Recurrent polymorphonuclear pleocytosis with increased red blood cells caused by varicella zoster virus infection of the central nervous system

Haug, Aaron; Mahalingam, Ravi; Cohrs, Randall J.; Schmid, Daniela; Corboy, John R.; Gilden, Don

doi:10.1016/j.jns.2010.01.019

Cited by 38 publications

(40 citation statements)

References 31 publications

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“…The detection of VZV DNA by PCR or detection of anti-VZV IgG antibody in CSF or both would confirm that VZV produced the neurologic disease. Importantly, the detection of anti-VZV IgG antibody, but not VZV DNA, in the CSF of our patient with VZV encephalitis parallels earlier findings in patients with VZV vasculopathy 6 and VZV myelopathy with brainstem involvement, 9 which showed that the detection of anti-VZV IgG antibody in CSF was superior to that of VZV DNA. More cases of VZV encephalitis need to be studied virologically.…”

Section: Sectionsupporting

confidence: 90%

Clinical Reasoning: A 57-year-old woman with ataxia and oscillopsia

et al. 2016

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A 57-year-old immunosuppressed renal transplant recipient experienced 2 months of oscillopsia, vertigo, ataxia, and headaches. The headaches were described as constant, bifrontal, dull, and associated with photophobia and nausea but no aura or positional component. She described rotational vertigo, both at rest and provoked by leftward head turn and gait instability that developed gradually over the last 4 weeks. Six months prior to presentation, she had a similar episode of headaches, dizziness, and ataxia that resolved spontaneously over 3 months. This was preceded by a dermatomal vesicular rash on the arm. She had undergone renal transplantation 12 years earlier. Three years ago, she had left C2-3 distribution zoster. She denied infectious or rheumatologic symptoms. Her only current medication was mycophenolate mofetil 360 mg PO BID.Neurologic examination. Visual acuity was 20/2022 OS and 20/20 OD. Extraocular movements were full without nystagmus. All attempts at fixation led to intermittent bursts of ocular flutter. There were also hypometric saccades to the left and hypermetric saccades to the right (video on the Neurology ® Web site at Neurology.org). Dix-Hallpike and other otolith repositioning maneuvers did not elicit vertigo or nystagmus. There was intention tremor in both arms without dysdiadochokinesia or dysmetria. Gait was wide-based and ataxic and the patient was unable to walk tandem without falling to the left. Romberg sign was absent and the remaining neurologic and general examinations were normal.

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Section: Sectionsupporting

confidence: 90%

Clinical Reasoning: A 57-year-old woman with ataxia and oscillopsia

et al. 2016

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“…1,7 The presence of neutrophils in early VZV vasculopathy is supported by their abundance in vesicular fluid of zoster patients 13 and in CSF throughout the protracted course of VZV vasculopathy, meningoencephalitis, encephalomyelitis, myelitis, and inflammatory brainstem disease. 9,[14][15][16][17] Although mechanisms of vascular remodeling triggered by VZV are unknown, neutrophils may play a role. When exposed to VZV, they produce reactive oxygen species which mediate smooth muscle cell proliferation and migration 18,19 and induce apoptosis and loss of vascular smooth muscle cells.…”

Section: Figure 3 T-cell Subsets In Varicella-zoster Virus (Vzv) Vascmentioning

confidence: 99%

Varicella-zoster virus vasculopathy

et al. 2013

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Objective: Pathologic changes in varicella-zoster virus (VZV)-infected arteries include inflammation, thickened intima, and paucity of smooth muscle cells. Since no criteria have been established for early vs late VZV vasculopathy, we examined inflammatory cells and their distribution in 6 normal arteries, and 2 VZV-infected arteries 3 days after onset of disease (early) and 10 months after protracted neurologic disease (late).Methods: VZV-infected temporal artery obtained 3 days after onset of ischemic optic neuropathy from an 80-year-old man, VZV-infected middle cerebral artery (MCA) obtained 10 months after protracted disease from a 73-year-old man, and 5 MCAs and 1 temporal artery from normal subjects, age 22-60 years, were examined histologically and immunohistochemically using antibodies against VZV and inflammatory cell subsets. Results:In both early and late VZV vasculopathy, T cells, activated macrophages, and rare B cells were found in adventitia and intima. In adventitia of early VZV vasculopathy, neutrophils and VZV antigen were abundant and a thickened intima was associated with inflammatory cells in vaso vasorum vessels. In media of late VZV vasculopathy, viral antigen, but not leukocytes, was found. VZV was not seen in inflammatory cells. Inflammatory cells were absent in control arteries. In varicella-zoster virus (VZV) vasculopathy, virus-infected regions are associated with a thickened intima composed of myofibroblasts, a paucity of smooth muscle cells in media, and disruption of internal elastic lamina.1 Similar morphologic changes have been found in other vascular diseases, such as pulmonary arterial hypertension (PAH) and atherosclerosis, 2 in which inflammation has emerged as a pathogenic component. For example, in PAH, inflammatory cells surrounding pulmonary artery lesions secrete CX3CL1, which induces vascular smooth muscle cell (VSMC) proliferation.3 In atherosclerosis, activated macrophages, in addition to other cells, secrete platelet-derived growth factor-BB and insulin-like growth factor-I, which promote VSMC migration 4 ; interleukin-1B also promotes VSMC proliferation. 5,6 We hypothesize that 1) after reactivation from trigeminal ganglia, virus spreads transaxonally to infect the adventitia, followed by transmural migration to the media 1,7 ; 2) inflammatory cells are recruited to virus-infected sites; and 3) inflammatory cells secrete factors that contribute to vessel wall changes seen in VZV vasculopathy. Characterization of immune cells involved in VZV vasculopathy could elucidate mechanisms of VZV-induced vascular remodeling and identify potential targets for therapy.

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“…Importantly, many cases of VZV vasculopathy are protracted, and VZV DNA is only found ~30 % of the time [18••]. The detection of anti-VZV IgG antibody in CSF with intrathecal synthesis is superior to detection of VZV DNA in CSF to diagnose VZV vasculopathy [19], recurrent myelopathy, and brainstem encephalitis produced by VZV [29]. …”

Section: Diagnostic Testsmentioning

confidence: 99%

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

Gilden

Nagel

Cohrs

et al. 2013

Curr Neurol Neurosci Rep

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Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines, and the virus reactivates to cause zoster (shingles), dermatomal distribution, pain, and rash. Zoster is often followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, vasculopathy, meningoencephalitis, and multiple ocular disorders. This review covers clinical, laboratory, and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system. Additional perspectives are provided by discussions of VZV latency, animal models to study varicella pathogenesis and immunity, and of the value of vaccination of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.

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Recurrent polymorphonuclear pleocytosis with increased red blood cells caused by varicella zoster virus infection of the central nervous system

Cited by 38 publications

References 31 publications

Clinical Reasoning: A 57-year-old woman with ataxia and oscillopsia

Clinical Reasoning: A 57-year-old woman with ataxia and oscillopsia

Varicella-zoster virus vasculopathy

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

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