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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Arterial ischemic stroke in a child with beta-thalassemia trait and methylentetrahydrofolate reductase mutation

Vesna Brankovic-Sreckovic1, Vedrana Milic Rasic, Valentina Djordjevic

  • 1Clinic for Child Neurology and Psychiatry, Medical Faculty, University of Belgrade, Serbia. vladas@infosky.net

Journal of Child Neurology
|July 11, 2007
PubMed

Insights

A young child with beta-thalassemia minor experienced a stroke due to combined genetic and acquired prothrombotic risk factors. This case highlights the potential for severe thromboembolism in seemingly mild genetic conditions.

Area of Science:

  • Pediatric Neurology
  • Hematology
  • Genetics

Background:

  • Procoagulable states from genetic and acquired disorders are known childhood stroke risk factors.
  • Thalassemia is associated with increased thromboembolic complications, though severe cerebral events are rare in beta-thalassemia minor.

Observation:

  • A 1-year-old boy presented with hemiparesis, seizures, microcytic anemia, and reactive thrombocytosis post-infection.
  • Magnetic resonance imaging confirmed ischemic infarction in the right middle cerebral artery territory.

Findings:

  • Genetic analysis revealed heterozygosity for beta(0)-thalassemia IVS-I-1 and homozygosity for methylenetetrahydrofolate reductase C677T.
  • The patient exhibited a hypercoagulable state resulting from synergistic genetic and acquired prothrombotic factors.

Implications:

  • This case underscores the importance of considering multiple prothrombotic risk factors in pediatric stroke.
  • Early identification and management of combined genetic and acquired risks are crucial for preventing severe outcomes in thalassemic children.

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