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Chapter 5 Summary and Future Directions The research discussed in this volume offers considerable hope that approaches to diagnosis and treatment of self-injurious behavior are reaching a level of complexity and sophistication that will make possible a range of preventive strategies and clinically significant treatments resulting in lasting changes in this behavior. What is needed next is a plan for promoting these procedures on a large scale, so that they are available to all who need them. They must be socially valid and lasting for years, rather than for days, weeks, or months if parents and families are to accept them and demand them for their children. Self-injurious behavior is a heterogeneous clinical phenomenon, currently best un- derstood with a developmental bio-behavioral perspective. It is certainly true that much of self-injurious behavior serves observable, external functions, such as gaining social attention or tangible reinforcers, and many of them are readily changed by altering social occasions for self-injurious behavior and the reinforcement contingencies that maintain it without necessarily addressing the bio- logical conditions that set the occasion for it. Functional analyses have provided em- pirical evidence for the complex picture of the antecedents and consequences that maintain self-injurious behavior and improved assessment instruments have led to a richer and better set of treatments for individuals with self-injurious behavior. There are also cases of self-injurious behavior, however, which may originally have been occasioned by social stimuli or contingencies but which, through extensive prac- tice, have now altered interoceptive stimuli, e.g., dopamine and/or opioid release, whose functions must also be altered, in order to allow social contingencies to be effective in treating self-injurious behavior. In still other cases, e.g., Lesch–Nyhan syndrome, there may be a strong genetic or neurobiological predisposition toward self- injurious behavior where using social contingencies without considering neurochemical deficiencies and maturational variables is very unlikely to produce lasting effects. The study of behavioral phenotypes in genetic syndromes associated with self-in- jurious behavior gives us hope that there are subtypes of self-injurious behavior, which, if considered sufficiently, will allow us to tune our algorithms in the treatment and prognosis for self-injurious behavior. The bio-behavioral models for self-injurious behavior also give plausible accounts for the variety of forms and functions of self-injurious behavior. In some cases the independent variable is behavioral (e.g., isolate rearing or suboptimal parenting by parents who are overwhelmed with a special needs child). In other cases, it is biological (e.g., dopamine dysregulation). In still other cases, the model is mixed (e.g., as in the

Chapter 5 Summary and Future Directions 2007 Assessment and Treatment of Child Psychopathology and Developmental Disabilities

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Page 1: Chapter 5 Summary and Future Directions 2007 Assessment and Treatment of Child Psychopathology and Developmental Disabilities

Chapter 5

Summary and Future Directions

The research discussed in this volume offers considerable hope that approaches todiagnosis and treatment of self-injurious behavior are reaching a level of complexityand sophistication that will make possible a range of preventive strategies and clinicallysignificant treatments resulting in lasting changes in this behavior. What is needed nextis a plan for promoting these procedures on a large scale, so that they are available toall who need them. They must be socially valid and lasting for years, rather than fordays, weeks, or months if parents and families are to accept them and demand them fortheir children.

Self-injurious behavior is a heterogeneous clinical phenomenon, currently best un-derstood with a developmental bio-behavioral perspective.

It is certainly true that much of self-injurious behavior serves observable, externalfunctions, such as gaining social attention or tangible reinforcers, and many of themare readily changed by altering social occasions for self-injurious behavior and thereinforcement contingencies that maintain it without necessarily addressing the bio-logical conditions that set the occasion for it. Functional analyses have provided em-pirical evidence for the complex picture of the antecedents and consequences thatmaintain self-injurious behavior and improved assessment instruments have led to aricher and better set of treatments for individuals with self-injurious behavior.

There are also cases of self-injurious behavior, however, which may originally havebeen occasioned by social stimuli or contingencies but which, through extensive prac-tice, have now altered interoceptive stimuli, e.g., dopamine and/or opioid release,whose functions must also be altered, in order to allow social contingencies to beeffective in treating self-injurious behavior. In still other cases, e.g., Lesch–Nyhansyndrome, there may be a strong genetic or neurobiological predisposition toward self-injurious behavior where using social contingencies without considering neurochemicaldeficiencies and maturational variables is very unlikely to produce lasting effects.

The study of behavioral phenotypes in genetic syndromes associated with self-in-jurious behavior gives us hope that there are subtypes of self-injurious behavior, which,if considered sufficiently, will allow us to tune our algorithms in the treatment andprognosis for self-injurious behavior.

The bio-behavioral models for self-injurious behavior also give plausible accountsfor the variety of forms and functions of self-injurious behavior. In some cases theindependent variable is behavioral (e.g., isolate rearing or suboptimal parenting byparents who are overwhelmed with a special needs child). In other cases, it is biological(e.g., dopamine dysregulation). In still other cases, the model is mixed (e.g., as in the

Page 2: Chapter 5 Summary and Future Directions 2007 Assessment and Treatment of Child Psychopathology and Developmental Disabilities

206 Self-Injurious Behavior in Intellectual Disabilities

bio-behavioral state model by Guess & Carr, 1991). A given self-injurious behaviorcase might fit one or several of these models depending on the genetic disposition andon the neurobiological and behavioral history.

The tools we have for exploring the above risk factors continue to improve. We nowhave better rating scales. The various methods of functional analysis (e.g., Journal ofApplied Behavior Analysis, 27, 1994, issue 2) have been a major advance in our ar-mamentarium. The study of genetic behavioral phenotypes with new genetic techniquessuch as linkage analysis (Dykens et al., 2000) and genomic analysis is another tool. Theuse of neurochemical assays of neurotransmitter functions, e.g., Lewis et al. (1996a,1996b, 1996c, 1996d), may also aid in predicting who will respond best to which drugtreatment. Together these tools will also help us with efforts to prevent self-injuriousbehavior.

Animal models of self-injurious behavior play a key role in discovering the biologicalcauses and treatments for different types of self-injurious behavior. They are critical forour understanding the mechanisms by which adverse events cause self-injurious be-havior and intellectual disability (Crnic & Nitkin, 1996). They permit us to experimentwith therapies that would never be permitted on humans without such prior testing.Finally, we can check our behavioral findings with genetic and neurobiological tech-niques that are too invasive to be used on humans. To be sure, care must be used incomparing a particular animal phenotype with an appropriate homology in humans.But once homology is established, one can then experiment with the methods of pro-ducing, preventing, and curing the disorder. For instance, gene therapy for Lesch–Nyhan syndrome is a real possibility for the future, but currently it requires the studyof the HPRT mouse model, in order to understand the purine salvage pathway inLesch–Nyhan syndrome and how the genetic defect can be cured or prevented.

It is easy to forget that only 40 years ago the self-injurious behavior cases of the typediscussed in this chapter were written off as hopeless, confined to physical and chemicalrestraints in highly restrictive environments. Today there are humane and effectiveinterventions for the majority of self-injurious behavior cases in mostly unrestrictedsettings. That is a paradigm shift in treatment and prognosis that was brought about bythe behavioral analytic revolution. We now think differently about and have differentexpectations for people with intellectual disabilities and self-injurious behavior.

It is only 20 years since our knowledge of the neurobiological causes of self-injuriousbehavior began to grow, and the rate of growth has been exponential ever since. Wenow have a few drugs based on a clear neurobiological rationale that selectively im-prove self-injurious behavior without serious side effects, e.g., naltrexone, the atypicalantipsychotics, and the serotonin reuptake inhibitors. We now have behavior pheno-types whose self-injurious behavior is differentially affected by selected drugs. Thereare now drugs coming on the market, which are likely to work even better. There iseven the prospect of gene therapy for certain self-injurious behavior-related geneticsyndromes. Lastly, there is a prospect of non-invasive training-induced recovery fromlesion-induced susceptibilities to self-injurious behavior. Truly we have come a longway with research on self-injurious behavior, but we still have a long way to go in orderto address all of the aspects of this multiply caused and multiply-affected devastatingdisorder.