The Impact of American Content on California Verbal Learning Test Performance: A New Zealand Illustration

2002 ◽  
Vol 16 (3) ◽  
pp. 290-299 ◽  
Author(s):  
Suzanne Barker-Collo ◽  
Anna Clarkson ◽  
Ainsleigh Cribb ◽  
Mary Grogan
2020 ◽  
pp. 135245852096441
Author(s):  
Zhizheng Zhuo ◽  
Yunyun Duan ◽  
Decai Tian ◽  
Xinli Wang ◽  
Chenyang Gao ◽  
...  

Background: The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function is unknown. Objectives: The aim of this study was to study the multimodal brain MRI alterations in MOGAD and to investigate their clinical significance. Methods: A total of 17 MOGAD, 20 aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4 + NMOSD), and 28 healthy controls (HC) were prospectively recruited. Voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) were compared between groups. Clinical associations and differential diagnosis were determined using partial correlation and stepwise logistic regression. Results: In comparison with HC, MOGAD had GM atrophy in frontal and temporal lobe, insula, thalamus, and hippocampus, and WM fiber disruption in optic radiation and anterior/posterior corona radiata; DC decreased in cerebellum and increased in temporal lobe. Compared to AQP4 + NMOSD, MOGAD presented lower GM volume in postcentral gyrus and decreased DC in cerebellum. Hippocampus/parahippocampus atrophy associated with Expanded Disability Status Scale ( R = −0.55, p = 0.04) and California Verbal Learning Test ( R = 0.62, p = 0.031). The differentiation of MOGAD from AQP4 + NMOSD achieved an accuracy of 95% using FA in splenium of corpus callosum and DC in occipital gyrus. Conclusion: Distinct structural and functional alterations were identified in MOGAD. Hippocampus/parahippocampus atrophy associated with clinical disability and cognitive impairment.


2004 ◽  
Vol 10 (4) ◽  
pp. 482-488 ◽  
Author(s):  
JACOBUS DONDERS ◽  
MICHAEL T. MINNEMA

One hundred sixty-seven children with traumatic brain injury (TBI), selected from an 8-year series of consecutive referrals to a Midwestern rehabilitation hospital, completed the California Verbal Learning Test–Children's Version (CVLT–C) and the Wechsler Intelligence Scale for Children–Third Edition (WISC–III) within 1 year after injury. A large proactive interference (PI) effect, defined as performance on the second list that was at least 1.5 standard deviations below that on the 1st one, was statistically significantly more common in this clinical sample (21%) than in the CVLT–C standardization sample (11%). Other performance discrepancies, including retroactive interference, rapid forgetting, and retrieval problems, occurred at approximately the same rate in the clinical and standardization samples. Children with anterior cerebral lesions were about 3 times less likely to have a large PI effect than children without such lesions, but the former group performed worse on the first CVLT–C list. The impact of pediatric TBI on a wide range of CVLT–C quantitative variables was mediated by speed of information processing, as assessed by the WISC–III Processing Speed factor index. It is concluded that failure to release from PI is somewhat common, although certainly not universal, in children with TBI. Unlike with adults, anterior cerebral lesions are not associated selectively with an increased risk for PI after pediatric TBI but rather with a reduced efficiency of allocation of cognitive resources. Deficits in speed of information processing appear to be primarily responsible for the learning deficits on the CVLT–C after pediatric TBI. (JINS, 2004, 10, 482–488.)


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 2004-2004 ◽  
Author(s):  
Jeffrey Scott Wefel ◽  
Stephanie L. Pugh ◽  
Terri S. Armstrong ◽  
Mark R. Gilbert ◽  
Minhee Won ◽  
...  

2004 Background: RTOG 0825 evaluated overall survival (OS) and progression-free survival (PFS) differences in patients with newly diagnosed GBM treated with standard chemoradiation, maintenance temozolomide and placebo (Arm 1) or bevacizumab (Arm 2). While OS was equivalent, PFS was longer in Arm 2. Longitudinal NCF testing was performed to evaluate clinical benefit. Methods: NCF was evaluatedat baseline and while on study and progression free with the Hopkins Verbal Learning Test-Revised (HVLT-R), Trail Making Test (TMT) and Controlled Oral Word Association (COWA). Change in NCF from baseline was categorized using the reliable change index. Differences between treatment arms were compared at follow-up evaluations. Additionally, baseline (B) and early changes (EC) (B to week 10) in NCF were examined as prognostic factors. Results: 542 patients consented and 507 randomized patients participated, with test completion rates at weeks 0 (B), 10, 22, and 34 of 94-97, 69-73, 59-64, and 53-58%, respectively. Mean test performance at B was equivalent between arms and ranged from -0.8 to -4.8 SDs below healthy population norms with global NCF on a composite variable at -2.0 SDs. There were no statistically significant between arm differences in frequency of improvement through week 34. Decline on COWA (verbal measure of executive function) at week 34 relative to baseline was more common (16.1 vs 5.7%) in patients in Arm 1 (p<0.05); whereas, there were trends for more decline in Arm 2 on a visuomotor measure of executive function (TMT B, p< 0.06; 22.2 vs 35.4%). B performance and EC in global NCF, memory, executive function and processing speed were prognostic for OS. At B, global NCF was prognostic for PFS. EC in global NCF, memory and executive function were prognostic for PFS. Conclusions: There was a statistically significant difference in the frequency of decline on a verbal test of executive function at week 34 favoring Arm 2. However, this was not found at earlier time points and was not found on a visuomotor test of executive function. B and EC in NCF were prognostic for OS and PFS. Longitudinal modeling is ongoing to further evaluate the impact of treatment on patients’ NCF. Support: U10 CA21661, U10 CA37422 and Genentech, Inc. Clinical trial information: NCI-2009-01670.


2010 ◽  
Vol 16 (3) ◽  
pp. 332-341 ◽  
Author(s):  
Frauke Fink ◽  
Paul Eling ◽  
Eva Rischkau ◽  
Nicole Beyer ◽  
Bernd Tomandl ◽  
...  

The California Verbal Learning Test (CVLT) is recognized as a standard clinical tool for assessing episodic memory difficulties in multiple sclerosis (MS), but its neural correlates have not yet been examined in detail in this patient population. We combined neuropsychological examination and diffusion tensor imaging (DTI) analysis in a group of MS patients ( N = 50) and demographically matched healthy participants ( N = 20). We investigated the degree of impairment of the uncinate fascicle (UF), the superior longitudinal fascicle (SLF), the fornix (FX) and the cingulum (CG). The patients were impaired on all CVLT parameters and the DTI parameters correlated moderately with disease-related variables. Regression analyses in the complete study sample showed that CVLT learning scores correlated with impairment of the right UF. This association reached marginal significance in the patient sample. In contrast to other studies claiming retrieval deficits, our results suggest that encoding and consolidation deficits may play a major role in verbal memory impairments in MS. The findings also provide evidence for an association between degree of myelination of prefrontal fibre pathways and encoding efficiency. Finally, DTI-derived measurements appear to reflect disease progression in MS. The results are discussed in light of functional MRI studies investigating compensatory brain activity during cognitive processing in MS.


2021 ◽  
Author(s):  
Melanie Marcille ◽  
Sandra Hurtado Rúa ◽  
Charles Tyshkov ◽  
Abhishek Jaywant ◽  
Joseph Comunale ◽  
...  

Abstract Quantitative susceptibility mapping (QSM), an imaging technique sensitive to brain iron, has been used to detect paramagnetic rims of iron-laden active microglia and macrophages in a subset of multiple sclerosis (MS) lesions, known as rim+ lesions, and are consistent with chronic active lesions. Because of their potential impact on disease progression and tissue damage, investigating the influence of rim+ lesions on disability and neurodegeneration is critical to establish the impact of these lesions on the disease course. This study aimed to explore the relationship between chronic active rim+ lesions, identified as having a hyperintense rim on QSM, and both clinical disability and imaging measures of neurodegeneration in patients with MS. The patient cohort was composed of 159 relapsing-remitting multiple sclerosis patients. The Expanded Disability Status Scale (EDSS) and Brief International Cognitive Assessment for Multiple Sclerosis, which includes both the Symbol Digit Modalities Test and California Verbal Learning Test-II, were used to assess clinical disability. Cortical thickness and thalamic volume were evaluated as imaging measures of neurodegeneration. A total of 4,469 MS lesions were identified, of which 171 QSM rim+ (3.8%) lesions were identified among 57 patients (35.8%). In a multivariate regression model, as the overall total lesion burden increased, patients with at least one rim+ lesion on QSM performed worse on both physical disability and cognitive assessments, specifically the Symbol Digit Modalities Test (p=0.010), California Verbal Learning Test-II (p=0.030), and EDSS (p=0.001). In a separate univariate regression model, controlling for age (p<0.001), having at least one rim+ lesion was related to more cortical thinning (p= 0.03) in younger patients (< 45 years). Lower thalamic volume was associated with older patients (p=0.038) and larger total lesion burden (p<0.001); however, the association did not remain significant with rim+ lesions (p=0.10). Our findings demonstrate a novel observation that chronic active lesions, as identified on QSM, modify the impact of lesion burden on clinical disability in MS patients. These results support further exploration of rim+ lesions for therapeutic targeting in MS to reduce disability and subsequent neurodegeneration.


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