Child neuropsychology, or paediatric neuropsychology, refers to the study of brain–behaviour relationships within the context of an immature but rapidly developing brain and the implementation of the knowledge gained into clinical practice. Child neuropsychology informs our understanding of typical child development by providing a framework within which to explore and map parallels between brain maturation and cognitive and socio-emotional development. For example, research has demonstrated that improvements in skills such as processing speed are closely associated with increases in myelination during infancy and childhood. Similarly, adolescent risk-taking behaviours have been linked to critical periods in frontal lobe development and connectivity. To date, the primary focus for the field of child neuropsychology has been the generation of a developmentally informed knowledge base that facilitates optimal understanding of the impact of early brain injury, insult or disruption on subsequent brain development and child function, guiding the design of evidence-based interventions to minimise disability.
Child neuropsychology takes its foundations from adult neuropsychological models, utilising pre-existing understandings of cerebral localisation and integrated brain systems to develop an appreciation of the functioning of the young brain. While adult models originally formed the basis of our knowledge of brain disorders in children, it quickly became evident that adult neuropsychology relates to a more ‘static’, tightly organised system, which is unable to easily accommodate the dynamic impact of brain pathology resulting from either brain insult or environmental disadvantage in early childhood (Anderson, Spencer-Smith, Leventer, Coleman et al., 2009; Anderson, Spencer-Smith, & Woods, 2011; Dennis, 1989; Dennis, Spiegler, Jaranek, Bigler, & Fletcher, 2013; Dennis, Spiegler, Simic, Sinopoli et al., 2014).
In an attempt to adapt adult-based models to be relevant for implementation with infants, children and adolescents, child neuropsychologists initially drew from a range of associated fields to establish a knowledge base from which to understand the unique consequences of early brain disruption. Developmental, cognitive and social psychology specialities and the neurosciences have been crucial elements for mapping the expected changes that occur within the brain throughout infancy and childhood, until the brain reaches relative stability and maturity in early adulthood. Of specific relevance are research findings that support parallels between spurts within the brain and increments in cognitive and socio-emotional abilities (Anderson, Northam, Hendy, & Wrennall, 2001; Beauchamp & Anderson, 2010; Gogtay, Giedd, Lusk, Hayashi et al., 2004; Hudspeth & Pribram, 1990; 1992; Luciana, 2003). While not surprising, these convergent findings support the close relationship between brain and behaviour. Knowledge of typical development is especially important in child neuropsychology, as it provides a template for measuring deviations relating to early damage and subsequent interruption to normal growth processes across a range of functional domains – neurologic, cognitive, socio-emotional – not just at the time of insult, but also in the longer term. The likelihood that ongoing development may be influenced by an early cerebral insult or disruption in childhood is not novel or unreasonable. The challenge for the child neuropsychologist is to grapple with the interactions between biologic, cognitive, social and developmental factors to reach an understanding of how these factors affect the child and lead to observed outcomes.
This chapter aims to explore the domain of child neuropsychology, taking a developmental, biopsychosocial approach to describe a field where comprehensive assessment and diagnosis of brain dysfunction are central to clinical practice. Clinical experience tells us that there is no definitive formulae that can predict outcome from early brain insult: some children with severe injuries do well, while others with comparatively minor insults experience lifetime disability. It is our premise that, to fully understand the long-term consequences of brain dysfunction during childhood, it is essential to address the ‘totality’ of the child – the medical, cognitive and psychosocial experiences that interact to influence recovery and development. Further, the importance of viewing children as more than simply ‘little adults’ will be canvassed, with emphasis on the dynamic path of maturation and development and the potential for disruption to this process.
Child neuropsychology: historical perspectives
Plasticity, vulnerability and critical periods
The earliest theoretical contributions to child neuropsychology can be traced to descriptions of plasticity and recovery of function following childhood brain damage. Researchers such as Kennard (1936; 1940) and Teuber (1974) are well known for their seminal works describing relative sparing of function following early brain insult, with the Kennard Principle, interpreted by Teuber, suggesting that: if you’re going to have brain damage, have it early. These early theorists documented relatively good recovery following early brain insult. For example, studies following recovery trajectories for aphasia note that, where injury severity is equivalent, there is greater improvement in children than in adults (Alajouanine & Lhermitte, 1965; Lenneberg, 1967). Such results are interpreted according to a theory of recovery of function where the young child’s brain is seen to be less differentiated than that of the mature adult and more capable of transferring functions from damaged cerebral tissue to healthy tissue. While there continues to be considerable debate regarding the conclusions drawn from this early research, the resultant theories represent an important contribution to the field of child neuropsychology, not least because they acknowledge the unique processes that may be acting in the developing brain following cerebral insult.
Notions of critical periods of development, while not constituting specific neuropsychological theory, have also added breadth to our understanding of the mechanisms at play following early brain insult. Mogford and Bishop (1993) define a critical period as “the time window during which external influences have a significant effect” (p. 252). Consistent with this view, others have argued that early brain insult will have different consequences at different times throughout development and, in some instances, may be more detrimental than later injury, because some aspects of cognitive development are critically dependent on the integrity of particular cerebral structures at certain stages of development (Dennis, Spiegler et al., 2013; Dennis et al., 2014). Thus, if a cerebral region is damaged or dysfunctional at a critical stage of cognitive development, it may be that the cognitive skill subsumed by that region is irreversibly impaired. Further, research suggests that, while there may be some functional plasticity early in life, the time frame may be quite restricted, and not necessarily related to age in a linear manner. For example, children with prenatal lesions, or those sustaining insults during the first few years of life, appear to exhibit particularly severe impairment (Anderson, Spencer-Smith et al., 2009; Anderson, Spencer-Smith, & Wood, 2011; Crowe, Catroppa, Babl, & Anderson, 2012; Dennis, Spiegler et al., 2013).
A perusal of the field of child neuropsychology since it has emerged as a distinct entity yields only a handful of attempts to formulate brain–behaviour paradigms of a truly developmental nature. To date, no theoretical framework has succeeded in integrating biological, psychological and environmental dimensions in a clinically meaningful way. However, two seminal models from the late 1980s, Byron Rourke’s non-verbal learning disability (1989) and Maureen Dennis’ multidimensional age at insult approach (1989) have both had, and continue to have, a major influence on the field. In fact, it may be argued that there has been little theoretical progress outside these two models over several decades.
Non-verbal learning disability (NVLD)
In the 1980s, Rourke (1988; 1989; 1995) described his clinically driven notion of NVLD to account for a consistent pattern of neurobehavioural deficits observed in children with a history of early, generalised cerebral dysfunction resulting from brain insult occurring during the perinatal period or in infancy. The hallmark characteristics of NVLD include: (i) bilateral tactile–perceptual deficits, more marked on the left side of the body; (ii) impaired visual recognition and discrimination and visuospatial organisational deficiencies; (iii) bilateral psychomotor coordination problems, more marked on the left side of the body; and (iv) difficulties managing novel information. Children with NVLD may also demonstrate a range of intact skills, primarily within the auditory/verbal domain. Rourke lists these as: (i) simple motor skills; (ii) auditory perception; (iii) rote learning; (iv) selective and sustained attention for auditory–verbal information; (v) basic expressive and receptive language; and (vi) word reading and spelling.
Rourke’s model is particularly noteworthy from a developmental perspective as it incorporates knowledge of the changing brain, the neuro dimension, with the development of a specific cognitive profile, the psych dimension, in a truly brain–behaviour model. Rourke (1988) continued to build on this model for almost 20 years, providing further descriptions of social and cognitive characteristics of NVLD and their relevance across disorders, arguing that the timing of the insult is of primary importance. NVLD theory explains the spectrum of children’s neurobehavioural abilities and disabilities, as well as the development trajectories of the three principle axes of relevance in brain–behaviour relationships: left–right; up–down; and anterior–posterior. Further elements for incorporation in such models might include explanations of interactions among biologic, cognitive and psychosocial factors from a dynamic, developmental framework.
One of the greatest contributions of the NVLD model is linking cognitive characteristics to an underlying neurologic explanation: the ‘white matter hypothesis’. Rourke’s model is based on the assumption that normal development of white matter is essential for intact child development. NVLD occurs when there is disruption to white matter development during critical stages of early childhood. In support of the NVLD hypothesis, there is evidence of white matter pathology in many of the disorder groups that present with symptoms of NVLD, including traumatic brain injury, hydrocephalus, prematurity and cranial irradiation (Rourke, 1989). However, early brain insult does not always lead to symptoms consistent with NVLD, with some early insults, such as cerebral infection, presenting with language problems or executive dysfunction, but intact non-verbal skills (e.g., Anderson, Bond, Catroppa, Grimwood et al., 1997; Dennis, Simic, Taylor, Bigler et al., 2012; Dennis, Wilkinson, Koski, & Humphreys, 1995; Ewing-Cobbs & Barnes, 2002; Ewing-Cobbs, Prasad, Landry, Kramer, & DeLeon, 2004) or global cognitive impairments (e.g., Anderson, Spencer-Smith et al., 2009).
Developmental stage at insult and cognitive outcome
The second influential theory for the child neuropsychology field has been proposed by Maureen Dennis (1989), based on her extensive research into child brain disorders, including traumatic brain injury and spina bifida. Dennis’ ‘heuristic’ does not propose a specific neurological mechanism for her theory, although other researchers have offered possible biological explanations. Rather, it focuses primarily on age/developmental stage at time of insult and progression in cognitive skills with time since insult. Her heuristic describes the impact of brain damage on language development. She divides skill development into several levels: (i) emerging, where an ability is in the early stages of acquisition, but not yet functional; (ii) developing, where a capacity is partially acquired but not fully functional; and (iii) established, where abilities are fully matured.
Dennis integrates these developmental skill levels with three crucial age-related variables – age at time of lesion, age at testing and time since insult. Age at lesion, she argues, determines the nature of the cognitive dysfunction. For example, early lesions disrupt the onset and rate of language development, while later lesions are associated with a specific symptom pattern, such as high-level language dysfunction (e.g., impaired pragmatic skills). Time since injury refers to differing performance patterns identified at different stages of recovery, with increases in some cognitive skills, but failure to develop others. Age at testing is also important, as even healthy children vary in their ability to perform cognitive tasks at different developmental stages. In this context, Dennis highlights that, while early brain insults appear to cause relatively few problems early post-injury, with ongoing development, children may ‘grow into’ deficits as they fail to acquire age-expected skills. Dennis’ model does not propose a specific neurological mechanism, but rather implies that the full impact of childhood brain injury is not clear until brain maturation is achieved in early adulthood. There is a range of research that supports the general thrust of Dennis’ model. Many studies note the greater impact of younger age at insult (e.g., Anderson, Catroppa, Morse, Haritou, & Rosenfeld, 2005a; 2009; Crowe et al., 2012), and others describe a pattern of increasing functional impairment with time since injury (e.g., Ewing-Cobbs, Fletcher, Levin, Francis et al., 1997; Ewing-Cobbs, Prasad, Landry et al., 2004).
Current multi-dimensional theoretical approaches
Advances in the neurosciences, particularly neuroimaging and neurogenetics, have led to theories that propose a complex relationship between risk factors, which interact and vary over time to determine functional outcomes...