Environmental Influences on Brain Development
The process of early brain development is constantly modified by environmental influences. Child abuse and neglect constitute one aspect of these environmental influences, which present the maturing child's brain with experiences that will crucially and potentially adversely affect the child's future development and functioning. The younger the infant, the more these environmental factors are mediated by the primary caregiver(s). In order to consider these effects, it is necessary to summarise current knowledge about the processes of neurodevelopment in infancy and early childhood. Brain Growth and MaturationFor obvious reasons, much of the work on the development of the brain has been carried out in animals, although increasing knowledge is being gained about human development. The volume of the human brain increases more during the first year of life than at any other time in life (Gilles, 1993). The human brain grows from an average weight of 400 gm at birth to 1.000 gm at 12 months, the growth spurt continuing to 24 months (Schore, 1994). From birth to 4 years of age, the cerebral cortex's use of glucose rises, reaching more than twice the glucose usage of adults' brain and continuing thus until the age of 10 years (Chugani, 1998). The stepwise sequence of neurodevelopment is genetically predetermined and not alterable by environmental forces. It proceeds from lower to higher brain centres, from the brain stem to the cerebral cortex, in a caudal to rostral direction (Nelson & Bloom, 1997). Most of the brain's neurons are formed and migrate to their assigned position during embryonic and early postnatal life. However, exceptions include the olfactory region (Huttenlocher, 1994) and hippocampal neurons in animals, including primates, which continue to be formed in adult life (Gould, McEwen, Tanapat, Galea, & Fuchs, 1997). Neurotrophins are chemicals of central importance to the regulation of the survival, differentiation, and maintenance of function of neurons in the brain. The synthesis and secretion of neurotrophins is dependent on, and regulated by, neuronal activity, which is itself related directly to environmental input (Thoenen, 1995). During the first 2 years of life, there is sequential growth, prodigious proliferation, and overproduction of axons, dendrites, and synapses in different regions of the brain [*1].
This process is genetically determined. However, not all the synaptic connections survive, many being subsequently "pruned" due to lack of use (Singer, 1995). During this period of plasticity, or potential for change, the determination of which synaptic connections will [Page 100] persist is environmentally regulated, being dependent on information received by the brain. A competitive process operates, determining which neurons and neural connections will survive. The competition is, for instance, for potential binding sites on the receiving neuron. To quote Courchesne, Chisum, and Townsend (1994) "neurons that fire together, wire together". Synaptic connections that are not utilised gradually disappear. The progressive neuronal maturation and the establishment of synaptic connections are reflected in changes in the infant's increasing functional maturity. Sensitive PeriodsDuring early brain development there are sensitive periods during which particular experiences affect brain maturation. Although certain experiences are essential for orderly brain development to proceed, the occurrences of some noxious experiences will cause harm to the developing organism. Descriptively, sensitive periods could be conceived of as a brief opening of a window (Bateson, 1979) of vulnerability, of need, and also of opportunity. Sensitive periods have been observed to exist in the development of many different animals as well as in humans. Although generally applied to stages of early development, they can also occur later in life, for instance in animals (but not humans) at the point when maternal responsiveness needs to develop towards her young. Bornstein (1989) points out that the study of sensitive periods has in the past often focused on associating an experience with an observed change, which is postulated to be a consequence of that experience. Bornstein suggests that an understanding of sensitive periods needs also to include
Applying Bomstein's terms to child development, the respective issues of interest here are
The complex interconnections between different areas of the brain, each with their own timetable for critical periods of maturation, contribute to the varied outcomes and developmental complications of early detrimental experiences (Kandel & Jessel, 1991). Greenough and Black (1992) distinguish between two aspects of this environmentally dependent maturational process of the brain. They describe one aspect as experience-expectant, that is, development that will not happen unless a particular experience occurs during its critical period. In this early phase, development is actually reliant on environmental influences. The predetermined sequences of expected experiences allow for an orderly process of synaptic connections, each stage building and depending on the establishment of the previous one. Greenough and Black further suggest that these early experiences have been selected through the process of evolution and are expected to occur reliably in the particular species and at a particular time in development. This species-typical development is genetically determined and its organisation is designed to buffer the developing brain in a regulatory and orderly development in the face of a variety of environmental influences (Bjorklund, 1997). In turn, typical and expectable environmental factors and circumstances are themselves species-specific, presumably evolved to ensure the stability of development. As far as the human infant is concerned, new stimuli are expected to be presented in a way which is "safe, nurturing, predictable, repetitive, gradual and attuned to the infant's or child's developmental stage" (Perry & Pollard, 1998). The overproduction of synapses tends to be found in situations in which a source of information can be relied upon to guide the elimination of unused synapses. They include the handling of young infants, responsive gaze, and talking to the infant. The absence of these interactions with the infant would be unusual and contributes to the elimination of synaptic connections. Neglect and failure of environmental stimulation during critical periods of brain development may lead to permanent deficits in cognitive abilities. Experience-expectant development has been especially well studied in animals' visual cortex (e.g. Wiesel, 1982). In experiments now regarded as classical, Hubel and Wiesel (1979) showed that by temporarily blocking the visual input to one eye of a cat during a critical period of development, irreversible structural and functional changes are produced in the brain's visual cortex, leading to permanent impairment of vision in that eye. In humans, profoundly deaf children do not continue to vocalise in later infancy (Scarr, 1993) presumably because species-typical auditory experiences, which are required for the development of language, fail to reach the appropriate brain area. Irreversible reduction in visual acuity (amblyopia) occurs if an eye is deprived of visual input due to, for instance, a cataract or a squint beyond the age of 8-10 years (Taylor & Taylor, 1979). The other aspect of brain maturation has been termed experience-dependent by Greenough and Black. Here too, environmental inputs actively contribute to brain structure, but unlike the experience-expectant process, here the experiences are not predetermined, nor are synapses anticipating the experiences at any particular stage. Experience-dependent processes generate new synapses in response to the environmentally determined experiences, which vary between individuals. For instance, rats reared for 30 days after weaning, in group complex environments were found to have 20-25% more synapses per neuron in the upper visual cortex than rats reared socially or individually in standard cages (Turner & Greenough, 1985). More recent work has shown that in rodents, neuro-genesis continues throughout adult life in the dentate gyrus of the hippocampus. Mice exposed to an enriched environment were found to have more new neurones in the dentate gyrus of the hippocampus than control mice (Kempermann, Kuhn, & Gage, 1997). Similar findings have been reported in adult rats trained in hippocampus-dependent tasks (Gould, Beylin, Tanapat, Reeves, & Shors, 1999). Both groups of authors found that these experience-dependent responses in the hippocampus enhance the survival of new neurons that had already been generated, rather than stimulating their production. In humans, Davidson (1994) raises the possibility that during an experience-dependent period of plasticity, exposure of the young child to particular affective interactions could lead to pre-frontal asymmetric structural and enduring changes in the brain that [Page 101] would carry significant consequences for later behaviour and affect. These individual experiences that contribute to brain development are an example of the non-shared environment about which Plomin, Owen, and McGuffin (1994) have written. They point out that the genetic studies of human behavioural dimensions and disorders provide the best available evidence for the importance of non-heritable, environmental factors to human development. Neural PlasticityThe process of neural plasticity in response to learning and the acquisition of new memories continues throughout childhood and into adulthood. Although the processes of plasticity enable the brain's structure and function to continue to be modulated in response to environmental input and the organism's needs, there is evidence that plasticity in the adult brain is limited, no longer leading to structural changes and operating mainly by regulating the efficacy of certain connections between neurons (Singer, 1987). With increasing age, the balance between plasticity and stability is progressively weighted towards the latter. Maturation is associated with decreased structural responsivity in the brain to new information (Tucker, 1992) or to injury. Synaptogenesis can be visualised by its active utilisation of glucose on PET (positron emission tomography) scanning (Chugani, 1998). Using this means, it has been possible to demonstrate that in humans, critical periods are proportionally longer. In contrast to animals, the course of human development is far more protracted and includes neotony, or the retention of embryonic or juvenile characteristics by retardation of development (Bjorklund, 1997). While this allows for a longer period of plasticity and maxima1 learning capacity, it equally prolongs the vulnerability for the developing child's brain. Synaptogenesis and pruning occur in functionally differentiated neural systems at their respective periods of maturation, at different ages early in the child's life (Thatcher, 1994). In some areas of the brain, maturation occurs more slowly and later than in other areas, extending into the second year of life in the frontal lobes. These areas are concerned with reasoning and abstract thought, and more global aspects of behaviour such as the regulation of goal-directed behaviour in time, as well as with affect inhibition (de Haan et al., 1994). In this area of development, object (and person) constancy are an example of what Greenough and Black (1992) term an expected experience. This is related to the secure base that Bowlby, in his conceptualisation of attachment, described as a biologically determined "environment of evolutionary adaptedness" (Bowlby, 1969). Regulation of Infants' Affect and ArousalAn important aspect of the primary caregivers' interaction with the developing infant is to respond sensitively to the infant by gauging their emotion accurately. This is necessary in order for the caregiver to regulate the affect, arousal, and behaviour of the young infant, to help the infant deal with frustration, and to direct and focus the infant's attention. Young infants have not developed the capacity to regulate their own level of arousal and impulses, are unable to obtain their own gratification, and require help in learning to plan their actions. The development of these executive functions requires the maturation of the frontal lobes, from the end of the first year. The frontal lobes are involved with the expression and self-regulation of emotion including the inhibition of automatic or habitual emotional responses, and with regulating responses to emotionally arousing situations. This orderly development is dependent on appropriate input and sensitive interaction with the primary caregivers at the sensitive period. Using rat pups in the first days of life, Hofer has detailed the interactions between the pups and their mothers, showing that the maternal regulation includes both physiological and behavioural modulation of the pups (Hofer, 1994). The early mother-infant interaction is thus a bio-behavioural system. In the brain of the infant who sees the responsive mother's face, brain stem dopaminergic fibres are activated, which trigger high levels of endogenous opiates. These endorphins are bio-chemically responsible for the pleasurable aspects of social interaction and social affect and are related to attachment (Schore, 1996). The pleasurable arousal also activates the sympathetic nervous system. The sensitive caregiver's role is to modulate the infant's arousal, which could also follow intense displeasure, fear, or frustration, by calming the infant and restoring her or him to a tolerable emotional state (van der Kolk & Fisler, 1994), free of anxiety. One aspect of early child abuse and neglect is the absence of these sensitive interactions between the parent(s) and the young child. Some depressed mothers are withdrawn and disengaged in their interactions with their infants, whereas others are insensitive, intrusive, and sometimes angry (Cohn & Tronick, 1989). In the absence of experiences of external modulation of affect, the infant brain is unable to learn self-regulation of affect, part of the process of ontogenesis. Such deficits may only become apparent later, when the child is expected to have matured for that particular task and these deficits may then become manifest by aggression or hyper-vigilance. OntogenesisOntogenesis, which is defined as the development of the self through self-regulation, is an active process in development. Ontogenesis is conceptually located between two other interacting influences that determine the direction of development, namely the child's genetic endowment and the environment. Development therefore constitutes more than the resultant of the interaction between nature and nurture, with the notion of ontogenesis allowing for the modification of the process by the contribution and adjustment of the individual child (Cicchetti & Tucker, 1994). They point to the importance of an historical analysis in understanding the complex process of the brain's self-organising system. The nature of the resolution of developmental tasks and challenges, a process that may be more or less adequately accomplished, will determine what is integrated into the brain's structure and contributes, in a probabilistic way, to later adaptation. Whatever the contribution of ontogenesis, it is far more effective to address adverse risk factors or actual ill-treatment before, or at an early stage of the critical period of neural development than to attempt to alleviate the later effects. Animal studies clearly indicate that recovery may be limited if treatment for the precipitating causes of the abnormal or unanticipated neural activity is [Page 102] offered after the closure of the critical period when neuronal "misconstruction" is completed (Courchesne et al., 1994).
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