Remotely delivered environmental enrichment intervention for traumatic brain injury: Study protocol for a randomised controlled trial.

INTRODUCTION: Individuals with moderate-severe traumatic brain injury (m-sTBI) experience progressive brain and behavioural declines in the chronic stages of injury. Longitudinal studies found that a majority of patients with m-sTBI exhibit significant hippocampal atrophy from 5 to 12 months post-injury, associated with decreased cognitive environmental enrichment (EE). Encouragingly, engaging in EE has been shown to lead to neural improvements, suggesting it is a promising avenue for offsetting hippocampal neurodegeneration in m-sTBI. Allocentric spatial navigation (ie, flexible, bird's eye view approach), is a good candidate for EE in m-sTBI because it is associated with hippocampal activation and reduced ageing-related volume loss. Efficacy of EE requires intensive daily training, prohibitive within most current health delivery systems. The present protocol is a novel, remotely delivered and self-administered intervention designed to harness principles from EE and allocentric spatial navigation to offset hippocampal atrophy and potentially improve hippocampal functions such as navigation and memory for patients with m-sTBI. METHODS AND ANALYSIS: Eighty-four participants with chronic m-sTBI are being recruited from an urban rehabilitation hospital and randomised into a 16-week intervention (5 hours/week; total: 80 hours) of either targeted spatial navigation or an active control group. The spatial navigation group engages in structured exploration of different cities using Google Street View that includes daily navigation challenges. The active control group watches and answers subjective questions about educational videos. Following a brief orientation, participants remotely self-administer the intervention on their home computer. In addition to feasibility and compliance measures, clinical and experimental cognitive measures as well as MRI scan data are collected pre-intervention and post-intervention to determine behavioural and neural efficacy. ETHICS AND DISSEMINATION: Ethics approval has been obtained from ethics boards at the University Health Network and University of Toronto. Findings will be presented at academic conferences and submitted to peer-reviewed journals. TRIAL REGISTRATION NUMBER: Version 3, ClinicalTrials.gov Registry (NCT04331392).

Examining moderators of cognitive recovery trajectories after moderate to severe traumatic brain injury.

OBJECTIVES: To examine the influence of cognitive reserve-related moderator variables on recovery trajectories during the first year after traumatic brain injury (TBI). Using mixed effects models, we measured (1) the level of cognitive function at 2 and 12 months postinjury and (2) the trajectories of cognitive recovery during the first 12 months postinjury. DESIGN: Repeated-measures design with neuropsychological testing at 2, 5, and 12 months postinjury. SETTING: Large, urban inpatient neurorehabilitation program. PARTICIPANTS: Patients (N=75) with moderate-to-severe TBI. INTERVENTIONS: Not applicable. PRIMARY OUTCOMES: neuropsychological composite scores including simple speed of processing, complex speed of processing, memory, untimed executive functions, and attention span. Primary predictors: age, estimated premorbid intelligence quotient (IQ), and years of education. RESULTS: Only age significantly moderated trajectories. Decreasing age significantly enhanced recovery of speed of processing, both simple (2-12mo postinjury, P<.001) and complex (2-12mo postinjury, P<.05; 5-12mo postinjury, P<.005). Decreasing age and increasing estimated premorbid IQ were associated with higher performance at 2 and 12mo postinjury for simple speed of processing (premorbid IQ, 2 and 12mo), complex speed of processing (age, 2 and 12mo), untimed executive functions (premorbid IQ, 2 and 12mo), and memory (premorbid IQ, 2 and 12mo). CONCLUSIONS: Recovery of speed of processing (both simple and complex) was favorably moderated by younger age. Older age is associated with more neuronal loss and less integrity of white matter, and speed of processing is associated with white matter networks. The recuperative effects of younger age may therefore be attributable to greater reserve capacity (as indexed by white matter integrity). Lower age and higher estimated premorbid IQ were associated with higher functioning on a variety of cognitive outcomes. This may reflect the buffering effects of reserve capacity or premorbid differences in age and IQ-related cognitive functioning. Implications for rehabilitation and recovery mechanisms are discussed.