Herpes zoster–associated voiding dysfunction: A retrospective study and literature review

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Herpes Zoster–Associated Voiding Dysfunction: A Retrospective Study and Literature Review Po-Hong Chen, MD, Hsiu-Fang Hsueh, MD, Chang-Zern Hong, MD ABSTRACT. Chen P-H, Hsueh H-F, Hong C-Z. Herpes zoster–associated voiding dysfunction: a retrospective study and literature review. Arch Phys Med Rehabil 2002;83:1624-8. Objectives: (1) To describe the demographic features of patients with voiding dysfunction associated with herpes zoster; (2) to discuss the pathophysiology of voiding dysfunction associated with herpes zoster; and (3) to suggest the best management policy. Design: A retrospective study. Setting: A university-affiliated medical center in Taiwan. Participants: Four hundred twenty-three patients (mean age, 55.5y) admitted with the diagnosis of herpes zoster from 1988 to 2000. Interventions: Not applicable. Main Outcome Measures: Dermatomal distribution of skin eruptions, urologic symptoms, treatment (catheterization, urecholine), clinical course of voiding dysfunction, and outcome. Results: Seventeen (mean age, 61.2⫾14.1y) of 423 patients (4.02%) with voiding dysfunction related to this virus infection were identified. Ten (58.8%) were men, and 7 (41.2%) were women. The incidence of dysfunction was as high as 28.6% if only lumbosacral dermatome–involved patients were considered. We classified urologic manifestations caused by herpes zoster into 3 groups: cystitis-associated (n⫽12), neuritis-associated (n⫽4), and myelitis-associated (n⫽1). Urinalysis revealed pyuria in all patients with cystitis-associated voiding dysfunction and microscopic hematuria in all patients with neuritis-associated voiding dysfunction. All patients, although receiving different treatment regimens for voiding dysfunction, regained a normal or balanced bladder within 8 weeks. No major urologic sequelae were noted. Conclusion: Voiding dysfunction, although a transient course, is not uncommon in patients with herpes zoster involving lumbosacral dermatomes. Treatment with intermittent catheterization (our preferred choice) or indwelling catheter placement is recommended if the patients have prolonged difficulty in urination. This disease entity usually has a benign clinical course, and almost every patient will either regain normal voiding or, at least, balanced bladder function. Key Words: Cystitis; Herpes zoster; Myelitis; Neuritis; Rehabilitation; Urination disorder. © 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

From the Department of Physical Medicine and Rehabilitation, Kuo General Hospital, Tainan, Taiwan (Chen); Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, Tainan, Taiwan (Hsueh); and Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA (Hong). No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Reprint requests to Po-Hong Chen, MD, Dept of Physical Medicine and Rehabilitation, Kuo General Hospital, Tainan, Taiwan, e-mail: [email protected]. 0003-9993/02/8311-6774$35.00/0 doi:10.1053/apmr.2002.34602

Arch Phys Med Rehabil Vol 83, November 2002

ERPES ZOSTER, A COMMON viral infection, caused H by the varicella-zoster virus (VZV), is usually a localized disease characterized by unilateral radicular pain and a vesicular eruption that is generally limited to the dermatome innervated by the nerve from a single spinal or cranial sensory ganglion. In contrast to varicella, which follows primary exogenous VZV infection, herpes zoster is the result of reactivation of an endogenous infection that has persisted in latent form within sensory ganglia after an earlier attack of varicella. Therefore, it occurs most often in the elderly population, especially in those with compromised immune systems.1 As with varicella, the incidence of complicated and atypical zoster herpes has been increasing with the increasing prevalence of human immunodeficiency virus infection in the general population.1 Voiding dysfunction, commonly found in many patients of a large medical institution, has been considered as an uncommon complication of herpes zoster in the general population. Urologic alterations produced by herpes zoster infection were first described by Davidsohn in 1890. Today, fewer than 120 cases have been reported in the literature.2 Most articles in the literature are case reports, and only few of them discuss this disease entity in detail. Among the sporadic reports in the literature, patients who had voiding dysfunction associated with herpes zoster can be generally classified into 3 groups: cystitis associated, neuritis associated, and myelitis associated.2,3 Cystitis-associated voiding dysfunction is caused by the direct invasion of VZV into the bladder wall, resulting in herpetic cystitis and followed by voiding dysfunction. Neuritis-associated voiding dysfunction has been, in general, thought to result from a retrograde spread of infection by the VZV in the dorsal root ganglia into the sacral motoneurons, leading to a sacral motor neuritis and causing a flaccid bladder. Myelitis-associated voiding dysfunction is caused by herpetic myelitis and can be manifested as a spastic bladder in the patients with suprasacral spinal cord injury (SCI). In this study, we reviewed the medical records of all patients admitted to a universityaffiliated medical center with the diagnosis of herpes zoster. Demographic features of all patients with voiding dysfunction associated with herpes zoster were identified. Pathomechanisms of urologic manifestations caused by herpes zoster infection were classified and discussed. Rehabilitative management of voiding dysfunction was also described. METHODS In this retrospective study, we searched the medical center’s database for all patients admitted to a university-affiliated medical center between 1988 and 2000 with a major diagnosis of herpes zoster by using the International Classification of Diseases, 9th revision, code 053. All patients with the diagnosis code 053 (the International Classification of Diseases, 9th revision code for herpes zoster), either major or minor, were identified, including those with diagnosis subcategories in code 053. All medical records of the identified patients were reviewed in detail, and those with urologic complications were picked out. We analyzed the demographic features. Patients

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ZOSTER-ASSOCIATED VOIDING DYSFUNCTION, Chen Table 1: Dermatomal Distribution of Skin Eruption Patients (%)

Cranial nerves* Cervical dermatomes Thoracic dermatomes Lumbar dermatomes Sacral dermatomes Disseminated† Total

Including Cranial Nerve Involvement

Excluding Cranial Nerve Involvement

Patients With Voiding Dysfunction (%)

230 (54.4) 42 (9.9) 90 (21.3) 22 (5.2) 34 (8.0) 5 (1.2) 423 (100)

42 (21.8) 90 (46.6) 22 (11.4) 34 (17.6) 5 (2.6) 193 (100)

0 (0) 0 (0) 1 (5.9) 2 (11.8) 14 (82.3) 0 (0) 17 (100)

* Including trigeminal and facial nerves. † Disseminated distribution sparing lumbosacral dermatomes.

with a history or other concomitant etiologies of voiding dysfunction were not included for analyses. Those with dysuria caused by painful vesicles around anogenital area were also excluded. According to the clinical manifestations, natural courses, and results of laboratory tests (if available), all herpes zoster–induced voiding dysfunctions were classified into 3 groups: cystitis associated, neuritis associated, and myelitis associated.3 Final outcome in those with voiding difficulty was also reviewed. If the medical records were incomplete or patients failed to return for follow-up in this hospital, we made telephone calls to ascertain the final outcome. RESULTS A total of 423 patients (222 women, 201 men) with a mean age of 55.5 years (range, 2–93y) were enrolled in this study. The dermatomal distribution of skin eruption is summarized in table 1. Twenty-three of the 423 patients had difficulty in urination. However, 6 patients (all with sacral dermatomal involvement) were dropped because painful vesicles around anogenital area (dysuria) was noted. Of the remaining 17 (4.02%) patients who had real voiding dysfunction, the der-

matomes of involvement were as follows: 14 in the sacral area, 2 in the lumbar, and 1 in the thoracic. The mean age was 61.2⫾14.1 years, ranging from 19 to 77 years (table 2). Ten (58.8%) of the 17 patients with voiding dysfunction were men, and 7 (41.2%) were women (table 2). All of these 17 patients were treated with intravenous acyclovir 500mg every 8 hours for 5 days. Tables 2 and 3 summarize the characteristics of all 17 patients, including demographic data, urologic manifestations, results of urinalysis (in terms of high-power fields) and urodynamic study (if done), management and natural course of voiding dysfunction, concomitant neurologic manifestations, and classification of voiding dysfunction. Urination difficulty in 12 (70.6%) of the 17 patients was clinically classified as cystitis-associated voiding dysfunction. Most of the patients complained of dysuria; in addition, they had either urinary frequency or retention. Filling sensation of the bladder was normal. On physical examination, they had normal sacral sensation and sphincter reflexes. Initial urinalysis revealed mild to moderate pyuria in all patients, whereas the results of other tests were negative (table 2). Their urologic symptoms were transient and correlated with the emergence

Table 2: Demographic Data and Clinical Manifestations of the 17 Patients With Voiding Dysfunction

Sex

Affected Dermatome

Urologic Symptoms

Constipation

Urinalysis*

1 2 3 4

63 43 70 19

M F F M

R S3–4 L S1–3 R L2–3 L T4–6

Urinary retention Dysuria, frequency Dysuria, frequency Overflow incontinence

Yes No Yes No

RBC 5–8 WBC 10–12 WBC 10–15 Negative

5 6 7 8 9 10 11 12 13 14 15

77 64 75 56 49 66 64 58 60 75 70

M M M F F M M M M F F

R S2–4 R S2 L S2 R S2 L S3–4 L S2–3 L S2–3 R L2–S2 R S2 L S2–3 L L5

Dysuria, frequency Dysuria, frequency Overflow incontinence Urinary retention Urinary retention Urinary retention Urinary retention Dysuria, frequency Dysuria, frequency Urinary retention Urinary retention

Yes Yes No Yes No No Yes No No Yes Yes

16 17

63 69

M F

Left S3 Right S3

Dysuria, frequency Urinary retention

No Yes

WBC 5–7 WBC 7–10 WBC 10–12 WBC 5–7 WBC 10–12 RBC 5–7 WBC 7–10 WBC 5–7 WBC 7–10 WBC 5–7 WBC 8–10; RBC 6–8 WBC 7–10 RBC 28–31

Patient No.

Age (y)

Concomitant Neurologic Manifestations or Diagnosis

Menigoencephalitis No No Herpetic myelitis with Brown-Se´quard syndrome No No No No No No No No No No Left drop foot No No

Abbreviations: M, male; F, female; R, right; L, left, RBC; red blood cell count; WBC, white blood cell count. * Positive findings in the urinalysis are shown in terms of hpfs; within normal limit if not shown.

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ZOSTER-ASSOCIATED VOIDING DYSFUNCTION, Chen Table 3: Results of Urodynamic Study, Management, Clinical Course, Classification, and Outcome of the 17 Patients With Voiding Dysfunction

Patient No.

Urodynamic Study

Management

Clinical Course of Voiding Dysfunction

Classification

Outcome*

Normal voiding after 6wk of indwelling catheter Normal voiding Normal voiding Normal voiding after 2wk of indwelling catheter Normal voiding Normal voiding Normal voiding Normal voiding Normal voiding Normal voiding after 6wk of indwelling catheter Normal voiding Normal voiding Normal voiding Normal voiding Balanced bladder after 2wk of ICP training Normal voiding Balanced bladder after 3wk of ICP training

1

Not done

Indwelling catheter

8wk

Neuritis-associated

2 3 4

Not done Not done Not done

Catheter drainage Catheter drainage Indwelling catheter

2d 7d 4wk

Cystitis-associated Cystitis-associated Myelitis-associated

5 6 7 8 9 10

Not done Not done Not done Not done Not done Bladder atony

Catheter drainage Catheter drainage Catheter drainage Catheter drainage Indwelling catheter Indwelling catheter

7d 2wk 2d 2d 4d 7wk

Cystitis-associated Cystitis-associated Cystitis-associated Cystitis-associated Cystitis-associated Neuritis-associated

11 12 13 14 15

Not done Not done Not done Not done Bladder atony

8d 3d 12d 4d 5wk

Cystitis-associated Cystitis-associated Cystitis-associated Cystitis-associated Neuritis-associated

16 17

Not done Bladder atony

Indwelling catheter Catheter drainage Catheter drainage Indwelling catheter ICP training; urecholine orally Catheter drainage ICP training; urecholine orally

3d 4wk

Cystitis-associated Neuritis-associated

* No postvoid residual was checked after regaining normal voiding except patients 15 and 17.

and resolution of the visible skin rash. Only short-term (⬍2wk) intermittent catheter drainage or indwelling catheterization was prescribed for these patients. No cystoscopic examination was performed on these patients. All patients regained normal voiding function before discharge, and no major urologic sequelae were noted during the outpatient follow-up period (range, 2wk–12mo). Four (23.5%) of the 17 patients were classified as having neuritis-associated voiding dysfunction (ie, a flaccid bladder). They clinically manifested with urinary retention and a reduced or absent filling sensation. On physical examination, they had reduced or absent sacral sensation and sphincter reflexes. Initial urinalysis revealed mild pyuria in 1 patient, and microscopic hematuria in the others (table 2). The course of urine retention was prolonged (⬎2wk). Urodynamic studies were performed on 3 patients, and all revealed an acontractile bladder. An intermittent catheterization program (ICP) and urecholine 25mg every 4 hours by mouth were prescribed for 2 patients and indwelling catheter for the other 2. The former patients developed a balanced bladder after 2 to 3 weeks of ICP training, whereas the latter remained with an indwelling catheter for 6 weeks. Similarly, there was no major sequela noted in these 4 patients during the outpatient follow-up period (range, 1–20mo). However, patient 15 in this group developed left drop foot along with herpes zoster. On physical examination, she had some atrophy of her left pretibial and calf muscles. Manual muscle testing of the lower left leg revealed a grade of 1/5 in the ankle dorsiflexion and great toe extension and 1⫹/5 in the ankle plantarflexion. Left Achilles’ reflex was absent. Electrodiagnostic studies revealed acute L5–S1 radiculopathy. Electrodiagnostic results are summarized in table 4. The concomitant sequela of herpes zoster in this patient provided indirect evidence of proximal invasion of VZV into the spinal cord and the motoneurons (discussed later). One (5.9%) of the 17 patients was classified into the myelitis-associated voiding dysfunction group (table 3). Urine retenArch Phys Med Rehabil Vol 83, November 2002

tion did not appear until this patient developed a herpetic thoracic myelitis (left fourth to fifth thoracic spinal cord; table 2), which was confirmed by magnetic resonance imaging and cerebrospinal fluid (CSF) analyses (ie, elevated VZV titer in the CSF). The patient had overflow incontinence at the time during spinal shock. Fortunately, he did not present with complete paralegic myelopathy and instead he presented with Brown-Se´ quard syndrome with weakness and loss of proprioception in his lower left extremity, and decreased sensation to light touch and pin prick in the right. Initial urinalysis was normal (table 2). His urologic symptoms subsided 2 weeks after placement of an indwelling catheter. No further urologic sequela was noted during the outpatient follow-up period (6wk). DISCUSSION Voiding dysfunction is commonly found in many patients with neuromuscular disorders. The usual causes include brain lesions (uninhibited bladder), suprasacral spinal cord lesions (spastic automatic bladder), sacral spinal cord or peripheral nerve lesions (flaccid autonomous bladder), and postganglionic detachment of neural connection inside the bladder detrusors caused by overdistension of the bladder (atonic bladder).4 Herpes zoster is a rare etiology of voiding dysfunction. This low rate is probably because of the relatively lower incidence of sacral dermatomal involvement by VZV.5 This study was performed in a university-affiliated medical center. The pattern of the patient population in this hospital is similar to that in any local general hospital in Taiwan. Therefore, the study results should reflect the actual epidemiologic status in the general population of the country. In this study, we identified 17 patients with voiding dysfunction associated with herpes zoster. The incidence was 4.02% in the 423 patients and increased to 8.81% in 193 patients when excluding those with cranial nerve rather than spinal involvement. This incidence was higher than that (3.5%) reported by Broseta et al2 and

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ZOSTER-ASSOCIATED VOIDING DYSFUNCTION, Chen Table 4: Results of Electrodiagnostic Examination in Patient No. 15 Tested Nerve or Muscle

Motor NCS Left peroneal nerve Left tibial nerve Sensory NCS Left sural nerve Left superficial peroneal nerve Needle electromyography examination Tibialis anterior Peroneus longus Gastrocnemius Biceps femoris (short head) Tensor facia lata L5, S1 paraspinalis

Results

No response Reduced CMAP amplitude (513␮V), reduced NCV (30.8m/s) No response No response Fibrillation Fibrillation Fibrillation Fibrillation Fibrillation PSW 1⫹

potentials potentials potentials potentials potentials

3⫹; 3⫹; 1⫹; 2⫹; 3⫹;

PSW PSW PSW PSW PSW

3⫹ 3⫹ 2⫹ 3⫹ 3⫹

Abbreviations: NCS, nerve conduction study; CMAP, compound muscle action potential; NCV, nerve conduction velocity; PSW, positive sharp wave.

Yamanishi et al,6 which could be because of the higher percentage (29%) of lumbosacral dermatomal involvement of VZV in our patients than that described in the literature (18%).7 Among the sporadic reports in the literature since 1970, most patients (78%) with voiding dysfunction have the sacral dermatomes involvement. Lumbar and thoracic dermatomes were affected in 16% and 6% of the patients, respectively.8 In our study, we found similar distribution pattern, with sacral dermatomes affected in 82.3% of those with voiding dysfunction, followed by lumbar and thoracic in 11.8% and 5.9%, respectively. On the other hand, when taking only lumbosacral dermatome–involved patients into account, voiding dysfunction appeared in 16 (28.6%) of 56 patients. Therefore, more than 25% of patients with herpes zoster infection involving lumbosacral dermatomes developed voiding dysfunction. This should be considered as clinically significant. Furthermore, similar to the findings of Cohen and Fowler,8 men (58.5%) were affected more commonly than women (41.5%). However, this finding was not statistically significant. There are several bladder disorders associated with herpes zoster infection. The most common type is an ipsilateral herpetic hemicystitis. Classically, patients in this group may present with dysuria, urinary frequency or retention, pyuria, and hematuria.2,3 The pathomechanism of this entity is probably because of the spread of VZV along the visceral and somatic nerves.5 Therefore, cystoscopic finding may confirm the presence of a herpetic hemicystitis, a grouping of vesicles in the urethral and bladder mucosa, in some cases.2,9 In our patients, 70.6% were clinically classified into the group with cystitis-associated voiding dysfunction. They presented with transient dysuria and urinary frequency or retention. Initial urinalysis revealed mild to moderate pyuria, but no hematuria, either microscopic or gross, was noted (table 2). The clinical course of voiding dysfunction usually correlated with the resolution of skin rash, and the symptoms improved shortly. None of our patients had received a cystoscopic examination at the time of clinical presentation because the clinical course was transient (ie, ⬎2wk), and the diagnosis was clinically obvious. All patients regained normal voiding function after a short course of intermittent catheterization or indwelling catheter placement. In recent reports, cystoscopy has been infrequently performed on the patients with cystitis syndrome, although it had been standard procedure before the 1970s.2,3,5,6,8,10-12 If cost-benefit analysis is taken into consideration, cystoscopy may not be necessary because zoster cystitis runs a short, benign course,

and complete spontaneous recovery is the likely outcome.2,13 While managing such a case, it is recommended to observe the urologic presentation closely, to prescribe intermittent catheterization or indwelling catheter placement if necessary, and to treat the VZV infection aggressively with antiviral agents. The second type of bladder disorder is neuritis-associated voiding dysfunction (ie, a flaccid bladder). It is probably caused by the spread of the VZV infection from the dorsal root ganglion into the sacral motoneurons, roots, or peripheral nerves, which causes interruption of the detrusor reflex.3 Most patients reported in the literature had a zosteroid eruption in the S2– 4 dermatomes. However, some with skin rash in the lumbar or even in the lower thoracic dermatomes also developed urologic alterations. This can be explained as an adjacent spread of the nonsacral VZV infection into the sacral segments, which is supported by Braverman et al14 in their study of 3 patients with herpes zoster polyradiculopathy. They also postulated that the virus spread proximally as well as distally, caused a local neuritis in the spinal nerve, and subsequently spread to the motor axons peripherally. One of our patients (no. 15) also developed drop foot, and the electrodiagnostic (table 4) examination revealed acute L5–S1 radiculopathy. Four (23.5%) of our 17 patients had a flaccid bladder, and 3 had skin rash in the S2– 4 dermatomes. Urinary retention was the typical presentation in those patients, and voiding function recovered within a relatively prolonged period (ie, 4 – 8wk), similar to the recovery time reported in the literature.6 Yamanishi6 reported performing cystometrography on 7 patients with herpes zoster–associated urinary retention and it was performed on 3 of our patients; all showed a detrusor areflexia. In addition, in other studies,3,6,10 cystoscopic examination in patients with a flaccid bladder did not always reveal the presence of herpetic cystitis, suggesting a true neurologic involvement rather than bladder involvement alone. Therefore, some of the patients probably had both cystitisand neuritis-associated voiding dysfunction, and some had only 1 of the 2 dysfunctions. In our 4 patients, all had microscopic hematuria, and 1 had mild pyuria in the urinalysis (table 2). Accordingly, we believe that they had both cystitis- and neuritis-associated voiding dysfunction. Physiatrists prescribed ICP training and oral urecholine for 2 of our 4 patients. All patients developed a balanced bladder after 2- to 3-week training, and no urologic sequela was noted during the follow-up period. Both physiatrists and urologists Arch Phys Med Rehabil Vol 83, November 2002

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ZOSTER-ASSOCIATED VOIDING DYSFUNCTION, Chen

were consulted for the voiding dysfunction of the other 2 patients, and their primary physicians decided to prescribe placement of indwelling catheter. Foley catheters were placed for 6 weeks, and the patients regained normal voiding function after multiple attempts to remove the catheter. In a recent report by Yamanishi et al,6 clean intermittent catheterization was also performed in all 8 patients with herpes zoster–associated bladder dysfunction. Many researchers15-21 have provided evidence supporting intermittent catheterization as the safest bladder management option for patients with SCI. We also recommend intermittent catheterization as the best and safest management option. Myelitis-associated voiding dysfunction, the third type of bladder disorder, presents as a spastic bladder seen in patients with suprasacral SCI. Transverse myelitis is a very rare complication of herpes zoster, usually affecting mainly the dorsal and ventral horns with only minor long tract involvement. Chang et al22 reported that 5 of 93 patients with herpes zoster developed myelopathy. In 3 patients, it manifested as segmental amyotrophy, whereas 2 had more prominent long tract signs. The clinical course of neurogenic bladder caused by long tract involvement was similar to that of a patient with SCI. Fortunately, the prognosis of zoster myelitis is good, with most patients having complete recovery.22 One (5.9%) of our 17 patients developed zoster myelitis in the left fourth and fifth thoracic cord, confirmed by magnetic resonance imaging and CSF analyses and manifesting with symptoms similar to Brown-Se´ quard syndrome. No cystometrography was performed to verify the voiding dysfunction, and the patient regained normal voiding function 2 weeks after placement of an indwelling catheter. Nevertheless, urodynamic studies and ICP training are still highly recommended when treating a patient with voiding dysfunction associated with transverse myelitis caused by herpes zoster. A fourth variety of bladder disorder was described by Rankin and Sutton.3 To explain urinary retention associated with herpes zoster in lower thoracic or higher lumbar segments, they postulated that activation of the lumbar sympathetic outflow by VZV infection can bring about a contraction of the internal sphincter.3 However, this hypothesis was later disputed by Richmond.23 CONCLUSION Voiding dysfunction is not an uncommon complication of herpes zoster involving lumbosacral dermatomes (28.6% in our patients). In this study, we presented 17 patients with voiding dysfunction, manifesting in 3 varieties of dysfunction as described in the literature. Treatment with intravenous acyclovir is part of the standard management of herpes zoster in our hospital. While managing a patient with urologic complaints associated with herpes zoster, it is recommended to observe the clinical manifestation closely and to perform intermittent catheter drainage to prevent bladder overdistention. If there is a prolonged course of bladder dysfunction, urodynamic studies should be arranged to identify a true neurogenic bladder. Cystoscopic examination is not necessary in most cases. In our opinion, ICP training with and without a parasympathomimetic agent (ie, urecholine) is the best choice for management of these patients. Because voiding dysfunction associated with

Arch Phys Med Rehabil Vol 83, November 2002

herpes zoster usually runs a short and benign course, no major urologic sequela will remain if one bears the differential diagnosis in mind. References 1. Oxman MN, Alani R. Varicella and herpes zoster. In: Fitzpatrick TB, Eisen AZ, editors. Dermatology in general medicine. 4th ed. New York: McGraw-Hill; 1993. p 2543-72. 2. Broseta E, Osca JM, Morera J, Martinez-Agullo E, Jimenez-Cruz JF. Urological manifestations of herpes zoster. Eur Urol 1993;24: 244-7. 3. Rankin JT, Sutton RA. Herpes zoster causing retention of urine. Br J Urol 1969;41:238-41. 4. Cardenas DD, Mayo ME. Management of bladder dysfunction. In: Braddom RL, editor. Physical medicine and rehabilitation. 2nd ed. Philadelphia: WB Saunders; 2000. p 561-77. 5. Constantian HM. Herpes zoster causing bladder atony. J Urol 1969;102:689-92. 6. Yamanishi T, Yasuda K, Sakakibara R, et al. Urinary retention due to herpes virus infections. Neurourol Urodynam 1998;17: 613-9. 7. Dumitru D. Herpes varicella-zoster virus. In: Dumitru D, editor. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. p 803-4. 8. Cohen LM, Fowler JF. Urinary retention associated with herpes zoster infection. Int J Dermatol 1993;32:24-6. 9. Gibbon NO. A case of herpes zoster with involvement of the urinary bladder. Br J Urol 1956;28:417-21. 10. Ray B, Wise GJ. Urinary retention associated with herpes zoster. J Urol 1970;104:422-5. 11. Izumi AK, Edwards J. Herpes zoster and neurogenic bladder dysfunction. JAMA 1973;224:1748-9. 12. Pryor J. Herpes zoster-induced bladder paralysis. Arch Phys Med Rehabil 1973;54:528-9. 13. Chancellor MG, Blaivas JG. Infectious neurologic diseases. In: Chancellor MG, Blaivas JG, editors. Practical neuro-urology: genitourinary complications in neurologic disease. Boston: Butterworth-Heinemann; 1995. p 180. 14. Braverman DL, Ku A, Nagler W. Herpes zoster polyradiculopathy. Arch Phys Med Rehabil 1997;78:880-2. 15. Jacobs SC, Kaufman JM. Complications of permanent bladder catheter drainage in spinal cord injury patients. J Urol 1978;119: 740-1. 16. Maynard FM, Diokno AC. Clean intermittent catheterization for spinal cord injured patients. J Urol 1982;128:477-80. 17. Maynard FM, Diokno AC. Urinary infection and complications during clean intermittent catheterization following spinal cord injury. J Urol 1984;132:943-6. 18. Perkash I, Giroux J. Clean intermittent catheterization in spinal cord injury patients: a follow-up study. J Urol 1993;149:1068-71. 19. Chai T, Chung AK, Belville WD, Faerber GJ. Compliance and complications of clean intermittent catheterization in the spinal cord injured patient. Paraplegia 1995;33:1161-3. 20. Larsen LD, Chamberlin DA, Khonsari F, Ahlering TE. Retrospective analysis of urologic complications in male patients with spinal cord injury managed with and without indwelling urinary catheters. Urology 1997;50:418-22. 21. Weld KJ, Dmochowski RR. Effect of bladder management on urological complications in spinal cord injured patients. J Urol 2000;163:768-72. 22. Chang CM, Woo E, Yu YL, Huang CY, Chin D. Herpes zoster and its neurological complications. Postgrad Med J 1987;63:85-9. 23. Richmond W. The genito-urinary manifestations of herpes zoster. Three case reports and a review of the literature. Br J Urol 1974;46:193-200.