The hippocampus is particularly susceptible to perinatal HII (Nyakas, Buwalda, & Luiten, 1996). Many previous animal and human studies have demonstrated atrophy of the hippocampus and memory impairments following HII (Isaacs et al., 2003; Maneru et al., 2003; Mikati et al., 2005; Quamme, Yonelinas, Widaman, Kroll, & Sauve, 2004; Yonelinas et al., 2002). One particular study by Vargha-Khadem and colleagues reported decreased hippocampal volumes of 39–57% below normal on volumetric MRI analysis of adolescents who experienced HII either during infancy or early childhood. Furthermore, although these children

all had IQs within the normal range, they exhibited impairments in both their episodic memory and their delayed HSP inhibitor verbal and visual memory (Vargha-Khadem et al., 1997).

Adults who experienced HII very early in life showed impairment on the VPC task in comparison with controls (Munoz, Chadwick, Perez-Hernandez, Vargha-Khadem, & Mishkin, 2011). The memory impairments in persons who experienced HII early in life have previously not been noted to occur until school age, at the earliest. One explanation for this could be that the hippocampus does not reach maturity until 5–7 years of age, so it is not until this point that the memory impairments become evident (Bachevalier & Vargha-Khadem, 2005). Conversely, memory impairments in children who have experienced perinatal HII may be present from Cell Cycle inhibitor the

time of the injury, but may go unnoticed until they enter school because relatively few demands are placed on memory during infancy or early childhood. No prior studies have tested infants with a history of perinatal HII for memory impairments while they are mafosfamide still in infancy. This study examined visual behavioral and electrophysiological measures of memory independently as well as in relation to one another in both typically developing infants and a small group of infants with a history of perinatal HII at 12 months of age. Our aims were to both better elucidate the relationship between behavioral and electrophysiological measures of memory in typically developing 12-month-old infants as well as to explore any potential differences between typically developing infants and those with a history of HII. The final sample consisted of 34 12-month-old infants: 25 control infants (CON; mean age = 381 days, SD = 15 days; 14 female infants) and nine infants who experienced a hypoxic-ischemic injury in the perinatal period (HII; mean age = 383 days, SD = 15; three female infants). Inclusion criteria for all infants were birth at greater than or equal to 35-week gestational age and weight less than 10 pounds. HII infants were recruited from the neonatal neurology clinic at Boston Children’s Hospital.