Our purpose was the study the magnetic resonance (MR) signal intensity of the perirolandic gyri perinatally and to correlate it with the histological findings in formalin-fixed brains, focusing on myelination. MRI of 20 neurologically normal neonates and infants, of 37-64 weeks postconception (PCA), were studied retrospectively. We reviewed four formalin-fixed brains of infants 37-46 weeks PCA microscopically. The posterior cortex of the precentral gyrus (P-PRE) and the anterior cortex of the postcentral gyrus (A-PST) had different signal intensity from the adjacent surrounding cortex. On T1-weighted images P-PRE and A-PST gave higher signal 41-44 weeks PCA; on T2-weighted images, they gave lower signal 37-51 weeks PCA. Histological examination revealed very little myelination of the nerve fibres within both the P-PRE and the A-PST, while considerable myelination was present in the internal capsule and central corona radiata. The changes in signal intensity in the perirolandic gyri may reflect not only the degree of myelination but also the more advanced development of the nerve cells, associated with rapid proliferation and formation of oligodendroglial cells, synapses and dendrites. They could be another important landmark for brain maturation.
This study aimed to investigate the most useful clinical and magnetic resonance imaging (MRI) parameters for differentiating isocitrate dehydrogenase (IDH)-mutant and -wildtype glioblastomas in the 2016 World Health Organization Classification of Tumors of the Central Nervous System.Methods: This multicenter study included 327 patients with IDH-mutant or IDH-wildtype glioblastoma in the 2016 World Health Organization classification who preoperatively underwent MRI. Isocitrate dehydrogenase mutation status was determined by immunohistochemistry, high-resolution melting analysis, and/or IDH1/2 sequencing. Three radiologists independently reviewed the tumor location, tumor contrast enhancement, noncontrastenhancing tumor (nCET), and peritumoral edema. Two radiologists independently measured the maximum tumor size and mean and minimum apparent diffusion coefficients of the tumor. Univariate and multivariate logistic regression analyses with an odds ratio (OR) were performed. Results:The tumors were IDH-wildtype glioblastoma in 306 cases and IDH-mutant glioblastoma in 21. Interobserver agreement for both qualitative and quantitative evaluations was moderate to excellent. The univariate analyses revealed a significant difference in age, seizure, tumor contrast enhancement, and nCET ( P < 0.05). The multivariate analysis revealed significant difference in age for all 3 readers (reader 1, odds ratio [OR] = 0.960, P = 0.012; reader 2, OR = 0.966, P = 0.048; reader 3, OR = 0.964, P = 0.026) and nCET for 2 readers (reader 1, OR = 3.082, P = 0.080; reader 2, OR = 4.500, P = 0.003; reader 3, OR = 3.078, P = 0.022).Conclusions: Age and nCET are the most useful parameters among the clinical and MRI parameters for differentiating IDH-mutant and IDH-wildtype glioblastomas.
Dynamic MRI was performed on 22 patients with extra-axial intracranial tumours. Serial images were obtained every 30 s for 3 min using a spin-echo sequence (TR 200, TE 15 ms) after rapid injection of Gd-DTPA, 0.1 mmol/kg body weight. The contrast medium enhancement ratio (CER) was correlated with the histology of the tumours. Meningiomas and extra-axial metastases showed a sharp rise, then a gradual decline. Although both had a definite early peak of CER, metastases showed a more rapid decline. Neuromas and extra-axial lymphoma showed a slow, steady increase with no peak within 180 s. This study indicates that the CER is helpful in the differentiation of extra-axial tumours.
This article reviews many of the applications of intravascular ultrasound (US) imaging for peripheral arterial diseases. In vitro studies demonstrate an excellent correlation between ultrasound measurements of lumen and plaque cross-sectional area compared with histologic sections. In vivo clinical studies reveal the enhanced diagnostic capabilities of this technology compared with angiography. Intravascular US imaging can provide valuable information on the degree, eccentricity, and histologic type of stenosis before intervention, and on the morphological changes in the arterial wall and the extent of excision after intervention. Intravascular US may also serve as a superior index for gauging the diameter of balloon, stent, laser probe, and/or atherectomy catheter appropriate for a proposed intervention. Significant new insights into the mechanisms of balloon angioplasty and atherectomy have been established by intravascular US findings. Intravascular US imaging has been shown to be a more accurate method than angiography for determining the cross-sectional area of the arterial lumen, and for assessing severity of stenosis. Quantitative assessment of the luminal cross-sectional area after the balloon dilatation should be more accurate than angiography as intimal tears or dissections produced by the dilatation may not be accurately evaluated with angiography. At the present time, intravascular US is still a controversial imaging technique. Outcome studies are currently being organized to assess the clinical value and cost effectiveness of intravascular ultrasound in the context of these interventional procedures.
A 59-year-old man with progressive cognitive decline and mood disturbances was admitted to the hospital. Brain magnetic resonance imaging revealed marked white matter hyperintensity (WMH) and widespread lobar cerebral microbleeds. Because he had untreated hypertension, we started antihypertensive treatment and found a significantly improved cognitive function and WMH regression. We diagnosed him with cerebral amyloid angiopathy (CAA) based on the modified Boston Criteria with the rare apolipoprotein E (ApoE) ε2/ε 4 genotype. The mechanism underlying reversible leukoencephalopathy in CAA may be related to the loss of autoregulation of brain circulation: cerebrovascular amyloid β deposits damaged the blood-brain barrier of the capillaries, which led to vasogenic edema induced by blood pressure surges.
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