ABSTRACT Non-neurological factors such as the “expectation as etiology” or the “good old days” bias (EE/GOD bias) may partially explain persistent symptoms following mild traumatic brain injury (MTBI). What is less clear from existing research is the degree to which EE/GOD bias is related to other psychological correlates of persistent post-concussive symptoms (PPCS). We examined whether the EE/GOD bias was related to illness perception beliefs, intolerance of uncertainty, suggestibility, and domain identification. Participants with MTBI history and without (controls) reported frequency and severity of current PPCS; the MTBI group additionally reported premorbid PPCS. Participants also completed measures of psychological factors potentially associated with PPCS. Consistent with previous studies of the EE/GOD bias, the MTBI group endorsed less premorbid PPCS than current PPCS and when compared to the current symptom report of the control group. The MTBI group also endorsed more current PPCS than the control group. Higher EE/GOD bias was associated with several aspects of illness identity, including belief that symptoms would be more chronic, greater illness-related psychological distress, and greater cogniphobia. Higher EE/GOD bias was also related to higher intolerance of uncertainty and stronger personal identification with memory abilities. Regression showed that perceived symptom timeline, cogniphobia, and domain identification were unique predictors of EE/GOD bias. Findings confirm that the EE/GOD bias is seen in individuals with self-reported history of MTBI and corresponds to other psychological processes that potentially explain ongoing MTBI symptoms, providing greater insight into the potential mechanisms of PPCS. Future studies should examine the EE/GOD bias and associated psychological correlates in a clinical population and also assess for potential neuropsychological correlates. Findings suggest that psychological factors and premorbid symptom report should be considered in clinical assessment and also suggest potential mechanisms of treatment of individuals with acute MTBI or prolonged MTBI symptoms.
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