On Knowing More: Future Issues for Developmental Approaches to Understanding Persons with Intellectual Disability
Abstract and Keywords
In this chapter, we summarize the contributions to this volume and to the evolving field of developmental research on intellectual disability (ID). The developmental theory and methodology reviewed in this volume reflect a level of precision and sophistication that could not have been imagined in our previous volumes from 1990 and 1998. These advances have led to an increasingly nuanced understanding of syndrome-specific cognitive and social developmental pathways, gene-brain-behavior relations, and transactions of individuals with their families and environments.
In the opening chapter of this volume, we offered the adage that “the more you know the less you know.” The book's many excellent contributions highlight this state of affairs, documenting both considerable advances and vast gaps in our understanding of the development of persons with ID. By encouraging authors to provide the framework for their own chapters, we hoped to provide greater insight into the ways in which the development of persons with ID is conceptualized, studied, and discussed.
Partly as a result, the contributions are organized in different ways, with a range of emphases and implications. Some chapters primarily concern single topical areas, which are examined across different syndromes. Others are focused on a single syndrome and provide insight into the etiology-related profiles or development of that specific group. In some cases, the emphasis is on what can be learned about the development of one or more syndromes; in others the lesson concerns development more generally. In some chapters, the focus is on the person's own development, while in others the effects on others in that person's life are highlighted.
Such cross-chapter diversity represents significant progress in studying ID from a developmental perspective. Consider the history of our several volumes on this topic. The title of our volume from two decades ago, Issues in the Developmental Approach to Mental Retardation (Hodapp, Burack, & Zigler, 1990b) implied a single developmental framework for understanding ID. That volume included the work of the small group of developmental researchers concerned with ID. Although the theory espoused was not entirely uniform, much discussion was based on the initial conceptualization of the developmental approach by Zigler (1967, 1969) and colleagues (Zigler & Balla, 1982; Zigler & Hodapp, 1986). Several chapters were focused on individuals with familial IDs (then called familial mental retardation), those whose ID is not due to any specific organic insult but who simply fall at the low end of the IQ curve (see Hodapp, Burack, & Zigler, 1990a; Zigler, 1967, 1969)). With the emphasis on persons with familial ID, developmental conceptualizations mostly concerned Piagetian-type cognitive sequences (Hodapp, 1990; Weisz & Zigler, 1979) and structures (Weiss, Weisz, & Bromfield, 1986; Weisz & Yeates, 1981). In this (p. 396) framework, development among persons with ID was generally considered to be typical, albeit at a slower rate and with a lower eventual asymptote (see Weisz, 1990; Weisz, Yeates, & Zigler, 1982; for a slightly differing perspective, see Mundy & Kasari, 1990).
In contrast to his developmental formulations about persons with familial ID, Zigler (1967, 1969) had long contended that “all bets were off” with regard to the uniformity of development among persons with clear physiological or neurological damage. He noted that, “if the etiology of the phenotypic intelligence (as measured by an IQ) of the two groups differs, it is far from logical to assert that the course of development is the same, or even that similar contents in their behaviors are mediated by exactly the same processes.…” (Zigler, 1969, p. 533).
Even in that earlier volume, however, attempts were made to extend the so-called developmental approach to individuals with different genetic etiologies. Although articulated when the Zeitgeist was to study persons with ID as a single population with a common defect, Zigler's perspective was more prophetic than he realized. In particular, many syndromes are now associated with specific developmental profiles, with relative strengths in some domains of functioning and relative weaknesses in others (Burack, 1990; Burack, Hodapp, & Zigler, 1988; Dykens, Hodapp, & Finucane, 2000). In parallel with the wider field of developmental psychology, researchers of persons with ID began calling into question the universality of Piagetian developmental structures, or relations across areas, even if Piagetian sequences might in many cases remain tenable.
Within this context, the developmental approach found a champion in Cicchetti, who, along with colleagues, argued for a liberal, or expanded, developmental approach. As articulated by Cicchetti (1990) in our original volume, meaningful organization across developmental structures might be found even among persons with specific syndromes, including those with Down syndrome (DS; Cicchetti, 1990; Cicchetti & Pogge-Hesse, 1982). Rather than use the difference in the development of children with DS as a reason for abandoning traditional developmental theory, Cicchetti and Pogge-Hesse (1982) used it as an opportunity to expand developmental theory and to provide lessons about development more generally (see also Hodapp & Burack, 1990). The second chapter on a specific syndrome, by Dykens and Leckman (1990), concerned fragile X syndrome (FXS). That chapter reflected research on a little understood syndrome and highlighted the nature of potential etiology-related patterns and trajectories of development.
The need to differentiate by etiology was clearly articulated throughout our second edited volume, the Handbook of Mental Retardation and Development (Burack, Hodapp, & Zigler, 1998). With overview chapters on genetics (Simonoff, Bolton, & Rutter, 1998) and neuropsychology (Pennington & Bennetto, 1998), essential differences in behavior were highlighted across various etiological groups. Such profiles of relative strengths and weaknesses in different etiological group were considered in sensorimotor processing (Dunst, 1998), early communication (Mundy, 1998), language (Fowler, 1998; Tager-Flusberg & Sullivan 1998), symbolic play (Beeghly, 1998), attention (Iarocci & Burack, 1998), and metacognitive processing (Bebko & Luhaorg, 1998). Granted, at this time, more fine-tuned analyses revealed similarities among some syndromes on certain developmental domains (Hodapp & Dykens, 1994; Hodapp, 1997) and that the behavioral effects of etiologies were probabilistic (Dykens, 1995; Rondal, 1995)—rarely does every person with a syndrome show every characteristic, nor is every characteristic found in every person with the syndrome. Still, etiology-related behavioral characteristics vary greatly from one syndrome to another, and most individuals with a specific syndrome show many of their syndrome's behavioral characteristics.
Beyond the emphasis of etiology per se, Zigler's original developmental approach was also expanded in other ways in our earlier volumes. One, in line with his focus on the noncognitive lives of persons with ID, Zigler (1970) had emphasized that social-personality-motivational processes were identical for those with and without ID, but that the behavior of persons with ID is influenced by their life experiences, which often included some combination of institutionalization, social and educational exclusion, and histories of failure. For example, to avoid inevitable failure, these persons are more likely to use outer-directed, rather than self-chosen strategies, and to choose small-but-safe rewards rather than bigger but less certain rewards (Hodapp & Zigler, 1986; Zigler, 1970; Zigler & Balla, 1982). By including social and emotional domains within the purview of the developmental approach, the researchers highlighted the humanity—the “whole person”—of persons with ID.
But a whole-person approach would only be complete when persons with ID were also considered (p. 397) within their actual environments, and within the context of how they are influenced by and influence these environments. By our first volume in 1990, the environment had already been extensively addressed in two ways. One was the centuries-old discussion of the influence of the environment on IQ, now reframed within developmental ideas of risk and resilience (e.g., Sameroff, 1990). The second was the work by Zigler and colleagues on how different social-educational environments influenced the personality-motivational characteristics of persons with ID (e.g., Merighi, Edison, & Zigler, 1990).
Although both areas imply bidirectional person—environment interactions, neither highlighted the continuing, ongoing transactions between persons with ID and the world around them. Again influenced by advances in the broader field of developmental psychology (Bronfenbrenner, 1979, 1986), researchers began to consider persons with ID within the contexts of many different aspects of the environment (also see Sameroff, 1990). By our second volume in 1998 (Burack, Hodapp, & Zigler, 1998), one of those environments—the family—had begun to receive extended attention. In addition to a chapter on the broader environment (Greenbaum & Auerbach, 1998), that second volume featured individual chapters on mothers (Marfo, Dedrik, & Barbour, 1998; Shapiro, Blacher, & Lopez, 1998), siblings (Stoneman, 1998), and the larger family (Stoneman, 1998). This broader theoretical perspective on the systems of influences on the developing child was needed in order to consider the potential variability in development that may be associated with unique experiences and environmental conditions. The understanding of the genetic constraints on development are now balanced with a more nuanced understanding of the way choices in parenting styles, siblings, and family relations may be powerful determinants of variability in development. There is now a clearer commitment to the importance of considering the impact of the disability on both the individuals and on meaningful others in their lives. The path was open for fuller, more elaborated developmental approaches to children and adults with disabilities.
Summing Up: “The More We Know …”
If the prior two decades are seen as a prelude to the current volume, advances are evident on a number of levels. Most important, the research reviewed in these chapters is characterized by a level of precision and diversity that could not have been imagined in 1990 or in 1998. Beyond advances in clinical or behavioral genetics, electroencephalograms, or magnetic resonance imaging, the sophistication in understanding the domains and even the subdomains of development for specific etiological groups is apparent. For example, researchers can no longer simply note that children with DS have a relative weakness in language, but rather must juxtapose areas and subareas of grammar, vocabulary, and pragmatics. On topics in which we once only had questions and theories, we now have concrete evidence, and our subsequent questions and theories have become increasingly sophisticated. The cycle continues as increasing precision leads to new findings, questions, and theories, which in turn lead to new studies and evidence, leading to even further questions and theories.
In a similar way, virtually every chapter in this volume is characterized by links of etiology to subdomains within the general field of developmental psychology. More fine-tuned relations between genetics and particular areas of cognitive functioning are presented with regard to specific etiological groups, as are more detailed understandings of neuropsychological processes and brain—behavior relations. Such precision led to better understandings of specific syndromes, but also to advances in the relevant scientific subfields. Increasingly, we have fine-tuned profiles of relative strengths and weaknesses across many different subareas of cognition for increasing numbers of etiological groups.
At this point, a few general conclusions seem justified. For example, researchers and practitioners must now abandon their earlier notions of some universal deficit as underlying behavioral functioning for all persons with ID. There is no single “core” deficit that accounts for behavioral functioning for all persons with IDs. Similarly, individuals with specific etiologies often are prone to etiology-related maladaptive behavior and psychopathology, such as the extremely high prevalence rates of hyperphagia in Prader-Willi syndrome (Dykens & Cassidy, 1999), increased rates of fears and anxieties in Williams syndrome (Dykens, 2003), and social avoidance and autistic symptoms (and ASD itself) in high percentages of children with FXS (Philofsky et al., 2004; Scambler et al., 2007).
Even the relations with and impact on the family are increasingly studied within the context of etiology. Accordingly, we see a movement to determine whether—and why—families of children with DS seem to cope better than families of children with other ID conditions (Hodapp, 2007). (p. 398) Do certain child characteristics “elicit” reactions from others (e.g., Fidler, 2011, Chapter 23, this volume), or might characteristics of the mother, father, or family overall most influence parent—family functioning? How does the child's cognitive-linguistic profile, behavior problems, or other characteristics predispose reactions from mothers, fathers, siblings, or the family as a whole (Hodapp, 2004)? Such questions are actively being studied by today's developmentally-oriented researchers.
Going Forward: “The More We Will Know …”
We end this chapter by discussing three issues for future work. In various ways, all are foreshadowed in many of this volume's chapters.
Greater Understanding of Etiology-related Trajectories and Profiles
As researchers increasingly examine development in children with different genetic etiologies, they appreciate how an individual child's developmental rate can change. Some changes seemingly relate to changes in the children themselves—for example, changes related to puberty or brain maturation—whereas others may relate to task difficulties. Young children with DS, who often show relatively high IQs in the infant and toddler years, may slow in their development as they experience difficulties in mastering their language's earliest grammatical relations. This issue of “age-related” versus “task-related” slowing, earlier discussed in relation to children with DS (Hodapp & Zigler, 1990), is now examined in terms of children with Williams syndrome, autism, and other conditions. The workings of such age- and task-related changes—both the “when” and the “why”—will increasingly be examined in future years.
Increased attention will also undoubtedly be devoted to the development of etiology-specific profiles. For example, in many cases of the early cognitive-linguistic development of children with different genetic disorders, very slight advantages and disadvantages at earlier ages may, over time, grow into the etiology-specific profiles that are evident among older children. This is seen in the recent work on the growing connection between cognitive-linguistic weaknesses and sociability among infants and toddlers with DS. For example, in examining mother—child interactions, Fidler, Philofsky, Hepburn, and Rogers (2005) found that infants with DS show particular difficulties in means—ends thinking, or tasks that involve the idea that objects (e.g., stick, stool) can be used as a means for obtaining desired other objects. Such deficits seemingly then relate to increased amounts of looking to others for solutions to difficult problems among these children. Eventually, “the coupling of poor strategic [i.e., means—ends] thinking and strengths in social relatedness is hypothesized to lead to the less persistent and overly social personality-motivational orientation observed in this population” (Fidler, 2006, p. 147). Although much remains to be studied, such early developments—and their effects on emerging cognitive-linguistic profiles and personality-motivational characteristics—may hold the key to understanding many etiology-related behaviors among persons with DS and other genetic etiologies of ID.
Understanding Better the Role of Genetics
A second future area of increased work involves genetics. Three aspects of upcoming genetic studies seem noteworthy. One area is how particular genetic anomalies eventually predispose children to certain behavioral outcomes. For example, what is it about having a third chromosome 21 (i.e., DS) that ultimately leads to specific behavioral profiles, trajectories, or personality styles? What is it about having a missing part of the long arm of chromosome 15 (deletion form of Prader-Willi syndrome) that predisposes individuals to show extreme, sometimes even life-threatening, hyperphagia (i.e., overeating)? Why is FXS so tied to gaze aversion and other symptoms of ASD? Such questions are increasingly studied, and ideas of critical genetic regions and pathways from gene to brain to behavior are increasingly raised.
Two, “background genetics” play an essential role, as the genetic contribution to most behavioral characteristics does not solely involve trisomy, deletion, or other genetic anomaly. As shown by behavior geneticists for typically developing children, a person's personality, general intelligence, specific intellectual abilities (the various “s” factors in intelligence), and other behavioral characteristics are partially attributable to their genetic inheritance. Over the next few years, researchers will likely examine heredibility for components of intelligence, language, personality, and maladaptive behavior/psychopathology (e.g., depression, anxiety) among children with different etiological conditions. Similarly, we do not yet know whether one of behavior genetics' most intriguing findings—that for many behavioral traits hereditability rates rise (instead of decline) as children get older (Plomin & Spinath,2006) (p. 399) —will replicate for children with any or all of the different genetic etiologies.
A final genetic issue concerns interactions between genes and environment, or so-called G × E interactions. G × E interactions concern the ways in which specific environments do not affect everyone equally, but instead most affect those who already show certain genetic susceptibilities. One potential example for IDs involves the connections between child abuse and subsequent antisocial behavior. As Caspi et al. (2002) demonstrated, only those children who experienced child abuse and had a particular variant of the MAOA gene were at high risk of becoming antisocial; neither child abuse nor the presence of the MAOA variant, by itself, was usually enough for antisocial behavior to develop. These types of relationships among factors may be particularly essential to outcome as children with IDs are four to ten times more likely to be abused as compared to nondisabled children (Fisher, Hodapp, & Dykens, 2007).
Beyond child abuse per se, the general concept of G × E interactions should prove helpful to developmentally oriented research on ID. Especially for children with particular genetic syndromes, almost all outcomes are probabilistic, with not every individual showing any expected outcome. Some variability in outcome may be associated with polymorphisms that alter the expression or function of genes, and these may interact with poor or stressful environments that lead to less-than-optimal developmental outcomes. In this regard, the impact of poverty on the outcomes of children and adults with specific etiologies and their families would be especially informative as children with disabilities more often reside in single-parent, poorer, and minority families (Emerson, 2007; Fujiura & Yamaki, 1997)
Connecting Person—Environmental Reactions to Etiology-related Characteristics
A third focus of future research is how certain child characteristics elicit reactions from others in their environment (see Fidler, 2011, Chapter 23, this volume). This listing of potential elicitors is fairly long, with many elicitors appearing more often among persons with certain genetic conditions (Hodapp & Dykens, 2009). For example, compared to other children (with or without IDs), children with DS are more likely to have immature faces, with large and round faces, large eyes, and lower-set facial features. Among children and adults without disabilities, such “baby faces” elicit warm, caring, and caretaking responses from others (Zebrowitz, 1997). So, too, do such caregiving responses appear to occur in reaction to faces of children with DS, at least as compared to same-aged children without disabilities and to those with other, more angular and adult-like faces (Fidler & Hodapp, 1999). In the same way, children with particular conditions are also more likely to display other eliciting characteristics (Hodapp & Dykens, 2009). Certain of these characteristics relate to personality; others relate to the presence, type, timing, or severity of psychopathology-maladaptive behaviors; health problems; motor or physical problems or other caregiving challenges; or even the onset of specific problems (e.g., onset of schizophrenia in adolescence-young adulthood; Seltzer et al., 2004). Although few potential elicitors have yet received sustained research attention, each likely influences family members and others in the child's environment.
Conversely, certain conditions show what might be termed “associated characteristics” (Hodapp, 1999). For example, infants with DS continue to be born to mothers who are on average older, more educated, more likely to be married, and of higher family socioeconomic status (Grosse, 2010). As compared to parents of children without disabilities, the parents of children with DS are slightly less likely to divorce (Urbano & Hodapp, 2007). Are these differences due to characteristics of the child (e.g., most children with DS display a more sociable personality), to characteristics of their parents or families (older, more educated parents), to the child's having a more well-known syndrome, or to some combination of the above? Such advantages and disadvantages may even change over the child's development. In a recent comparison of families of children with autism versus families of children without disability, Hartley et al. (2010) found that divorce rates were comparable for the two groups early on, but were higher among the families with children with autism as the children got older. In future studies, many of these elicitation factors, as well as how they operate as the child develops, should be discussed.
Conclusion: Up the Spiral Staircase?
We began this concluding chapter, as well as the book itself, with the idea that the more one knows, the less one knows. In some ways, this idea seems depressing. Why study anything, after all, if one ends up further behind than one started?
Ultimately, however, we feel that science progresses, and that even as we end with more questions (p. 400) than which we started, a general upward progression can be cited. This issue, long discussed in the philosophy of science (e.g., Kuhn, 1970), also applies to studies of individuals with ID when examined with developmental approaches. Do we know more today than we did when Zigler (1967) formally began developmental approaches over 40 years ago? Do we know more today compared to the information reviewed in our own volumes in 1990 and 1998?
To us, the answer seems obvious. We know much more today about development in specific etiological conditions, in specific areas and subareas of development, in connections among these subareas themselves, and in how different behavioral subareas connect to underlying brain structures. Similarly, concerning the environment, we know much more about mothers, fathers, siblings, and families as a whole, about schools, communities, and the workings of environments and gene—environment and environment—person interactions more generally. Some of this knowledge even links diverse levels of environment together, whereas some concerns the lifespan development of the person with specific etiologies or changing interpersonal (mostly familial) environments in which they live.
Ultimately, then, we may indeed be left with more questions over time, but our questions become more specific, more interesting, and (we hope) more relevant to the lives of these individuals. In some sense, we are becoming more “differentiated” and, to some extent, also more “hierarchically integrated.” And, as we have been repeatedly instructed by Werner (1948) and other developmental thinkers, increasing differentiation and hierarchic integration constitute the hallmarks of higher levels of development, of any living organism (or living field of study).
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