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Updated: Feb 4, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
Published on: August 30, 2020
Hemiparesis without Responsible Hematomas in Patients with Subarachnoid Hemorrhage Undergoing Early Aneurysmal Repair
Takatoshi Sorimachi1, Kazuma Yokota1, Akihiro Hirayama1
1Department of Neurosurgery, Tokai University, Kanagawa, Japan.
Objective:
The presence of hemiparesis on arrival in patients with subarachnoid hemorrhage (SAH) is presumed to affect prognosis; intracranial hematomas with mass effect responsible for hemiparesis are frequently observed in these patients. The aim of this study was to clarify characteristics and outcomes of patients who presented with hemiparesis on arrival with no responsible hematomas (hemiparesis without hematoma) having mass effect demonstrated on computed tomography.
Methods:
Consecutive patients with SAH treated with surgery for ruptured cerebral aneurysms within 5 days of onset between 2003 and 2015 were retrospectively reviewed.
Results:
Hemiparesis without hematoma was present in 25 of 858 surgically treated patients (2.9%). Internal carotid artery aneurysms were significantly more common in patients with hemiparesis without hematoma than in the other patients (P < 0.05). In 19 of 21 surviving patients (90.5%) with hemiparesis without hematoma on arrival, the hemiparesis improved at discharge. Favorable outcomes were achieved in 16 of 25 patients with hemiparesis without hematoma (64%) and in 13 of 59 patients with hemiparesis with hematomas (22.0%); this difference was significant (P < 0.05).
Conclusions:
Hemiparesis can be expected to improve in patients with SAH with hemiparesis without hematoma, and such patients appear to have a better prognosis than patients with SAH with hemiparesis and responsible hematomas. A possible major mechanism of hemiparesis without hematoma based on the characteristics identified is a combination of transient ipsilateral hemispheric functional failure caused by the impact of aneurysmal rupture and transient ischemia of the perforators originating from the internal carotid artery.
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