Capture by misleading information and its false acceptance in patients with traumatic brain injury

Abstract

Exposure to misleading information, presented after a critical episode, can alter or impair memory reports about that episode. Here, we examine vulnerability to misleading information in patients with traumatic brain injury (TBI). The ability to initiate an effective retrieval strategy and inhibit irrelevant or interfering information requires participation from the prefrontal cortices, which are susceptible to damage following brain injury. We report that TBI patients are more prone to interference effects produced by misleading information during a cued-recall task and are more likely to accept this information as the product of 'remembering' compared with healthy controls. The results are consistent with a model proposing that patients are captured by highly accessible responses eliminating their opportunity to engage in recollection. Correlations between the cued-recall interference task and other executive measures helped elucidate the processes underlying 'capture'. In TBI patients, reduced recollection produced by a misleading prime was associated with impaired prospective remembering when engaged in a background task. A common functional deficit that may underlie poor performance on both tasks is the failure to inhibit previously relevant but currently irrelevant information. Subjective reports pertaining to the subject's cued-recall response were indexed by electrodermal activity. In control subjects, larger skin conductance responses (SCRs) were associated with a greater frequency of guess reports, suggesting that SCRs provide a marker for uncertainty regarding the candidacy of a selected response. TBI patients did not show this relationship, suggesting that impairments of post-retrieval evaluation might also underlie greater false acceptance of misinformation. Discussion focuses on the role of the prefrontal cortex and cognitive processes that mediate the selection and evaluation of memories.

The anatomy of apathy: A neurocognitive framework for amotivated behaviour

“…Whilst FDG-PET estimates general metabolic activity (and presumably underlying neuronal loss), research using more specific metabolic imaging techniques has implicated dopaminergic neuromodulatory systems in the development of apathy in PD. Apathetic PD patients have reduced dopamine and/or noradrenaline receptor binding capacity within bilateral VS ( Remy et al, 2005 ). They have reduced striatal dopamine binding capacity even at the time of PD diagnosis, and before they have commenced dopaminergic therapy ( Santangelo et al, 2015 ).…”

“…Apathy is a core feature of several other neurodegenerative disorders that affect particularly frontal and subcortical brain regions, such as frontotemporal dementia (FTD), progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) ( Litvan et al, 1998 , Litvan et al, 1996 ). It was the most common neurobehavioural disorder in a large imaging study that combined patients with these diagnoses as well as AD ( Rosen et al, 2005 ). The presence of apathy in these groups correlated with reduced GM volume in ACC, OFC, middle frontal gyrus, anterior insula and caudate ( Rosen et al, 2005 ).…”

Electrophysiological markers of cognitive deficits in traumatic brain injury: A review

“…Impaired awareness of deficits in TBI patients has been identified as a significant factor in determining successful outcome, in terms of rehabilitation (Lam et al, 1988), vocational status (Sherer et al, 1998a;Wise et al, 2005), functional independence, (Trudel et al, 1998) and caregiver distress (Prigatano and Fordyce, 1986). Research in our laboratory has found that TBI participants show reduced error awareness on simple laboratory error detection tasks (O'Keeffe et al, 2007;O'Keeffe et al, 2004) and are more likely to falsely yet assuredly accept misleading information as the product of 'remembering' (Dockree et al, 2006b).…”

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

“…Such assessments are also taking advantage of computerized and virtual assessment techniques as well as the ability to automate the assessment (Cernich et al, 2007;Iverson et al, 2005;Schatz & Putz, 2006;Slobounov et al, 2006). Likewise, various cognitive neuroscience measures either by themselves or combined with functional neuroimaging methods hold great promise for more accurate assessment of the effects of TBI on behavior and cognition (Bergemalm & Lyxell, 2005;Casson et al, 2006;Chan, 2001;Chen et al, 2007;Cicerone et al, 2006;Dockree et al, 2006b;Jantzen et al, 2004;Mendez et al, 2005;O'Keeffe et al, 2007a;O'Keeffe et al, 2007b;Scheibel et al, 2007;Suh et al, 2006). These types of studies applied to PPCS will likely advance the field rather than another round of testing with traditional "clinical" neuropsychological measures (Heitger et al, 2004(Heitger et al, , 2005.…”