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Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
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Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
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Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review

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Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review
Journal Article

Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review

2025
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Overview
Background and Clinical Significance: Intracerebral hemorrhage (ICH) is a very rare complication following endovascular closure of direct carotid-cavernous fistulas (CCFs). When reported, ICH typically appears within the first 48 h after CCF closure. We performed an extensive literature review, starting from the case of a 48-year-old patient presenting with an intracerebral hemorrhage after CCF closure. Case Presentation: A 48-year-old woman with arterial hypertension developed an intracerebral hemorrhage in the right frontal lobe 12 days after successful closure of a traumatic CCF. The patient exhibited acute neurological deterioration in a previously hypoperfused territory. A narrative review identifies the classical molecular theory of hemodynamic dysregulation, known as Normal Perfusion Pressure Breakthrough (NPPB), as the principal pathophysiological mechanism. Other mechanisms such as oxidative stress, microglial activation, blood–brain barrier disruption, metalloproteinase expression, and possible genetic alterations such as ICA1L variants are also implicated. Conclusions: This case underscores the importance of considering molecular mechanisms in the pathophysiology of delayed post-endovascular treatment of ICH, as well as the need for hemodynamic monitoring and follow-up in patients with vascular comorbidities.