Data are summarized from 152 single-subject analyses of the reinforcing functions of self-injurious behavior (SIB). Individuals with developmental disabilities referred for assessment and/or treatment over an 11-year period were exposed to a series of conditions in which the effects of antecedent and consequent events on SIB were examined systematically by way ofmultielement, reversal, or combined designs. Shook, Keith Slifer, and G. Linden Thorn for the special panel concluded that, although much is known about SIB at the present time, thorough understanding and eventual reduction in the frequency of SIB will require continued research on all aspects of the disorder, induding prevalence, etiology, treatment, and prevention.In an attempt to define the general parameters of SIB as a clinical disorder, a number of investigators have conducted group surveys using methods roles they played in developing or maintaining the clinical environments that accommodated this research. Michael Dorsey is now at the South Bay

Because there are potentially serious limitations to differential reinforcement of other behavior (DRO) (which is probably the most widely used treatment procedure for behavior problems), we examined an alternative procedure--noncontingent reinforcement (NCR). Three females with developmental disabilities, all of whom engaged in severe self-injurious behavior, participated. During a pretreatment functional analysis, each subject's self-injury was shown to be differentially sensitive to social attention as a maintaining consequence. Next, each subject was exposed to a DRO treatment and an NCR treatment. During DRO, attention was delivered contingent on the absence of self-injury for prespecified intervals. During NCR, attention was delivered on a fixed-time schedule that was not influenced by the subject's behavior. Results showed that both procedures were highly effective in reducing self-injury, probably because the functional reinforcer for self-injury was used during treatment. Furthermore, there was evidence that NCR attenuated several of the limitations of DRO. These results are particularly interesting in light of the long experimental history of NCR as a control rather than as a therapeutic procedure.

IntroductIonOne-third of the US population is clinically obese (BMI ≥30 kg/m 2 ) (1), a condition associated with increased morbidity and health-care costs (2). Although the origins of this problem are complex, caloric intake in excess of expenditure is the primary cause of weight gain. Food intake is influenced by a convergence of processes in the brain, including homeostatic mechanisms, motivation, cognitive control, and decision making (3). Research has shown that obese individuals find food more reinforcing compared to healthy weight (HW) individuals (4,5). The motivational value of food can be measured by determining the extent to which an individual will work to obtain food (3) and is influenced by a variety of factors including food composition (6,7) and hunger (3).In experimental settings, obese individuals show increased food motivation, compared to HW individuals, by working more for food rewards than nonfood rewards (4) and by consuming more food in laboratory settings than individuals who demonstrate lower levels of food motivation (4,8). In addition, obese individuals, compared to overweight and HW individuals, report higher levels of eating disinhibition and hunger on the Three Factor Eating Inventory (EI) (9), which measures dietary restraint (conscious effort to control dietary intake), eating disinhibition (release of control under emotional or situational triggers), and hunger (feeling hunger and its relationship to eating) (10).Functional neuroimaging studies are beginning to examine brain mechanisms underlying food motivation. Positron emission tomography studies in HW adults, examining brain activations during food consumption, show changes in regional cerebral blood flow (rCBF) in prefrontal regions, including ventromedial prefrontal cortex (PFC), as well as insular cortical regions (11)(12)(13)(14)(15). In these studies, researchers manipulated food motivation by increasing participant hunger through fasting (4.5-36 h) and measuring responses to a liquid meal (11-13,15) or chocolate (14). rCBF increased during hungry states in the hypothalamus, insula, and the orbitofrontal cortex (11,14,15). Meal consumption was associated with increased rCBF in prefrontal regions such as the ventromedial PFC (11,13,15). It should be noted that re-analysis of rCBF results (11,13,15) using a random effects as opposed to fixed effects analysis revealed decreases rather than increases in dorsolateral prefrontal regions (16,17). One out of three adults in the United States is clinically obese. Excess food intake is associated with food motivation, which has been found to be higher in obese compared to healthy weight (HW) individuals. Little is known, however, regarding the neural mechanisms associated with food motivation in obese compared to HW adults. The current study used functional magnetic resonance imaging (fMRI) to examine changes in the hemodynamic response in obese and HW adults while they viewed food and nonfood images in premeal and postmeal states. During the premeal condition, obese participants...

Objective: To investigate the neural mechanisms of food motivation in children and adolescents, and examine brain activation differences between healthy weight (HW) and obese participants. Subjects: Ten HW children (ages 11-16; BMI o 85%ile) and 10 obese children (ages 10-17; BMI 495%ile) matched for age, gender and years of education. Measurements: Functional magnetic resonance imaging (fMRI) scans were conducted twice: when participants were hungry (pre-meal) and immediately after a standardized meal (post-meal). During the fMRI scans, the participants passively viewed blocked images of food, non-food (animals) and blurred baseline control. Results: Both groups of children showed brain activation to food images in the limbic and paralimbic regions (PFC/OFC). The obese group showed significantly greater activation to food pictures in the PFC (pre-meal) and OFC (post-meal) than the HW group. In addition, the obese group showed less post-meal reduction of activation (vs pre-meal) in the PFC, limbic and the reward-processing regions, including the nucleus accumbens. Conclusion: Limbic and paralimbic activation in high food motivation states was noted in both groups of participants. However, obese children were hyper-responsive to food stimuli as compared with HW children. In addition, unlike HW children, brain activations in response to food stimuli in obese children failed to diminish significantly after eating. This study provides initial evidence that obesity, even among children, is associated with abnormalities in neural networks involved in food motivation, and that the origins of neural circuitry dysfunction associated with obesity may begin early in life.

Self-injurious behavior (SIB) is maintained by automatic reinforcement in roughly 25% of cases. Automatically reinforced SIB typically has been considered a single functional category, and is less understood than socially reinforced SIB. Subtyping automatically reinforced SIB into functional categories has the potential to guide the development of more targeted interventions and increase our understanding of its biological underpinnings. The current study involved an analysis of 39 individuals with automatically reinforced SIB and a comparison group of 13 individuals with socially reinforced SIB. Automatically reinforced SIB was categorized into 3 subtypes based on patterns of responding in the functional analysis and the presence of self-restraint. These response features were selected as the basis for subtyping on the premise that they could reflect functional properties of SIB unique to each subtype. Analysis of treatment data revealed important differences across subtypes and provides preliminary support to warrant additional research on this proposed subtyping model.