Repetitive and stereotyped behaviors in autism

Repetitive and stereotyped behaviors (RSB) are considered a core symptom of autism spectrum disorders (ASD). This defining symptom has been known since the original series of 11 children described by Kanner. Some of the repetitive behaviors exhibited by these children included jumping, spinning and other rhythmic body movements. Longitudinal studies using either retrospective parental interviews and/or systematic observation reveal that RSB in autistic children unfold with aging, becoming increasingly prevalent between 3 to 5 years of age. The quantity and severity of RSB are directly related to negative outcomes and appear to be co-dependent with social and communication symptoms.

Some people believe that repetitive behaviors like hand-flapping may benefit the child as they may serve as a way of coping with frustrations (e.g., when the environment becomes unpredictable) or a way of communicating. A Neurodiversity proponent, Ms. Julia Bascom, has gone so far as to state that they are a part of her personality, “Is flapping my hands or intensely and obsessively loving something ‘weird’ or wanting to be myself the psychological equivalent of diabetes, or is it a natural and beautiful part of human diversity/” (http://www.thedailybeast.com/articles/2015/02/25/they-don-t-want-an-autism-cure.html).

Contrary to Ms. Bascom’s statement people with obsessive-compulsive disorders are unable to control their thoughts and/or activities. Patients often fall into a spiral of thoughts and actions that gets hardwired into their brain. You can wash your hands until they become raw and the skin ulcerated or your repetitions are so time-consuming as to become disabling. In some cases repetitive behaviors, such as head banging, may give rise to brain damage or death. Bruxism or teeth grinding, is a motor movement disorder or RSB that may lead to dental fractures and wearing down of the tooth enamel. Attrition of the teeth may necessitate placement of steel crowns under general anesthesia. In one ASD study bruxism was reported to occur in approximately one-fifth of surveyed children (Williams et al, 2004).

In the case of my grandson Bertrand his obsession was spinning objects. This materialized probably by his third year of life. Bertrand did not appear to be upset prior to or while spinning objects. His behavior was similar to that of an addict where triggers from the environment (e.g. in the case of an alcoholic the trigger could be passing by a bar) prompted the ritualistic behavior. Anything that could spin looked to Bertrand like a wheel. Once engaged nothing would draw him out of the same.

Contrary to the opinion of Neurodiversity proponents repetitive behaviors are not a social lubricant. Some of these repetitive behaviors, just as in an addiction, hijack your brain and make you numb to other activities, or at least they become less pleasurable. The more you perform them the harder it is to quit. In time, performing the repetitive behavior is the only thing that makes an individual feel well.

The prefrontal cortex controls the urges stemming from subcortical centers. Failure of this executive center to inhibit other areas of the brain may lead to problems in impulse control including tantrums or maladaptive behaviors. Indeed many times maladaptive behaviors coalesce and frequently manifest as a number of behaviors rather than single exemplars. In autism the prefrontal lobes appear to be affected thus providing vulnerability to repetitive behaviors as well as for faulty programming of planned sequences or theory of mind. Also, similar to an addiction, certain alterations in risk genes for autism (e.g., DRD2) are found as an inheritable component of addictive behaviors (Hettinger et al., 2012).

The available data makes us believe that although anxiety may play a role in some cases of RSB, in others it may be a manifestation of an addictive behavior. It also makes us wonder whether fixation in certain interests, like playing video games, may all stem from the same causative mechanism.

References

Hettinger JA, Liu X, Hudson L, et al. DRD2 and PPP1R1B (DARPP-32) polymorphisms independently confer increased risk for autism spectrum disorders and additively predict affected status in male-only affected sib-pair families. Behav Brain Funct 8:19, 2012.

Williams GP, Sears LL, Allard A. Sleep problems in children with autism. J Sleep Res 13:265-8, 2004.

20 responses to “Repetitive and stereotyped behaviors in autism

  1. I am very glad to see this blog post.I was a great object spinner and finger flapper before my cerebral folate deficiency was found and treated.I can tell you that doing these things produces a drug-like “high” in the brain.It was,as you say,very addicting,much the same way,I would imagine,a drug addiction was.As a child,I would go into a severe meltdown if I could not do these things when I wanted.I would sit in school and flap and spin for hours instead of doing any work.I think it is something common to all types of autism,it’s just that the more severe the autism,the more intense the actions,the more severe the addiction,and the more it interferes with other aspects of one’s life.And as with any addiction,it is very difficult to give up without doing something else to take its place,or as in my case,rewiring the brain.I think this is one reason those in the the neurodiversity movement defend this behavior.The desire for stereotypy simply went away after I started treating my cerebral folate deficiency,after 40+ years of doing it.That was 2009.

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  2. I’ve also written about my twiddling which is a self-stimulatory behavior. It is very much like a drug addiction which I can’t quit. I can control it to a certain extent, but I sort of feel like a drug addict going through withdrawal when I do it. I’m wondering how many individuals in the ND movement actually do these forms of self-stimulation. I’m wondering about the etiology of the prefrontal controlling subcortical structures. the term subcortical structure is vague and not very specific, but perhaps that is because the etiology of twiddling is not known. A likely candidate would be the nucleus accumbens which controls pleasure and addictive behavior. I remember you telling me that there were tracts that connected from the prefrontal cortex to the nucleus accumbens but they were excitatory rather than inhibitory and GABA was not the neurotransmitter involved (if i’m remembering correctly) I guess GABA is the main neurotransmitter you’ve concentrated on in your research as the space in the abnormal minicolumns is influenced by inhibition by GABA. I know purkinje cells which have been found to be lacking in many autistic cerebella also use both GABA and norepinephrine as inhibitory neurotransmitters.

    I also wondered if norepinephrine could be involved in this since, as you probably know, the dorsal tegmental bundle goes from the locus coereleus to various parts of the brain thought to be involved in autism including parts of the limbic system and terminating at the superior cerebellar peduncle. I know studies have shown stimulation of the superior cerebellar peduncle is reinforcing in rates, so I was wondering if that had anything to do with the etiology of twiddling, but I guess I’m just speculating from a limited knowledge of neuroscience and I’m not sure even the best experts (yourself included) really know the exact etiology of these self-stimulations. I guess the nucleus accumbens and other pleasure centers are more influenced by dopamine than by GABA or norepinephrine counfounding things further. I wish I could know what was going on in my brain. Sorry if this comment was too long.

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    • I think that I would only be able to speculate just like yourself. There is not much known about RSBs. Still the possible mechanisms and clinical consequences of the same merit much more research than what is done at present. I remember chairing the Developmental Brain Disorders Branch for several years and none of the grants received had ever anything to do with either RSB nor sensory disorders (which is another area in need of research).

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  3. Manuel Casanova,
    Your site is quite interesting.
    “Contrary to Ms. Bascom’s statement, people with obsessive-compulsive disorders are unable to control their thoughts and/or activities.”
    The animal, control system, deterministic, network is physically expected to “control” behavioral events. However, future events are expected to be unpredictable. see (Chaotic systems)
    “People” i.e. animals, are not physically expected to control behavioral events.
    Best wishes, Joe Ray Newton joernewton@att.net

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  4. Thank you for your comments Joe. Curiously I have been interested in systems theory and chaos for the last 20 years. Some of my articles try to explain the hierarchical arrangement of modules within the cerebral cortex and how cognition may be developed through emergent properties.

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    • Manuel thanks for the reply. I first was exposed (1954) to chaotic control systems in old Fords with the I-beam front axel. These Fords, upon hitting a bump (the perturbation) at a particular speed (frequency) would immediately (bifurcate) shimmy (vibrate) at high amplitude. Of course I didn’t know all the physics then.
      Subsequent training and experience with nuclear missile control systems demonstrated chaotic behavior, which again I didn’t understand. Later university aerospace engineering explained the Ford and missile chaotic behavior. This chaos I’ve demonstrated to doctor Mark G Lipe and others with my 1971 Ford pickup again with I-beam axles. .
      The animal information system is little different; it just has trillions of loops and components.
      I will search the NLM and read your pubs.
      Joe

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    • Manual,
      Your “Significant neuronal soma volume deficit in the limbic system in subjects with 15q11.2-q13 duplications”
      is unusually interesting as it directly indicates hypothesized increased volume differentials, now supported by many gene-imaging studies of multiple diagnoses. These differentials also apply to other timing factors such as action potential velocity, neuron integration and AP coordination.. Med Hypotheses. 1999 Jan;52(1):77-83.
      Future studies should focus on these timing factors.

      I’ve read papers on hierarchy and they are ambiguous which makes them impossible.
      Hierarchical arrangement is something I doubt of a massively parallel control system network and I believe it might mislead neuroscientist.
      Best wishes Joe

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  5. Thanks. I may not be able to do it now as I am preparing to travel to Columbia SC for an all day symposium tomorrow; however, I will send you a couple of our papers (chapters). Later on at your convenience send me your email and remind me of this (my email is m0casa02@louisville.edu)

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  6. Aren’t repetitive movements among the clearest sign of neurological impairment? My son, Conrad, used to bounce back and forth from one foot to the other, waving a flag or piece of string. When he was excited, he would swing both shoulders back, then forward, and I have seen this same motion so often in even high functioning autistic adults. Aren’t these called athetoid movements?

    My oldest son, less afflicted than Conrad, used to wiggle his hands in small circles when he was excited. He has recovered to a much greater degree than Conrad, but often has distinctive movements of his lower arms when he walks fast. Both of my two oldest sons were very athletic, as are both of their younger brothers.

    Conrad was very jaundiced at birth, and from my reading, I think his autism was really kernicterus. That would mean damage of the basal ganglia and relay nuclei in the auditory pathway. Subcortical damage at birth would disrupt maturation of the cerebral cortex, especially the language areas. This is my view, and I would appreciate discussion with neurologists like you.

    The ideas of “neurodiversity” proponents totally neglect all that has been learned by research in neurology since the days of Broca, Wernicke, and others in the 19th and 20th centuries.

    Patience, aka Eileen Nicole Simon

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    • Neurodiversity proposes many things that fly in the face of science. I think they feel justified as long as nobody challenges them. Many repetitive movements can be asses as motor movement abnormalities and in certain cases do suggest a neurological impairment. To say that it is a personality trait is absurd.

      In the case of your son kernicterus has often been associated with motor abnormalities. There have been a number of studies.blogs writen on the subject of kernicterus or jaundice and autism. Considering that extreme prematures have a strong risk for kernicterus may explain why they are also linked to autism.

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  7. Good question. Different forms of Neurodiversity type thinking have been around since the ancient Greeks. From there we had the era of the Romantics and divine madness and even the antipsychiatry movement of the 60’s. Right now many of the members are either self-diagnosed or suffer from a borderline personality disorder.

    We all fight for accommodations, however, neurodiversity’s stance on research and lack of treatment for everybody (including conditions like bipolar) is dangerous and could prove deadly.

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    • I have read before that neurodiversity had its roots in the antipsychiatry movement of the 1960s.One complaint I have with neurodiversity,is it remains stuck in that past.That it ignores all we have learned in the last couple of decades about the immune,metabolic,and genetically controlled mechanisms behind the various forms of both autism,and schizophrenia.Maybe ignore is the wrong term,perhaps willful ignorance is more like it.As for why such a philosophy based on scientific neo-luddism has become so popular,is anybody’s guess.It has been suggested that those sympathetic to neurodiversity might be on the mild end of the spectrum themselves,and see themselves in the advocates of neurodiversity.Others may see the explanation offered by neurodiversity as an easy way out.A simple explanation to avoid all of the hard work involved in research,and finding causes for these disorders.

      The acceptance of self-diagnosis is a disgrace.This seems to be one of neurodiversity’s dirty little secrets,that only those “in the know” seem to be aware of.

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      • I am also scratching my head. No science to back arguments only their imagination. Considering that many appear to be self-diagnosed or have a personality disorder not autism does not seem to matter.

        People are living in a dream world shaded by Neurotribe’s verbiage. It is of concern that some of the praises for the same come from parents and individuals that do not seem to grasp the meaning of the message.

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  8. Thank you for your comment above that neurodiversity’s stance on research and treatment is dangerous. Medical education includes learning about neurological disorders and the brain structures affected. Why are so many well-educated doctors now sympathetic to the neurodiversity movement?

    Autism begins in early childhood. Its clear neurological signs are (1) language disorder, (2) repetitive movements, (3) oculomotor deficit, (4) diminished environmental awareness, and (5) sometimes seizures. Terms like “communication” and “social” disorders were euphemistic attempts to minimize the stigma of brain damage.

    Everyone with an MD degree should know cortical structures like the frontal, parietal, occipital, and temporal lobes, plus subdivisions like the pre-central gyrus, and special circuits like the angular gyrus. They have been taught about subcortical structures like the basal ganglia, and sensory pathways in the brainstem that course through the midbrain tectum, geniculate bodies and thalamus toward target structures in the cortex. Maturation of the target structures depends upon integrity of the earlier developing brainstem pathways, and autism results from disrupted maturation.

    Thank you for pointing out that self-diagnosed members of the neurodiversity community are likely afflicted with borderline personality disorder. That they write best-selling books and their ideas are taken seriously by medical “experts” is appalling. Is there some way the neurodiversity movement can be stopped? They would have us discard everything that has been learned about the brain.

    Patience, aka Eileen Nicole Simon

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  9. Thank you for asking me to expand on my personal experience and ideas on autism. My experience began with the difficulties I had in childbirth. Before I had ever heard the word autism, I was trying to go beyond what pediatricians were telling me not to worry about.

    WF Windle in the October 1969 Scientific American presented his surprise finding of damage in the brainstem auditory pathway caused by asphyxia at birth (in monkeys). Then I found the article he wrote with MD Faro on subsequent maturational failure of the cerebral cortex in monkeys subjected to asphyxia at birth (Experimental Neurology 24:38-53 (1969). These papers were soon to be forgotten, except by me.

    Autism is associated with myriad genetic defects, prenatal rubella infection, prenatal exposure to valproic acid (Depakote) or alcohol. Darby and Clark (1992) proposed that autism results from injury of a “final common pathway” in many organic disorders. Despite great hopes for a cure, the final common pathway appears to be in the brain.

    Increased prevalence of autism must be the result of some recent interference with infant development. I posted a website conradsimon.org 16 years ago in memory of my son Conrad. I received many email messages asking how soon after birth Conrad’s umbilical cord was clamped. Clearly it was before he was breathing.

    Clamping the umbilical cord immediately after birth became standard protocol in the mid 1980s. Dr. George Malcolm Morley explains why this is wrong on his website autism-end-it-now.org. The brainstem auditory system as a “final common pathway” is something I can discuss further.

    Patience, aka Eileen Nicole Simon

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    • Thanks. The comments are very helpful. It is interesting that you and others like Jonathan are careful to cite the relevant medical literature and are better read than even some physicians. I do not see that from the Neurodiversity side, where assertions are made without any regards to available contradictory evidence.

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    • Thanks for the comments. You sound like a loving mother and one that has done her homework trying to understand autism. As I said in my response at corticalchauvinism, I find it curious that others in the Neurodiversity camp have not done their homework but use their imagination as proof of an argument.

      Manuel F. Casanova, M.D. SmartState Endowed Chair in Childhood Neurotherapeutics Professor of Biomedical Sciences Departments of Pediatrics and Biomedical Sciences University of South Carolina School of Medicine Greenville Campus Greenville Health System ________________________________

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