Masato Naraoka1, Toshio Fumoto2, Yuchen Li2, Takeshi Katagai2, Hiroki Ohkuma2. 1. Department of Neurosurgery, Hirosaki University School of Medicine and Hospital, Hirosaki, Japan. Electronic address: nessun@hirosaki-u.ac.jp. 2. Department of Neurosurgery, Hirosaki University School of Medicine and Hospital, Hirosaki, Japan.
Abstract
OBJECTIVE: Early brain injury after subarachnoid hemorrhage (SAH), which is considered a main factor leading to poor outcome, is believed to be caused by the increase of intracranial pressure (ICP) and/or the presence of subarachnoid blood clots (SBC) itself. The purpose of this study was to examine whether ICP or SBC is more important to neurologic deficit in the presence of apoptosis or edema. METHODS: A total of 50 rats were allocated to 3 groups: an endovascular perforation SAH model (the SAH group), a cisterna magna saline injection model (the saline injection group), and a cisterna magna sham injection model (the sham injection group). Statistical analysis of correlations among the ICP, the grade of clot volume, neuronal apoptosis, brain water content (brain edema), and neurologic deficit was performed. RESULTS: In the SAH group, each of increased ICP and clot volume was correlated with neuronal apoptosis and brain edema. In the saline injection group, increased ICP was associated with apoptosis, but it did not correlate with brain edema. Neuronal apoptosis (r = 0.75; P < 0.01) and brain edema (r = 0.89; P < 0.01) correlated independently with neurologic deficit in the SAH group. CONCLUSIONS: The present study suggests that neuronal apoptosis is caused mainly by increased ICP, whereas brain edema is induced by SBC, and increased ICP could aggravate it in the presence of SBC. Brain edema could affect neurologic deficit, but apoptosis alone may be less influential. Not only ICP but also SBC seem important for brain damage in the acute stage of SAH.
OBJECTIVE: Early brain injury after subarachnoid hemorrhage (SAH), which is considered a main factor leading to poor outcome, is believed to be caused by the increase of intracranial pressure (ICP) and/or the presence of subarachnoid blood clots (SBC) itself. The purpose of this study was to examine whether ICP or SBC is more important to neurologic deficit in the presence of apoptosis or edema. METHODS: A total of 50 rats were allocated to 3 groups: an endovascular perforation SAH model (the SAH group), a cisterna magna saline injection model (the saline injection group), and a cisterna magna sham injection model (the sham injection group). Statistical analysis of correlations among the ICP, the grade of clot volume, neuronal apoptosis, brain water content (brain edema), and neurologic deficit was performed. RESULTS: In the SAH group, each of increased ICP and clot volume was correlated with neuronal apoptosis and brain edema. In the saline injection group, increased ICP was associated with apoptosis, but it did not correlate with brain edema. Neuronal apoptosis (r = 0.75; P < 0.01) and brain edema (r = 0.89; P < 0.01) correlated independently with neurologic deficit in the SAH group. CONCLUSIONS: The present study suggests that neuronal apoptosis is caused mainly by increased ICP, whereas brain edema is induced by SBC, and increased ICP could aggravate it in the presence of SBC. Brain edema could affect neurologic deficit, but apoptosis alone may be less influential. Not only ICP but also SBC seem important for brain damage in the acute stage of SAH.