Bruce Perry is an internationally recognised authority on child trauma, and, like Allan Schore, is frequently cited in the child development and child protection literature. In this post, I look at Perry’s paper “Childhood Experience and the Expression of Genetic Potential: What Childhood Neglect Tells Us About Nature and Nurture”. I’ve chosen this paper because it tackles the nature/nurture issue head-on and also because it’s the source of the cover illustration for Graham Allen’s Early Intervention: The Next Steps. (The illustration also appears in a recent article in The Telegraph.)
On first reading, I found Perry’s paper slightly disconcerting due to its variable style. The opening section gets quite lyrical;
“Are we born evil – natural born killers or the most creative and compassionate of all animals? Are we both? Does our best and our worst come from our genes or from our learning? Nature or nurture?” (p.80)
“Humankind’s transient but magnificent rebellion against nature is allowed by the brain” (p.81).
That’s followed by a densely factual account of brain development and function, a brief review of historical studies of infant neglect, a detailed account of a study co-authored by Perry involving brain scans and finally a highly speculative section on socio-emotional growth derived from the concept of attachment. Stylistic issues aside, my first problem with this paper was that Perry frames human survival primarily in terms of social relationships.
Survival and instinctive behaviours
Although, oddly, Perry doesn’t actually mention Bowlby in this paper, he begins with what’s essentially an expansion on Bowlby’s environment of adaptedness ;
“Three key brain-mediated capabilities must be present for our species to survive: individual survival, procreation and the protection and nurturing of dependents. Failure in any of these three areas would lead to extinction of our species. The brain, therefore, has crucial neural systems dedicated to (1) the stress response and responding to threats – from internal and external sources; (2) the process of mate selection and reproduction and (3) protecting and nurturing dependents, primarily the young.” (p.81)
My reservation about this claim is that although Perry is right about the three capabilities, the first – individual survival – doesn’t map directly onto (1), a neural system dedicated to a stress response, because survival requires more than just a response to threat. It also requires the ability to find food and shelter, for example. I suppose the reflexes that underlie rooting, suckling, foraging, hunting and nest-building (used by many species for their sleeping arrangements) could at a stretch be classified as responses to threat (of starvation, predation or hypothermia), but these behaviours come into play in order to avert threat, rather than as a response to it. Not only are they not responses to stresses or direct threats, but stresses or threats usually disrupt them. In addition of course, the brain has ‘crucial neural systems’ dedicated to many functions other than the three listed.
Perry then goes on;
“The primary strategy we use to meet these objectives is to create relationships. Relationships which allow us to attach, affiliate, communicate and interact to promote survival, procreation and the protection of dependents. It is the brain that allows humans to form the relationships which connect us – one to another – creating the myriad groups – that have been the key to our success on this planet.” (p.81)
Creating relationships has certainly been an important factor in our ecological ‘success’ but whether it is the primary strategy is debatable. Our problem-solving capability and language have been also been crucial, demonstrated by the fact that human beings have been more successful, than say, chimpanzees, who are social primates par excellence.
So although I wouldn’t dispute Perry’s conclusion that
“… some of the most powerful and complex neural systems in the human are dedicated to social affiliation and communication.” (p.81),
I get the impression that he sees human ecological success in terms of social affiliation and communication, rather than social affiliation and communication being two factors that contribute to human ecological success. The nature of Perry’s model might explain the absence of a detailed discussion of the role of genetic factors in development.
Normal and abnormal: genetic variation
The next section of the paper consists of an excellent summary of brain development and function, listing eight key processes. My one reservation is about Perry’s conclusion. He says:
“The eight key neurodevelopmental processes described above are dependent
upon the genome and environmentally-determined microenvironmental cues …. Disruption of the pattern, timing or intensity of these cues can lead to abnormal neurodevelopment and profound dysfunction.” (p.85)
What bothered me was the implicit assumption that there is such a thing as ‘normal’ neurodevelopment. In a large population, the measures of many characteristics, such as height or weight, fall into a ‘normal’ distribution – when represented as a graph, they form a bell-shaped curve. The majority of individuals cluster around the middle of the curve – the 50th percentile. In the case of head circumference (the measure Perry uses in cases of neglect), as head size increases above or decreases below the 50th percentile, fewer and fewer individuals have those larger or smaller head sizes. With regard to measures used in medicine, approximately 95% of the population is generally considered to form the ‘normal range’. So around 2.5% of the population with the smallest head sizes and around 2.5% with the largest head sizes are considered to have ‘abnormal’ head sizes, but in a statistical sense only – it doesn’t mean there’s necessarily anything wrong with the individuals concerned.
The bell-shaped curve reflects the range of genetic and environmental factors that contribute to differences between individuals. I think Perry’s (and Bowlby’s and Schore’s) omission of a discussion about genetic variation between individuals is significant. It’s especially significant in Perry’s case, since his paper claims to be about
genetic potential. Each of these authors appears to employ a model of genetic development similar to the one popular during the early days of genetic research – of an unfolding species-specific genetic blueprint
. For example, Perry says;
“Sensitive periods are different for each brain area and neural system, and therefore, for different functions. The sequential development of the brain and the
sequential unfolding of the genetic map for development mean that the sensitive periods for neural system [sic] (and the functions they mediate) will be when that system is in the developmental ‘hot zone’ – when that area is most actively organizing.” (p.88, my emphasis)
which means that;
“The simple and unavoidable conclusion of these neurodevelopmental principles
is that the organizing, sensitive brain of an infant or young child is more malleable to experience than a mature brain. While experience may alter the behavior of an adult, experience literally provides the organizing framework for an infant and child. Because the brain is most plastic (receptive to environmental input) in early childhood, the child is most vulnerable to variance of experience during this time.” (p.88)
Although at one level Perry’s conclusion is correct, he doesn’t mention that individual variations in genetic endowment are also involved in neural development; I get the impression that he sees human genetic endowment as standard issue (any exceptions being immediately obvious), so that as a general rule experience alone provides the organizing framework for brain development. This isn’t the case, of course. Deletions, insertions and duplications of genetic material, both inherited and occurring spontaneously between generations, combined with epigenetic changes (the environment acting on genetic expression) that can also be inherited, result in each individual being genetically as well as environmentally unique. This means that the only way one can safely use the term ‘abnormal’ in relation to development is in a statistical sense – in terms of the normal range for any particular characteristic. But Perry’s paper isn’t about genetic endowment, it’s about genetic potential.
Perry explains genetic potential like this;
“Genes are designed to work in an environment. Genes are expressed by microenvironmental cues, which, in turn, are influenced by the experiences of the individual. How an individual functions within an environment, then, is dependent upon the expression of a unique combination of genes available to the human species. We don’t have the genes to make wings. And what we become depends upon how experiences shape the expression – or not – of specific genes we do have. For thousands of years, the genetic potential to use “joysticks” was not expressed – nor that for written language or reading. Yet when experiences are provided in a structured, patterned and appropriately timed way, that potential can be expressed and neural systems which mediate all of those functions will develop.”(p.86; Perry’s emphasis)
There are several ambiguities in this paragraph; notably about genetic design and genetic expression and potential.
Firstly, as far as I’m aware, there’s no evidence that genes are designed to do anything. Genes are molecular units that behave in certain ways in the presence of other molecular units or in certain chemical and physical microenvironments. How an individual functions in response to those microenvironments is dependent not upon the expression of a unique combination of genes available to the human species, but to the individual human being. Genetic endowment alone, regardless of environment, can, for example, result in a failed conception, a miscarriage or an individual born with ‘profound dysfunction’.
Secondly, the term genetic expression usually refers to the chemical (in most cases a protein) that’s produced using information from a gene; using the term ‘genetic expression’ in relation to broader human potential is, I feel, a bit confusing. Being able to read, write or use joysticks aren’t abilities encoded in our genes, they are affordances– a range of things we have the potential to do as a consequence of genetic expression.
Normal and abnormal: environmental variation
Perry points out that animals raised in enriched environments have been found to have larger, more complex and functionally more flexible brains than those raised in more deprived environments, and that animals raised in the wild tend to have larger brains than their domesticated offspring. He concludes;
“It is plausible, however, that abnormal microenvironmental cues and atypical patterns of neural activity during sensitive periods in humans could result in malorganization and compromised function in a host of brain-mediated functions. Indeed, altered emotional, behavioral, cognitive, social and physical functioning has been demonstrated in humans following specific types of neglect.” (p.90)
I’m not convinced that Perry has fully thought through the implications of what he considers to be ‘normal’ and ‘abnormal’ microenvironmental cues. Perry clearly approves of the hunter-gatherer lifestyle – or at least the social aspects of it;
“The genetic potential for healthy socio-emotional functioning – to be empathic, to share, to invest in the welfare of the community – is better expressed in children living in hunter-gatherer bands or extended families or close-knit communities in comparison with our compartmentalized modern world.” (p.96)
And he disapproves of aspects of the modern developed world, questioning the size of households, the amount of television we watch and the way our children are segregated from adults in schools (p.96). What Perry fails to recognize, I feel, is that lifestyle isn’t necessarily based on free choice. Nor does he recognize that something that’s beneficial in some respects might be damaging in others.
Children raised in hunter-gatherer communities are essentially brought up in ‘the wild’. Animals and humans raised in the wild are at high risk of death from starvation, injury or disease, so we would expect their brains to reflect such an ‘enriched’ environment because of the constant need to be on the alert for risk factors. Domesticated animals (and humans) clearly don’t face the same challenges, so we’d expect their brains to reflect that difference. It doesn’t follow, of course, that an animal kept confined in a concrete pen, or a neglected child, is better off than a member of its species engaged in hunting and foraging. But hunter-gatherer communities have no choice about living in large groups, because nuclear family units wouldn’t have the resources to ensure a constant food supply or protection from attack. That doesn’t mean a high risk of starvation, injury or disease is a good thing, nor does it mean that people are necessarily happier when living in close proximity to large numbers of other people. One has only to read the Old Testament to learn some salutary lessons about how extended families can malfunction; I don’t think it’s any coincidence that when they’ve had the option, many families have chosen to live as nuclear units.
Perry clearly doesn’t think that a high risk of starvation, injury or disease is beneficial to children’s development, and despite his doubts about ‘electronic activities’ (p.97) believes that some modern technologies (reading, writing and joysticks) are benign. In short, he picks and chooses which aspects of modern life he considers to be damaging, but doesn’t provide a coherent explanation as to why. Suggesting that it’s because we’ve departed from a hunter-gatherer lifestyle doesn’t hold water, because there are aspects of hunter-gatherer lifestyles that Perry would object to. I think he needs to clarify what he means by ‘abnormal microenvironmental cues’, ‘atypical patterns of neural activity’ and ‘altered emotional, behavioral, cognitive, social and physical functioning’ – altered from what, exactly? What does he consider to be the norm and why?
Following his discussion of neurodevelopment, Perry introduces the topic of neglect, which he defines as ‘the absence of critical organizing experiences at key times during development’(p.88). He then considers two forms of neglect, one involving sensory deprivation and the other affecting the development of socio-emotional potential.
“Two forms of “neglect” will be considered below: extreme multi-sensory
neglect in childhood and a more subtle, insidious decrease in our opportunities to
elaborate our socio-emotional potential caused by the sociocultural changes in how
we choose to live. The sensory deprivation neglect results in obvious alterations in
neurobiology and function while the second form has an almost invisible toxic
impact on the developing child – and ultimately, society.” (p.88)
Perry claims that neglect has – ironically – been neglected by researchers mainly because it’s difficult to “see”, citing specifically emotional neglect (p.88) and the importance of touch in early development and referring to Rene Spitz’ work with institutionalized infants (p.89). I wouldn’t dispute that emotional neglect is harmful, nor that tactile experience is important for the development of proprioceptive and motor function, but, as far as I recall, Spitz (and Harlow with his baby monkeys) made some assumptions about what was missing from the environment of the deprived infants. In addition to emotional engagement and tactile deprivation, there were clearly questions over the adequacy of nutrition – vitamin D levels, for example – and precisely what sensory stimuli were absent. Spitz’ children would have been very susceptible to viral infections, also difficult to “see”. For example, Spitz (1957) describes deprived children rotating their heads around the sagittal axis (i.e. from side to side) and interprets this movement as the children using a universal human signifier for ‘no’ – despite the fact that head-shaking isn’t a universal human signifier for ‘no’ and that it can result from middle ear infections (common in infants, especially if they are supine for long periods) or from impaired development of the cerebellum.
The outcomes of neglect
Perry then moves on to clinical findings in relation to neglect and presents the results from a study he co-authored comparing children subjected to different types of neglect. To summarise, institutionalized and neglected children tend to show low IQs, developmental delays and small head size. This developmental trend is reversed when children are placed in good foster homes or adopted, younger children making better progress than older ones. Perry’s investigation of head size leads him to conclude that neglect results in impaired brain development and he supports this conclusion by referring to evidence from brain scans.
Perry and Pollard (1997) investigated four groups of children;
“Global Neglect (GN; n = 40); Global Neglect with Prenatal Drug Exposure (GN+PND; n = 18); Chaotic Neglect (CN; n = 36); Chaotic Neglect with Prenatal Drug Exposure (CN+PND; n = 28). Measures of growth were compared across group [sic] and compared to standard norms developed and used in all major pediatric settings”. (p.92)
Global neglect is defined by “a history of relative sensory deprivation in more than one domain (e.g., minimal exposure to language, touch and social interactions)” and chaotic neglect as “far more common and was considered present if history was obtained that was consistent with physical, emotional, social or cognitive neglect.” (p.92)
Perry and Pollard found that for the global neglect group, the mean head circumference was below the 5th percentile, but such a dramatic variation from the norm wasn’t seen in the chaotic neglect group. For the global neglect group, 17 MRI or CT scans were available – 11 of them were judged ‘abnormal’ by neuroradiologists. 26 scans were available for the chaotic neglect group, but only 3 were judged ‘abnormal’.
The material on clinical and neurobiological findings raises many unanswered questions. Why were the children in institutions? Were their parents dead, ill or did they lack the resources or ability to care for their children? Were genetic or physiological causes for the children’s poor development ruled out? Why were children neglected at home? What specific factors necessary for healthy development were absent? Why were CT and MRI scans available? Had brain damage or a medical condition been previously suspected?
Until these questions are answered, all that Perry’s data can tell us is that specific groups of children, raised in specific conditions (characterized by unspecified inadequacies), showed delayed or abnormal development. All we have is a correlation between neglect and poor development. We don’t know if the neglect caused the poor development, or if it did, which elements of the neglect caused what developmental deficits.
But Perry doesn’t identify precisely which sensory domains were neglected or how, or what aspects of physical, emotional, social or cognitive input were missing. Specifying the components of neglect isn’t important if you’re interested only in the degree of neglect, but it becomes very important if you’re mapping neglect onto brain abnormalities or want to compensate for specific factors that might have been absent in early development.
What Perry does tell us is that two particular brain anomalies were identified from the CT and MRI scans; enlarged ventricles or cortical atrophy. (You can see abnormalities of the ventricles and cortex in the right-hand image of Perry’s Figure 1, below.)
Perry’s Figure 1
The ventricles are spaces in the brain that join up with the central canal of the spinal cord and are filled with cerebro-spinal fluid. The lateral ventricles are visible in the centre of the CT scan images. Cortical atrophy means that the cortex of the brain has shrunk, usually due to the degeneration of cells.
It’s possible that the neglect experienced by the children resulted in these two brain anomalies; but there are other possible causes. Enlarged ventricles occur in around 1% of pregnancies for a variety of reasons, unlikely to be due to global or chaotic neglect as defined by Perry, but he doesn’t mention the possibility of enlarged ventricles occurring prenatally. Perry and Pollard’s data indicate that the globally neglected children also showed low height and weight, and the authors do mention that nutrition might be involved. Cortical atrophy can also have a variety of medical causes. In short, although neglect is a possible cause, it’s only one of several possibilities.
Support for the hypothesis that neglect rather than genetic make up or medical conditions caused the brain abnormalities comes from the finding that a year after neglected children were placed in foster care, head size had increased, the increase being inversely correlated with the child’s age (younger children showed greater increases). Even so, in the Perry and Pollard study the youngest children’s head size was still below the 30th percentile – we aren’t told whether the youngest children eventually ‘caught up’ with their non-neglected peers and we don’t know whether the children would have had small heads regardless of whether or not they were neglected. In addition, the head circumference data are presented as means – we aren’t told the range of measurements involved for each age range. It could be that the group mean is artificially high because one child’s head size increased significantly, or artificially low because one child’s head size remained small.
Although some parts of Perry’s paper are very useful – the sections on brain development and the summary of the history of child neglect research, for example – in general I found it frustrating, for three reasons. These are that Perry conflates correlation with causality, fails to take adequately take into account individual variations and doesn’t define neglect with sufficient accuracy.
Correlation and causality Running through this paper is an implicit assumption that if that neglect is associated with developmental and brain abnormalities, those abnormalities must be caused by neglect. This is a basic error of data analysis. Although it’s likely that neglect causes developmental problems – otherwise it wouldn’t be called ‘neglect’ – it’s impossible to tell from Perry’s data whether;
• neglect caused the brain abnormalities
• the brain abnormalities caused the neglect (if the brain abnormalities were also present in parents or neglect was a response to the children’s behaviour)
• there were other causes for the abnormalities, or
• which components of neglect were responsible for which brain abnormalities.
Individual variation Perry doesn’t seem to take individual variation into account; in his Figure 1 he compares a neglected brain on the 3rd percentile with a non-neglected one on the 50th percentile, when a comparison with a 3rd percentile non-neglected brain would probably have been more informative. And his graph of the increase in head-size when children of different ages are fostered, presents mean values for each age group rather than the range of head sizes for each group.
Defining neglect There’s no question that children need certain conditions for healthy development. A nutritious balanced diet, fresh air, exercise and sunlight, a stimulating environment and consistent, caring stable relationships suggest themselves. The absence of any of these factors can cause deficits in development – the child might not reach their genetic potential as Perry suggests. But apart from making a distinction between extreme (global) neglect and more common (chaotic) neglect, Perry doesn’t discriminate between the different components of neglect and their possible effects. It’s important that we know what components of neglect have what outcomes because if we don’t, whether or not a child has been ‘neglected’ ends up being a matter of personal judgement. In his closing section, for example, Perry suggests that living in small social units and watching several hours of television a day is detrimental. He’s entitled to his view of course, but provides no evidence to support his claim, apart from pointing out the decline in the number of people who vote in Presidential elections (p.97).
Why Perry’s paper worries me
What worries me about Perry’s paper is that, despite its weaknesses, because it’s relevant to a highly specialised domain, it’s unlikely to be read by the geneticists and the evolutionary, developmental and molecular biologists who are in a position to critique it. Perry’s work has been cited, uncritically, in a number of policy documents. His argument in this paper is superficially plausible because, like Bowlby, he constructs it by juxtaposing several indisputable ideas (e.g. human lifestyles have changed, children are developing, neglect can be harmful) but the definitions of underlying concepts and the causal links between them, by contrast, are rather tenuous. But a busy social worker, school nurse, health visitor or even doctor, is quite likely not to notice the weaknesses in the definitions or causal links. Perry’s paper is likely to be seen as providing evidence that neglect (sometimes seen by professionals as synonymous with parenting strategies of which they personally disapprove) causes abnormal brain development. Or worse, that abnormal brain development will be assumed to be caused by neglect, rather than by one or more of many possible causes.
Perry, B.D. and Pollard, D. (1997). “Altered brain development following global neglect in early childhood”. Society For Neuroscience: Proceedings from Annual Meeting, New Orleans.
Spitz, R.A. (1957). No and yes : on the genesis of human communication. New York : International Universities Press.
Normal distribution curve from: http://en.wikipedia.org/wiki/Percentile_rank