• Jill Del Pozzo, Lisa Spielman, Belinda Yew, Danielle M Shpigel, Enna Selamanovic, and Kristen Dams-O'Connor.
• Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
• J. Neurotrauma. 2024 Aug 1; 41 (15-16): 193719471937-1947.

AbstractTraumatic brain injuries (TBIs) can lead to long-lasting cognitive impairments, and some survivors experience cognitive decline post-recovery. Early detection of decline is important for care planning, and understanding risk factors for decline can elucidate targets for prevention. While neuropsychological testing is the gold standard approach to characterizing cognitive function, there is a need for brief, scalable tools that are capable of detecting clinically significant changes in post-TBI cognition. This study examines whether a clinically significant change can be detected using the Brief Test of Adult Cognition by Telephone (BTACT) in a sample of individuals with chronic TBI and investigates whether potentially modifiable factors are associated with cognitive decline. Ninety participants aged 40 or older with complicated mild-to-severe TBI participated in two telephone-based study visits ∼1 year apart. Demographic, head trauma exposure, comorbid medical conditions, physical, and psychosocial functioning data were collected via self-report. The BTACT, a brief measure of global cognitive function, was used to assess cognitive performance across six domains. A reliable change index for quantifying clinically significant changes in BTACT performance was calculated. Results revealed cognitive decline in 10-27% of participants across various cognitive domains. More specifically, only depressive symptoms, including depressed affect and anhedonia, were significantly associated with cognitive decline after correcting for multiple comparisons using false discovery rate (FDR). Other factors such as the number of blows to the head, male gender, dyspnea, increased anxiety symptoms, seizures, illicit drug use, and fewer cardiovascular comorbidities should be considered hypothesis generating. Importantly, age was not a significant predictor of cognitive decline, which challenges the assumption that cognitive decline is solely related to the natural aging process. It suggests that there are unique factors associated with TBI that impact cognitive function, and these factors can affect individuals across the lifespan. The BTACT is a brief and sensitive tool for identifying clinically meaningful changes in cognitive function over a relatively brief period (i.e., 1 year) in a sample of individuals in the chronic stages of TBI (i.e., x̄ = 6.7 years post-TBI). Thus, the BTACT may be useful in surveillance efforts aimed at understanding and detecting decline, particularly in situations where in-person cognitive screening is impractical or unfeasible. We also identified potentially modifiable targets for the prevention of post-TBI cognitive decline. These findings can offer insights into treatment goals and preventive strategies for individuals at risk for cognitive decline, as well as help to facilitate early identification efforts.

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