Herpes Zoster and Neurogenic Bladder Dysfunction

Izumi, Allan K.

doi:10.1001/jama.1973.03220270044011

Cited by 12 publications

(6 citation statements)

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“…A combination of both conditions could also happen. Cystitis associated with herpes zoster is ipsilateral hemicystitis, which usually occurs simultaneously with skin rash 7 . Patients with herpes cystitis may present with dysuria, urinary frequency or retention, pyuria, and hematuria.…”

Section: Commentsmentioning

confidence: 99%

Herpes zoster‐associated voiding dysfunction in hematopoietic malignancy patients

Imafuku¹,

Takahara²,

Uenotsuchi³

et al. 2007

Int J Dermatology

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Section: Commentsmentioning

confidence: 99%

Herpes zoster‐associated voiding dysfunction in hematopoietic malignancy patients

Imafuku¹,

Takahara²,

Uenotsuchi³

et al. 2007

Int J Dermatology

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“…Zoster paresis (weakness) is manifest by arm weakness or diaphragmatic paralysis (Brostoff, 1966; Stowasser et al, 1990) after cervical distribution zoster, leg weakness after lumbar or sacral distribution zoster, and by urinary retention after sacral distribution zoster (Izumi and Edwards, 1973; Jellinek and Tulloch, 1976). Magnetic resonance imaging (MRI) of patients with zoster paresis reveals involvement not only of the posterior horn and posterior roots, but also of the anterior roots and anterior horn at the spinal level corresponding to the patient’s clinical deficit (Hanakawa et al, 1997; Umehara et al, 2011).…”

Section: Neurologic Complications Of Zostermentioning

confidence: 99%

Varicella-zoster

Gilden

Nagel

Cohrs

2014

Handbook of Clinical Neurology

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“…Arm weakness or diaphragmatic paralysis [21, 22] occurs after cervical distribution zoster, abdominal muscle weakness and hernia after thoracic distribution zoster [23, 24], leg weakness after lumbar or sacral distribution zoster and urinary retention after sacral distribution zoster [25, 26]. Magnetic resonance imaging (MRI) of patients with zoster paresis reveals involvement of both anterior and posterior roots at the spinal level that corresponds to the patient’s clinical deficit [27].…”

Section: Neurological Complications Of Vzv Reactivationmentioning

confidence: 99%

Complications of Varicella Zoster Virus Reactivation

Nagel

Gilden

2013

Curr Treat Options Neurol

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Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, myelopathy, multiple ocular disorders and vasculopathy that can mimic giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without rash. Diagnosis of VZV-induced neurological disease may require examination of CSF, serum and/ or ocular fluids. In the absence of rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV DNA by PCR and for anti-VZV IgG and IGM. Detection of VZV IgG antibody in CSF is superior to detection of VZV DNA in CSF to diagnose vasculopathy, recurrent myelopathy, and brainstem encephalitis.Oral antiviral drugs speed healing of rash and shorten acute pain. Immunocompromised patients require intravenous acyclovir. First-line treatments for post-herpetic neuralgia include tricyclic antidepressants gabapentin, pregabalin, and topical lidocaine patches. VZV vasculopathy, meningoencephalitis, and myelitis are all treated with intravenous acyclovir. KeywordsVaricella zoster virus; Complications; Herpes zoster; Cranial nerves; Zoster paresis; Pathology; Treatment; Postherpetic neuralgia; Vasculopathy; Temporal artery infection; Myelopathy; Meningoencephalitis; Cerebellitis; Ocular disorders; Zoster sine herpete; Diagnostic tests IntroductionVaricella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause herpes zoster (shingles) which is * Address correspondence and reprint requests to Dr. Don Gilden, Department of Neurology, University of Colorado School of Medicine, 12700 E. 19th Avenue, Box B182, Aurora, CO 80045. Telephone: 303-724-4326; Fax: 303-724-4329; don.gilden@ucdenver.edu. Conflict of InterestMaria A. Nagel and Don Gilden declare that they have no conflict of interest. Human and Animal Rights and Informed ConsentThis article does not contain any studies with human or animal subjects performed by any of the authors. (Table 1). VZV reactivation also produces chronic radicular pain without rash (zoster sine herpete). NIH Public Access NEUROLOGICAL COMPLICATIONS OF VZV REACTIVATION Herpes zosterHerpes zoster is the most common manifestation of VZV reactivation. Zoster is characterized by a vesicular eruption on an erythematous base in one to th...

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Herpes Zoster and Neurogenic Bladder Dysfunction

Cited by 12 publications

References 8 publications

Herpes zoster‐associated voiding dysfunction in hematopoietic malignancy patients

Herpes zoster‐associated voiding dysfunction in hematopoietic malignancy patients

Varicella-zoster

Complications of Varicella Zoster Virus Reactivation

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