INTRODUCTION Herpes zoster is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV) that is the cause of varicella. Gilbert for this comments. The findings were compared with lesions in classical acute HZO. Brain magnetic resonance imaging (MRI) revealed left orbital myositis and periorbital skin eruptions appeared two days after this MRI study. Varicella zoster virus (VZV) is an exclusively human, neurotropic double-stranded DNA alphaherpesvirus. All patients with acute herpes zoster ophthalmicus should receive antiviral therapy with the goal of preventing ocular complications. Link between VZV reactivation and CNS disease.
inactivated influenza vaccine) and live vaccines (e.g. However, this is rarely the case because the majority of VZV meningitis will not present with a rash. The notion that virus spreads transaxonally after reactivation from trigeminal and other cranial nerve ganglia is supported by the demonstration of afferent fibers from trigeminal ganglia to intracranial blood vessels, venous sinuses, and dural structures [1, 2]. Evidence for productive VZV infection of affected arteries was first provided by virologic analysis of a patient who died after VZV vasculopathy; the infected arteries contained Cowdry A inclusion bodies, multinucleated giant cells, herpes virions, and both VZV DNA and antigen . Granulomatous angiitis of the CNS associated to Hodgkin lymphoma is a rare disease. Immunohistochemical analyses using antibodies directed against VZV, endothelium, and smooth muscle actin and myosin revealed the presence of VZV antigen in the outermost arterial layer (adventitia) early in infection and later in the media and intima layers, consistent with both transaxonal spread of reactivated VZV to the arterial adventitia followed by transmural spread of virus . Moreover, virus-infected arteries revealed a disrupted internal elastic lamina, a thickened intima composed of cells expressing α smooth muscle actin and smooth muscle myosin heavy chain, but not endothelial cells expressing CD31 and decreased numbers of medial smooth muscle cells .
The loss of medial smooth muscle cells and the presence of cells expressing myosin in the thickened intima suggest that some of these latter cells are of medial smooth muscle origin. Simplex often causes recurrently acute disease, while zoster consequences are more chronic.15 Herpes simplex keratitis often responds well to treatment within a week, though repeated episodes are common and increase the risk of scarring. Early VZV vasculopathy was distinguished by the presence of abundant neutrophils in the adventitia that were absent in late VZV vasculopathy. Human Vaccines. Nucleic acid amplification methods such as PCR have greatly improved the detection of viral pathogens. Finally, a thickened intima was associated with inflammation in vasa vasorum vessels in early VZV vasculopathy, consistent with a role for virus-induced inflammation in vessel wall remodeling [7, 8]. Together, the findings point to the role of altered arterial caliber and contractility, produced in part by abnormal accumulation of smooth muscle cells and myofibroblasts in the thickened neointima and by disruption of the media associated with the presence of viral antigen and inflammatory cells, in VZV-associated stroke.
Although the exact incidence of VZV vasculopathy is unknown, recent studies from the United Kingdom, Europe, and Asia have indicated that stroke after zoster is not uncommon. A study of 7760 adults with zoster and 23 280 matched controls without zoster that analyzed medical records from the Taiwan National Health Research Institute revealed a 30% increased risk of stroke in the year after zoster, a risk that was further increased 4-fold when zoster was in the ophthalmic division of the trigeminal nerve . Use of the same database for additional analysis of 658 individuals with ophthalmic-distribution zoster and 1974 controls confirmed a 4.5-fold increased risk of stroke in the year after zoster in the former group compared with controls and no found effect of antiviral treatment on the difference in rates . Some limitations of the 2 studies included key confounders such as body mass index and atrial fibrillation, and the analysis of the risk of stroke at only a single time-point (1 year after zoster). Pre-Existing Chronic Pain Influences the Severity of Acute Herpes Zoster Pain-A Prospective Observational Cohort Study on ResearchGate, the professional network for scientists. Limitations of this study included the use of antiviral treatment as a proxy for zoster, which may have resulted in false-positive exposures as some people with herpes simplex virus infection may have received treatment. BC CDC August 2012.