Scholarlink

<p>Spontaneous subarachnoid hemorrhage (SAH) is most often caused by rupture of an intracranial aneurysm. However, in approximately 15–20% of cases, no clear source of bleeding can be identified. While angiogram-negative perimesencephalic SAH is characterized by localized blood clot distribution and is generally associated with favorable outcome, angiogram-negative non-perimesencephalic SAH presents a more diffuse blood pattern resembling aneurysmal hemorrhage and is linked to worse outcome, and its causes and etiology remain unclear. We hypothesize that rupture of small terminal artery aneurysms followed by parent vessel occlusion may account for a subset of angiogram-negative non-perimesencephalic SAH. Over a 10-year period, we reviewed the imaging studies of 524 patients with SAH admitted to our institution to identify patients with angiogram-negative non-perimesencephalic SAH. Clinical data, imaging findings, and outcomes were analyzed. Follow-up data were supplemented prospectively. Seventy two patients (14%) were identified with angiogram-negative SAH. Of these, 45 patients (63%) presented with perimesencephalic SAH, while 27 patients (37%) had non-perimesencephalic patterns on CT imaging. Among the non-perimesencephalic group, 9 patients (33%) exhibited small brain infarctions correlated with parent artery occlusion. These patients (mean age 68&#xa0;years) presented with severe SAH (Fisher grade 3 or 4) and Hunt and Hess grades ranging from 2 to 4. Chronic arterial hypertension was present in 8 of 9 cases. All patients required cerebrospinal fluid diversion, and two developed vasospasm. At follow-up, 5 patients had a good outcome, 2 had moderate disabilities, and 2 patients were dead. This series suggests that ruptured aneurysms of small terminal arteries combined with occlusion of these arteries may cause angiogram-negative non-perimesencephalic SAH. In these patients, characteristic localized infarcts in the territory of the occluded terminal artery support this mechanism. The clinical outcome in these cases is similar to that observed in aneurysmal SAH, underscoring the need for diligent management.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Simultaneous subarachnoid hemorrhage and cerebral infarction due to aneurysm rupture and occlusion of the parent terminal artery: A cause of angiogram-negative non-perimesencephalic subarachnoid hemorrhage

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月11日

查看全文
  • Shadi Al-Afif,
  • Heinrich Lanfermann,
  • Yannick A. Wilken,
  • Harold F. Hounchonou,
  • Marie Middendorff,
  • Joachim K. Krauss,
  • Omar Abu-Fares

摘要

Spontaneous subarachnoid hemorrhage (SAH) is most often caused by rupture of an intracranial aneurysm. However, in approximately 15–20% of cases, no clear source of bleeding can be identified. While angiogram-negative perimesencephalic SAH is characterized by localized blood clot distribution and is generally associated with favorable outcome, angiogram-negative non-perimesencephalic SAH presents a more diffuse blood pattern resembling aneurysmal hemorrhage and is linked to worse outcome, and its causes and etiology remain unclear. We hypothesize that rupture of small terminal artery aneurysms followed by parent vessel occlusion may account for a subset of angiogram-negative non-perimesencephalic SAH. Over a 10-year period, we reviewed the imaging studies of 524 patients with SAH admitted to our institution to identify patients with angiogram-negative non-perimesencephalic SAH. Clinical data, imaging findings, and outcomes were analyzed. Follow-up data were supplemented prospectively. Seventy two patients (14%) were identified with angiogram-negative SAH. Of these, 45 patients (63%) presented with perimesencephalic SAH, while 27 patients (37%) had non-perimesencephalic patterns on CT imaging. Among the non-perimesencephalic group, 9 patients (33%) exhibited small brain infarctions correlated with parent artery occlusion. These patients (mean age 68 years) presented with severe SAH (Fisher grade 3 or 4) and Hunt and Hess grades ranging from 2 to 4. Chronic arterial hypertension was present in 8 of 9 cases. All patients required cerebrospinal fluid diversion, and two developed vasospasm. At follow-up, 5 patients had a good outcome, 2 had moderate disabilities, and 2 patients were dead. This series suggests that ruptured aneurysms of small terminal arteries combined with occlusion of these arteries may cause angiogram-negative non-perimesencephalic SAH. In these patients, characteristic localized infarcts in the territory of the occluded terminal artery support this mechanism. The clinical outcome in these cases is similar to that observed in aneurysmal SAH, underscoring the need for diligent management.