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Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
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A Patient-Derived Xenograft Model for Venous Malformation
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Published on: June 15, 2020

A virulent vasculopathy.

A Molloy1, D Forde, C De Gascun

  • 1Department of Neurology, Cork University Hospital, Cork, Ireland. annamolusa@gmail.com

BMJ Case Reports
|June 16, 2012
PubMed
Summary
This summary is machine-generated.

Varicella zoster virus (VZV) can cause arteriopathy in immunocompetent adults. Prompt antiviral treatment led to the resolution of neurological symptoms and imaging findings in a VZV-negative patient.

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Area of Science:

  • Neurology
  • Infectious Diseases
  • Vascular Medicine

Background:

  • Arteriopathy is a rare complication of primary varicella zoster virus (VZV) infection.
  • This complication is particularly uncommon in immunocompetent adults.

Observation:

  • A 39-year-old VZV-negative woman presented with transient expressive aphasia and right upper limb paresthesia.
  • Symptoms followed a prodrome of malaise, arthralgia, and a generalized rash.
  • Neurological symptoms were linked to focal cerebritis and vasculopathy.

Findings:

  • Varicella zoster virus (VZV) infection was confirmed via cerebrospinal fluid PCR analysis.
  • Imaging demonstrated focal cerebritis and vasculopathy consistent with VZV infection.
  • The patient had no detected immunocompromise but had a known infectious contact.

Implications:

  • Early antiviral therapy can lead to the resolution of VZV-induced vasculopathy and neurological deficits.
  • Highlights the importance of considering VZV in adult-onset neurological events, even in VZV-negative individuals.
  • Underscores the potential for VZV to cause cerebrovascular complications in immunocompetent hosts.