Episodic thinking involves the ability to re-create past and to construct future personal events, which contain event-specific (episodic) and general (semantic) details. The richness of episodic thought for past events improves as children move into adolescence. The current study aims to examine changes in episodic future thinking and to establish the cognitive underpinning of these changes. Typically developing children (n = 14) and adolescents (n = 15) were tested using an adapted version of the Child Autobiographical Interview (CAI) that required generation of past and future personally relevant events. Relational memory and executive skills were also examined. Significant developmental gains were found in richness of events recall across temporal directions (past and future) and across different types of details (episodic and semantic). Developmental gains in richness of past events were also shown to correspond to developmental gains in generation of future events. Moreover, developmental changes in relational memory and (to a lesser extent) executive functions were found to relate to increases in the amount of episodic (but not semantic) details provided. Our study highlighted the similarities between past and future episodic thinking in typically developing children and adolescents. It also raises a possibility that children with developmental and neurological disorders with impaired relational memory and/or executive skills may be at risk of difficulties with episodic thinking.
BackgroundThe longitudinal rate and profile of cognitive decline in persons with stable, treated, and virally suppressed HIV infection is not established. To address this question, the current study quantifies the rate of cognitive decline in a cohort of virally suppressed HIV+ persons using clinically relevant definitions of decline, and determine cognitive trajectories taking into account historical and baseline HAND status.MethodsNinety-six HIV+ (clinically stable and virally undetectable) and 44 demographically comparable HIV- participants underwent standard neuropsychological testing at baseline and 18-months follow-up. We described clinically relevant cognitive trajectories based on standard definitions of historical and baseline HAND status and cognitive decline. Historical, moderate to severe HAND was formally diagnosed at the start of the cART era in 15/96 participants based on clinical neurological and neuropsychological assessment. The same standard of care has been applied to all participants at St. Vincent’s Hospital Infectious Disease Department for the duration of their HIV infection (median of 20 years).ResultsRelative to HIV- controls (4.5%), 14% of HIV+ participants declined (p = .11), they also scored significantly lower on the global change score (p = .03), processing speed (p = .02), and mental flexibility/inhibition (p = .02) domains. Having HAND at baseline significantly predicted cognitive decline at follow up (p = .005). We determined seven clinically relevant cognitive trajectories taking into account whether participant has a history of HAND prior to study entry (yes/no); their results on the baseline assessment (baseline impairment: yes/no) and their results on the 18-month follow up (decline or stable) which in order of prevalence were: 1) No HAND history, no baseline impairment, 18-month follow-up stable (39%), 2) No HAND history, baseline impairment, 18-month follow-up stable (35%), 3) History of HAND; baseline impairment, 18-month follow-up stable (9%) 4) No history of HAND, baseline impairment, 18-month follow-up decline (7%), 5) History of HAND, no baseline impairment, 18-month follow-up stable (3%), 6) No HAND history, no baseline impairment, 18-month follow-up decline (3%) 7) History of HAND, baseline impairment, 18-month follow-up decline (3%). There was no relationship between cognitive decline (taking into account historical and baseline HAND) and traditional HIV disease biomarkers.ConclusionsDespite long-term viral suppression, we found mostly subclinical levels of decline in psychomotor speed and executive functioning (mental flexibility and cognitive inhibition); well-established markers of HAND progression. Moreover, 57% of our cohort is undergoing slow evolution of their disease, challenging the notion of prevalent neurocognitive stability in virally suppressed HIV infection.
Accelerated long-term forgetting (ALF) is characterized by adequate recall after short, but not long delays. ALF is not detected by standardized neuropsychological memory tests. Currently, the prevailing conceptualization of ALF is of a temporal lobe seizure-related phenomenon. Nevertheless, Mayes and colleagues (2003) proposed that ALF may occur when any of the components of the brain network involved in long-term memory formation, or their interaction, is disrupted. This disruption does not have to be caused by temporal lobe seizures for ALF to occur. Here, we investigate this possibility in a group of school-age children who have sustained traumatic brain injury (TBI) (n = 28), as TBI typically disrupts the brain network that is important for long-term memory formation and recall. Healthy control children (n = 62) also participated. Contrary to the dominant conceptualization of ALF being a seizure-related phenomenon, children with TBI showed ALF. Sustaining a severe TBI and diffuse subcortical damage was related to ALF. Individually, 8 of the 13 children with severe TBI presented with ALF. ALF would remain undetected on standardized testing in six of these eight children. One child had the opposite pattern of dissociation, an impaired score on standardized testing, but an average long-term memory score. This is the first study, to our knowledge, to show ALF in patients with TBI, which has remained undiagnosed and untreated in this patient population. Our study also challenges the dominant hypothesis of ALF being a temporal lobe seizure-related phenomenon, and raises a possibility that short-term and long-term memory systems may be independent.
Objectives. Autobiographical memory (AM) is a complex function that involves reexperiencing of past personal events (episodic memory) scaffolded by personal facts (semantic memory). While AM is supported by a brain network and cognitive skills that are vulnerable to disruption by child traumatic brain injury (TBI), AM has not been examined in this patient population.Design. Cross-sectional study.Methods. Participants included children with severe closed TBI (n = 14) and healthy control (NC) children (n = 20) of comparable age, sex, and socioeconomic status. Participants completed (1) the Child Autobiographical Interview (Willoughby et al., 2012, Front. Psychol., 3, 53), which required recall of autobiographical events and distinguished episodic (internal) from non-episodic (external) details, and self-rating of event phenomenological qualities, and (2) a battery of neuropsychological tests.Results. Children with TBI recalled significantly fewer internal details relative to NCs, but the between-group difference was eliminated when specific probes were provided. The groups did not differ in either recall of external details or in ratings of events' phenomenological qualities. The gap between the groups in recall of internal details increased with age, as the greater number of internal details was associated with older age in the NC group, but not in the TBI group. Poorer verbal memory and lower IQ were related to recall of fewer internal details in the TBI group.Conclusions. This study unveils, to our knowledge for the first time, that severe child TBI is associated with a selective deficit in autobiographical memory that involves episodic, but spares semantic details, and identifies the risk factors for this impairment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.