Validity of high resolution magnetic resonance imaging in detecting giant cell arteritis: a meta-analysis.

OBJECTIVES: This study was designed to evaluate the performance of high-resolution magnetic resonance imaging (HR-MRI) in detecting giant cell arteritis (GCA), evaluate superficial extracranial artery and other MRI abnormalities, and compare three-dimensional (3D) and two-dimensional (2D) techniques. METHODS: PubMed, Web of Science, and Cochrane Library were screened up to March 7, 2021, and further selection was performed according to the eligibility criteria. Quality Assessment of Diagnostic Accuracy Studies-2 was used for quality assessment, and heterogeneity assessment and statistical calculations were also performed. RESULTS: In total, 1851 records were retrieved from online databases, and 15 studies were finally included. Regarding the performance of HR-MRI, the superficial extracranial artery had 75% sensitivity and 89% specificity, respectively, with an area under the receiver operating characteristic curve (AUC) of 0.91. Positive and negative post-test possibilities were 86% and 20%, respectively, with clinical diagnosis as reference. When referenced with temporal artery biopsy, the sensitivity was 91%, specificity was 78%, AUC was 0.92, and positive and negative post-test possibilities were 78% and 10%, respectively. 3D HR-MRI and 2D HR-MRI had 70% and 72% sensitivity, respectively, and 91% and 84% specificity, respectively. CONCLUSIONS: HR-MRI is a valuable imaging modality for GCA diagnosis. It provided high accuracy in the diagnosis of GCA and played a potential role in identifying GCA-related ischemic optic neuropathy. 3D HR-MRI had better specificity than 2D HR-MRI. KEY POINTS: HR-MRI helps clinicians to diagnose GCA. Superficial extracranial arteries and other MRI abnormalities can be assessed with HR-MRI. HR-MRI can help in assessing GCA-related optic neuropathy.

Intracranial Calcification is Predictive for Hemorrhagic Transformation and Prognosis After Intravenous Thrombolysis in Non-Cardioembolic Stroke Patients.

AIM: Hemorrhagic transformation is the major complication of intravenous thrombolysis. Calcification is used widely as an imaging indicator of atherosclerotic burden and cerebrovascular function. The relationship between intracranial calcification and hemorrhagic transformation has not been explored fully. We aimed to identify and quantify calcification in the main cerebral vessels to investigate the correlations between quantitative calcification parameters, hemorrhagic transformation, and prognosis. METHODS: Acute, non-cardiogenic, ischemic stroke patients with anterior circulation who received intravenous thrombolysis therapy in the First Hospital of Jilin University were retrospectively and consecutively included. All included patients underwent a baseline CT before intravenous thrombolysis and a follow-up CT at 24 hours. A third-party software, ITK-SNAP, was used to segment and measure the calcification volume. A vascular non-bone component with a CT value ＞130 HU was considered calcified. Hemorrhagic transformation was determined based on the ECASS II classification criteria. RESULTS: The study included 242 patients, 214 of whom were identified as having calcification. Thirty-one patients developed hemorrhagic transformation. The calcification volume on the lesion side (0.1ml) was associated with hemorrhagic transformation (p=0.004, OR=1.504, 95% CI: 1.140-1.985). Ninety-six patients had poor prognoses. The poor prognosis group had more calcified vessels than the good prognosis group (p=0.014, OR=1.477, 95% CI: 1.083-2.015). CONCLUSIONS: The arterial calcification volume on the lesion side is associated with hemorrhagic transformation after thrombolysis. The higher the number of calcified vessels, the greater the risk of poor prognosis.

Neurochemical and behavioral effects of the intrahippocampal co-injection of beta-amyloid protein1-40 and ibotenic acid in rats.

The present study was designed to investigate the effects of the intrahippocampal co-injection of beta-amyloid protein1-40 (Abeta(1-40)) with ibotenic acid (Ibo) on learning and memory in normal and aging model rats, and to explore the mechanism underlying the effects of the co-injection. The normal and aging rats were bilaterally injected Abeta(1-40) (4 microg for each side) with Ibo (2 microg for each side) into the hippocampus. Two weeks after the intrahippocampal injection, the exploratory behavior and learning-memory ability of the rats were tested by using open field, Y-maze and passive avoidance task. And the changes of membrane fluidity in hippocampal mitochondria, the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in hippocampus were also examined. The co-injection of Abeta(1-40) with Ibo induced tested rats a remarkable decrease in the explorative behaviors and a significant decline in learning-memory ability (P < 0.01). The neurochemical changes induced by the co-injection included a significant decrease in membrane fluidity of hippocampal mitochondria (P < 0.01), a significant decrease in the activity of SOD (P < 0.01), as well as a remarkable increase in the content of MDA (P < 0.01). The results suggest that co-injection of Abeta(1-40) with Ibo may induce an increase of hippocampal damage by peroxidation and a serious deficit in the learning and memory of the rats. The results also suggest that the co-injection of Abeta(1-40) with Ibo may provide a useful animal model for the Alzheimer's disease (AD) research.

Distribution of wall shear stress in carotid plaques using magnetic resonance imaging and computational fluid dynamics analysis: a preliminary study.

BACKGROUND: Wall shear stress is an important factor in the destabilization of atherosclerotic plaques. The purpose of this study was to assess the distribution of wall shear stress in advanced carotid plaques using high resolution magnetic resonance imaging and computational fluid dynamics. METHODS: Eight diseased internal carotid arteries in seven patients were evaluated. High resolution magnetic resonance imaging was used to visualize the plaque structures, and the mechanic stress in the plaque was obtained by combining vascular imaging post-processing with computational fluid dynamics. RESULTS: Wall shear stresses in the plaques in all cases were higher than those in control group. Maximal shear stresses in the plaques were observed at the top of plaque hills, as well as the shoulders of the plaques. Among them, the maximal shear stress in the ruptured plaque was observed in the rupture location in three cases and at the shoulder of fibrous cap in two cases. The maximal shear stress was also seen at the region of calcification, in thrombus region and in the thickest region of plaque in the other three cases, respectively. CONCLUSION: Determination of maximal shear stress at the plaque may be useful for predicting the rupture location of the plaque and may play an important role in assessing plaque vulnerability.

Behavioral and neurochemical effects of the intrahippocampal co-injection of beta-amyloid protein 1-40 and ibotenic acid in rats.

The authors investigated the effects of bilateral intrahippocampal co-injection of Abeta1-40 (4 microg for each side) with ibotenic acid (Ibo, 2 microg for each side) on rats' performance in the open field behavior, Y-maze, and passive avoidance task, and also examined some neurochemical changes in hippocampus two weeks after the co-injection. The results showed that the co-injection of Abeta1-40 with Ibo induced a decrease in exploratory activity and a significant decline in learning-memory ability of the tested rats (p < .01). The neurochemistry changes induced by the co-injection included a significant decreased in membrane fluidity of hippocampal mitochondria (p < .01), a significant decrease in the activity of SOD (p < .01), and a remarkable increase in the content of MDA (p < .01). These results suggest that the co-injection of Abeta1-40 with Ibo may induce an increase of hippocampal damage by peroxidation, and a serious learning and memory impairment of the rats. The results also suggest that the co-injection of Abeta1-40 with Ibo may provide a useful animal model for Alzheimer's disease (AD) research.