Varicella zoster virus vasculopathy

Nagel, Maria A.; Traktinskiy, Igor; Azarkh, Yevgeniy; Kleinschmidt‐DeMasters, Bette K.; Hedley-Whyte, Tessa; Russman, Andrew; VanEgmond, Eve M.; Stenmark, Kurt R.; Frid, Maria G.; Mahalingam, Ravi; Wellish, Mary; Choe, Alexander; Cordery-Cotter, R.; Cohrs, Randall J.; Gilden, Don

doi:10.1212/wnl.0b013e3182267bfa

Cited by 148 publications

(131 citation statements)

References 38 publications

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“…After VZV reaches the arterial adventitia, virus spreads transmurally to infect all layers of the cerebral arteries, resulting in the characteristic pathology of granulomatous arteritis. Virological and immunological analyses of VZV-infected arteries have revealed disruption of the internal elastic lamina and progressive intimal thickening, with cells expressing smooth muscle actin but decreased smooth muscle cells in the media (14). The pathophysiology of VZV vasculopathy appears to be similar in children.…”

Section: Pathophysiology Of Vzv Vasculopathymentioning

confidence: 99%

Varicella Zoster Virus: A Common Cause of Stroke in Children and Adults

Amlie‐Lefond

Gilden

2016

Journal of Stroke and Cerebrovascular Diseases

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Background-Varicella zoster virus (VZV) is a neurotropic exclusively human herpesvirus. Primary infection causes varicella (chickenpox), after which virus become latent in ganglionic neurons along the entire neuraxis. As cell-mediated immunity to VZV declines with advancing age and immunosuppression, VZV reactivates to produce zoster (shingles). One of the most serious complications of zoster is VZV vasculopathy.

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Section: Pathophysiology Of Vzv Vasculopathymentioning

confidence: 99%

Varicella Zoster Virus: A Common Cause of Stroke in Children and Adults

Amlie‐Lefond

Gilden

2016

Journal of Stroke and Cerebrovascular Diseases

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“…6 With reactivation, VZV spreads centripetally from the dorsal root ganglia along the axon, with transmural migration to blood vessels of the CNS. 7 Infection and inflammation of the vessels can result in ischemic stroke by narrowing the arterial lumen or inducing arterial thrombosis. 8 Patients frequently pre sent with one or more of focal neurologic deficits, subacute onset of headache or changes in mental status.…”

Section: Discussionmentioning

confidence: 99%

Multifocal strokes in a 56-year-old man with HIV infection

Lefkowitz

Gold

Casaubon

et al. 2015

CMAJ

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A 56-year-old man presented with a oneday history of vomiting, vertigo and blurred vision in both eyes preceded by a three-week history of fever, night sweats and a 5-kg weight loss. He had no recent history of travel or contact with sick people. His past medical history was notable for untreated HIV infection diagnosed eight months previously, after treatment for presumed Pneumocystis jirovecii pneumonia. At that time, his CD4 count was 0.072 × 10 9 /L. He was immune to hepatitis B virus infection secondary to a previous natural infection, and he had remote idiopathic retinal vasculitis. He had had chickenpox as a child. There was no history of hypertension, diabetes mellitus, smoking, dyslipidemia, atrial fibrillation or cardiac disease. He denied intravenous drug use.On examination, the patient was afebrile, his blood pressure was 133/83 mm Hg, and his heart rate was 57 beats/min and regular. He was somnolent but rousable and answered questions appropriately. Findings on cardiovascular, respiratory and abdominal examinations were normal. Neurologic examination showed bilateral eye deviation to the right as well as horizontal, vertical and torsional nystagmus in primary position, which worsened with rightward gaze. There was rightsided miosis but no ptosis. Speech and swallowing were normal. Muscle tone, power and reflexes were normal. There was decreased sensation to pinprick in the right cheek and the left arm and leg. The patient had marked ataxia in his right arm and leg (appendicular ataxia). Dermatologic examination revealed several crusted skin lesions distributed over his body, with a single vesicle overlying his right zygoma. There were no peripheral findings of infective endocarditis.The patient's leukocyte count was 2.4 (normal 4.0-11.0) × 10 9 /L, hemoglobin A 1C concentration 6% (normal 4%-6%) and low-density lipoprotein cholesterol 2.76 mmol/L. Blood cultures for bacteria were negative. Tests of the patient's serum were negative for syphilis and cryptococcal antigen. The erythrocyte sedimentation rate was 41 (normal 0-10) mm/h.Magnetic resonance imaging of the brain showed small acute infarcts in the left frontal cortex and deep white matter (the territory supplied by the left middle cerebral artery) and in the right lateral medulla and right cerebellar hemisphere (the territory supplied by the right posterior inferior cerebellar artery) (Figure 1

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“…Indeed, stroke following zoster ophthalmicus is of high clinical importance 83,84 . VZV that reactivates in the trigeminal nerve can travel via the ophthalmic sensory nerves to the face and via afferent sensory fibres to the internal carotid artery and its intracranial branches 85,86 . Thereafter, the virus establishes infection in the arterial wall, which leads to inflammation, arterial weakening, aneurysm formation, occlusion and stroke 87 .…”

Section: Neurological Complications Of Zostermentioning

confidence: 99%

“…Thereafter, the virus establishes infection in the arterial wall, which leads to inflammation, arterial weakening, aneurysm formation, occlusion and stroke 87 . Infected cerebral arteries contain multinucleated giant cells, Cowdry A inclusions (accumulations of viral DNA and protein in the cell nucleus) and herpesvirus particles, as well as VZV DNA and VZV antigens 81,85 .…”

Section: Neurological Complications Of Zostermentioning

confidence: 99%