Zoster sine herpete

What is herpes zoster sine herpete?

Some cases of VZV reactivation result in a condition known as zoster sine herpete. Patients experience pain and weakness in a dermatology distribution, and a tender, housemasters, unilateral patch or plaque is apparent, but there are no visible signs of cutaneous vesicles. Like typical herpes zoster (shingles), zoster sine herpete tends to be preceded by synesthesia.

This condition presents a diagnostic dilemma; however, VZV DNA may be detected by polymerase chain reaction (PCR) assay of oropharyngeal swabs in patients with zoster peripheral facial palsy. Because such studies are not routine, the true incidence and prevalence are unknown

Classic zoster sine herpete (Z SH) is defined clinically as dermatology distribution pain without rash. Z SH was designated as a nosologic entity based on virologist confirmation in 3 men over age 60 with chronic thoracic-distribution radicular pain, with amplifier avarice zoster virus (VZV) DNA found in C SF of the first 2 patients1 and in blood mono nuclear cells (Mn Cs) in the third patient. Herein, we describe a patient who developed radicular pain without rash in the same dermatology as his initial cervical-distribution zoster episode, but with a remarkably prolonged interval between episodes, and in whom Z SH was neurologically confirmed by the detection of anti-VIZ immunoglobulin G (IgG) antibody in C SF with serum/C SF ratios indicative of nontheatrical antibody synthesis.

Case report.

In 2008, a 77-year-old man developed right C8-distribution zoster; he was not treated with an antiviral agent or steroids and his rash and pain resolved completely. One year later, he developed colon cancer and was treated every other week for 7 months with a protocol using leucine, 5-fluorouracil, oxaliplatin, and folic acid.3 In November 2009, right C7–8-distribution pain recurred, but in the absence of rash. In December 2009, he developed a painless right foot drop. In February 2010, neurology examination revealed C7–8 thigmesthesia and alloyed and an incidental right personal palsy. All deep tendon reflexes were reduced or absent. Cervical MRI revealed degenerative changes at C5–6 and C6–7 without root compression. The C SF was a cellular; cytology was negative, and C SF protein was 87 mg%. A presumptive diagnosis of Z SH was made, and he was treated with val acyclovir, 1 g 3 times daily for 14 days, and prefabbing, 150 mg at night. A few days after treatment, he experienced a dramatic reduction in pain, and 2 months later, was pain-free. Virology studies of the C SF and serum obtained before antiviral treatment revealed no amplifier VZV or herpes simplex virus (VHS) DNA and no anti-VHS IgG antibody. In contrast, anti-VIZ IgG antibody was present, and the serum/C SF ratio of anti-VIZ IgG antibody was markedly reduced (4.9) compared to ratios for albumin (70) and total IgG (150), indicative of nontheatrical synthesis of anti-VIZ IgG.

  • The psychophysiology mechanisms underlying reactivation of and neurological complications associated with avarice zoster virus are currently not completely characterized.
  • Italian researchers reported that patients with zoster sine herpete (Z SH), pain in the absence of an antecedent rash, reported greater severity and longer duration of pain than patients with typical herpes zoster (HZ) eruption.
  • The authors also reported increased use of opioids in patients with Z SH than those with HZ.

Primary infection with avarice zoster virus (VZV), a ubiquitous neurotic human alphanumerical, causes chicken pox, after which VZV becomes latent in cranial nerve, dorsal root, and autonomic ganglionic neurons along the entire neurosis.2 VZV can later become reactivated—even decades after the primary infection—following decline of cell-mediated immunity against VZV, due to increasing age-, disease-, or drug-related presupposition.2,3 Reactivated VZV is associated with neurological complications, including VZV psychopathy, electroencephalograms, myelitis, ocular disease, and stroke, and when traveling in retrograde to the skin, causing HZ (also referred to as shingles) and prosthetic neuralgia (PHN).3 PHN is the most frequent and significant neurological complication of VZV reactivation, occurring in over 40% of patients with zoster aged >60 years with an overall annual incidence rate of 3.2 cases per 1000 in the US.3,4 Studies addressing the economic burden of HZ reported that it is associated with an increase in health care costs in the 12 months following the initial diagnosis, with up to nearly 4-fold cost increases associated with PHN during the same period

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