4949702, E-Mail [email protected]

Natural Vertigo And Dizziness Relief

Natural Vertigo And Dizziness Relief

Are you sick of feeling like the whole world Is spinning out of control. Do You Feel Weak Helpless Nauseous? Are You Scared to Move More Than a Few Inches From The Safety of Your Bed! Then you really need to read this page. You see, I know exactly what you are going through right now, believe me, I understand because I have been there & experienced vertigo at it's worst!

Get My Free Ebook

Post a comment