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Introduction <p>Developmental venous anomaly (DVA) is a common cerebral vascular variant, typically considered benign and clinically silent. We report an exceptional case of a symptomatic infratentorial DVA in a 9-year-old child that became clinically evident after a minor head trauma.</p> Case Report <p>The patient presented with neurological symptoms indicative of posterior fossa involvement, including headache, nausea, and ataxia. MRI revealed a cluster of abnormally dilated medullary veins in the right cerebellar hemisphere converging into an enlarged collector vein, consistent with a DVA. Significant cerebellar edema was identified in association with detected vascular malformation. The patient was managed conservatively with antiedematous therapy and analgesics, which led to rapid resolution of symptoms and complete recovery.</p> Conclusion <p>This case demonstrates that DVAs can become acutely symptomatic secondary to significant vasogenic edema following even minor head trauma, likely due to transient hemodynamic disturbance without thrombosis or hemorrhage. Our findings challenge the perception of DVAs as invariably benign entities and warrant further investigation into their post-traumatic pathophysiology.</p>

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Trauma-Induced Cerebellar Edema: A Rare Presentation of Infratentorial Developmental Venous Anomaly in a Pediatric Patient

  • 期刊论文

  • 发表日期：

    2025年5月19日

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  • Mirko Micovic,
  • Bojana Zivkovic,
  • Ivan Vukasinovic,
  • Aleksandra Nedeljkovic,
  • Zarko Nedeljkovic,
  • Vladimir Bascarevic

摘要

Introduction

Developmental venous anomaly (DVA) is a common cerebral vascular variant, typically considered benign and clinically silent. We report an exceptional case of a symptomatic infratentorial DVA in a 9-year-old child that became clinically evident after a minor head trauma.

Case Report

The patient presented with neurological symptoms indicative of posterior fossa involvement, including headache, nausea, and ataxia. MRI revealed a cluster of abnormally dilated medullary veins in the right cerebellar hemisphere converging into an enlarged collector vein, consistent with a DVA. Significant cerebellar edema was identified in association with detected vascular malformation. The patient was managed conservatively with antiedematous therapy and analgesics, which led to rapid resolution of symptoms and complete recovery.

Conclusion

This case demonstrates that DVAs can become acutely symptomatic secondary to significant vasogenic edema following even minor head trauma, likely due to transient hemodynamic disturbance without thrombosis or hemorrhage. Our findings challenge the perception of DVAs as invariably benign entities and warrant further investigation into their post-traumatic pathophysiology.