Meta-Analysis of Hippocampal Volume and Episodic Memory in Preterm and Term Born Individuals.

Preterm birth (< 37 weeks gestation) has been associated with memory deficits, which has prompted investigation of possible alterations in hippocampal volume in this population. However, existing literature reports varying effects of premature birth on hippocampal volume. Specifically, it is unclear whether smaller hippocampal volume in preterm-born individuals is merely reflective of smaller total brain volume. Further, it is not clear if hippocampal volume is associated with episodic memory functioning in preterm-born individuals. Meta-analysis was used to investigate the effects of premature birth on hippocampal volume and episodic memory from early development to young adulthood (birth to 26). PubMed, PsychINFO, and Web of Science were searched for English peer-reviewed articles that included hippocampal volume of preterm and term-born individuals. Thirty articles met the inclusion criteria. Separate meta-analyses were used to evaluate standardized mean differences between preterm and term-born individuals in uncorrected and corrected hippocampal volume, as well as verbal and visual episodic memory. Both uncorrected and corrected hippocampal volume were smaller in preterm-born compared to term-born individuals. Although preterm-born individuals had lower episodic memory performance than term-born individuals, the limited number of studies only permitted a qualitative review of the association between episodic memory performance and hippocampal volume. Tested moderators included mean age, pre/post-surfactant era, birth weight, gestational age, demarcation method, magnet strength, and slice thickness. With this meta-analysis, we provide novel evidence of the effects of premature birth on hippocampal volume.

Long-Term Risk for Mood and Anxiety Disorders After Pediatric Traumatic Brain Injury: A Population-Based, Birth Cohort Analysis.

OBJECTIVE: To determine whether exposure to traumatic brain injury (TBI) before 10 years of age is associated with development of a mood or anxiety disorder by 25 years of age, and whether sex or injury severity influences this risk. SETTING: Olmsted County, Minnesota. PARTICIPANTS: A total of 5518 persons born from January 1, 1976, through December 31, 1982. DESIGN: Population-based, birth cohort study. Children sustaining TBI before 10 years of age (index date) were confirmed by manual record review and classified by injury severity using the Mayo Classification System. Each TBI case was age- and sex-matched to 2 referents from the same birth cohort without a history of TBI at the index date. Cox proportional hazards models were fit to compare the risk of a subsequent clinically diagnosed mood or anxiety disorder by 25 years of age between TBI cases and referents. Separate analysis was performed stratified by sex and injury severity. MAIN MEASURES: Incidence of mood and anxiety disorders determined through clinical diagnostic codes and manual record review. RESULTS: The study included 562 children (238 females [42.3%] and 324 males [57.7%]) with TBI before 10 years of age (mean [SD] age at TBI: 4.7 [2.8] years). At least 1 mood or anxiety disorder was diagnosed for 115 persons with TBI and 215 referents. No statistically significant association existed between childhood TBI status and anxiety disorder (adjusted hazard ratio [aHR], 1.01 [95% confidence interval (CI), 0.71-1.43]; P = .97) or mood disorder (aHR, 1.16 [95% CI, 0.92-1.47]; P = .21). However, females who sustained TBI had a significantly increased risk of a subsequently diagnosed mood disorder compared with age-matched female referents (aHR, 1.40 [95% CI, 1.04-1.89]; P = .03). CONCLUSIONS: This study suggests that isolated TBI before 10 years of age is not significantly associated with an increased risk of anxiety or mood disorder by 25 years of age, though females may be at an increased risk.

Risk factors for development of long-term mood and anxiety disorder after pediatric traumatic brain injury: a population-based, birth cohort analysis.

OBJECTIVES: The objective of this study was to identify characteristics associated with an increased risk of anxiety and mood disorder prior to 25 years of age, in children who sustained a traumatic brain injury (TBI) prior to age 10. METHODS: This population-based study identified 562 TBI cases from a 1976-1982 birth cohort in Olmsted County, Minnesota. TBI cases were manually confirmed and classified by injury severity. Separate Cox proportional hazards regression models were fit to estimate the association of TBI and secondary non-TBI related characteristics with the risk of a subsequent clinically determined anxiety or mood disorder. Multivariable-adjusted population attributable risk (PAR) estimates were calculated for TBI characteristics. RESULTS: Older age at initial TBI and extracranial injury at time of initial TBI were significantly associated with an increased risk of anxiety (adjusted HR [95% CI]: 1.33 [1.16, 1.52] per 1-year increase and 2.41 [1.26, 4.59]), respectively. Older age at initial TBI was significantly associated with an increased risk of a mood disorder (adjusted HR 1.17 [1.08-1.27]). CONCLUSION: In individuals sustaining a TBI prior to age 10, age at injury greater than 5 years old was the largest contributor to development of a mood or anxiety disorder.

Neuropsychological Functioning in Alexander Disease: A Case Series.

Limited information is known about neuropsychological outcomes in Alexander disease, a rare leukodystrophy. Two pediatric cases are summarized. Case 1 (evaluations at 6, 7, 9, and 12 years of age) represents Type I Alexander disease with associated seizures. Case 2 (evaluations at 12, 13, and 16 years of age) represents Type II Alexander disease without additional complications. Case 1 experienced declines in intellectual functioning, visual motor skills, receptive vocabulary, verbal memory, and academic achievement. Case 2 experienced variable neurocognitive change and academic functioning, with average word reading and spelling. Verbal memory also remained intact. Taken together, individuals with Alexander disease may experience cognitive decline to variable degrees. Type I Alexander disease, associated with earlier onset and additional neurological complications, may presage greater cognitive decline than Type II. Due to variability in functioning over time, it is critical to follow individuals across development to make recommendations for educational and treatment planning.

Age-associated increase in mnemonic strategy use is linked to prefrontal cortex development.

Memory functioning undergoes dynamic changes between childhood and adulthood. Spontaneous use of elaborative strategies, which can enhance the recall of information, expands with age and contributes to age-associated improvement in memory functioning. Findings from lesion and neuroimaging studies suggest that the ability to use elaborative strategies is dependent upon intact functioning of the prefrontal cortex (PFC), particularly the dorsolateral PFC region. Because the PFC undergoes protracted maturation, we examined whether age difference in the structure of the PFC is correlated with age-associated increase in strategy use. Here, we investigated the relationship between PFC volume and spontaneous strategy use in a sample of 120 participants aged 5-25 years. We assessed semantic clustering during recall with a standardized word-list recall task (California Verbal Learning Task children's version, CVLT-C) and computed PFC regional volumes from participants' structural brain images. We observed an age-associated increase in the use of semantic clustering and an age-associated decrease in volumes of the PFC. Further, we found that smaller PFC volume was linked to increased use of semantic clustering. Importantly, the volume of the right dorsolateral PFC partially explained the relation between age and the use of semantic clustering. These findings suggest that PFC maturation supports the development of strategy use and lends further support for the notion that brain-behavior relations change across development.