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Understanding and Treating Self-Injurious Behavior

Few things are more puzzling and disturbing to parents and caregivers than self-injurious behaviors (SIB) exhibited by individuals with autism. SIB is a deliberate harm to one’s own body that may result in tissue damage, such as open cuts and bruises, and that may lead to inflammation and infection. It is often associated with intellectual and developmental disabilities (IDD), including autism, and can be exacerbated by co-existing psychiatric disorders such as mood disorders. The most common types of SIB are excessive scratching, head banging, and biting of the extremities, especially the wrist.

Individuals with autism spectrum disorders (ASD) often struggle with communication, social interactions, repetitive behaviors and inflexible daily routines. SIB is not part of these core symptoms, but can derive from deficits and excesses in these three domains. It is often a chief concern of caregivers.

Currently, two major causal theories of SIB exist in the scientific literature: environmental and biological. Because of the overlap between the two, a combination of these two models is more plausible. The environmental, or operant model, proposes that SIB is learned and maintained by environmental consequences, such as positive or negative reinforcement. The biological model proposes that SIB is a neuropathology resulting from interactions of neurotransmitter systems. SIB may also occur as a way to minimize physical pain resulting from other medical conditions.


Applied Behavior Analysis: After more than 40 years of research, applied behavior analysis (ABA) has demonstrated its profound effect on individuals with autism (Matson, 2008; Eikeseth, 2008). It is a branch of psychology which focuses on the science of behavior and uses a systematic approach to assessing and intervening (Baer et al., 1968). ABA observes what happens before (antecedents) and after (consequences) the behavior and, using a functional behavior analysis (FBA), determines the environmental factors that may be encouraging or maintaining the SIB. Essentially, SIB is seen as a nonverbal request for a preferred outcome.

In order of increasing complexity, the three types of FBA are indirect, descriptive, and experimental. Indirect FBA involves interviewing caregivers about the situations and settings in which SIB occurs using questionnaires and rating scales. This type of analysis is considered a first step in FBA.

Descriptive FBA involves observing the frequency of SIB in the natural environment (e.g., home, school) and recording what happens before and after the SIB. Indirect and descriptive FBA do not involve environmental manipulations. They seek to identify patterns and correlations rather than discover clear cause-and-effect relationships. If FBA identifies obvious conditions maintaining the SIB, an intervention plan involving one or more strategies may be devised.

However, in cases where it is unclear why an individual engages in SIB despite caregiver interview and direct observation in the natural setting, experimental FBA may be necessary. Experimental FBA exposes the individual to situations which vary the presence and absence of attention, preferred leisure materials, and tasks (work). The frequency of SIB is then compared across these situations to delineate the reasons for the behavior. The changes in frequency or intensity of SIB under the different situations often explain why the behavior is occurring and facilitate a treatment plan. During treatment, the behavior analyst attempts to teach the individual a more appropriate way to produce the desired consequence (attention, materials, escape, and so forth).

Common Treatment Modalities: Engaging in SIB often results in an individual receiving desired consequences such as social attention and interaction, leisure materials, food, avoidance of non-preferred activity or work requests, or a caregiver’s compliance with a previously denied request. To minimize the occurrence of SIB in these situations, minimal attention should be given to SIB. This includes giving no direct eye contact, reprimands, or verbal reasoning and assurance. Attempts to redirect the behavior may inadvertently increase SIB if the SIB is maintained by social attention. Instead, social interactions should be given in the absence of SIB. That is, positive interaction should occur when the individual engages in any other behavior. Ignoring SIB may initially increase the SIB, but will ultimately decrease the likelihood that the individual will engage in SIB to gain attention. Another way to minimize SIB in such cases is to make available more leisure items, attention, or opportunities for other preferences so that the individual does not need to engage in SIB to acquire them.

Redirection to another activity and time-out may also worsen the situation if the desired consequence of the SIB is to avoid a particular task. To minimize escape-maintained SIB, task difficulty can be altered, breaks from the task can be given more often, or the individual can be taught to ask for help or a break.

Teaching alternative ways to communicate is one of the most effective methods for decreasing SIB and maintaining treatment gains (Durand & Carr, 1985) if the reason for the SIB can be identified. However, functional communication training must allow the individual to reach the same desired outcome as the SIB. The mode of functional communication must fit the communication needs and abilities of the individual (e.g., pictures, micro-switches, hand signs), and the functional communication program must be incorporated into all aspects of the individual’s daily activities. Over time, the individual learns that functional communication is a much easier and efficient way to get what he or she wants.

When the reason for SIB cannot be identified, the SIB is often said to be maintained by automatic or sensory reinforcement via the “pleasurable” sensations it creates. Providing equivalent, alternate sensory stimulation (such as a massage) or blocking the sensory stimulation (with protective devices) to undo the reinforcing properties of the SIB may be effective. In many cases, drug therapy is considered.

Although the Federal Drug Administration (FDA, 2006) has recently approved Risperdal for treatment of irritability associated with autism (i.e., tantrums, aggression, and SIB), there is no single, well-established medication for treatment of SIB. Rather, pharmacotherapy of SIB often involves the use of medications developed for other psychiatric disorders in a trial-and-error fashion (called ‘off-label’ use). Because there is no existing practice guideline or a simple litmus test to indicate which medication will work best for whom, identifying the right medication for each individual relies heavily on the treating clinician’s expertise and clinical experience.

Current research findings point to the interactions of multiple neurotransmitter systems associated with SIB. Among these, medications acting on the dopamine, opiate, and serotonin systems have been studied most extensively.

Dopamine: Dopamine is a major regulator of motor behavior, emotions, and reinforcement systems. Dopaminergic treatment of SIB is primarily based on the effects of medications that either increase (agonists, such as stimulants) or decrease (antagonists, such as antipsychotics) dopamine functioning. Stimulant medications (e.g., Ritalin) developed for attention-deficit hyperactivity disorder (ADHD) have been effective in reducing SIB in a small number of individuals.

Antipsychotic medications used for treating schizophrenia are the most widely studied drugs in autism. Early attempts with thioridazine and haloperidol indicated that they nonselectively targeted all behaviors, including SIB, mainly through sedation. Such global behavioral suppression, however, was also accompanied by unacceptable levels of involuntary repetitive movement (extrapyramidal symptoms or EPS) in a significant number of individuals. Newer antipsychotic drugs (including Risperdal) are more selective for treating SIB with fewer side effects (RUPP, 2002; 2005; Zarcone et al., 2001). Ironically, there is no convincing evidence of primary involvement of the dopamine system in autism.

Opioids: The opiate system is a mysterious part of the brain which is best known for mediating pain. The opiate model contends that individuals engaging in SIB have unusually high tolerance for pain (hyper-analgesia) due to elevated levels of endogenous opiates (Sandman & Touchette, 2002). In fact, researchers have found that 80% of SIB occurred on only 5% of the body area, and during SIB, those same areas produced pain relief (not pain) and led to an increase in endogenous opioids (Symon & Thompson, 1997). Consequently, SIB produces a feeling of euphoria that requires successively higher amounts to attain the same level of sensation. Tolerance is built with repeated opiate self-administration, followed by increased physical dependence, and compulsive, euphoria-seeking SIB.

In this situation, attempts to prevent SIB by eliminating the sensory stimulation it causes may not be successful as the individual will seek to avoid the adverse withdrawal symptoms by engaging in SIB. While studies report improvements with naltrexone in a small number of individuals with autism, several clinical trials so far indicate mixed results (Campbell et al., 1993; Willemsen-Swinkels et al., 1995; 1996).

Serotonin: Serotonin is a major regulator of mood, sleep, and appetite. The logic of using selective serotonin reuptake inhibitors (SSRIs) is based on the similarity of repetitive SIB to obsessive compulsive behaviors and symptoms of affective mood disorders, both of which are successfully treated with SSRIs (Aman et al., 1999). Moreover, many years of research indicate elevated levels of serotonin in the bloodstream of individuals with autism (Schain & Freedman, 1961), providing further support for SSRIs to potentially reverse some of the symptoms of serotonin dysregulation in autism. Still, controlled clinical trials show mixed results (Remington et al., 2001; Niederhofer et al., 2003).


Dynamic interactions between and within environmental and biological mechanisms make SIB complex and difficult to understand and treat. While there is no single medication or behavioral procedure that eliminates SIB, research so far has shown that ABA and newer antipsychotic medications such as Risperdal may alleviate this debilitating condition in some people with autism. Much of the research examining the effects of medications is based on small open trials and anecdotal reports. The limited efficacy reported with each class of medication strongly indicates the interaction of multiple neurotransmitter systems. This interaction is further complicated by environmental consequences that contribute to SIB. Thus, the origin of a particular individual’s SIB and the variables maintaining it may largely depend on that individual’s environmental and biological histories. More systematic, empirical data on the basic neurological mechanisms of SIB and analysis of biological and behavioral interactions are needed to fully conquer SIB and its impact on peoples’ lives.

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