Autism Spectrum Disorder: A Chaser
A species hinging upon communication, human beings are often tasked to present complex concepts through verbal communication, emotional displays, and socially-appropriate bodily cues. However, one condition with genetic predispositions presents a unique struggle for families and for those that experience it – autisms. Accepted as a disorder of the brain (and classified as a neurodevelopmental disorder in the Diagnostic and Statistical Manual, 5th Edition [DSM-5]), autism has often found itself in the popular press as a disease with no origin but plenty of theories of causality.
Speculative causes for autisms range from vaccinations to dyes to atypical neurodevelopment. Many treatments also exist for autism; few of them actually have scientific basis. Nontraditional alternative medicines, psychoactive medications, nutritional supplements, and behavioral treatments all battle for the attention of parents daily and there is much to be dissected about autism’s causes, effects, and treatments that are effective and ineffective regardless of ease.
This Medium will cover, pardon the pun, the spectrum of the Autism Spectrum Disorder. Classified in the DSM-5, Autism Spectrum Disorder (ASD), is a collapsed version of what was considered Autism and Asperger’s Disorder in the DSM-IV-TR. We will look at some basic and technical information of ASD’s etiology and presentation, examine disorders that can commonly occur with ASD, and look at treatments.
Examinations of ASD require a fundamental explanation both of the disorder and its classifications. The DSM-5 overhauled the classification of Autism and Asperger’s from the DSM-5. They list the diagnostic criteria of ASD as follows. We will look at each passage to discuss the pragmatic representation of these abilities that I have experienced in clinical settings.
A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive; see text):
In short, this must be present. I must see, as a clinician, a developmental shortcoming in social communication and interaction. It must be across contexts or situations. For example, you must have this problem with social communication and interaction in school, at home, on the playground, at work, and at the dinner table.
It cannot be that you choose not to talk at a certain time, that you don’t like someone so you refuse interaction, or that you have a biological condition.
The first step of any diagnosis is that I must rule out an organic, biological, or medication cause. I must also rule out other diagnoses such as schizophrenia. This is done in a long interview where I meet with the client/person in a face-to-face setting for 2 hours to do a biopsychosocial assessment that assesses problems from multiple angles.
Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
This is an example behavior. Typically in those with autism, this is hallmark. I will see a marked problem with social-emotional reciprocity. That is, they will have difficulty reading and returning emotions. I often also see this represented in facial expressions which are often very “flat”. There may not be smiles, frowns, etc. as these are all social cues.
Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures: to a total lack of facial expressions and nonverbal communication.
This is another example and it is, again, hallmark. This is an example of the exact same behavior as you see above. However, this example is much more clued in on the non-verbal. The prior example was keyed to verbal or contextual information of speech, communication, and linguistics.
Deficits in developing, maintaining, and understanding relationships, ranging, for example, from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers.
This is also hallmark. I see this in almost every person with ASD. This speaks to behaviors and relationships that result from behaviors. Most often, I’ll see a large absence of interest in select peers who do not interest the person with ASD. They may like the person, but they do not show interest in them. Those with ASD are not selfish. They are not self-absorbed. They simply show interest when interest is present. If interest is not present, interest will not be expressed.
After all, it’s simply polite to pretend that you’re interested in someone while simultaneously tuning them out. This is a social skill.
What the DSM-5 did here in this area is remove the concept of Autism as a checklist of behaviors. Instead, the DSM-5 allowed for room for clinical judgment. Those who do not know differential diagnosis believe that mental health should be something that is delineated.
However, the reality of human behavior is that it happens on a continuum. No behavior if categorical. You don’t just feel depressed. You have a wide range of behaviors, expressions, and precipitating factors of depression. Continuum diagnosis allows for this continuum of human behavior expressions based upon a whole multitude of variables including age, height, weight, socioeconomic status, early intervention, race, gender, sexuality, and any other variable that makes one person different from another. Yes, even hair color can affect the expression of a certain disorder. After all, those with red hair may express anxiety due to social disapproval based on recessive genes.
B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history (examples are illustrative, not exhaustive; see text):
This is the second required area of ASD. I must see some sort of restricted, repetitive pattern of behavior, interest, or activities. These do not have to range from simple to complex. They merely have to be restricted (that is fixated or bound to a certain thing) and repetitive.
If someone must play video games on a certain time at a certain place with a certain game, this qualifies.
This is different from Obsessive-Compulsive Disorder as these rituals lack obsession. Obsessions are intrusive and unwanted. Compulsions are demands that you carry them out to alleviate the intrusive, unwanted thought. Upon carrying out the action, the person feels a stress release that reinforces the ritual.
ASD stereotypy and ritualism are not intrusive and unwanted. They are fixations and preoccupations, but they are not intrusive and unwanted. They present no distress, and doing the behavior does not release from stress. The behaviors may self-soothe and relax, but the thoughts of the behavior do not cause distress that is then released by action.
Below are some of the example behaviors of this requirement:
Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
I tend to see this in many persons with ASD. Often times, these behaviors are self-soothing. I tend to see rocking in those with ASD. Sometimes, I’ll see idiosyncratic behaviors such as tapping of the hand with fingers. These behaviors may self-soothe, but the intent of them is not to release stress. Often, they’re intended to reinforce an attempt at homeostasis through stimuli that are familiar.
In other words, if you’re experiencing something you don’t like (a screaming child), your response will be to do something you DO like (leaving the room). The response is the same, but it’s often nonverbal and behavioral instead of verbal due to potential language delay
Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
I see this manifestation in nearly every person with ASD that I’ve ever treated. The disruption to familiar schedules is absolutely devastating. It can literally destroy an entire day. If there is a change to the schedule that is expected, any disruption to that expected schedule will obliterate the entire day.
This can also appear like OCD, but note that the requirement of the ritual is not based in stress and catharsis. It’s based in familiarity of ritual and schedule along with the preference to adhering to the schedule.
Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
I see this one very regularly as well. Interests will typically be very specific and they will be rigid. For example, someone with ASD may develop an interest in Pokemon. They will then collect every Pokemon game, buy every Pokemon card, get every Pokemon plushie, but every Pokemon side item, watch every Pokemon TV show, and generally appear like a “creepy Pokemon fan.”
However, they are just fixated upon Pokemon. It holds their interest, and what holds their interest is worth pursuing. Do note that interests can change. However, it must be on the schedule of the person with ASD. Change that is rooted in the desire of another person is a violation of ritual.
Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse re sponse to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement).
I tend to see this one in nearly every single client/person with ASD. I generally see more hypereactivity than I see hyporeactivity. This is the classic example of those with ASD. They cannot block out stimulus. Everything floods in.
It is incredibly painful when it happens.
The response to this event is typically an activation of the sympathetic nervous system located in the amygdalae in the limbic system in the medial temporal lobes. In short, the amygdalae are little almonds with tubes that sit not too far behind your eyes. This structure is responsible for emotion, some memories, and decision-making.
When you experience stress of any kind, the amygdalae make a decision and send out a signal to fight or run to the brain. The brain then sends out, from the motor cortex, the behavior that is desired. Along the way, the brain sends out the signal to activate the sympathetic nervous system to do any of this. Your body then sends out adrenals and a signal shoots from your brain to the rest of your body to either fight the stress or run.
Now imagine you have no clue what the hell just happened to your body when all of this happened. You’re a young kid who just experienced this overload, you’re in pain, and your body is sending you this weird signal to run or fight.
The response of many with ASD from this hypereactivity is to develop specific behaviors, reactions, or activities that keep this chain reaction from happening. If it gets bad enough, someone with ASD may accept any similar stimulus over the unfamiliar one. Sometimes, this means hitting yourself in the head until you bleed because what is happening in your brain is so painful (overstimulation) that the response is to replace it with something you know.
The behaviors that you know and that keep you calm are self-soothing. The ASD community sometimes call these behaviors “stimming.”
Stimming is not, as a word, a diagnostic term. Professionals use the term stereotypy, ritualized, or stereotyped. Stimming is a term adopted by the ASD community to dispel a perceived stigma of stereotyped or ritualized. Stereotype, for example, can mean a negative belief structure of someone. Ritualization can, for example, mean a set of behaviors that are required for participation.
The psychiatric field uses neither term in that manner.
C. Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life).
We previously stuck to diagnosing ASD in childhood. The DSM-IV-TR allowed for Pervasive Developmental Disorder NOS (not otherwise specified) for adult diagnoses. However, I rarely diagnose ASD as developed in adulthood. Typically, the diagnosis is historic and reproduced in multiple forms of treatments prior to reaching me.
D. Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning.
This is standard for every single disorder. I cannot, as a professional, diagnose someone who does not have clinical significance in the domain of social, occupational, or other areas of functioning.
If someone as ASD and they are functioning well, I cannot diagnose it. In fact, if someone has a schizophrenia or a bipolar disorder, I cannot diagnose it if there’s not impairment. However, those who come to my clinic are typically there because there’s impairment.
This is where there’s a fundamental difference between laypersons, undergraduates, non-licensed people, and anyone else who likes to use the DSM for self-diagnosis. Professionals are keenly aware of the requirement on every disorder for impairment in some setting of life.
E. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level.
This is crucial. Some expressions of ASD may actually be because of intellectual functioning and disability. I typically request an IQ test on a new diagnosis of ASD. I need to know that the functional state is not better explained by intellectual disability. I also must know that it’s not better explained by a biological or medical condition. For example, Broca’s aphasia (a piece of the brain causes a loss in the ability to produce speech) may better explain ASD symptoms of not communicating or doing so poorly with a limited vocabulary.
Finally, a note:
Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder. Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for autism spectrum disorder, should be evaluated for social (pragmatic) communication disorder.
The DSM-5 created a new diagnosis for those who simply have problems with pragmatic speech. This means issues with speech on a social level. This diagnosis is meant to separate those who may just have problems communicating socially from those who have ASD. So for those who may have problems with social communication but have no stereotypy, hyperstimulation, developmental delays outside of speech, inflexibility, etc may qualify for pragmatic communication disorder under the DSM-5.
Diagnostically, we must look for impairment in social communication and interaction, restricted types of behaviors, and an early childhood onset. There must be impairment. We can also accept historic reports of ASD.
We cannot accept self-diagnosis or anecdote in lieu of professional assessment.
One reason for this is a principle in psychiatry known as insight. Insight is the concept that the person who presents knows the causes and effects of the disorder. Typically speaking, most of those I see with ASD have poor insight into the causes of ASD.
Many of those who experience ASD are well aware of the effects of ASD, however. They know the experience of ASD. They know what it feels like, smells like, tastes like, and how it affects their life. This is the case for every disorder. The effects and treatments of the disorder are understood well before the causes.
For this reason, experience of a disorder in effects is not acceptable for explanation of disorder in cause. Even if someone has full insight into the disorder, they still are not qualified to assess, diagnose, and treat that disorder. They are not governed by an ethics board, licensed by a legal board in their state, and they are not educated in the execution of treatment.
Another reason is something called differential diagnosis. You may hear this on television, but differential diagnosis requires having a vast knowledge base of every single disorder in the DSM. It requires being keenly oriented to parsing out difficult information that may not be presented clearly by someone who cannot communicate clearly for whatever reason.
Having a license means that you have the experience, knowledge, and background. You have the training. You have the base from which to draw for a vast diversity of expressions of ASD or any other disorder.
We are educated, trained, and licensed to handle any behavior, thought, or feeling that someone with ASD (or those without) reports. This was done over 2 years of education, 2 years of training, and years of practice with adults who have a wide array of behaviors, thoughts, feelings, and expressions of behaviors.
MHPs know a large amount of treatments, and we are keenly aware of both the benefits and the risks of those treatments. We weigh them against the needs of my client, their family, greater society, and we implement a treatment plan accordingly in keeping with my state’s laws and regulations, the laws and regulations of insurance companies, and the expectations of all involved.
Experiencing ASD or any other disorder does not prepare any particular person for negotiating this incredibly rocky terrain. In fact, treatments for ASD could cause someone’s suicide. It could cause someone’s death. It could cause families to break up. It could cause someone to hurt themselves.
Therapists are trained, licensed, and insured to do any of this. Someone who experiences a disorder is not. This increases their liability based upon limited insight, knowledge, and expertise in this area.
Much in this same vein, someone with a heart murmur is not qualified to do open-heart surgery on others. Mental health is just as delicate. People can, and do, die if mental health procedures and interventions are done incorrectly.
Every therapist has a story of at least one client that said, “I’m OK,” left the office, and killed themselves. Therapists are equipped to handle that in full.
I typically notice ASD in children around the age of 2. Prior to this, we tend to send children to neurologists as there is evidence that brain development for those with ASD is different from typical development.
This is why those with ASD often prefer to be called neuro-atypical. The brain shows the effects of ASD.
The first signs of ASD tend to be a lack on emotional reciprocity with mothers. After this, behaviors that are more complex tend to stand out. Sometimes, the child may never play with toys, be able to do unusual things like counting up to 100 before learning their name, or developing rituals such as lining up cars, trucks, or other toys.
Autism affects boys more than girls.
This is, I cited in the other piece, to the order of 4:1. We are very good at identifying ASD and differential diagnosis of it. There is still some debate on the rates and if they are reflected by diagnostic criteria, but we do know that we’ve gotten much better at diagnosing it.
Girls tend to be able to mask developmental delays in social communication and interaction better. However, girls with ASD also tend to have intellectual disabilities in higher rates. Why is still unknown.
The etiological cause of ASD is unknown.
According to Tsai (1999), a strong preliminary suggestion of neurochemical genesis exists within literature. However, other research has indicated that as many as 15 or more genes could constitute a genetic genesis (Volker & Lopata, 2008). Another theory puts for that physiological abnormalities in the cerebellum may be a cause (Belmonte, et al, 2004). One missing theory, however, is one that the media and some parents favor – immunization. According to the Center for Disease Control (CDC), however, this is not the case as thimerosal has been excluded as a causal factor (Center for Disease Control, 2009, para. 1). The DSM-5 notes that genetic cause estimations range from 37% to higher than 90%. 15% of ASD appears to be associated with genetic mutations such as Fragile X Syndrome.
Simply put, we have no single cause. However, evidence points toward genetics, neurology, and possibly environment all resulting in a developmental delay in early childhood. ASD is not caused by vaccines. It is not caused by bad parenting. It is not contagious.
Many treatments for autism exist both in the biomedical as well as homeopathy. The use of complementary and alternative medicines (CAMs) has been reported, in research, to be on the rise for both children and for adults with estimations of near 50% increase in expenditures on CAMs; this finding was found by Hanson, Curtis & Ware (2007) as they found that 74% of surveyed children with ASD have used CAM. These CAMs, according to Hanson, Curtis & Ware (2007) include modified diet, vitamins and minerals, supplements, mind-body interventions, and body stimulation methods. However, research indicates that while these may be cost-effective, natural, and appealing alternatives, they also have their flaws. According to Maurice, Green & Luce (1996), there is a very small window of time for autistic children to have the most effective treatment. That treatment, however, is not the use of CAMs which often do not work effectively. Under the purview of Maurice, Green & Luce (1996), two CAMs were examined: Facilitated Communication (FC) and Sensory Integration Therapy (SIT). FC, which aimed to increase communication, had shown no evidence of effective outcomes with outcomes that were uncontrolled in experimentation. SIT, aiming to improve sensory processing, had not shown any effective results and potentially increased self-harming behavior found in autistic persons.
In continuation, other CAMs cited such as vitamins, minerals, and supplements (Vitamin B-6, Magnesium, Vitamin B-12, Folic Acid, and Melatonin) had minimal results (Tsai, 1999). In the case of B-6 and Magnesium, which can help with symptoms of schizophrenia and autism, researchers could not verify the methodologically unsound results despite stellar outcomes (Tsai, 1999). For B-12 and Folic acid, meant to restore normal functioning to the brain, research originally showed promising results but these could not be replicated either (Tsai, 1999). Melatonin, meant to regulate sleep cycles, could assist with the sleep problems but did nothing for the autism itself (Tsai, 1999). Even within the large amounts of required supplemental treatments, however, autism remained untreated.
While the CAM and supplemental treatments do not treat autism, one form of nutritional treatment does boast to treat autism based upon theoretical dietary sensitivity – the gluten-free, casein-free diet. The foundation of the dietary treatment, the removal of casein and gluten from the diet, is one that is unfounded according to Ahearn (2010). Based upon the concept of selective stimulus that is known to occur in autism, the autistic’s food is restricted to just a certain range to attempt to placate either the selectivity or to deal with unspoken pain. However, the problem with this becomes clear as often the autistic person is required to eat separate meals – further casting out an already ostracized child. This, however, is in vain as the diet has no scientific evidence to state it works in treatment of autism (Ahearn, 2010).
In following of the research on CAMs, vitamin, mineral, supplemental, and dietary treatments and cures for autism, a return is required to the causes of the disorder. Strong evidence suggests that autism is genetic (Volker & Lopata, 2008) as well as neurological/neurochemical (Tsai, 1999). In his evaluation of the neurochemical, Tsai (1999) examined many of the various psychoactive pharmaceuticals which can treat the various behaviors associated with autism and his findings were numerous. However, to begin the discussion Tsai (1999) outlines that of those with ASD, 60% have poor attention, 40% are hyperactive, 88% show preoccupation, 37% have obsessive tendencies, 16 to 89% show stereotyped utterance, 70% show stereotyped gestures, 17 to 74% have anxiety, 9 to 44% have inappropriate affect, 24 to 43% have history of self-injury, and 8% have tics, and one third have taken or are on psychoactive medication.
Keeping this in mind, Tsai (1999) found that serotonin-related Fenfluramine showed no significant result, Clomipramine had significant results in behaviors and affect with few side-effects, Fluoxetine improved ritualistic behaviors but with many side-effects, Fluvoxamine showed increased agitation in children but lessened compulsion and aggression in adults, Sertaline showed promise in open trials but had many side-effects, and Buspirone remained relatively unstudied. Dopamine studies showed that Haloperidol improved self-care and affect in certain doses with better results in older children but with harmful side-effects that limited trials, Pimozide treated aggression and self-injury but resulted in parkisonian symptoms, and L-dopa only found negative results (Tsai, 1999). Tsai, however, cautions against the use of these as complete treatments due to the small sample sizes.
Neurosurgery for those with ASD does not exist despite some indication that physiology may play a part. We cannot repair the parts in question.
Though all of these medications treat various symptoms well, none truly teach the behaviors and coping mechanisms required by both the autistic and their families. Research points to a method of treatment that has been scientifically validated – Applied Behavior Therapies/Analysis (ABA) (Volker & Lopata, 2008; Maurice, Green & Luce, 1996). Through the teaching of appropriate and inappropriate behaviors through the use of cognitive behaviorist therapy, the child or an adult can learn appropriate, socially-acceptable behaviors well before the window closes and the only recourse is psychoactive medications. For families that must care for autistic children, however, stress must be addressed proactively with problem focusing, social support, positive reframing, emotional regulation, and compromise coping to lessen daily stress both on the parent as well as the child (Pottie & Ingram, 2008).
There are also therapies which can help to model behaviors, examine behaviors for antecedents before consequences erupt, and increase motivation and choice. Along with family therapies, a therapist will utilize a host of approaches to treat someone with ASD ranging from cognitive therapies, behavioral therapies, solution therapies, supportive therapies, individual therapies, family therapies, and a whole host of other intervention strategies that act to assist the family in whole.
Comorbidity, that is a diagnosis that goes along with ASD, is high in ASD. It is the rule. It is not the exception. According to the DSM-5, 70% of those with ASD will have some other diagnosis. Diagnoses that go along with ASD include intellectual disability and language disorder. I will often consider an intellectual disability along with a diagnosis of ASD if the impairment is so profound that it is causing a complete lack of language development.
As the DSM-5 has moved away from reliance upon just IQ score for intellectual disability, and considers need of assistance, I may see a rise in this depending on clinical requirements.
I also frequently see ASD and Attention Deficit Hyperactivity Disorder. I will also typically diagnose an anxiety disorder as well. Often, this will be in the form of Generalized Anxiety Disorder, Social Anxiety Disorder, or Anxiety Disorder NOS.
I often also see depression with ASD. This tends to be Major Depression. I also see lots of sleep problems with those with ASD. I’ll often diagnose a learning disorder on some subject. Typically, this will be English or Reading due to problems with abstract metaphorical nuance.
In short, comorbidity is the rule. It is not the exception.
This piece covered a lot of material on ASD as a diagnosis, treatments of ASD, and associated clinical features. In doing so, I aimed to present factual information along with clinical expertise. This information is meant to educate those who may be wholly ignorant of the causes of ASD.
It is meant to assist in dispelling some of the myths of ASD. It’s also meant to counteract some of the misconceptions of mental health, diagnosis, and the professional nature of psychiatry when it comes to neurodevelopmental disorders such as ASD.
The experience that one may have with ASD is highly individualized. The experience that every person with ASD has is highly individualized. For every person who says they do not experience stereotypy, there are many more than do according to Tsai (1999) who details:
60% have poor attention
40% are hyperactive
88% show preoccupation
37% have obsessive tendencies
16 to 89% show stereotyped utterance
70% show stereotyped gestures
17 to 74% have anxiety
9 to 44% have inappropriate affect
24 to 43% have history of self-injury
8% have tics
33% have taken or are on psychoactive medication