Autism and Comorbid Features: Autistic Regression

Autism Spectrum Disorder (ASD) has been associated with multiple syndromes of genetic etiologies. This poses the question of whether there is a direct correlation between ASD and these syndromes. The possible causes of ASD are due to genetic instability or genetic factors such as tuberous sclerosis complex, a neurocutaneous autosomal dominant disorder; fragile X syndrome, the most common inherited form of human mental retardation; Angelman Syndrome, characterized by developmental delays, mental retardation, speech impairment, gait ataxia and a “happy behavior,” marked by laughing, smiling, and excitability; Prader-Willi, characterized by hypotonia, developmental delay and mental retardation; Gilles de la Tourette, characterized by multiple motor and one or more vocal “tics”; Down’s syndrome, the most common chromosomal cause of mental retardation in United States; and Neurofibromatosis type 1, an autosomal dominant condition caused by decreased production of the protein neurofibromin. According to Zafeirious and colleagues (2007), autism is associated with another genetic syndrome more than 90% of the time. Although autism and genetic factors have been strongly correlated, the exact genetic background and epidemiological data of autism is unclear (Hrdlicka, 2008; Zafeirious, et al., 2007) [See table 1].

There are several medical conditions that have been recognized with relatively high frequency in individuals with Autistic Spectrum Disorder (ASD). About 30% of individuals with Autism Spectrum Disorder (ASD) also have seizure disorders; 2-5% has fragile X syndrome; and 1-3% has tuberous sclerosis. Rutter, Greenfield, and Lockyer (1967) reported that among 63 children with Infantile psychosis, 48% were hyperkinetic at the time of first hospitalization, 43% had morbid preoccupation, 37% had obsessive phenomena, 70% had stereotyped behaviors, 25% had self-injury, and 60% had anxiety or fear ( Strømme, et al. 2000.) In addition to these coexisting medical or psychiatric conditions, many autistic individuals also develop other behavioral and/or psychiatric symptoms in addition to the core autistic symptom domains (e.g. impairment in social interaction, impairment in communication, and restricted, repetitive and stereotyped patterns of behavior, interests, and activities), that may be considered clinical manifestations of comorbid psychiatric disorders.

Regression in individuals with Autism Spectrum Disorder defined as “a) loss of both language and social skills or b) loss of either language or social skills” associated with some neuro-psychopathologies – such as intellectual impairment, seizures, ADHD, gastrointestinal, sleep concerns, Anxiety Disorders, depression and psychosis (schizophrenia) – has been controversial, poorly understood and mistreated (Hansen, et al, 2008; Tuchman, 2006.) The prevalence of developmental regression in autism is one of the more puzzling features of this disorder due to problems in the definition used. Individuals with regression performed significantly less well on communication than those without regression. A study which examined the prevalence of regressive autism found that 15% of autistic individuals lost both language and social skills and 41% lost either language or social skills (Hansen, et al, 2008.)

It is believed that environmental factors may have relevance to the regression as well as progressive degenerative disease of the brain. There are several hypotheses to explain autistic regression such as a slow viral infection, an autoimmune phenomenon, an insufficiency of growth factors during the development, abnormalities of an excitatory neurotransmitter and recurrent seizures or abnormal electrical activity in the brain. For instance, recurrent seizures can cause specific cognitive, language, or behavioral abnormalities. Seizures or the interictal epileptiform activity are responsible for the deterioration of the individual (Hrdlicka, 2008; Oslejsková, et al., 2008; Engel, et al., 2001; Deonna, 1991). The age of regression is higher in autistic individuals with seizures when compared to individuals with regression without epileptic seizures. Moreover, it has been observed that autistic regression has different clinical implications than individual with epilepsy (Danielsson, et al., 2005).

According to Tuchman and Rapin (1996), developmental regression occurred greater in individuals with autism and epileptiform EEG than in individual without epileptiform EEG. The clinical implications of regression in individuals with epilepsy are different from the clinical implications of regression with autism (Danielsson, 2005) In addition, in a case-control study, autism is more prevalent in individuals with Down syndrome than it does in the general population, and when autism is comorbid with Down Syndrome, regression in language and other skills, as measured by the Autism Diagnostic interview-Revised (ADI-R), are reported to occur in up to 50% of the cases (Castillo, et al., 2008). Individuals with autism and comorbid Fragile X, were found to be significantly more impaired in overall imitation abilities, oral-facial imitation, and imitations of actions and joint attention than individual without Fragile X (Rogers, et al., 2003). Data from retrospective studies have suggested that the pathogenesis of autism with developmental regression differs from that of autism without regression (Ball, et al., 2007; Linda, et al., 2007).

Autism and regression represent a challenge from a pharmacological treatment point of view. The treatment should be designed accordingly with the features of regression. The pharmacological management would be different from the autism without regression. When autism with regression is suspected, clinicians should re-evaluate the comorbid conditions.

Table 1 1) Tuberous sclerosis complex 2) Fragile X syndrome 3) Down syndrome 4) Neurofibromatosis type 1 5) Angelman, Prader-Willi and isodicentric 15q chromosome syndromes 6) Anorexia nervosa 7) ARX syndrome 8) Charge, Goldenhar and Moebius syndromes 9) Chromosome 2q37 deletion syndrome 10) Chromosome 13 deletion syndrome 11) Cohen syndrome 12) Cole–Hughes macrocephaly 13) Cowden and other hamartoma syndromes 14) De Lange syndrome 15) Duchenne muscular dystrophy 16) Giles de la Tourette syndrome 17) Hypomelanosis of Ito 18) Lujan–Fryns syndrome (X-linked mental retardation with marfanoid habitus) 19) Mitochondrial disorders 20) Phenylketonuria 21) Smith–Lemli Opitz syndrome 22) Smith Magenis syndrome 23) Sotos syndrome 24) Steinert’s myotonic dystrophy 25) Timothy syndrome 26) Turner’s syndrome (monosomyX) 27) Velocardiofacial (catch 22) or 22q11 deletion or Di George syndrome 28) Williams syndrome 29) 47,XYY syndrome 30) Some other syndromes are: Ehlers Danlos, Joubert (which was strongly associated with autism, Leber’s congenital amaurosis, Coffin Siris, Biedl Bardet, Kleine Levin, Myhre, Apert, neuroaxonal dystrophy, HEADD, Klinefelter, San Filippo syndrome, Noonan, 10p deletion, etc. 31) Environmental factors [ e.g. see our previous blog] 32) ADHD 33) Seizure Disorders 34) Sensory Problems 35) Bowel Disorders Zafeiriou, D., Ververi, A. and Vargiami, E. (2007). Childhood autism and associated comorbidities. Brain and Development: Volume 29, Issue 5, Pages 257-272. (32-35 are not listed in Zafeiriou’s article).

Autism and Environmental Factors

In 2007, the Centers for Disease Control and Prevention’s Autism and Developmental Disabilities Monitoring Network (ADDM) released the data that about 1 in 150 8-year-old children in multiple areas of the United States had an Autism Spectrum Disorder (ASD). Changes in the diagnostic criteria and the awareness of autism will not alone explain this epidemiological explosion. Are there environmental factors that with an underlying genetic susceptibility are responsible for the rise in autism?

Currently, no definitive cause has been identified for autism. Autism is a very complex neurobehavioral disorder that may result from a cocktail of factors possibly comprising of genetic and environmental interactions. Understanding autism presents significant challenges that would require the input of genetic, biological, neurological and psychological researchers working together to comprehend the many facets of this disorder. In 2007, the Institute of Medicine's Forum on Neuroscience and Nervous System Disorders suggested that a complex interplay of environmental stressors, genetic mutations, and other biological factors likely play a significant role in the development and/or progression of autism spectrum disorder (ASD).

The idea that environmental factors are the sole cause of autism has been very controversial. Some studies suggest that individuals exposed to specific heavy metals and other toxic insults are likely to precipitate dysfunctions in the limbic system, and the temporal and frontal lobes, which are observed in autism spectrum disorder. Evidence shows that exposure to the following agents might cause neuro-toxicity and may interfere with the normal childhood neurodevelopment during pregnancy and the first years of development: mercury, aluminum, arsenic, lead, manganese, thallium, clay, coal, soil, uranium, xenobiotic agents (including carcinogens such as nitrosamines, hydrazines, and pesticides) (Exley & Esiri , 2006; Wasserman, et al., 2007; Opler, et al., 2004; Bowler, et al., 2006; Haas, et. al., 2003;).

The neuro-toxicity hypothesis in autism has gained considerable popularity. Heavy metals were considered as possible agents contributing to the etiology of autism. It was hypothesized that some children who had ingested lead through pica and other eating habits, “became” autistic. Fetal exposure to certain chemicals such alcohol, cocaine and sodium valproate have been associated with behavioral deficits seen in autism (Shearer & Larson, 1982; Jackson & Garrod, 1978). Nanson,1992; Harris et al., 1995; Fombonne, 2002; David at al., 1992; Moore et al., 2000; Schneider and Przewlocki, 2005).

Recent attention from the media has centered on Thimerasol as a contributing agent to autism. Thimerasol is a mercury containing preservative in the MMR vaccine (Measles, Mumps and Rubella). In combination with gastrointestinal vulnerability or mitochondrial dysfunction, thimerasol may possibly lead to autism. However, it is critical to point out that larger and controlled studies have not provided consistent support of this hypothesis (Volkmar, 2000; CDC & NIH, 2003).

A number of researchers and institutions are now studying the possible role of a wide range of toxic chemicals, genetic predisposition, and the interplay between these two in altering brain development and social behaviors during early life. A major study, for instance, is underway at The University of California, Davis (UCDavis) and Childhood Autism Risks from Genetic and the Environment (CHARGE) The UC Davis Institute is using a large sample of autistic children to investigate if there is a correlation between the onset of autism and chemical exposures during early childhood.

Therapeutic Effects of Omega-3 Fatty Acids on Challenging Behaviors of Autistic Individuals

There are enormous amounts of both anecdotal and randomized, double-blind, placebo-controlled studies about the neurobehavioral mechanisms of Omega-3 Fatty Acids in psychiatric disorders and Autism Spectrum Disorders (ASD) (Meguid, et. al. 2008; Kidd, 2007; Clayton, et. al., 2007; Sliwinski , et. al., 2006; Amminger, et al., 2006; Vaisman, et. al., 2006; Parker, et. al. 2006; Gustafsson, et. al., 2004; Longan, 2003; Marangell, et. al., 2003; Bell, et. al, 2002; McCrone, 2002; Peet, 2002; Vancassel, et al., 2001; Fenton, et. al., 2000; Stoll, et. al. 1999; Bourre, et. al. 1993; Hibbeln, et. al., 1995.)

Essential fatty acids such as omega-3 are long-chain polyunsaturated fatty acids found in various plants and marine animals that cannot be synthesized in the human body, and are important for normal cellular function. The three major omega 3 fatty acids are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).

(Lippincott Williams and Wilkins, 1999)

Normally, we can convert ALA to EPA and DHA, which are the forms that we can metabolize. However, recent evidence shows that the capacity to produce EPA and DHA from ALA is limited and unlikely to supply requirements, especially in rapidly growing young children (Agostoni, et. al. 1995).

Omega-3 fatty acids are considered an important element in normal brain development. According to several researchers (Bourre, et al. 1991, 1993; Yehuda, et al., 1999 & Vancassel, et al., 2001), the human brain is the second organ that contains the highest concentration of polyunsaturated fatty acids (PUFA). In the nervous system, one out of every three fatty acids belongs to the polyunsaturated fatty acids group (Bourre, et al., 1991 & Yehuda, et al., 1999). Some studies suggest that the levels of polyunsaturated fatty acids are lower in autistic individuals, in comparison with normal populations (Kidd, 2007.)

Autism Spectrum Disorder has a very complex etiology and core symptom domains such as “qualitative impairment in social interaction”, “qualitative impairments in communication” and “restricted repetitive and stereotyped patterns of behavior, interests and activities” (DSM-IV). Evidence from research studies have hypothesized that the core symptoms domains are in part due to a developmental disorder of the central nervous system (Trottier, et al., 1999).

Meguid and colleagues (2008) evaluated the correlation between omega-3 and challenging behaviors in a study of 30 children with autism in comparison with 30 healthy children (control group). They found that autistic children treated with linolenic acid (an omega-3) showed 71% reduction in challenging behaviors. Amminger and colleague (2006) provided preliminary evidence that omega-3 fatty acids may be an effective treatment for challenging behaviors in children with autism (hyperactivity and stereotypy behaviors).

A possible explanation for the therapeutic effects of omega-3 on autism has to do with its relationship with pro-inflammatory mediators such as Serotonin. While it is commonly known that Serotonin is a neurotransmitter that regulates neuronal activity in the brain, it is also a product of platelet cells involved in inflammatory reactions. It has a similar action to histamine, in that it also dilates arterioles and increases the permeability of venules.

Eicosapentaenoic acid (EPA), an Omega-3 fatty acid, acts to reduce pro-inflammatory reactions by suppressing the production of mediators such asThromboxane A2 that lead to platelet aggregation and stimulation, and thus release Serotonin and Histamine. Given that Serotonin levels in autistic individuals are elevated above normal and, as some studies suggest, may be related to the pathology of autism, it would be reasonable to consider if Omega-3 can potentially lower Serotonin levels and produce a positive behavioral response in autistic individuals (Anderson, et al., 1987; Sliwinski, 2006.) Serotonin (5-hydroxytryptamine, 5-HT) is derived from the essential amino-acid Tryptophan. Serotonin regulates mood and abnormalities and has been associated with depression, aggression, obsessive-compulsive behaviors, feeding behaviors and obesity.

Croonenberghs and colleagues (2008, 2007, 2005, and 2002) suggested that abnormalities in the inflammatory response system (IRS), may induce some of the behavioral symptoms of autism, such as social withdrawal, resistance to novelty and sleep disturbances. Disorders in the peripheral and central metabolism of Serotonin (5-HT) may play a role in the pathophysiology of autistic disorder (Sliwinski, 2006.) Again, polyunsaturated fatty acids (PUFAs – Omega-3, in particular DHA) are potent suppressors of the Inflammatory Response System (IRS), and currently used as treatment, for instance, of rheumatoid arthritis (Chen, et al., 2005; Young & Conquet, 2005.)

Polyunsaturated fatty acids (PUFA) supplementation may play an important role in ameliorating autistic problematic behavior. Some of the best sources of omega 3 fatty acids are fish, corn, soybean oil and safflower oil. Unfortunately, many fish such as shark, swordfish, and tuna are high in mercury and other toxins, but salmon and shrimp, for instance, tend to have lower levels of mercury. Some studies reported that mercury levels in several USA brands of fish oil capsules are undetectable. High doses of omega-3 may have harmful effects, such as an increased risk of bleeding.

According to the FDA the maximum safe dietary dosage is no more than 3g/day of EPA and DHA from supplements and no more than 2g/day of Omega-3 from the diet (FDA, 2004.)

Autism Spectrum Disorder and Sexuality

Last week we have the opportunity to attend to a sexuality training sponsored by Long Island DDSO and the Cody Center for Autism & Developmental Disabilities. In this training we reviewed why individuals with autism need sexuality training and support, how to provide support to them and how to address problematic sexual behaviors. Autism Spectrum Disorder and sexuality is a very challenging topic due to the complexity of the sexual development and understanding of sexuality of individuals with deficits in social skills, communication and sensory issues [e.g. high level of physiological arousal, hypersensitive to tactile stimuli, sex education, interpersonal relationships, same-sex attraction, bisexuality and transgender problems] (Lawson, 2005; Hutt, Hutt, Lee and Ounsted, 1964; Grandin & Scariano, 2002). In our society, this subject is generally not well received and is filled with taboos, which raises ethical, clinical and legal dilemmas for support professionals. Can we respond to consumers’ sexual questions or behaviors? Why do we need to provide sexuality training to all consumers, if some consumers probably will not understand any information that we provide about sexuality anyway? Most of the time we are underestimating our influences and power to facilitate healthy sexuality. As support professionals we should take advantage and use any “teachable moments” (TV shows, movies, songs, magazines) to share information or teach social skills. I think that we should develop a sexuality support plan that facilitates a healthy sexuality instead of simply eradicate the maladaptive sexual behaviors (Realmuto & Ruble, 1999).

Due to the cardinal symptoms of Autism Spectrum Disorder such as an inability to form social relationships, speech and communication impairment and an “obsessive insistence on the preservation of sameness" (Hutt, et al., 1964), autistic individuals may display problems in sexual behaviors such of inappropriate masturbation, inappropriate touching of self or others and poor menstrual hygiene. Keep in mind that autistic individuals are entitled to sexual fulfilment in the same way as anyone else, but the most important component to address the misbehavior is to determine the causes of the inappropriate sexual behavior. The maladaptive sexual behaviors can have multiple functions and triggers such as history of learned behaviors, partner selection, and medical reasons, physiological or sensory causes (distressing or confusing physical changes associated with puberty). According to Hingsburger and colleagues (1991), deviant sexual behaviors “may arise from living in a system in which appropriate sexual knowledge and relationships are not supported.” Dalldorf (1983) has suggested that persistent masturbation in some autistic individuals may be caused due to a lack of alternative outlets for sexual tension and a predisposition for self-stimulatory behavior. Moreover, some studies hypothesize that socially unacceptable sexual behaviors may be related to the core symptom domains of autism (Realmuto and Ruble, 1999.) Dr. Lorna Wing in her book Autistic children: a guide for parents and professionals(1985) reports that sexual development and interest varies with physical development in autism, but in general is delayed. According to DeMyer's survey of parents (1979), she found that parents of boys with autism believe that their child is not interested in sexuality. However, while the initiation of menstruation and sexual drive are usually tolerated calmly, exhibitionism and masturbation are sometimes problems that manifest. Masturbatory activities is very frequent in autism probably due to the biological implication in Autism Spectrum Disorder [neurological and neurobiochemical](Wing, 1985).

Excessive masturbation in public areas and touching of self or others’ private parts are concerns for support professionals working with autistic individuals, especially when they are in the community. Sometimes these issues become a chronic situation or involve inappropriate targets such a family members or individuals who are lower functioning. In these cases the support professionals need to develop special treatment strategies such as incidental teaching, augmentative communication, teach about relationship boundaries or use antiandrogen therapy [flutamide (brand name Eulexin), bicalutamide (brand name Casodex), and leuprolide depot, etc. – medication used in the treatment of advanced prostate cancer, which decrease libido] (Realmuto & Ruble, 1999.)

We found the research on autism and sexuality somewhat limited, which makes it more difficult to provide the professional support that our autistic community needs in this area. The autistic community needs our support in accepting and understanding their sexual needs and rights, and in teaching autistic individuals appropriate sexual behaviors and how to execute their rights with responsibility.

Epidemiological Diagnostic and Treatment Trends of Autism in the Tri-State Area

I would like to analyze a few epidemiological patterns on autism diagnosis’s and treatment that may help to enlighten the increasing incidence of autism.

Epidemiological data collected from online surveys conducted by the Interactive Autism Network (IAN) show that in the state of Connecticut, 41% of families with a member with autism reported that this member was diagnosed with autistic disorder, in comparison with 35% in the state of NY and 38% in the state of NJ. The tri-state area shows a lower percentage of autistic individuals diagnosed with autistic disorder when compared with the entire nation with 44%. However, the state of NY and NJ show higher percentage of individuals diagnosed with Pervasive Developmental Disorder, Not Otherwise specified (PDD, NOS), 42% and 33% respectably when compared with 29% in the nation,. The state of Connecticut shows 14% of individuals diagnosed with Asperger’s syndrome in comparison with 10% in NY with and 9% in NJ. However, the state of Connecticut shows a similar percentage as the nation with 15% of individuals diagnosed with Asperger’s Syndrome. This data indicates how autism spectrum diagnosis’s varies in the tri-state area from the national pattern. Although diagnosis data is reported by the parent and is not based on medical charts or on school reports, this data seems to suggest that in the tri-state area, PDD, NOS represents a difference to the national pattern.

Another interesting parameter is the type of treatment used. We have hundreds of autism treatments available. Many types of treatments have little or no clear scientific evidence to support their effectiveness. In the tri-state area the top treatment has been Speech and Language Therapy with 71% in NY, 70% in NJ and 67% in CT, which are all higher with respect to the national trend of 65%. Occupational therapy ranked in second place with 62% in NY and NJ and 60% in CT, higher than the national percentage of 52%. Moreover, state use of medications such as psychotropic drugs differs from the national pattern of 40%, when compared with 38% in NY, 32% in NJ and 33% in CT. The use of Applied Behavior Analysis (ABA) is greater in the tri-state area (NY 42%, NJ 54% and CT 43%) in comparison with the national pattern of 29%. The state of NJ ranked higher in the use of ABA than NY and CT.

One way of interpret these diagnostic and treatment trends is to view them as a reflection of state changes in diagnostic practices, such as improved identification, availability of services, and other similar factors.

[Disclaimer: the data presented here is based on information submitted over the internet by parents of children with autism spectrum disorders (ASD) from the United States who volunteered to participate in the Interactive Autism Network survey developed by Kennedy Krieger Institute and sponsored by Autism Speaks.]

Why Do Some Autistic Individuals Have Severe and Recurrent Problem Behaviors?

Parents and staff often ask these questions when they are witness to an autistic adult individual who is engaged in what psychologists call, problem behaviors. An autistic individual may be hitting or punching himself or others, throwing a tantrum, running away (elopement), screaming or yelling loud in an agitated manner or assaulting others in different ways.

There are two major frames of thought for analyzing these problem behaviors. We can think of them from a biological perspective, that is, view the behavior as a result of brain dysfunction and biochemical imbalances. We can also view these problem behaviors from a social environmental perspective (Bauman & Kemper, 2004; Hollander & Evdokia, 2007; Iwata, Vollmer, & Zarcone, 1990).

At this time, I would like to focus solely on the latter social environmental perspective and discuss the role the social environment plays in the occurrence and recurrence of severe problem behaviors. To begin answering this question, we must analyze not just the behavior itself, but also the sequence of environmental events surrounding that behavior. This type of analysis is what we call a functional behavior analysis, whereby we assess the role of the social and physical context and consequences (observable/measurable events) that surrounds the severe problem behaviors. The reason for analyzing the surrounding events is that this perspective assumes an existing relationship between the behavior and the environment. Another way of understanding this relationship is to view the severe problem behaviors as purposeful and working within a function of antecedent contexts and consequences (if “X”, then “Y”). For instance, when an autistic individual becomes agitated or self-abusive, most of the time a family member or staff will give him more attention, which may be what he wants. This relationship between the self-abusive behavior and “attention giving” may become strengthened, conditioning the maladaptive behavior by the positive consequences. Thus, a functional analysis accounts for the fact that social environmental events can either trigger or give purpose to the maladaptive behavior (Center for Autism and Related Disabilities, SUNY, 2008).

We can have two types of consequences to a maladaptive behavior: a positive reinforcement or a negative reinforcement. By using the words positive and negative, I do not make any value judgment about these reinforcers, meaning that I say nothing about whether they are “good” and “bad” things. Positive reinforcements are environmental stimuli that are introduced immediately after the behavior and subsequently increase the likelihood of occurrence of a particular behavior. For example, if an autistic individual gets agitated and a staff member takes him for a walk- an activity that he enjoys-, it is likely that through time the agitated behavior may increase in frequency and possibly intensity. The effect of the staff providing a walk to the autistic individual, contingent upon the agitation increases the frequency of the behavior over time. In this example there exists a temporal relationship between the behavior and the positive consequence of going for a walk. Therefore, we can say that the autistic individual learned how to get a walk with staff, by getting agitated (Austin and Carr, 2000; Cooper, Heron and Heward, 2007.)

Negative reinforcements are aversive environmental stimuli that are removed immediately after the behavior and subsequently increase the likelihood of occurrence of a particular behavior. Negative reinforcements are often seen in problem behaviors when we engage an autistic individual in task demands and compliance situations. The autistic individual tries to escape from a situation because it becomes an aversive event to him or her. It can consequently be negatively reinforced when that event or demand is removed, which may make the maladaptive behaviors more likely in the future. For example, an autistic individual may throw herself on the floor to avoid going back to engaging in a task. The negative reinforcer in this case would be the consequence of no longer engaging in that task as a response to this maladaptive behavior. Occasionally, self-injurious behaviors follow a negative reinforcement function and the misunderstanding of the behavior may lead to an unintentional escalation of the behavior. Therefore, it is imperative to perform an accurate functional analysis to understand the behavior because in the case of self-injurious behaviors the plan of ignoring the behavior may seem to be a good strategy for changing the behavior if the motivation (function) for the behavior is to seek attention, but it could be that the individual's contingency relationship (temporal cause-effect relationship) may be characterized differently. In another situation, an autistic individual may choose to engage in self-injurious behavior to avoid complying with staff instructions, for instance, to do laundry, take a shower or attend his day program. The autistic individual maintains his or her own non-compliance behaviors by negatively reinforcing that behavior through escape and avoidance of the aversive stimulus, such as doing laundry. In this scenario, we could try to modify the behavior not by ignoring it, but by increasing the motivational components of the low non-preferred activity to do laundry. Occasionally, a poor management of this situation may escalate to verbal and physical aggression and property destruction (Repp and Horner, 1999).

There are different contingencies that may strengthen severe problem behaviors such as attention-seeking, obtaining tangible items (e.g. food), escape-avoidance from a difficult task and self-stimulation (boredom or lack of structure) (Center for Autism Spectrum Disorder, 2005). If parents and staff members can understand the function of the severe problematic behaviors, they can change the stimulus that maintains the maladaptive behaviors and subsequently work to alter the frequency and motivational conditions of these problematic behaviors.

Who knows What Is High-Functioning Autism?

High-Functioning Autism (HFA) has been a controversial term which occasionally refers to and sometimes is used interchangeably with Asperger’s Syndrome and Pervasive Developmental Disorder, not otherwise specified (PDD, NOS). Great confusion and controversy about the definition of High-Functioning Autism (HFA) continue, with the main issue being whether or not Asperser’s Syndrome is truly distinct from autistic disorder (Asperger, 1944; Wing, 1981; Baron-Cohen, 2002; Freeman, et. al. 2002; Klin, et. al. 2000; Volkmar & Klin, 2001; Young & Brewer, 2002). Goldstein, et. al. (2002) stated that the diagnostic criteria between Asperger’s Syndrome and High-Functioning Autism (HFA) overlap and are unclear according to the DSM-IV (1994). Blacher et. al. (2003) stated that “definitional and boundary issues are major research concerns in the area of Asperser’s Syndrome and High-Functioning Autism (HFA). The term Asperger’s Syndrome was first described by Dr. Hans Asperger in 1944, but was not widely used in the United States until after 1981, when his work was translated into English. In addition, when classification of Asperger’s Syndrome is compared in the DSM-IV and ICD-10 with PDD, NOS, Dr. Szatmari (2000) considers that the conceptualization is deeply unsatisfying to many parents, front-line clinicians and academic researchers. Given that HFA is not classified in the DSM-IV or ICD-10, some would say that it isn’t a diagnosis.

In 1991, Dr. Frith in her book “Autism and Asperger’s Syndrome” mentions that many professionals felt Asperger’s Disorder was simply a milder form of autism and they used the term “High-Functioning Autism” to describe these individuals. Dr. Szatmari stated that by not specifying symptom differences, the differentiation of Asperger's Syndrome from High-Functioning Autism becomes confused. Eric Schopler et. al. (1992) in his book, High-Functioning Individuals with Autism, proposed that Asperger’s Syndrome and High-Functioning Autism did not have any difference and he recommended that the term Asperger’s Syndrome be discarded. Wing (1998) concluded that Asperger's syndrome and High-Functioning Autism were synonymous and stated that Asperger's Syndrome and High-Functioning Autism are not distinct conditions. She recommended that Asperger's Syndrome be used for "children and adults who have autistic features, but who talk grammatically and who are not socially aloof".

Moreover, Ozonoff, et. al. (2000), suggested that Asperger's Syndrome and High-Functioning Autism involve the same fundamental symptomatology, but differing only in the severity. According to Gilbert (1998), there are no widely accepted diagnostic guidelines specifically for High Functioning Autism (Gillberg, 1998). When individuals diagnosed with Asperger’s Syndrome are compared with those with HFA, they generally have lower Full Scale IQs, with less apparent Verbal/Performance IQ discrepancies.

Due to the confusion in the diagnostic criteria and definitions between Asperger’s Syndrome, PDD, NOS and High-Functioning Autism, Dr. Pomeroy (1992) presents a model for subtyping the Pervasive Developmental Disorder (PDD). He suggested that it is justifiable to define three subtypes of PDD without mental retardation (a) a group with higher verbal skills than performance skills, b) a group with language impairment, and c) a group with non-language impairment.).

There is no consensus within the scientific community that Asperger's syndrome is indeed separate and distinct from High-Functioning Autism. Also it remains unclear whether Asperger’s Syndrome is different from the autistic spectrum disorders. The Autism Society of America states that “more advanced”, "high-functioning", or "mild" autism are subjective terms and that there are no clear clinical definitions for them. Researchers and clinicians are working to determine if Asperger’s Syndrome is a form of High-Functioning Autism or if it is a different entity with different etiology and treatment. The problem arises in individuals within the spectrum with borderline cognitive ability (IQ>70 or above) who sometimes are described as High-Functioning Autism. Some researchers report differences in verbal skills, for example, between Asperger’s Syndrome and High-Functioning Autism (Fitzgerald & Corvin, 2001). Some researchers are still using Asperger’s Syndrome interchangeably with High-Functioning Autism, while others use only High-Functioning Autism/PPD (HFPDD) (Kamio, 2007). However, making the diagnosis based on verbal skills or IQ differences are not supported by the research data (Fitzgerald & Corvin, 2001).

So, then, to return to the question: Who knows what is High-Functioning Autism? Based on the current status of the scientific knowledge and diagnostic classifications (DSM-IV & ICD-10), a lot of clinicians and researchers would say that they know the “right answer”- that is, they are the ones who know what is High-Functioning Autism (HFA) -, but without a much needed consensus of a differential diagnosis and treatment, the scientific community is unable to have a clear dialogue to better understand the phenomenon of High-Functioning Autism (HFA), Asperger’s Syndrome (AS) and Pervasive Developmental Disorder, not otherwise specified (PDD, NOS).