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A reciprocal relationship between perceptual learning and functional brain changes towards perceptual learning effectiveness has been demonstrated previously; however, the underlying neural correlates remain unclear. Further, visual perceptual learning (VPL) is implicated in visual field defect (VFD) recovery following chronic stroke. We investigated resting-state functional connectivity (RSFC) in the visual cortices associated with mean total deviation (MTD) scores for VPL-induced VFD recovery in chronic stroke. Patients with VFD due to chronic ischemic stroke in the visual cortex received 24 VPL training sessions over 2 months, which is a dual discrimination task of orientation and letters. At baseline and two months later, the RSFC in the ipsilesional, interhemispheric, and contralesional visual cortices and MTD scores in the affected hemi-field were assessed. Interhemispheric visual RSFC at baseline showed the strongest correlation with MTD scores post-2-month VPL training. Notably, only the subgroup with high baseline interhemispheric visual RSFC showed significant VFD improvement following the VPL training. The interactions between the interhemispheric visual RSFC at baseline and VPL led to improvement in MTD scores and largely influenced the degree of VFD recovery. The interhemispheric visual RSFC at baseline could be a promising brain biomarker for the effectiveness of VPL-induced VFD recovery. [ABSTRACT FROM AUTHOR]

Early neurological deterioration (END) in lenticulostriate artery (LSA) infarction is associated with perforating artery hypoperfusion. As middle cerebral artery (MCA) tortuosity may alter hemodynamics, we investigated the association between MCA tortuosity and END in LSA infarction. We reviewed patients with acute LSA infarction without significant MCA stenosis. END was defined as an increase of ≥ 2 or ≥ 1 in the National Institutes of Health Stroke Scale (NIHSS) total or motor score, respectively, within first 72 h. The MCA tortuosity index (actual /straight length) was measured. Stroke mechanisms were categorized as branch atheromatous disease (BAD; lesions > 10 mm and 4 axial slices) and lipohyalinotic degeneration (LD; lesion smaller than BAD). Factors associated with END in LD and BAD were investigated. END occurred in 104/390 (26.7%) patients. A high MCA tortuosity index (adjusted odds ratio, aOR 10.63, 95% confidence interval [2.57–44.08], p = 0.001) was independently associated with END. In patients with BAD, high initial NIHSS score (aOR 1.40 [1.03–1.89], p = 0.031) and presence of parental artery disease (stenosis < 50%; aOR 10.38 [1.85–58.08], p = 0.008) were associated with END. In patients with LD, high MCA tortuosity (aOR 41.78 [7.37–237.04], p < 0.001) was associated with END. The mechanism causing END in patients with LD and BAD may differ. [ABSTRACT FROM AUTHOR]

Two different stroke mechanisms are involved in small vessel disease: branch atheromatous disease (BAD) and lipohyalinotic degeneration (LD). We compared mechanisms of stroke in lenticulostriate arteries (LSA) vs. anterior pontine arteries (APA) and verified factors associated with stroke mechanisms, including shape of middle cerebral artery (MCA) and basilar artery (BA). We retrospectively reviewed patients with acute ischemic stroke with penetrating artery territory confirmed by MRI. The mechanisms of stroke were categorized based on diffusion-weighted imaging; BAD was defined as lesion larger than 10 mm in LSA and lesions involving basal pontine in APA. Other lesions were classified as LD. The shapes of MCA and BA were classified as straight, with one angle, or with two angles (U, C or S shape, respectively) using anterior–posterior view. The study included 221 patients. LD was more common in LSA infarcts, but BAD was more common in APA infarcts (p < 0.001). Low initial National Institutes of Health Stroke Scale [Adjusted Odds ratio (aOR) = 0.78; p < 0.001], absence of hyperlipidemia [aOR = 0.31; p = 0.002], previous statin use [aOR = 4.35; p = 0.028] LSA infarcts [reference = APA territory; aOR = 11.07; p < 0.001], and S-shaped vessels (reference = straight shaped vessels; aOR = 3.51; p = 0.004) were independently associated with LD. Angulations in the mother vessels may be more associated with true small vessel disease more with LD than BAD. [ABSTRACT FROM AUTHOR]

Multimodal magnetic resonance imaging (MRI) has emerged as a promising tool for diagnosing ischemic stroke and for determining treatment strategies in the acute phase. The detection and quantification of the penumbra and the infarct core regions aid the assessment of the potential risks and benefits of thrombolysis by providing information on salvageable tissue or ischemic lesion age. In this study, we proposed a fully automated and real-time algorithm to compute parameter maps of perfusion-weighted images (PWIs) and to identify an infarct core from diffusion-weighted images (DWIs). DWI and PWI were obtained using a 1.5 Tesla MRI scanner for 15 patients with acute ischemic stroke. Parameter maps of PWI were computed using restricted gamma-variate curve fitting and Fourier-based deconvolution. The ischemic penumbra was identified using time-to-maximum (Tmax) > 6 s as the mutual optimal threshold, while the infarct core was segmented using an adaptive thresholding on DWI. When the penumbra on PWI was compared with that generated using commercial software Pearson's linear correlation coefficient between penumbra volumes was 0.601 (p = 0.030), and the Dice coefficient was 0.51 ± 0.15. The infarct core on DWI was compared with the manually segmented gold standard. Dice coefficient between the manually drawn and automated segmented infarct cores was 0.62 ± 0.18. The processing times for PWI and DWI were 222.9 ± 16.4 and 53.4 ± 4.8 s, respectively. In conclusion, we demonstrate a fully automated and real-time algorithm to segment the penumbra and the infarct core regions based on PWI and DWI. [ABSTRACT FROM AUTHOR]

Purpose: To compare F-18-fluoro-2-deoxy- D-glucose (F-18 FDG) positron emission tomography/computed tomography (PET/CT) imaging at two different circulation times after injection of F-18 FDG in order to measure atherosclerosis in carotid arteries. Methods: We assessed 12 patients with recent symptomatic plaques in the carotid arteries. F-18 FDG PET/CT carotid plaque imaging was performed for 20 min at 2 h after F-18 FDG injection in five patients and at 3 h in seven patients. We measured vessel wall uptake using the maximal standardized uptake value (SUV), and the mean and maximal blood target-to-background ratios (TBR) of the symptomatic carotid arteries. Blood pool activity (BPA) was measured as the mean SUV of the superior vena cava (SVC) and jugular vein of these 12 patients, and in 14 age- and gender-matched patients who underwent whole-body F-18 FDG PET/CT examinations 1 h after injection. Results: F-18 FDG PET/CT revealed visible F-18 FDG uptake in all patients with symptomatic carotid plaques. Maximal SUV did not differ between groups evaluated at 2 h and 3 h (2.62 ± 0.45 vs 3.00 ± 0.85, p = 0.335). However, mean (2.04 ± 0.22 vs 3.54 ± 0.62, p < 0.05) and maximal (1.65 ± 0.15 vs 2.70 ± 0.42, p < 0.05) TBR values that were normalized to BPA in the SVC differ significantly. Conclusions: Symptomatic carotid plaques are visualized for a relatively short period of imaging time on ≥1-h PET/CT images. Quantitative parameters of atherosclerotic carotid arteries are preserved or even increased over time, whereas those of blood pools are decreased. [ABSTRACT FROM AUTHOR]