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Varicella Vasculopathy


Learning objectives

  • Role of VZV infection in stroke
  • Clinical features and diagnosis
  • Diagnosis and treatment

Introduction

  • A viral induced vasculopathy with vascular inflammation due to active initial chicken pox infection or reactivation of the virus.
  • The vasculopathy can lead to ischaemic infarction of the brain and spinal cord, as well as aneurysm formation, subarachnoid and cerebral haemorrhage, carotid dissection.
  • Rarely can even cause peripheral arterial disease. It can occur without a rash and diagnosis is by Anti VZV IgG on CSF.

Aetiology

  • Primary infection with VZV in childhood manifests as chickenpox, and then VZV enters a dormant period in the dorsal root ganglia
  • Reactivation as cell mediated immunity falls later is seen in later life or when on immunosuppression
  • Inflammatory changes of both large and small arteries. There is a granulomatous angiitis of the nervous system in patients with herpes zoster.
  • The VZV vasculopathy occurring up to 6 months later suggesting some chronic arterial damage.
  • It may affects both immunocompetent and immunocompromised patients and is often multifocal.
  • There is no relationship between VZV and Giant cell arteritis

Clinical

  • Headache, fever, malaise and then focal neurological findings and can cause a vasculopathy or myelopathy.
  • Retinal necrosis, and cerebellitis have been seen. Post herpetic neuralgia is also seen.
  • There may be no or minimal rash (zoster sine herpete).
  • There may also be simply zoster infection with ipsilateral infarcts.
  • Headache may be seen.
  • Monocular visual loss due to involvement of blood supply to retina with resultant CRAO.
  • A myelitis due to VZV may occur with long tract signs

Investigations

  • Elevated anti-VZV IgM antibody, indicating active infection
  • Brain Imaging: Is almost always abnormal. Ovoid rounded lesions can be superficial or deep. Classically lesions are seen on imaging at the grey-white matter junction.
  • Angiography: can affect large and small arteries. May be presence of stenosis or occlusion. Can be segmental constriction, often with postste-nic dilatation. Aneurysm formation may be seen especially in those with HIV.
  • CEMRA: Contrast-enhanced vessel wall imaging high-resolution MRI (HRMR) has revealed vessel wall thickening and enhancement in multiple intracranial vasculopathies, including varicella zoster virus (VZV) vasculopathy.
  • CSF: Mildly raised WCC (< 10-100) and red cells may also be seen. Oligoclonal bands are commonly with IgG directed against VZV. The diagnostic value of detecting anti-VZV IgG is more effective than detecting VZV DNA. A negative PCR does not exclude the diagnosis. A negative anti-VZV IgG antibody tests in the can reliably exclude the diagnosis of VZV vasculopathy.

Management

  • Standard stroke care. ABC. HASU bed.
  • IV Aciclovir 10 mg/kg TDS for at least 14 days is the standard therapy which may be combined with Prednisolone 1mg/kg for the first 5 days

References

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