This page is dedicated to sharing information on Autism Spectrum Disorder, ASD. The material is taken from the book “Abnormal Psychology” and is presented here in an unedited form. ADDspeaker do not have the rights to this material, and we encourage you to purchase the book for yourself, if you are benefitting from the knowledge presented here.

NOTE: ADDspeaker do not agree with the book’s author on three areas:

  1. Definition of ASD (DSM-5 vs. ICD-11)
  2. Applied Behavioral Analysis (ABA)
  3. Medication for ASD do not (officially) exist, as correctly stated in the book.

Please read our comments at the end of this article for more on this discrepancy. The rest of this article is taken from the book “Abnormal Psychology” by Ronald J. Comer and ADDspeaker do not have any rights to this text. Please be advised to contact the copyright owner for approval for use of the material presented here.



Autism spectrum disorder (ASD) begins early in life and involves impairments in social interaction, social communication, and restricted, repetitive behaviors. ASD is a new term that evolved prior to DSM-5 (Lord & Bailey, 2002). Several disorders once viewed as distinct are now seen as falling on a continuum (a spectrum).

The most important of these “separate” disorders are autism (where children often cannot communicate and typically have intellectual disabilities) versus Asperger’s disorder (where intelligence and communication are in the normal range).

Even though DSM-5 changed the language, we occasionally refer to “classic autism” and “Asperger’s disorder” to help you understand past research (which typically studied the problems separately) and changing concepts.

Terminology is not terribly important, but the underlying question is:

Does ASD refer to variations on the same disorder, or has DSM-5 mistakenly given the same name to different problems?

One thing is not in question. ASD is defined far more broadly in DSM-5 (2013) than classic autism was defined in DSM-IV (1994). As a result, the symptoms of ASD include far less serious impairments, the prognosis is brighter, comorbid problems like intellectual disabilities are less frequent, and prevalence estimates are far higher.

We pay careful attention to changing definitions, and you should too. Many people think that ASD itself has changed, but mostly what has changed is the definition of ASD. The dictionary definition of autism, “absorption in one’s own mental activity,” grossly understates the disorder’s potentially severe social disturbances.

The classic autism – the severe end of the ASD spectrum – is characterized by profound indifference to social relationships, odd, stereotypical behaviors, and severely impaired or nonexistent communication.

Even those adults who achieve exceptionally good outcomes show severely disturbed social emotions and social understanding.

Consider the remarkable case of Temple Grandin, a woman who achieved what may be the most successful outcome of classic autism on record.


Judging from physical appearance alone, you would not expect children with ASD to have a serious psychological impairment. Motor milestones may be reached late, and movement may appear awkward or rather uncoordinated (Prior & Ozonoff, 2007). But most children are normal in physical appearance, and physi- cal growth is generally normal.


The normal physical appearance is one reason why ASD, which begins early in life, may go unrecognized. In retrospect, parents may recall abnormalities that seem to date to birth.

For example, a parent may remember that her ASD child was easy as a baby – too easy, perhaps uninterested in attention, cuddling, and stimulation. In 20 percent to 40 percent of cases of severe ASD, the baby develops normally for a time but either stops learning new skills or loses the skills acquired earlier (Volkmar, Chawarska, & Klin, 2005).

The National Institute of Mental Health hopes to improve the early identification of ASD, and researchers are working to identify early warning signs (Volkmar et al., 2005). One clever study used videotapes of one-year-olds’ birthday parties in this effort.

Normal children were compared with those later diagnosed with classic autism or with an intellectual disability. Infants with classic autism looked at others and oriented to their names less often than infants with an intellectual disability.

Both groups used fewer gestures, looked less at objects held by others, and engaged in more repetitive motor movements than normally developing babies (Osterling, Dawson, & Munson, 2002).

Findings like this cannot yet be used for early identification, but scientists are searching for more definitive markers (Lord et al., 2012). Problems in social communication skills are one promising focus (Ingersoll, 2011).


ASDs are characterized by a range of persistent deficits in social communication and social interaction – a very wide range of deficits.

Social communication problems include normal language accompanied by odd “body language” at one extreme to a total absence of verbal and nonverbal communication at the other.

Many children with classic autism fail to develop normal speech. Some learn a few words and then suddenly lose their language abilities. About half are mute (Volkmar et al., 1994). Children with ASD who do acquire language often speak oddly.

One example is dysprosody, subtle disruptions in the rate, rhythm, and intonation of speech. Another is echolalia, uttering phrases back, perhaps repeatedly. When the mother of a 11⁄2-year-old points to herself and says, “Who is this?” normal toddlers respond with “Mama.”

A 10-year-old child with classic autism and echolalia responds to the same question by repeating, “Who is this?” Even high-functioning people with ASD have trouble communicating or understanding abstractions.

Here is how Temple Grandin describes her struggles:

Autistics have problems learning things that cannot be thought about in pictures. The easiest words for an autistic child to learn are nouns, because they are directly related to pictures. . . . Spatial words such as “over” and “under” had no meaning for me until I had a visual image to fix them in my memory. Even now, when I hear the word “under” by itself, I automatically picture myself getting under the cafeteria tables at school during an air-raid drill, a common occurrence on the East Coast during the early fifties. When I read, I translate written words into color movies or I simply store a photo of the written page to be read later. When I retrieve material, I see a photocopy of the page in my imagination. I can then read it like a Teleprompter. . . . When I am unable to convert text to pictures, it is usually because the text has no concrete meaning. Some philosophy books and articles about the cattle futures market are simply incomprehensible. (pp. 29–31)

Problems with social communication spill over into many social interactions. Social impairments range from relatively mild problems with social or emotional reciprocity, for example, struggling with back and forth conversation, to extreme difficulties. Some children and adults with severe ASD have no interest in relationships. They treat other people as if they were confusing, foreign objects.


Some have suggested that ASD is characterized by the absence of a theory of mind – a failure to appreciate that other people have a different point of reference (Baron-Cohen, Tager-Flusberg, & Cohen, 1993).

Theory of mind is illustrated by the “Sally–Ann task” (see Figure 15.5). The child is shown two dolls, Sally, who has a basket, and Ann, who has a box. Sally puts a marble in her basket and then leaves. While Sally is gone, Ann takes the marble out of Sally’s basket and puts it into her own box. When Sally returns, the question is: Where will she look for her marble? Sally should look for the marble in her basket, where she left it, because she did not see Ann hide it. However, children with severe ASD often fail to appreciate Sally’s perspective – they lack a theory of mind.

In one early study, 80 percent of children with severe ASD said Sally would search in Ann’s box, whereas only 14 percent of children with Down syndrome made the same error (Baron-Cohen, Leslie, & Frith, 1985).

Theory of mind is not a “core” deficit in ASD, however. Many higher functioning children with ASD do have a theory of mind, while many with intellectual disabilities do not (Prior & Ozonoff, 2007; Tager-Flusberg, 2007).

Figure 15.5

Where will Sally (on left) look for the marble? Many children with autism answer “in the box,” evidence that they may lack a “theory of mind.” Source: Frith, U. 1989. Autism: Explaining the Enigma. Blackwell Publishing, Ltd.

ADDspeaker: The BBC have made an excellent documentary on Autism, which features Prof. Uta Frith, and we highly recommend it to anyone trying to understand Autism in more detail. Find it on iPlayer here


The social interaction deficits in ASD are emotional, not just cognitive (Losh & Capps, 2006). In fact, some children with severe ASD appear to be missing the basic motivation to form attachments. As infants, they do not seek out attachment figures in times of distress, nor are they comforted by physical contact.

As children, they show little interest in their peers, failing to engage in social play or to develop friendships. Throughout life, they avoid others in small but significant ways, for example, through gaze aversion, actively avoiding eye contact.


Another defining symptom of ASD is restricted, repetitive patterns of behavior, interests, or activities. Again, the DSM-5 provides a wide range of possible symptoms.

A high functioning adult with ASD may be unusually fascinated with some activity, perhaps collecting and endlessly reviewing baseball cards, but hide or no longer engage in the behavior. Children with severe ASD may literally spend most of their day flapping a string in front of their eyes.

Behaviors like string flapping seem to serve no other function than self-stimulation. One interpretation is that the child receives too little sensory input, and self-stimulation increases sensation to a more desirable level. We prefer an alternative interpretation.

Self-stimulation reduces sensory input by making stimulation monotonously predictable. Stereotyped behavior in ASD may help to make a terrifying world more constant and predictable.

Temple Grandin’s (1996) observations seem consistent with our view:

When left alone, I would often space out and become hypnotized. I could sit for hours on the beach watching sand drib- bling through my fingers. I’d study each individual grain of sand as it flowed between my fingers. Each grain was different, and I was like a scientist studying the grains under a microscope. As I scrutinized their shapes and contours, I went into a trance which cut me off from the sights and sounds around me. Rocking and spinning were other ways to shut out the world when I became overloaded with too much noise. Rocking made me feel calm. It was like taking an addictive drug. The more I did it, the more I wanted to do it. My mother and my teachers would stop me so I would get back in touch with the rest of the world. (pp. 44–45)


Although not required for the diagnosis, many people with ASD respond to sound, touch, sight, or smell in unusual ways. At the mild end, a child may find certain clothing intolerable, even painful, for example, wearing a leotard. At the severe end, a patient may respond as if he were deaf, even though his hearing is intact, an apparent sensory deficit (Lovaas et al., 1971).

The sensory deficit is “apparent,” because the sense organ is not impaired even though the response suggests otherwise. Even more puzzling, the “deaf” patient may scream in pain in reaction to a much quieter sound like the scratch of chalk on a blackboard. This suggests that the problem lies at some higher level of perception (Prior & Ozonoff, 2007).

Temple Grandin, who called this “sensory jumbling,” believes that this symptom is an understudied aspect of autism:

When I was little, loud noises were also a problem, often feeling like a dentist’s drill hitting a nerve. They actually caused pain. I was scared to death of balloons popping, because the sound was like an explosion in my ear. Minor noises that most people can tune out drove me to distraction. When I was in college, my roommate’s hair dryer sounded like a jet plane taking off. (p. 67)


Self-injurious behavior is one of the most bizarre and dangerous difficulties that can accompany severe ASD. The most common forms are repeated head banging and biting the fingers and wrists (Rutter, Greenfield, & Lockyer, 1967).

Injuries may involve minor bruises, or they can be severe – broken bones, brain damage, and even death. Self-injury is not suicidal behavior. The child with severe ASD does not have enough self-awareness to be truly suicidal. Fortunately, self-injury can be treated effectively with behavior therapy, using techniques we discuss shortly.


A fascinating ability sometimes associated with ASD is the rare child who shows savant performance – an exceptional ability in a highly specialized area of functioning. Savant performance typically involves artistic, musical, or mathematical skills. No one has an adequate theory, let alone an explanation, for savant performance.

Unfortunately, one thing does seem clear: The existence of savant performance does not indicate that, as many have hoped, children with classic autism really are normal or even superior in intelligence.

Most people with severe ASD do not show savant performance, and most have an intellectual disability (Fombonne, 2007). Past research showed that about a quarter of children with classic autism have IQs below 55, about half have IQs between 55 and 70, and only one-fourth have IQs over 70 (Volkmar et al., 1994; see Table 15.4). And for the most part, IQ scores are stable over time (Prior & Ozonoff, 2007).

Average IQs are higher in more recent samples — perhaps 50 percent fall below 70. However, this is primarily a result of broader definitions of ASD, a diagnosis that now includes less severely disturbed children. On a more optimistic note, some children are being diagnosed sooner and treated more successfully, so some of the IQ increase may be real (Chakrabarti & Fombonne, 2001; Volkmar & Lord, 2007).


Two psychiatrists independently described ASD at almost the same point in history. Importantly, however, they viewed the problem differently.

In 1943, psychiatrist Leo Kanner (1894–1981) of Johns Hopkins University identified a small group of severely disturbed young children with an inability to form relationships, delayed or noncommunicative speech, a demand for sameness in the environment, stereotyped activities, and lack of imagination. Kanner (1943) called the problem “early infantile autism.” Kanner’s patients suffered from what we have called classic autism in this chapter.

At about the same time, Viennese psychiatrist Hans Asperger (1906–1980) described children with similar social problems and stereotyped behavior. But Asperger’s (1944) patients had normal intellectual functioning and good communication skills. Asperger’s work received little attention until late in the twentieth century when his papers were translated into English. In 1994, Asperger’s disorder was listed in the DSM for the first time.

In the decade that followed, practitioners began to use broader and broader definitions of Asperger’s disorder. At first, links between the new diagnosis and classic autism seemed clear, and the idea of an autism spectrum (ASD) was born. Over time, however, the Asperger’s diagnosis began to be given to any child or adult with odd social interactions and highly focused interests. Web sites blossomed, and Albert Einstein, Thomas Jefferson, Sir Isaac Newton, and many others were posthumously diagnosed with Asperger’s disorder!

Experts became concerned about overdiagnosis, particularly about a false “epidemic of autism.” As we discuss further on, increased estimates of the prevalence of ASD reflect inflation of the diagnosis much more than a real increase in the disorder.

Vehement debates about how to define ASD in DSM-5 focused on the benefits versus the costs of containing diagnostic inflation (Huerta et al., 2012; McPartland et al., 2012; Skuse, 2012; Swedo et al., 2012; Tsai, 2012). Should ASD be defined more narrowly and perhaps more accurately? What would happen to people who no longer qualified for the Asperger’s disorder diagnosis? Would they be denied services?

In one of its most controversial changes, DSM-5 embraced the idea of an autism spectrum and of a broad definition of the disorder. Read through the diagnostic criteria in “DSM-5: Autism Spectrum Disorder.”

The impairments sound severe, and they often are tragic. But also note the least severe symptoms that meet diagnostic criteria. If these symptoms fall along a continuum, it is a very long line (see Thinking Critically About DSM-5).


For decades, classic autism was viewed as a very rare disorder, occurring in perhaps 4 of 10,000 children (Lotter, 1966). However, the diagnosis of ASD exploded after the introduction of Asperger’s disorder. The U.S. Centers for Disease Control and Prevention (CDC) now estimates that perhaps 200 in 10,000 children suffer from ASD (Blumberg et al., 2013). This startling 50-fold increase has created an uproar.

Many parents and some professionals believe that environmental factors, such as pollution or vaccines, caused an “epidemic of autism.”

The dramatic increase in the number of cases has been carefully and repeatedly documented (Barbaresi et al., 2005; Baron-Cohen et al., 2009; Fombonne, 2007; Kogan et al., 2009; Newschaffer, Falb, & Gurney, 2005).

In fact, the CDC reported an increase of 400 percent in the prevalence of ASD between 1998 and 2007, and another increase of another 300 percent by 2012 (Blumberg et al., 2013) (see Figure 15.6).

In the minds of many parents, the measles/mumps/rubella (MMR) vaccination, which used to contain thimerosal, a mercury-based organic compound, explains the upsurge in ASD.

Despite the fear, even hysteria, that vaccines cause autism, no scientific evidence links MMR to ASD (Offit, 2010; see Critical Thinking Matters in Chapter 2).

Similarly, no evidence ties environmental pollutants with the upsurge in ASD (Rutter, 2005; Wing & Potter, 2002). Of course, many popular media and Internet sites make claims that are not exactly based on science. Nevertheless, the “epidemic of autism” appears to be more of a reason for celebration than paranoia.

Leading experts agree that the increasing prevalence estimates are most likely due to increased awareness and broadened diagnostic criteria (Barbaresi et al., 2005; Charman, 2002; Miles, 2011; Newschaffer et al., 2005; Rutter, 2005; Wing & Potter, 2002).

One piece of evidence in support of this interpretation is the declining percentage of children diagnosed with ASD who have comorbid intellectual disabilities. The diagnosis is now being applied to less severely disturbed children (Blumberg et al., 2013).


We need to tackle another myth about the epidemiology of ASD. Parents of children with ASD were once thought to be especially intelligent, a finding that contributed to the mistaken view that children with ASD have superior intelligence. Researchers did repeatedly find that children treated for ASD had especially well-educated parents.

However, this is because well-educated parents are vigorous in seeking specialized treatment for their troubled children, so the parents of children treated for ASD are more educated than the average parent. In other words, a biased sample created a false correlation (Gillberg & Schaumann, 1982). In the general population, ASD is unrelated to parental education (Schopler, Andrews, & Strupp, 1979).

Two legitimate findings about the prevalence of ASD have inspired research on possible causes. Four times as many boys as girls suffer from ASD, suggesting a gender-linked etiology, as in fragile-X syndrome. ASD also is much more common among siblings of a child with ASD (Ozonoff et al., 2011), suggesting possible genetic causes.


Before discussing evidence on biological contributions to ASD, we first briefly consider – and reject – environmental explanations.


For many years, parents were blamed for causing ASD in their children. Psychoanalytic speculations said that ASD results from the infant’s defense against maternal hostility (Bettelheim, 1967).

Behaviorists viewed the disorder as caused by inappropriate parental reinforcement (Ferster, 1961). Both views blamed parents as cold, distant, and subtly rejecting of their children.

In fact, in 1960, Time Magazine published an account of these “refrigerator parents.” The article stated that the parents of children with autism “just happened to defrost long enough to produce a child” (Schreibman, 1988). Such harmful assertions are simply wrong.

Researchers have found no differences in the child-rearing styles of the parents of children with ASD when compared with those of the parents of normal children (Cantwell, Baker, & Rutter, 1979). And even if differences existed, common sense would force us to challenge the “refrigerator parent” interpretation.

How could a parent’s emotional distance create such an extreme disturbance so early in life? Even heinous abuse does not cause symptoms that approach the form or severity of the problems found in ASD. Moreover, if parents are emotionally distant, could this be a reaction to the child’s social disturbance? If an infant shows no normal interest in cuddling or mimicking, is it surprising if a parent grows a bit distant?

Speculation about poor parenting – or vaccines – can never be completely disproved. However, logic and mounting research on biological causes make it unfathomable to think that ASD has a psychological cause.

And as we hope you have come to understand, the rules of science require you to prove your hypothesis. Until a proven true, the community of scientists assumes a hypothesis is false.

Claims about “refrigerator parents” offer sad testament to the wisdom of this scientific principle.


In terms of its cause, ASD does not appear to be one disorder. Like intellectual disabilities, ASD includes several problems that look similar but actually have different biological causes. Known causes include fragile-X syndrome, Rett’s disorder, and a handful of other known causes of intellectual disability. Other suspected causes include genetics and brain abnormalities.


Genetic factors are widely thought to play an important role in ASD. The prevalence of ASD is much greater among siblings of a child with ASD, and several studies have found higher concordance among MZ than DZ twins (Smalley et al., 1988; Smalley & Collins, 1996; Steffenburg et al., 1989).

In the largest study to date, concordance rates were 60 percent for MZ twins and 0 percent for DZ twins (Bailey et al., 1995). For a broader spectrum of disturbances, the rates were 92 percent for MZ and 10 percent for DZ twins in the same study.

These results suggest that ASD is strongly genetic, but there is a puzzle. The DZ rates are too low. Recall that, in dominant genetic transmission, rates are 100 percent MZ and 50 percent DZ. The anomaly might be explained if ASD is caused by a combination of different genes or perhaps by a spontaneous genetic mutation (Gottesman & Hanson, 2004).

Recent research identified a “hot spot” on chromosome 16 (16p.11.2) that is linked with perhaps 1 percent of cases (Weiss et al., 2008). And one analysis suggested that, if all causes are included (such as fragile-X, Rett’s, and 16p.11.2), as many as 25 percent of cases of ASD can be attributed to various genetic causes (Miles, 2011).

Finally, three different research groups recently reported associations between ASD and spontaneous genetic mutations (Neale et al., 2012; Roak et al., 2012; Sanders et al., 2012).


Different causes could lead to similar abnormalities in brain development, structure, or function, thus producing similar symptoms. Some evidence indicates that the brains of children with ASD are larger than average. The problem seems to be developmental.

Brain growth appears to be unusually rapid in children with ASD, at least until the age of two or three. Then brain growth is arrested, so that cerebral and cerebellar brain volume are smaller than normal at later ages (Courchesne et al., 2001).

Still, no obvious brain abnormalities have been identified in ASD. Early theorizing about potential brain damage focused on the left cerebral hemisphere, where language is controlled.

However, the communication deficits in ASD are more basic, and current thinking focuses more on subcortical brain structures involved in emotion, perception, and social interaction (Waterhouse, Fein, & Modahl, 1996; Wing, 1988).

Two likely sites are the cerebellum, where sensorimotor input is integrated, and the limbic system, the area of the brain that regulates emotions (Bauman, 1996; Courchesne et al., 2001; Schreibman, 1988; Waterhouse et al., 1996).

Within the limbic system, the amygdalae are a particular focus, and recent evidence indicates that these structures follow the pattern of early rapid then slowed development (Mosconi et al., 2009).

The frontal lobe, the site of executive functioning, also may be involved (Moldin, 2003).

Recent theorizing also points to the functioning of mirror neurons, neurons that fire both when an individual performs an action and when the individual observes another performing the same action.

Mirror neurons were first identified in the 1990s and are known to be involved in many normal abilities that are impaired in ASD including imitation, understanding others’ intentions, empathy, and language learning. Research on ASD and the mirror neuron system is in its infancy, but it is exciting because of its potential relevance to several key symptoms (Oberman & Ramachandran, 2007).

The most promising research on neurotransmitters and ASD focuses on endorphins and neuropeptides (Polleux & Lauder, 2004). Endorphins are internally produced opioids that have effects similar to externally administered opiate drugs like morphine.

One theory suggested that ASD is caused by excess endorphins. According to this speculation, people with ASD are like addicts high on heroin. They lack interest in others, because their excessive internal rewards reduce the value of the external rewards offered by relationships (Panksepp & Sahley, 1987).

More recent theorizing has expanded to include various neuropeptides, substances that affect the action of neurotransmitters. Oxytocin and vasopressin, which affect attachment and social affiliation in animals, are two neuropetides that are the subject of active investigation (Waterhouse et al., 1996).

ASD is widely viewed as a brain disorder, but to date, it has defied explanation in terms of specific abnormalities.


Controversy exists about the degree to which treatment can help children with ASD. Some researchers are optimistic about new treatments, whereas others are skeptical, especially because a large number of dubious treatments have been promoted (see Critical Thinking Matters).

Everyone acknowledges, however, that there is no cure for ASD. Thus, the effectiveness of treatment must be compared against the unhappy course and outcome of the disorder.


Unfortunately, classic autism is a lifelong disorder. A recent review of 16 follow-up studies concluded that only about 20 percent achieve a “good” outcome, defined as living a somewhat normal and independent life. The outcome is “poor” for 50 percent, who require substantial supervision and support.

A major change in more recent years is that more children and adults with classic autism are cared for in their homes or communities instead of institutions (Howlin, 2007). More recent studies also find somewhat better outcomes, but this may be a result of including higher functioning individuals, not necessarily because of improved care.

Asperger’s disorder is generally thought to have a much more optimistic prognosis (Gillberg, 1991), but this has not yet been shown empirically (Howlin, 2007).

A more positive prognosis for classic autism is predicted by language skills at the age of five or six (Yirmiya & Sigman, 1996 and higher IQ (Schreibman, 1988). Recent research also shows that joint attention, coordinating attention with another person through gestures, social responding, or social initiation, predicts language development from preschool age to age nine (Anderson et al., 2007). Importantly, a quarter or more of young people with classic autism develop seizure disorders as teenagers (Wing, 1988). In adult life, affective disorders are common (Howlin, 2007).

Statistics offer a sobering view of ASD. Can treatment help?


A huge variety of medications have been tried for classic autism, ranging from antipsychotics to opiate agonists. Unfortunately, no medication is very effective, although temporary claims of success have fueled false hope more than once.

A cautionary tale can be told about secretin, a “breakthrough” medication in the late 1990s. Secretin is a hormone involved in digestion. It is sometimes used to test for gastrointestinal problems, which are common in classic autism. Widespread interest in the drug was sparked by three case studies of children who reportedly showed remarkable improvement in language and social behavior while taking secretin for a routine gastrointestinal workup (Horvath et al., 1998).

Rumors spread on the Internet, and thousands of desperate parents across the country sought secretin for their autistic children. Scientists quickly responded to the intense interest. Unfortunately, the news was not good. A double-blind study using random assignment found no improvement over placebo in 58 autistic children treated with a single dose of secretin (Sandler et al., 1999). Several subsequent studies also showed no benefit (Erickson et al., 2007). As with other “miracle” medications, the effects of secretin are not miraculous.

Even more troubling, desperate parents and at least some physicians have been attempting to treat classic autism with chelation therapy, administering agents that remove heavy metals from the body (presumably the mercury that does not cause ASD). Chelation can be dangerous to children’s health, and the National Institutes of Health recently canceled a proposed study of chelation and ASD because the risks far outweighed any potential benefits (Wall Street Journal, September 18, 2008).

In a similar vein of desperation (and quackery), the Chicago Tribune (November 23, 2009) reported that various potentially dangerous substances are being misused to “treat” ASD by attempting to reduce “inflammation” of the brain, an approach legitimate scientists find frightening.

About the only mention of this treatment in the scientific literature is a warning not to misinterpret research on brain development and try something like this (Pardo & Eberhart, 2007).

Some legitimate medications are known to help with some symptoms of ASD. Certain antipsychotics, particularly risperidone, help in behavior management. Medications used in treating obsessive–compulsive disorder (the SSRIs) may also help with some stereotyped behavior in ASD (Lewis, 1996).

However, no medication can be considered to be an effective treatment (Erickson et al., 2007; Lord & Bailey, 2002).


Intensive behavior modification using operant conditioning techniques called Applied Behavior Analysis (ABA) is the most promising approach to treating classic autism. ABA therapists focus on treating specific symptoms, including communication deficits, lack of self-care skills, and self-stimulatory or self-destructive behavior.

Even within these different symptom areas, behavior modification emphasizes very specific and small goals. In attempting to teach language, for example, the therapist might spend hours, days, or weeks teaching the pronunciation of a specific syllable.

Months of intensive effort may be needed to teach a small number of words and phrases. The lack of imitation among many children with classic autism is one reason why so much effort goes into achieving such modest goals.

If the first goal of ABA is to identify very specific target behav- iors, the second is to gain control over these behaviors through the use of reinforcement and punishment.

Unlike normal children, who are reinforced by social interest and approval, children with classic autism often do not respond to ordinary praise, or they may find all social interaction unpleasant. For these reasons, the child’s successful efforts must be rewarded repeatedly with primary reinforcers such as a favorite food, at least in the beginning phases of treatment.

An example helps to illustrate the level of detail of ABA programs. A common goal in treating echolalia is to teach the child to respond by answering questions rather than repeating them.

As an early step in treatment, a target behavior might be to teach the child to respond to the question “What is your name?” with the correct answer “Joshua.” In order to bring this specific response under the control of the therapist, initially it may be necessary to reward the child for simply echoing. Therapist: “What is your name?” Child: “What is your name?” Reward.

This first step may have to be repeated hundreds of times over the course of several days. A logical next step would be to teach the child to echo both the question and the response. Therapist: “What is your name? Joshua.” Child: “What is your name? Joshua.” Reward.

Again, hundreds of repetitions may be necessary. Gradually, the ABA therapist sets slightly more difficult goals, rewarding only increasingly accurate approximations of the correct response.

One such intermediate step might be to echo the question “What is your name?” in a whisper and repeat the response “Joshua” in a normal tone of voice. Over a period of days, even weeks, the child learns to respond “Joshua” to the question “What is your name?”

Similar detailed strategies are used to teach children other language skills. In the hope of speeding the process, some tried teaching sign language to children with classic autism (Carr, 1982).

Unfortunately, this was not a breakthrough. The communication deficits are more basic than receptive or expressive problems with spoken language.

Children sometimes use instrumental gestures to get what they want, but not expressive gestures to show how they feel (Frith, 2003). ABA remains a painfully slow process that differs greatly from the way in which children normally learn to speak.

The intensity and detail of ABA remind us that normal children come into the world remarkably well equipped to acquire language.

In addition to teaching communication skills, behavior therapists who work with children with ASD concentrate on reducing the excesses of self-stimulation, self-injurious behavior, and general disruptiveness, as well as teaching new skills to eliminate deficits in self-care and social behavior (Schreibman, 1988).

ABA programs have successfully eliminated some behavioral excesses, particularly self-injury, but the treatments are controversial because they typically rely on punishment. A gentle slap or a mild electric shock can reduce or eliminate such potentially dangerous behaviors as head banging, but are such aversive treatments justified?

This question confronts therapists, parents, and others concerned with the treatment and protection of children. Behavior therapists have been fairly successful in teaching self-care skills and less successful in teaching social responsiveness.

The struggle with social skills is unfortunate, because treatment outcomes for children with classic autism are especially positive when social responsiveness improves (Koegel, Koegel, & McNerney, 2001).

As Schreibman (1988) noted, “It is perhaps prophetic that the behavior characteristic which most uniquely defines autism is also the one that has proven the most difficult to understand and treat” (p. 118).

Although ABA focuses on specific target behaviors, ultimately the important question is: To what extent does treatment improve the entire disorder?

Research shows that autistic children can learn specific target behaviors, but do intensive training efforts bring about improvements that are clinically significant?

An optimistic answer to this question was provided by O. Ivar Lovaas (1927–2010), who was a psychologist at UCLA and an acknowledged leader in ABA for classic autism.

In a comprehensive report on the efforts of his research team, Lovaas (1987) compared the outcomes of three groups of children with autism: 19 children who received intensive ABA; 19 children who were referred to the program but who received less intensive treatment due to the unavailability of therapists; and 21 children who were treated elsewhere.

Children with extremely low IQ scores were excluded, and treatment began before the children were four years of age. The children in the treatment group received the types of interventions described above, including both reinforcement and punishment procedures. In fact, they were treated 40 hours a week for more than two years.

No differences among the three groups of children were found before treatment began.

Assessments following treatment were conducted between the ages of six and seven at the time when the children ordinarily would have finished the first grade of school.

In the intensive behavior modification group, nine children (47 percent) completed first grade in a normal school. Eight more children (42 percent) passed first grade in a special class for children who cannot speak.

In comparison, only one child (2 percent) in the two control groups completed first grade in a normal classroom, and 18 children (45 percent) completed first-grade classes for aphasic children.

Table 15.5 summarizes these outcomes, and also the strong relation between IQ and classroom placement. Note the low mean IQ levels of all the children, despite the investigators’ attempts to screen out the most severely impaired children.

These data are reason for considerable optimism. And a follow-up study indicated that many gains continued into late childhood and adolescence (McEachin, Smith, & Lovaas, 1993).

Other research shows significant, but notably smaller, gains with very intensive ABA approaches (Smith, Groen, & Wynn, 2000). Recent research indicates that activities designed to encourage joint attention and social coordination improve language learning in ABA treatments (Kasari et al., 2008), at least when children show prior evidence of joint attention (Yoder & Stone, 2006).

And a new study provocatively suggests that a very small percentage of people with ASD, especially those with higher social functioning, show essentially no symptoms of the disorder after treatment (Fein et al., 2013).

We applaud the efforts of Lovaas and others who have used ABA to teach skills to children with classic autism. Despite the fact that ASD apparently is caused by neurological abnormalities, the most effective treatment for the disorder is highly structured and intensive ABA (Rutter, 1996).

Still, we must raise cautions: Are the children who passed first grade functioning normally in other respects?

Because pretreatment IQ predicted outcome (Lovaas, 1987), does ABA work only with children who are high functioning? But perhaps the most important question about ABA is its cost.

The children in the intensive ABA group were treated for 40 hours per week for more than two years. The children in the “limited treatment” control group received almost 10 hours of weekly treatment, yet they showed few improvements. The expenses associated with early but effective treatment clearly are far less than those involved in a lifetime of care (Lovaas, 1987).

Still, we wonder: How do we justify devoting so many resources to ASD when, in comparison, we neglect intervention with children with intellectual disabilities?


Intellectual disabilities are defined by:

(1) deficits in intellectual functioning,

(2) deficits in adaptive skills, and

(3) an onset before age 18.

People who have IQs below 70 but function adequately in the world are not considered to have an intellectual disability.

IQ tests are reliable and valid (if imperfect) predictors of academic performance.

DSM-5 divides intellectual disability severity into mild, moderate, severe, and profound but no longer bases this on IQ scores.

Down syndrome is caused by an extra chromosome on the 21st pair and is the most common of the known biological causes of intellectual disability.

Fragile-X syndrome is a genetic disorder that often causes intellectual disabilities, especially in boys.

Other known biological causes include phenylketonuria (PKU), an inherited metabolic deficiency; infectious diseases transmitted to the fetus during pregnancy or birth, such as rubella, syphilis, and genital herpes; excessive maternal alcohol consumption or drug use during pregnancy; Rh incompatibility; and malnutrition, premature birth, and low birth weight.

So-called cultural-familial retardation typically involves a mild intellectual disability and no known specific cause. It is assumed to represent normal IQ variation.

A major policy goal is normalization of the lives of people with intellectual disabilities through mainstreaming in public schools and promoting care in the community.

Autism spectrum disorder (ASD) involves disturbances in social relationships and communication, as well as stereotyped activities.

DSM-5 views ASD as a single disorder, and eliminates problems once considered to be different, including autism, which typically involves extreme symptoms, including an intellectual disability, and Asperger’s disorder, characterized by similar but less severe difficulties like those found in autism except without communication problems and with normal intelligence.

Estimates of the prevalence of ASD increased dramatically over the last decade, a trend likely primarily due to increased awareness and a broader diagnosis and not new causes of ASD.

Several known causes of intellectual disabilities may also cause ASD, which appears to be caused by multiple, mostly unidenti- fied biological problems.

Applied behavior analysis is a promising treatment for autism, but the expense and effort involved are considerable.


For more information, please refer to the book “Abnormal Psychology” by Ronald J. Comer.

ADDspeaker’s comments:

ADDspeaker do not agree with the authors of this book in three areas;

Definition of ASD (DSM-5 vs. ICD-11)

At ADDspeaker, we do not agree with the DSM-5 definition of ASD, as it is understood and used in the book “Abnormal Psychology”, where ASD is viewed as a primarily behavioral disorder, but refer to the ICD-11 definition of ASD as a generalized neurodevelopmental disorder as of June 2018:

Autism spectrum disorder is characterized by persistent deficits in the ability to initiate and to sustain reciprocal social interaction and social communication, and by a range of restricted, repetitive, and inflexible patterns of behaviour and interests.

The onset of the disorder occurs during the developmental period, typically in early childhood, but symptoms may not become fully manifest until later, when social demands exceed limited capacities.

Deficits are sufficiently severe to cause impairment in personal, family, social, educational, occupational or other important areas of functioning and are usually a pervasive feature of the individual’s functioning observable in all settings, although they may vary according to social, educational, or other context.

Individuals along the spectrum exhibit a full range of intellectual functioning and language abilities.

Applied Behavioral Analysis (ABA)

At ADDspeaker, we dot agree with the books authors on the use of ABA in treatment of ASD. As we view ASD as a primarily physical condition with behavioral symptoms, using ABA to correct children’s behavior is not advised, since this is simply implementing a Pavlovian stimulus/response behavior in the child, through using methods of restricting movements (which is not behavioral, but psychically caused by dysregulation of the Motor Control System (verbal/nonverbal behavior) due to an impairment in the Inhibitory System, causing a age inappropriate, developmental level, as well a involuntary motor functions (verbal/nonverbal), which is not based on behavior, but on physical factors, not in the control of the person with ASD.

In short, we view ABA as a form of torture, not as a viable alternative to treating Autism. We recognize that some behavior of ASD is harmful to the self and others, and would like to ask the reader to investigate ECT treatment as a better option, in severe cases of ASD.

We recommend further reading on the topic on PubMed, e.g. this article:

Electroconvulsive therapy for self-injurious behaviour in autism spectrum disorders: recognizing catatonia is key.” – Wachtel LE et al. (2018)


Medication for ASD do not (officially) exist, as correctly stated in the book.

However, at ADDspeaker we have extensive experience in treating ASD symptoms with Guanfacine (Brand Name: INTUNIV, Shire Pharmaceuticals), especially in patients with comorbid ADHD, in our ADDspeaker Advisory Group (AAG), which is a group consisting of 200 dedicated persons who either have ADHD/Autism themselves, have it in their families or have a formal education in these areas.

The AAG have tested Guanfacine with the purpose of reducing symptoms of Autism, and we have ourselves experienced the efficacy of combining Guanfacine with other ADHD medication, and thereby significantly reducing both overall ADHD and Autism symptoms, with minimal side effects (<2 weeks of adjustment) and no significant longterm side effects (Personally I’ve been using Intuniv for more than 2 years, in combination with Lisdexamphetamine, Dextroamphetamine and Venlafaxine, without any side effects, at all).

Guanfacine is a drug originally developed and used since the late 70’s to treat high blood pressure. It has been tested on adults numerous times and a long history of scientific studies are available on PubMed as well. In 2016, INTUNIV was approved by the European Medicines Agency, EMA, for use in treating ADHD in children aged 6 – 17 years, but not in Adults. In the USA, Guanfacine (Brandname: TENEX and INTUNIV) have been used to treat ADHD for the past decade, with good efficacy and no long term side effects.

What we at ADDspeaker have found, is that Guanfacine in the form of INTUNIV (a medication used to treat symptoms of ADHD), seems to have a calming effect on the sensory overstimulation of the Amygdalae, which in turn relaxes the stress levels in the brain and subsequently having the effect of reducing frustration and aggression levels, overall.

Likewise, Guanfacine is known to have an effect on the Executive System in the Frontal Lobes, improving the Executive functions and thereby giving the person with ASD a better cognition, less aggressive behavior and more control over emotional self-regulation and emotional self-control.


Guanfacine is not approved for treatment of Autism symptoms, officially yet, neither by the FDA or the EMA. At ADDspeaker we are not educated psychiatrists or psychologists, but have extensive experience in research and real life, of ADHD and Autism, both personally and scientifically.

ADDspeaker is a not-for-profit grassroots-organization and we have no interests in pharmaceutical, religious, political or any other agenda, and our views are based on scientific, evidence based information, not emotions or personal beliefs.


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