Current Medical Diagnosis & Treatment in Psychiatry

Combined Interventions in Developmental Disabilities

Behavioral interventions can be highly effective in improving the quality of life for people who have developmental disabilities and display serious behavior problems. Sometimes behavioral methods are insufficient by themselves. Psychopharmacologic treatments can control psychopathologic symptoms and behavior in some people with mental retardation and related disabilities, much as they are effective in treating disorders (eg, major depression, bipolar disorder, anxiety disorder, schizophrenia) in non–developmentally delayed individuals.

In attempting to better understand how psychotropic drugs reduce problem behavior, it is helpful to elucidate the behavioral as well as neurochemical mechanisms of drug action. Behavioral mechanisms refer to psychological or behavioral processes altered by a drug. Neurochemical mechanisms refer to the underlying receptor-level events that are causally related to those changed behavioral processes. Some psychopathologic problems are associated so frequently with specific developmental disabilities that pharmacotherapy is often among the first treatments to be explored. Anxiety disorder, especially OCD, is commonly associated with autism and Prader-Willi syndrome. Anxiety disorder manifests itself as ritualistic, repetitive stereotypic motor responses (eg, rocking or hand-flapping) and rigidly routinized activities (eg, repeatedly lining up blocks, insisting that shoe laces be precisely the same length) that, if interrupted, provoke behavioral outbursts or tantrums. Selective serotonin reuptake inhibitors help reduce agitation, anxiety, and ritualistic behavior, including skin-picking and some self-injurious behavior associated with these problems. At times, aggression may result from an anxiety disorder. For example, a patient with autism who has severe anxiety may strike out against others who are crowding too closely, in order to keep them at a distance. Fluvoxamine reduces anxiety and the need for increased social distance, thereby diminishing the need to strike out against others to keep them at a distance. Aggression, in this example, serves as a social avoidance response that the fluvoxamine makes unnecessary. The behavioral mechanism of action is reduced anxiety and associated avoidance. The neurochemical mechanism is thought to be mediated by inhibition of serotonin reuptake with increased binding to the serotonin-2 receptors.

An individual with autism or mental retardation who strikes his or her head in intermittent bouts throughout the day may do so because head blows cause the release of ß-endorphin, which binds to the-opiate receptor, thereby reinforcing self-injury. In this way, a self-addictive, vicious cycle is established and maintained and through years of repetition becomes a firmly entrenched behavioral pattern. Administration of an opiate antagonist, such as naltrexone, blocks the reinforcing effects consequent to the binding of ß-endorphin to the opiate receptor. Naltrexone reduces such self-injurious behavior in approximately 40% of patients, primarily in those engaging in high-frequency, intense self-injury directed at the head and hands. Evidence indicates that elevated baseline levels of plasma ß-endorphin after bouts of self-injury are predictive of a subsequent therapeutic response to naltrexone.

Repetitive self-injurious behavior, such as head banging and self-biting, can be treated effectively with complementary behavioral and pharmacologic strategies, as described in the following case example.

A 13-year-old boy with autism and severe mental retardation was nonverbal and had no communication system at baseline. An observational functional assessment of the boy’s self-injurious behavior in his natural environment (a special education classroom) indicated that approximately two thirds of this behavior appeared to be motivated by the desire to obtain attention or to escape from situations he didn’t like or found disturbing. Self-injury dropped 50% from baseline during the first naltrexone treatment phase. Next the patient was taught to use pictorial icons to make requests and to indicate basic needs and wants to others around him (Figure 2-1). His selfinjury dropped subsequently by another 50% (a reduction of a total of 75% from baseline) when communication treatment was initiated. On follow-up 1 year later, during which time naltrexone treatment was continued, the boy’s self-injurious behavior had continued to drop to nearly zero. In this case, naltrexone blocked the neurochemical reinforcing consequences of self-injury, and the communication training provided an appropriate behavioral alternative to indicate basic needs and wants. In short, the combined treatments produced complementary, additive salutary effects.

Figure 2–1
Efficacy of treatments for self-injurious behavior. Nal, naltrexone.

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