Two experiments examined the development of recollection (recalling qualitative details about an event) and familiarity (recognizing the event) using the dual-process signal detection model. In Experiment 1 (n = 117; ages 6, 8, 10, 14, and 18 years), recollection improved from childhood to adolescence after semantic encoding but not after perceptual encoding and familiarity improved from ages 6 to 8 regardless of encoding condition. In Experiment 2 (n = 56; ages 6, 8, and 10 years), long duration compared to short duration of semantic encoding increased familiarity but not recollection. Age-related differences replicated those of Experiment 1, except no age difference in familiarity was found with long study duration. Overall, recollection and familiarity showed distinct developmental and functional characteristics. The dual-process signal detection model proved promising for developmental investigations.

Episodic memory is central to the human experience. In typically developing children, episodic memory improves rapidly during middle childhood. While the developmental cognitive neuroscience of episodic memory remains largely uncharted, recent research has begun to provide important insights. It has long been assumed that hippocampus-dependent binding mechanisms are in place by early childhood, and that improvements in episodic memory observed during middle childhood result from the protracted development of the prefrontal cortex. We revisit the notion that binding mechanisms are age-invariant, and propose that changes in the hippocampus and its projections to cortical regions also contribute to the development of episodic memory. We further review the role of developmental changes in lateral prefrontal and parietal cortices in this development. Finally, we discuss changes in white matter tracts connecting brain regions that are critical for episodic memory. Overall, we argue that changes in episodic memory emerge from the concerted effort of a network of relevant brain structures.

The ability to recollect details about past events improves during childhood. Most researchers favor the view that this improvement depends largely on the development of the prefrontal cortex, which is thought to have a protracted course of development relative to the medial temporal lobes (MTL). The primary goal of the present study was to test the hypothesis that the development of detail recollection is also associated with changes in MTL function. We collected functional magnetic resonance imaging data during an incidental encoding task in 80 participants, divided equally across four age groups: 8-year-olds, 10-to 11-year-olds, 14-year-olds, and young adults. Developmental differences in MTL activation profiles were observed. Fourteen-year-olds and adults engaged regions of the hippocampus and posterior parahippocampal gyrus selectively for subsequent detail recollection, whereas 8-and 10-to 11-year-olds did not. In 8-year-olds, these regions were recruited indiscriminately for detail recollection and item recognition; in 10-to 11-year-olds, activation in these regions did not consistently predict subsequent memory. These results suggest there are changes in the functional organization of the MTL, such that the hippocampus and posterior parahippocampal gyrus become increasingly specialized for recollection; these changes may be in part responsible for long-term memory improvements during childhood.

BACKGROUND Diabetic ketoacidosis in children may cause brain injuries ranging from mild to severe. Whether intravenous fluids contribute to these injuries has been debated for decades. METHODS We conducted a 13-center, randomized, controlled trial that examined the effects of the rate of administration and the sodium chloride content of intravenous fluids on neurologic outcomes in children with diabetic ketoacidosis. Children were randomly assigned to one of four treatment groups in a 2-by-2 factorial design (0.9% or 0.45% sodium chloride content and rapid or slow rate of administration). The primary outcome was a decline in mental status (two consecutive Glasgow Coma Scale scores of <14, on a scale ranging from 3 to 15, with lower scores indicating worse mental status) during treatment for diabetic ketoacidosis. Secondary outcomes included clinically apparent brain injury during treatment for diabetic ketoacidosis, short-term memory during treatment for diabetic ketoacidosis, and memory and IQ 2 to 6 months after recovery from diabetic ketoacidosis. RESULTS A total of 1389 episodes of diabetic ketoacidosis were reported in 1255 children. The Glasgow Coma Scale score declined to less than 14 in 48 episodes (3.5%), and clinically apparent brain injury occurred in 12 episodes (0.9%). No significant differences among the treatment groups were observed with respect to the percentage of episodes in which the Glasgow Coma Scale score declined to below 14, the magnitude of decline in the Glasgow Coma Scale score, or the duration of time in which the Glasgow Coma Scale score was less than 14; with respect to the results of the tests of short-term memory; or with respect to the incidence of clinically apparent brain injury during treatment for diabetic ketoacidosis. Memory and IQ scores obtained after the children’s recovery from diabetic ketoacidosis also did not differ significantly among the groups. Serious adverse events other than altered mental status were rare and occurred with similar frequency in all treatment groups. CONCLUSIONS Neither the rate of administration nor the sodium chloride content of intravenous fluids significantly influenced neurologic outcomes in children with diabetic ketoacidosis. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Health Resources and Services Administration; PECARN DKA FLUID ClinicalTrials.gov number, NCT00629707.)

The hippocampus is critically involved in episodic memory, yet relatively little is known about how the development of this structure contributes to the development of episodic memory during middle to late childhood. Previous research has inconsistently reported associations between hippocampal volume and episodic memory performance during this period. We argue that this inconsistency may be due to assessing the hippocampus as a whole, and propose to examine associations separately for subregions along the longitudinal axis of the hippocampus. In the present study, we examined age-related differences in volumes of the hippocampal head, body, and tail, and collected episodic memory measures in children ages 8-11 years and young adults (N = 62). We found that adults had a smaller right hippocampal head, larger hippocampal body bilaterally, and smaller right hippocampal tail compared with children. In adults, but not in children, better episodic memory performance was associated with smaller right hippocampal head and larger hippocampal body. In children, but not in adults, better episodic memory was associated with larger left hippocampal tail. Overall, the results suggest that protracted development of hippocampal subregions contribute to age-related differences in episodic memory.