Some macrophages expressing NG2 chondroitin sulfate proteoglycan (NG2) and the macrophage marker Iba1 accumulate in the ischemic core of a rat brain subjected to transient middle cerebral artery occlusion (MCAO) for 90 min. These cells are termed BINCs (for brain Iba1(+) /NG2(+) cells) and may play a neuroprotective role. Because BINCs are bone marrow-derived cells, they are able to invade ischemic tissue after the onset of an ischemic insult. In this study, chemokine-based mechanisms underlying the invasion of BINCs or their progenitor cells were investigated. We found that isolated BINCs expressed mRNA encoding CCR2 and CX3CR1 at high levels. Cultured astrocytes expressed mRNA encoding their ligands, MCP-1 and fractalkine. Recombinant MCP-1 and/or fractalkine, as well as astrocytes, induced the migration of BINCs in vitro. mRNA for MCP-1, fractalkine, CCR2, and CX3CR1 was expressed in the ischemic core during the acute phase of the ischemic event. Immunohistochemical studies revealed that vascular endothelial cells and astrocytic endfeet expressed MCP-1 and fractalkine, respectively, in the ischemic core during the acute phase. CCR2(+) /Iba1(+) monocytes attached to the inside of the vascular wall at 1 day postreperfusion (dpr), and there were CCR2(+) /CX3CR1(+) macrophage-like cells in the parenchyma in the ischemic lesion core at 2 dpr, which may be the progenitors for BINCs. These results suggest that CCR2(+) monocytes are first attracted to the ischemic lesion by MCP-1(+) endothelial cells and migrate toward fractalkine(+) astrocytic endfeet through the disrupted blood-brain barrier. Thus, chemokines may play a critical role in the accumulation of neuroprotective BINCs. © 2013 Wiley Periodicals, Inc.

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Summary:We evaluated the neuropsychological functions of 105 patients who underwent 108 surgeries for unruptured cerebral aneurysms. All patients completed the Wechsler Adult Intelligence Scale-Revised (WAIS-R) before and one month after surgery. The aneurysms were located mainly in the anterior cerebral artery, middle cerebral artery, or internal cerebral artery. Deep white matter hyper-intensities (DWMH), brain atrophy and cerebral infarction were evaluated using preoperative magnetic resonance imaging (MRI). Brain contusion (large: 10 mm or more in largest diameter; small: smaller than 10 mm), subdural fluid collection (thick: midline shift observed; thin: mass effect observed without midline shift) and cerebral infarction were evaluated on postoperative MRI and/or computed tomography. A decrease of four points or more in the WAIS-R score postoperatively was interpreted as deterioration.Although there was no statistical difference between the preoperative and postoperative WAIS-R scores, 25 of 108 surgeries (23%) showed deterioration of the WAIS-R score postoperatively.Brain contusion on MRI was observed in 15 surgeries (large: 7; small: 8), and six of those surgeries (40%) showed deterioration of the WAIS-R score. Deterioration of the WAIS-R score was observed more frequently in patients with large brain contusion (4 of 7, 57%) than in those without brain contusion (19 of 93, 20%) (p 0.05). Brain contusion occurred more frequently in patients with moderate or severe DWMH (5 of 23, 22%) than in those without DWMH (2 of 43, 5%) (p 0.05), and in patients with ACoA aneurysm (5 of 26, 19%) than in those with MCA aneurysm (1 of 33, 3%) (p 0.05). Although large brain contusion was observed postoperatively in patients with aneurysms localized to the ACoA operated through the pterional approach, damage was not apparent in patients operated with an interhemispheric approach. Subdural fluid collection was observed after 14 surgeries (thick: 5; thin: 9), and four of those patients (29%)