Clinical neuropsychology has been slow in adopting novelties in psychometrics, statistics, and technology. Researchers have indicated that the stationary nature of clinical neuropsychology endangers its evidence-based character. In addition to a technological crisis, there may be a statistical crisis affecting clinical neuropsychology. That is, the frequentist null hypothesis significance testing framework remains the dominant approach in clinical practice, despite a recent surge in critique on this framework. While the Bayesian framework has been put forward as a viable alternative in psychology in general, the possibilities it offers to clinical neuropsychology have not received much attention.

In the current position paper, we discuss and reflect on the value of Bayesian methods for the advancement of evidence-based clinical neuropsychology.

We aim to familiarize clinical neuropsychologists and neuropsychological researchers to Bayesian methods of inference and provide a clear rationale for why these methods are valuable for clinical neuropsychology.

We argue that Bayesian methods allow for a more intuitive answer to our diagnostic questions and form a more solid foundation for sequential and adaptive diagnostic testing, representing uncertainty about patients’ observed test scores and cognitive modeling of test results.

To develop and validate the Discrepancy-based Evidence for Loss of Thinking Abilities (DELTA) score. The DELTA score characterizes the strength of evidence for cognitive decline on a continuous spectrum using well-established psychometric principles for improving detection of cognitive changes.

DELTA score development used neuropsychological test scores from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort (two tests each from Memory, Executive Function, and Language domains). We derived regression-based normative reference scores using age, gender, years of education, and word-reading ability from robust cognitively normal ADNI participants. Discrepancies between predicted and observed scores were used for calculating the DELTA score (range 0–15). We validated DELTA scores primarily against longitudinal Clinical Dementia Rating-Sum of Boxes (CDR-SOB) and Functional Activities Questionnaire (FAQ) scores (baseline assessment through Year 3) using linear mixed models and secondarily against cross-sectional Alzheimer’s biomarkers.

There were 1359 ADNI participants with calculable baseline DELTA scores (age 73.7 ± 7.1 years, 55.4% female, 100% white/Caucasian). Higher baseline DELTA scores (stronger evidence of cognitive decline) predicted higher baseline CDR-SOB (ΔR2 = .318) and faster rates of CDR-SOB increase over time (ΔR2 = .209). Longitudinal changes in DELTA scores tracked closely and in the same direction as CDR-SOB scores (fixed and random effects of mean + mean-centered DELTA, ΔR2 > .7). Results were similar for FAQ scores. High DELTA scores predicted higher PET-Aβ SUVr (ρ = 324), higher CSF-pTau/CSF-Aβ ratio (ρ = .460), and demonstrated PPV > .9 for positive Alzheimer’s disease biomarker classification.

Data support initial development and validation of the DELTA score through its associations with longitudinal functional changes and Alzheimer’s biomarkers. We provide several considerations for future research and include an automated scoring program for clinical use.