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The Debate Over Brain Plasticity in Children


It was back in the 1900s that a Neuroscientist, Margaret Kennard, gained recognition for her research into the effects of early lesions on the developing brain and recovery of function. The legacy of her work was the belief that the younger a person is when they acquire a brain injury, the better the outcome. This belief has, however, been roundly challenged in more recent years by those who view brain development from the perspective of vulnerability, and propose the young brain is uniquely sensitive to injury (Anderson et al., 2009).

Kennard’s work led to the emergence of plasticity theory. Essentially, the brain is seen as a plastic entity, capable of recovery and reorganisation following injury. Proponents of this theory consider the young brain to be immature, less committed to any specialist skill or ability, and so less vulnerable to the effects of injury. Plasticity is therefore seen as optimal early in development.

The concept of brain plasticity is associated with remarkable transformational processes that occur during normal development. From the beginning, the smooth fetal brain follows a complex series of local tissue volume changes, evolving into a sulcated neonatal brain. This sulcated brain has an individually unique cortical folding pattern that dramatically increases the cortical surface area. In this sense, the young, rapidly developing brain is indeed highly plastic, with growth taking place at both physical and functional levels. Research suggests that the organisation of brain function in children involves predominantly local interactions, and that this shifts to a more distributed network in young adults (Dosenbach et al., 2010).

Over the course of normal development, the brain continues to demonstrate its inherent plasticity in the form of neurogenesis. Neurogenesis involves activity-dependent changes in synaptic structures and programmed cell death (Johnston, 2009). These neural processes may be either rapidly adaptive or involve more long-term changes as the child matures into adolescence (Kujala & Näätänen, 2010). Critical periods of maturational activity, when the brain is likely to be more vulnerable to the effects of injury, are separated by more stable periods.

During childhood, a variety of experiences stimulate the overproduction of synapses. These enhance plasticity by increasing the strength and development of neurotransmitter systems and excitatory/ inhibitory mechanisms (Harris et al., 2011), and the release of the brain-derived neuronal growth factor. This creates a proliferation of dendritic spines and neuronal circuits, ripe for pruning during adolescence. Huttenlocher and de Court (1987), for example, found that there was a burst in synaptogenesis in the occipital area in the early postnatal period, increasing at around two years old to a density about twice that in the adult brain, then reducing to adult levels by early adolescence. However, compared to adults, the number of synapses in the frontal lobes remains higher for adolescents well into their teens.

Magnetic resonance imaging has shown that in young people aged 7-19 years an initial increase in density is followed by thinning (Shaw et al., 2006). In fact, weakening connections have been found to be a better predictor of brain maturity than strengthening connections (Dosenbach et al., 2010).

Long-term plasticity is currently seen as a complex, multicomponent process, in which synapses and dendritic spines can also undergo morphological remodelling, and where long-term potentiation and depression are driven by sensory use or disuse, and by the acquisition of particular skills (Feldman, 2009).

In the course of normal development, plasticity is expressed functionally as children get older, progressing towards and reaching developmental milestones, e.g. talking and walking, and achieving optimum cognitive, behavioural and social efficacy. Many twentieth century developmental theorists (e.g. Piaget, Bruner, Vygotsky) discussed the ways in which children were thought to gradually acquire abilities to make sense of their world, and how cognitive structures adapted and expanded to accommodate and assimilate increasingly complex life experiences.

  • Piaget (in Durkin, 1995, pp.16-19), for example, proposed four sequential and age-related stages of development – sensorimotor (0-2 years), preoperational (2-7 years), concrete operational (7-11 years) and formal operational (11+ years). He believed that the cognitive development associated with these stages was not rigidly fixed, but contained its own rhythm, and that mental schemata had to be in place before the particular types of thinking and expression associated with each stage could occur.
  • Bruner described children as limited information processors in the areas of training, manipulation of cognitive strategies, expertise, memory and attention. Adults were seen as competent information processors whose support and guidance (scaffolding) was essential in promoting a child’s cognitive development.
  • Vygotsky (1978) introduced the concept of the zone of proximal development, which suggests that, even with support, a child’s development is limited by their actual mental age.

These early theories and the concept of normal developmental plasticity provide a sense of alignment, in that alongside bursts of brain development there is a relatively rapid and sequential acquisition of a vast array of intrapersonal and interpersonal skills maintained into adolescence. In fact, the human brain continues to mature until a person reaches their mid-twenties (Sowell et al., 2004).

Jacobs et al. (2007) point out that a number of interacting factors may contribute to the brain’s ability to recover from early damage in childhood and to compensate functionally. These may include:

  • the nature of the injury itself, including focal versus diffuse damage (e.g. acquired brain injury such as a stroke or tumour versus a traumatic brain injury)
  • the developmental ‘windows of opportunity’ associated with neuronal generation and peak periods of synaptogenesis. It has been proposed that injury prior to, or following, these bursts of synaptogenesis may correspond to level of outcome. 

There is no doubt that some degree of functional plasticity exists, in the sense of recovery of skills lost after an early brain injury. Where there has been a focal injury, the plasticity model argues for a relatively better functional outcome in childhood, and especially that recovery of language or motor abilities is likely to supersede the requirement for what have traditionally been seen as less critical skills. Indeed, some children with left hemisphere pathology have been observed to go on to develop age appropriate language skills, apparently without any of the aphasic difficulties that tend to accompany similar lesions in adults (Heywood & Canavan, 1987). However, more recent research looking at the effects of focal brain injuries in young stroke victims raises questions about certain aspects of executive functioning that might be affected by early injury into the long-term (Max et al., 2010).

Many studies have explored the effects of focal brain injuries in childhood. Less is known about the effects of diffuse injury following a traumatic brain injury (TBI), including mild TBI, on the developing brain, and repeated TBI as when babies are shaken. Impact injury is more likely to produce shearing injuries in infants and young children, possibly related to incomplete myelination. Furthermore, the relatively large head, weaker neck, and thin malleable bones of the skull allow force to transfer more effectively to the brain (Singer, 2006).

Anderson et al. (2009) note that in contrast to those who sustain a focal insult, those with a generalised injury such as a TBI tend to have a slower recovery and poorer outcome than adults with similar injuries. It is known that biomechanical forces during childhood trauma can have a destructive effect on the white matter fibres connecting areas of, for example, the frontal lobes (Oni et al., 2010) and the uncinate fasciculus (Johnson et al., 2011). The process of myelination is also considered to play an important role in healthy paediatric development, associated with the emergence over time of motor deficits after early focal lesions in the primate brain, and taking the longest to form in the frontal lobes (Kennard, 1940, in Dennis, 2010, p.1050; Prins & Giza, 2012). The protracted course of myelination in the frontal lobes, which are especially vulnerable to TBI, also highlights the potential for adverse effects on the development of executive functioning over time.

Gerrard-Morris et al. (2010) also examined the effects of TBI severity (severe, moderate, and complicated mild) on the cognitive development of 3-6 year olds over an 18 month period. They found a delayed effect, 12 months post-injury, for the manifestation of cognitive communication difficulties in children with severe TBI. This was assessed as ‘Pragmatic Judgement’, which drew on abilities to make inferences about pictured social interactions, to appreciate the intentions of the people in the pictures, and the use of social discourse. Indeed, frontal and temporal areas of the brain that are crucial for effective social cognition, are also noted to be particularly vulnerable in paediatric TBI (Yeates et al., 2004).

The phenomenon of cerebral plasticity, involving alterations in dendritic and synaptic structure and connectivity, is thought to increase in frequency after injury (Jacobs et al., 2007). However, Max et al. (2010) hypothesise that neuronal repair, especially if the injury were sustained during a phase of axonal pruning, may be hindered by the anomalous retention of axons that would normally have been destroyed, and/or the proliferation of neuronal reconnections. If the reconnections are inappropriate, this may result in dysfunctional behavioural recovery, or a ‘crowding effect’ (Aram & Eisele, 1994). In other words, functions normally controlled by the damaged parenchyma are transferred to another area of the brain, creating a depression of all abilities (Anderson et al. 2009). It is possible, then, that the adverse impact of an injury sustained at a critical period of synaptogenesis or pruning, when particular abilities and skills are developing rapidly or being honed, may be far greater than if these abilities or skills were already established.

One theory for the evidence of the later adverse effects following an early lesion is based on the Vygotsky/Bruner concept of scaffolding, in that the cognitive abilities acquired at one point during development are necessary to maintain a normal rate of subsequent intellectual growth (Banich et al., 1990). In this context the delayed effects of an early injury mean that the discrepancy in the acquisition of cognitive abilities and functional skills between a child without a brain injury and a child with a brain injury increases cumulatively over time. In the early stages of recovery, the differences may not be so noticeable, but over time accumulating deficits may also interfere with a child’s ability to interact with others at a social level (Max et al., 2010), leading to increasing isolation and loneliness (Yeates et al., 2004).

It may be that the true extent of an early brain injury only becomes evident as children move on from the structured environment of primary school, through the less structured environment of secondary school, and into late adolescence/early adulthood. Deficits in specific skills associated with particular types of cerebral pathology may only be revealed at the point when they are expected to become operational within the context of development.

More recently, researchers have begun to examine the impact of family environment on the social cognition of children who have sustained a paediatric TBI. A prospective longitudinal study over 4 years post-injury included 6-12 year old children with severe or moderate TBI, and controls with orthopaedic injuries (Yeates et al., 2004). They found that long-term social outcomes for the children with TBI were accounted for by severity of injury, specific cognitive abilities, social communication and problem-solving abilities. In addition, negative social outcomes for the child were further adversely affected by family environments with lower socioeconomic status, fewer family resources, and poorer family functioning. From the opposite perspective, Gerrard-Morris et al. (2010) concluded that the chances for cognitive recovery and development were enhanced by a supportive family environment.

It is possible that a child who sustains a severe brain injury very early in life may adapt with little overt awareness of the changes in their life. However, an adolescent who suffers a severe brain injury may be less cognitively impaired in some respects, but they may have considerably more self-awareness, and there can be major consequences with respect to self-image, self-esteem, social functioning, academic achievement, and expectations for future life goals.

Even where the effects of an early TBI are initially ‘hidden’, the temporally and developmentally defined emergence of difficulties with executive and social functioning can also impact at many different levels and interfere with a young adult’s quest for independence. Difficulties may eventually become apparent even in basic activities of daily living such as cooking, personal organisation, finding suitable employment, and building healthy friendships and relationships. Parental overprotection, which may naturally increase in the days and months after their child’s injury, can become problematic as the child reaches their late teens or early twenties and begins to express a desire for greater autonomy.

Interestingly, the plasticity theory is still alive and well. Johnston, for example, in 2009, concluded that ‘plasticity mechanisms are enhanced in the developing brain so that children can recover more fully from brain injuries than adults’ (p. 99-100). A survey in 1996 (Webb et al) also found belief in plasticity theory to still be active in professional practice. They asked different groups of professionals (neurosurgeons, neurologists, neuropsychologists, general practitioners, nurses, physiotherapists, occupational therapists, and speech therapists) to estimate the extent of recovery in four fictitious case studies of brain injury. The same accident and injury details from each of the four case studies were given for either a child (either aged 3 or 7 years) or an adult (either aged 48 or 55 years). Neuropsychologists did not differ from any other profession with respect to the view that children would have a better recovery than adults.

The research literature as a whole, however, provides stronger support for developmental vulnerability following an injury to the brain in childhood than it does for the plasticity model. There are multiple issues to consider that are associated with age at lesion, time since injury, and age at testing. These include the development of the brain itself, especially the rhythm and complexity of the physical and chemical changes that occur over time. More evidence is needed to determine the extent to which developmental vulnerability is associated with particular stages or phases of neurological activity. The nature, severity, and mechanisms of an injury are relevant, i.e. an acquired focal lesion or a traumatic brain injury. We also need to explore the delayed effects of brain injury, especially those that emerge later in the first two to three decades of life. This should include the recovering child’s interaction with their environment, the degree of richness and support in that environment – at home, at school, and socially – all of which can influence long-term outcome (Crone & Ridderinkhof, 2011).


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