Untangling the tangled relationship between cognitive and psychological comorbidities in epilepsy: Bidirectionality and mediation.

OBJECTIVE

Cognitive and psychological abnormalities are known to be frequently occurring complications of the epilepsies, but their patterns of co-occurrence, directions of effect, underlying mechanism(s), and causal pathways remain uncertain. The intent of this investigation was to advance understanding of these issues in patients with temporal lobe epilepsy (TLE).

METHODS

A total of 121 patients with TLE were administered a comprehensive neuropsychological battery, and symptoms of diverse psychological syndromes were assessed with a standardized psychological inventory. The cognitive and psychological data were reduced by factor analysis (FA) to broad- and narrowband indicators that were then examined by partial least squares structural equation modeling (PLS-SEM) to inform the presence, strength, direction, and mediators of cognitive-psychological relationships.

RESULTS

FA identified overarching metrics of cognition (g) and psychopathology (p) as well as their correlation and underlying factors wherein g contained three indicators (language/memory, perceptual/nonverbal reasoning, information/processing speed) and p contained two indicators (externalizing, internalizing). PLS-SEM demonstrated direct, bidirectional associations between internalizing psychopathology and language/memory, indicating these factors express a strong interdependency. Mediation modeling showed an index of functional brain reserve served to explain this selective, shared influence, as well the relationship between the broader concepts of p and g, indicating origin in a common psychological/cognitive mechanism.

SIGNIFICANCE: Neuropsychological and psychological comorbidities of TLE are represented by both broadband and narrowband indicators of clinical and theoretical relevance. These indicators exhibit multidimensionality, multimorbidity, and bidirectionality that point to a shared neurobiological core best expressed and explained by the mediating influence of brain functional reserve.