Environmental influences that affect specific developmental processes have maximal effects during the developmental stages when those processes are under way. These developmental time periods, referred to as either “critical” or “sensitive” periods, thus constitute a window of influence for experience that is crucially important for proper brain development or for vulnerability of the developing brain to pathogenic influences from the environment. Perhaps the paradigmatic example of this point is the effect of monocular occlusion, in which one eye is sutured closed and prevented from receiving any sensory input. In adult animals, monocular occlusion produces no effect on vision or on brain structure and function. When imposed early in development, however, it permanently alters both: It impairs vision in that eye, it reduces cortical representation of the sutured eye, and it expands cortical representation of the open eye. Binocular occlusion produces perhaps even more extraordinary reorganization of the brain during an early critical period, as neurons in the would-be visual area respond not to light or visual stimuli, but to auditory and somatosensory stimuli instead (Purves, Augustine, et al., 2000; Wiesel, 1982).
Sensitive periods in humans are most clearly identified for disturbances in development of gross sensory and motor functions. For example, problems that create an imbalance in the activity of the two eyes early in life can have a permanent effect on the function of the cortical visual system. Failure to correct congenital cataracts by about age 4 months in human infants produces irreversible impairments in the visual system (Purves, Augustine, et al., 2000). Similarly, correction of strabismus, a misalignment of eye orientation, by age 7 produces optimal prevention of permanent visual impairment (Flynn, Schiffman, et al., 1998), possibly because synaptic elimination in the visual cortex is complete by that time.
Evidence in humans for the existence of sensitive periods when exposure to specific environmental and experiential influences confers enhanced vulnerability to the development of MEB disorders is thus far modest and largely circumstantial. The effects on cognitive development of environmental deprivation and separation from human caregivers may be more severe during early development (Nelson, Zeanah, et al., 2007), an observation consistent with the effects of early separation that have been documented in nonhuman primates (O’Connor and Cameron, 2006; Sabatini, Ebert, et al., 2007). Furthermore, traumatic experiences in childhood and adolescence appear to predispose to the development of severe character pathologies in adulthood; these effects are distinct from the effects of trauma experienced later in life (Bierer, Yehuda, et al., 2003; Golier, Yehuda, et al., 2003; Goodman, New, and Siever, 2004). These effects of childhood maltreatment in humans are consistent with animal models of child abuse and neglect that