Background: Carotid atherosclerotic disease is recognized as an important risk factor for brain ischemic events. However, high-grade stenosis does not always cause ischemic strokes, whereas moderate-grade stenosis may often cause ischemic strokes. It has been reported that there is an association between carotid intraplaque hemorrhage (IPH) and new cerebral ischemic events. The purpose of this study was to elucidate the relationship between high-intensity signals (HIS) on maximum intensity projection (MIP) images from routine 3-dimensional time-of-flight magnetic resonance angiography (3D-TOF-MRA) and prior ischemic strokes in the patients with moderate carotid stenosis. Materials and Methods: Sixty-one patients with moderate carotid artery stenosis (50-69% stenosis based on North American Symptomatic Carotid Endarterectomy Trial criteria) were included. Carotid IPH was defined as the presence of HIS in carotid plaques on MIP images detected by 3D-TOF-MRA using criteria we previously reported. We analyzed the relationship between the presence of HIS in plaques and prior ischemic strokes defined as ischemic lesions on diffusion-weighted brain images. Results: HIS in carotid plaques were present in 27 (44%) of 61 patients. Prior ipsilateral ischemic strokes occurred more frequently in the HIS-positive group than the HIS-negative group (67 vs. 9%, p < 0.001). Furthermore, there were more smokers in the group with ischemic stroke than without it (62 vs. 25%, p = 0.005). In multivariate logistic regression analysis, HIS in carotid plaque (OR 23.4, 95% CI 4.62-118.3, p < 0.001) and smoking (OR 5.44, 95% CI 1.20-24.6, p = 0.028) were independent determinants of prior ischemic strokes after adjustment for age. Conclusions: HIS in carotid plaques on 3D-TOF-MRA MIP images are independent determinants of prior ischemic strokes in patients with moderate carotid artery stenosis, and they can potentially provide a reliable risk stratification of patients with moderate carotid artery stenosis.

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We investigated the expression of granulocyte colony-stimulating factor (G-CSF), G-CSF mRNA, and G-CSF receptor mRNA in astrocytoma cell lines, G-CSF in astrocytoma cyst fluid, and the effect of recombinant G-CSF on the proliferation of astrocytoma cells in vitro and in vivo. We first examined supernatants from astrocytoma cell lines for the presence of G-CSF by ELISA. G-CSF was expressed by 6 of 14 astrocytoma cell lines constitutively, and, was detected after stimulation with tumor necrosis factor-alpha (TNF-alpha) in four of eight cell lines which did not produce G-CSF constitutively. G-CSF mRNA was detected by reverse-transcriptase polymerase chain reaction (RT-PCR) in all cell lines studied, suggesting that astrocytoma cells have the potential to produce G-CSF. We also analyzed the presence of G-CSF by ELISA in five astrocytoma cyst fluids. G-CSF was detected in one case. Although, in vitro study, the growth of glioma cells was not affected by rG-CSF, in a mouse model, the administration of G-CSF significantly shortened the time to tumor appearance and accelerated tumor growth. These data suggest that G-CSF has a stimulatory effect on the proliferation of astrocytoma cells in vivo through the mediation of host factors.

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Whether plaques with severe stenosis already had severe stenosis at the onset of events or plaques with moderate stenosis progressed owing to an acute change, such as growth of an IPH, remains unclear, because no carotid imaging was carried out just before the events. This is the first case report which presents neurological symptoms and MRI at both baseline and follow-up in patients with asymptomatic moderate carotid artery stenosis and carotid IPH.