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A Sequential Process Model for Cognitive Diagnostic Assessment With Repeated Attempts.

ABSTRACT: When diagnostic assessments are administered to examinees, the mastery status of each examinee on a set of specified cognitive skills or attributes can be directly evaluated using cognitive diagnosis models (CDMs). Under certain circumstances, allowing the examinees to have at least one opportunity to correctly answer the questions and assessments, with repeated attempts on the items, provides many potential benefits. A sequential process model can be extended to model repeated attempts in diagnostic assessments. Two formulations of the sequential generalized deterministic-input noisy-"and"-gate (G-DINA) model were developed in this study. The first extension uses the latent transition analysis (LTA) approach to model changes in the attributes over attempts, and the second extension constructs a higher order structure of latent continuous variables and latent attributes to account for the dependences of the attributes over attempts. Accurate model parameter estimation and correct classifications of attributes were observed in a series of simulations using Bayesian estimation. The effectiveness of the developed sequential G-DINA model was demonstrated by fitting real data from a longitudinal mathematical test to the developed model and the longitudinal G-DINA model using the LTA approach. Finally, this article closes by discussing several important issues associated with the developed models and providing suggestions for future directions.

SUBMITTER: Hung SP

PROVIDER: S-EPMC6739742 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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A Sequential Process Model for Cognitive Diagnostic Assessment With Repeated Attempts.

Hung Su-Pin SP Huang Hung-Yu HY

Applied psychological measurement 20181212 7

When diagnostic assessments are administered to examinees, the mastery status of each examinee on a set of specified cognitive skills or attributes can be directly evaluated using cognitive diagnosis models (CDMs). Under certain circumstances, allowing the examinees to have at least one opportunity to correctly answer the questions and assessments, with repeated attempts on the items, provides many potential benefits. A sequential process model can be extended to model repeated attempts in diagn ...[more]

PMID: 31534286

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Project description:Given advantages in reperfusion therapy leading to mild stroke, less apparent cognitive deficits can be overseen in a routine neurological examination. Despite the widespread use of the Montreal Cognitive Assessment (MoCA), age- and education-specific cutoffs for the detection of post-stroke cognitive impairment (PSCI) are not established, hampering its valid application in stroke. We aimed to establish age- and education-specific MoCA cutoffs to better discriminate patients with and without acute PSCI. Patients with acute ischemic stroke underwent the MoCA and a detailed neuropsychological assessment. PSCI was defined as a performance < - 1.5 SD in ≥ 2 cognitive domains. As secondary data analysis, the discriminant abilities of the MoCAraw-score (not adding + 1 as correction for ≤ 12 years of education, YoE) cutoffs were automatically derived based on Youden Index and evaluated by receiver operating characteristic analyses across age- (< 55, 55-70, > 70 years old) and education-specific (≤ 12 and > 12 YoE) groups. 351 stroke patients (67.4 ± 14.1 years old; 13.1 ± 2.8 YoE) underwent the neuropsychological assessment 2.7 ± 2.0 days post-stroke. The original MoCA cutoff < 26 falsely classified 26.2% of examined patients, with poor sensitivity in younger adults (34.8% in patients < 55 years > 12 YoE) and poor specificity in older adults (55.0%, in > 70 years ≤ 12 YoE). By maximizing both sensitivity and specificity, the optimal MoCAraw cutoffs were: (i) < 28 in patients aged < 55 with > 12 YoE (sensitivity = 69.6%, specificity = 77.8%); (ii) < 22 and < 25 in patients > 70 years with ≤ 12 and > 12 YoE (sensitivity = 61.6%, specificity = 90.0%; sensitivity = 63.3%, specificity = 84.0%, respectively). In other groups the optimal MoCAraw cutoff was < 26. Age and education level should be considered when interpreting MoCA-scores. Though new age- and education-specific cutoffs demonstrated higher discriminant ability for PSCI, their performance in young stroke and adults with higher education level was low due to ceiling effects and MoCA subtests structure, and cautious interpretation in these patients is warranted.Trial registration: ClinicalTrials.gov Identifier: NCT05653141.

Project description:Mild traumatic brain injury (mTBI) results in broad neurological symptoms and an increased risk of being diagnosed with a neurodegenerative disease later in life. While the immediate oxidative stress response and post-mortem pathology of the injured brain has been well studied, it remains unclear how early pathogenic changes may drive persistent symptoms and confer susceptibility to neurodegeneration. In this study we have used a mouse model of repeated mTBI (rmTBI) to identify early gene expression changes at 24 h or 7 days post-injury (7 dpi). At 24 h post-injury, gene expression of rmTBI mice shows activation of the DNA damage response (DDR) towards double strand DNA breaks, altered calcium and cell-cell signalling, and inhibition of cell death pathways. By 7 dpi, rmTBI mice had a gene expression signature consistent with induction of cellular senescence, activation of neurodegenerative processes, and inhibition of the DDR. At both timepoints gliosis, microgliosis, and axonal damage were evident in the absence of any gross lesion, and by 7 dpi rmTBI also mice had elevated levels of IL1β, p21, 53BP1, DNA2, and p53, supportive of DNA damage-induced cellular senescence. These gene expression changes reflect establishment of processes usually linked to brain aging and suggests that cellular senescence occurs early and most likely prior to the accumulation of toxic proteins. These molecular changes were accompanied by spatial learning and memory deficits in the Morris water maze. To conclude, we have identified DNA damage-induced cellular senescence as a repercussion of repeated mild traumatic brain injury which correlates with cognitive impairment. Pathways involved in senescence may represent viable treatment targets of post-concussive syndrome. Senescence has been proposed to promote neurodegeneration and appears as an effective target to prevent long-term complications of mTBI, such as chronic traumatic encephalopathy and other related neurodegenerative pathologies.

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A Sequential Process Model for Cognitive Diagnostic Assessment With Repeated Attempts.

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A Sequential Process Model for Cognitive Diagnostic Assessment With Repeated Attempts.

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