The impact of the ClearRT™ upgrade on target motion tracking accuracy in Radixact® Synchrony® lung treatments.

Background: The objective was to investigate the change in segmentation error of Radixact® Synchrony® lung treatment after its kV imaging system was upgraded from Generation 1 to Generation 2 in the ClearRT™ installation. Materials and methods: Radixact® Lung Synchrony® plans were created for the Model 18023 Xsight® Lung Tracking "XLT" Phantom combined with different lung target inserts with densities of 0.280, 0.500, 0.943 and 1.093 g/cc. After Radixact® Synchrony® treatment delivery using the Generation 1 and Generation 2 kV systems according to each plan, the tracking performance of the two kV systems on each density insert was compared by calculating the root mean square (RMS) error (δRMS) between the Synchrony-predicted motion in the log file and the known phantom motion and by calculating δ95%, the maximum error within a 95% probability threshold. Results: The δRMS and δ95% of Radixact® Synchrony® treatment for Gen1 kV systems deteriorated as the density of the target insert decreased, from 1.673 ± 0.064 mm and 3.049 ± 0.089 mm, respectively, for the 1.093 g/cc insert to 8.355 ± 5.873 mm and 15.297 ± 10.470 mm, respectively, for the 0.280 g/cc insert. In contrast, no such trend was observed in the δRMS or δ95% of Synchrony® treatment using the Gen2 kV system. The δRMS and δ95%, respectively, fluctuated slightly from 1.586 to 1.687 mm and from 2.874 to 2.971 mm when different target inserts were tracked by the Gen2 kV system. Conclusion: With improved image contrast in kV radiographs, the Gen2 kV imaging system can enhance the ability to track targets accurately in Radixact® Lung Synchrony® treatment and reduce the segmentation error. Our study showed that lung targets with density values as low as 0.280 cc/g could be tracked correctly in Synchrony treatment with the Gen2 kV imaging system.

Mapping the contribution and strategic distribution patterns of neuroimaging features of small vessel disease in poststroke cognitive impairment.

OBJECTIVES: Individual neuroimaging features of small vessel disease (SVD) have been reported to influence poststroke cognition. This study aimed to investigate the joint contribution and strategic distribution patterns of multiple types of SVD imaging features in poststroke cognitive impairment. METHODS: We studied 145 first-ever ischaemic stroke patients with MRI and Montreal Cognitive Assessment (MoCA) examined at baseline. The local burdens of acute ischaemic lesion (AIL), white matter hyperintensity, lacune, enlarged perivascular space and cross-sectional atrophy were quantified and entered into support vector regression (SVR) models to associate with the global and domain scores of MoCA. The SVR models were optimised with feature selection through 10-fold cross-validations. The contribution of SVD features to MoCA scores was measured by the prediction accuracy in the corresponding SVR model after optimisation. RESULTS: The combination of the neuroimaging features of SVD contributed much more to the MoCA deficits on top of AILs compared with individual SVD features, and the cognitive impact of different individual SVD features was generally similar. As identified by the optimal SVR models, the important SVD-affected regions were mainly located in the basal ganglia and white matter around it, although the specific regions varied for MoCA and its domains. CONCLUSIONS: Multiple types of SVD neuroimaging features jointly had a significant impact on global and domain cognitive functionings after stroke on top of AILs. The map of strategic cognitive-relevant regions of SVD features may help clinicians to understand their complementary impact on poststroke cognition.

Chronic Ketamine Exposure Causes White Matter Microstructural Abnormalities in Adolescent Cynomolgus Monkeys.

Acute and repeated exposures to ketamine mimic aspects of positive, negative, and cognitive symptoms of schizophrenia in humans. Recent studies by our group and others have shown that chronicity of ketamine use may be a key element for establishing a more valid model of cognitive symptoms of schizophrenia. However, current understanding on the long-term consequences of ketamine exposure on brain circuits has remained incomplete, particularly with regard to microstructural changes of white matter tracts that underpin the neuropathology of schizophrenia. Thus, the present study aimed to expand on previous investigations by examining causal effects of repeated ketamine exposure on white matter integrity in a non-human primate model. Ketamine or saline (control) was administered intravenously for 3 months to male adolescent cynomolgus monkeys (n = 5/group). Diffusion tensor imaging (DTI) experiments were performed and tract-based spatial statistics (TBSS) was used for data analysis. Fractional anisotropy (FA) was quantified across the whole brain. Profoundly reduced FA on the right side of sagittal striatum, posterior thalamic radiation (PTR), retrolenticular limb of the internal capsule (RLIC) and superior longitudinal fasciculus (SLF), and on the left side of PTR, middle temporal gyrus and inferior frontal gyrus were observed in the ketamine group compared to controls. Diminished white matter integrity found in either fronto-thalamo-temporal or striato-thalamic connections with tracts including the SLF, PTR, and RLIC lends support to similar findings from DTI studies on schizophrenia in humans. This study suggests that chronic ketamine exposure is a useful pharmacological paradigm that might provide translational insights into the pathophysiology and treatment of schizophrenia.