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Help for Autism

Neuro-physiotherapy for Autism Spectrum Disorder

Judith Ann Miller Ph.D. & Dallas Shepard, RP




ABSTRACT

Autism Spectrum Disorder (ASD) was previously defined as a pervasive developmental disorder marked by deficits in social interaction, communication and behavior. In addition symptoms may include high anxiety difficulties with attention and impulsivity, and specific learning difficulties. ASD is characterized by the early onset of impairments in social and communication skills along with restricted and repetitive interest and activities. Recent research has shown that ASD has links to neuro-physiological disorders which include neural executive deficiencies, oxidative stress and mitochondrial dysfunction. This presentation is two-fold in that it first - introduces LENS (Low Energy Neurofeedback systems) training for Autism Spectrum Disorder. Secondly, NFR2 is introduced as an activation product designed to reduce oxidative stress and mitochondrial dysfunction for ASD. A brief literature review presents a description of LENS and progress reports of individual children diagnosed with ASD; followed by a description of how NFR2 works to alleviate stress for ASD. While the best is yet to come, this article acknowledges successful, innovative integrated treatments for ASD.


Coordinated Alternative Therapies - Dr. Julie Kibby, in a presentation to World Dreaming: World congress for Psychotherapy entitled: “The interface of psychotherapy and Autistic Spectrum Disorder reported: Autistic spectrum disorder is a condition of delayed speech development, impaired emotional responsiveness and a desire for sameness. In early life young people are described as being in a dream world separated from others. The etiology is multi-factorial but the awareness of transcriptor genes in forming neural synapses increasingly implicates environmental factors. There is anecdotal evidence of improvement through life experience but with increasing frequency and a plethora of treatment options. It is timely to consider the interface of this condition with psychotherapy. A consideration of ASD as a presentation of anxiety in mother and child is proposed; the infant brain bathed in glucocorticoids. Transcriptor genes are thereby induced or impeded. This study considers the diagnosis made through psychotherapy; the referral of a young male with treatment resistant depression; the therapy for an autistic adolescent with school refusal and depression; the enriching of the emotional environment of parents of children with ASD and treating the trauma of the sibling through therapy through a recognition of autistic features and the adaptation required by the therapist utilizing the Conversational Model. The potential of psychotherapy is affirmed where a new form of relatedness can be established (Kibby, 2010).”


History of ASD Treatment - Historically, the prognosis for individuals diagnosed with ASD in childhood has been poor: Levy and Perry (2011) found across studies that prior to 1990, only 25 percent of such individuals were classified as having “good” or “fair” outcomes based on an operationalized definition of a “good” or “fair” outcome for an adult with ASD as having achieved some form of formal education, maintaining employment, living independently, and sustaining social relationships. Currently, the state of affairs is not greatly improved.

Autism was first described by Dr. Leo Kanner, (1943) an Austrian-American Psychiatrist as a form of childhood schizophrenia and the result of cold parenting, then as a set of related developmental disorders, and finally as a spectrum condition with wide-ranging degrees of impairment. During the 1950s and 1960s, autism was thought to be rooted in cold and unemotional mothers, whom Bruno Bettelheim dubbed ‘refrigerator mothers.’ The ‘refrigerator mother’ concept was disproved in the 1960s to 1970s, as a growing body of research showed that autism has biological underpinnings and is rooted in brain development.

Current research is focused on identifying the biomarkers for autism and the connectivity or un-connectivity between different regions of the brain. Specific under connectivity is suspected between the prefrontal cortex and posterior regions (Just & Keller, 2004). Research has documented its presentation, etiology, and treatment. Individuals diagnosed with an ASD typically experience difficulty in three main areas: (1) communication; (2) social interaction; and (3) flexibility of thinking and behavior (Wing and Gould 1979).


The Advent of Neuro-physiological Therapy for ASD – Autism Spectrum Disorder (ASD) has traditionally been framed as a behavioral disorder and thus classified as a psychiatric disorder. Much research has been dedicated to neural executive deficiencies (Hammond, 2-011). Also, recent evidence has been linked to physiological abnormalities in ASD, which strongly implicate that ASD has a clear biological basis with features of known medical disorders. The past couple decades have revealed a strong correlation between oxidative stress and mitochondrial dysfunction and causes of autism (Chauhan & Chauhan, 2007, and Rossigignol & Frye, 2014).


Oxidative Stress and Mitochondrial Dysfunction Related to ASD A number of studies using peripheral biomarkers have linked oxidative stress, mitochondrial dysfunction and immune dysregulation in individuals with ASD (James et al., 2009a; Mostafa et al., 2010; Zhang et al., 2010; Napoli et al., 2013; Theoharides et al., 2013; Frye et al., 2013a).


The Gut-Brain Relationship as Related to ASDAs many as 90% of people with autism exhibit gastrointestinal (GI) dysfunction including bloating, abdominal pain, and alternating diarrhea and constipation, which can exacerbate core autism traits [Buie et al., 2010 & McElhanon, et al. 2014).


Innovative Treatments for ASD - A number of studies have reported improvements in autism using nutritional supplements and medications which can support mitochondrial function (Geier et al., 2011; Frye and Rossignol, 2012b; Rossignol and Frye, 2012b; Fahmy et al., 2013), reduce oxidative stress (Dolske et al., 1993; Chez et al., 2002; Adams and Holloway, 2004; Rossignol, 2009; Adams et al., 2011; Rossignol and Frye, 2011; Hardan et al., 2012; Ghanizadeh and Moghimi-Sarani, 2013), and decrease inflammation (Stefanatos et al., 1995; Shenoy et al., 2000; Boris et al., 2007; Bradstreet et al., 2007; Asadabadi et al., 2013; Taliou et al., 2013)


Neural Executive Dysfunctions - There is also mounting evidence that executive function deficits may contribute to the core symptoms of ASD (Hill, 2004). During the past two decades research on Neurotherapy for autism and Asperger’s Syndrome has shown significant success (Coben & Meyers, 2010; Coben & Pudolsky, 2007; Jarusiuwic, 2002; Kouijzer, de Moor, Gerits, Buiterlaar, & van Schie, 2009; Kouijzer, de Moor, Gerrits, Congedo, & van Schie, 209; Koupijze, van Schie, de Moor, Gerrits & Buitelaar, 2010; Pineda et al., 2007; Pineda et al., 2008; Scolnick, 2005; Siche, Fehmi, & Goldstein, 1995). This understanding has led to advanced treatment strategies for ASD, namely neurofeedback and NfRF2, an activation product that reduce oxidative stress and mitochondrial dysfunction.


Neurofeedback - A recent scientific literature review by Dr. Corydon Hammond, (2011) of the University of Utah, School of Medicine reported that neurofeedback has shown positive research support as a beneficial treatment for autism spectrum problems. Such findings have shown positive changes in brain function, attention, IQ, impulsivity and parental assessments of other problem behaviors such as communication stereotyped and repetitive behavior, reciprocal social interaction, and sociability. Dr. Hammond notes that neurofeedback while not a cure for these conditions seems to significantly improve chronic autistic symptoms.

Researcher Coben and Associates (2002 & 2010) review of positive findings with neurofeedback treatment of autism found a 41% reduction in overall autistic symptoms, including a 55% decrease in social interaction deficits and improvements in communication and social interaction deficits

A 2010 case study of nine (9) autism spectrum syndrome patients who received 40 to 60 neurofeedback sessions, found statistically significant improvements in measures of attention, impulsivity, auditory and visual attention, reading, spelling, arithmetic, EEG measures and an average full scale IQ score gain of 9 points (Thompson, Thompson & Reid, 2010).


The Neuro-feedback Application: Low Energy Neurofeedback Systems (LENS) – LENS as developed by Dr. Len Ochs of Ochs Labs, Inc., is designed to restore the brain’s neurochemistry by gently releasing repressions and enhancing mental efficiency. This system utilizes low energy biofeedback signal to connect neurological pathways compromised by physical and emotional trauma. Treatments are non-invasive, painless, and can lead to dramatic improvement in chronic debilitating neurological conditions. It is an exceedingly mild form of non-cognitive biofeedback that takes information from the brain directly and the client does not have to do anything but sit quietly in the treatment chair. The neurological activity from a single site location is processed through a biofeedback loop in the computer and a return stimulation is sent back to the brain with slight modifications. The feedback signals can have a remarkable therapeutic effect as they allow the brain to re-connect its own blocked nerve pathways.


Progress Reports: LENS Application for ASD Children - This section presents progress reports for children diagnosed with ASD who were successfully treated with LENS. While most are experiencing continual therapy, their progress is remarkably encouraging.

Timothy F – Timothy is a 6-year-old, non-verbal very active intelligent boy attending a local rural school. He began his second month of LENS training on a very cold day and when he walked to his van with his grandparents he said: “Cold”. A few days later he woke his grandfather from a nap and said: “You gotta get up”. He has progressed to singing Christmas Carols and speaking in phrases. His past behavior was to flop on the floor as he entered the therapy room and his grandmother would pick him up and hold in in the chair. The technician was insightful enough to say to the grandmother: “You don’t have to pick him up, he’s a big boy, he can get up by himself”. He immediately jumped up and said: “Big boy”. He sat in the chair by himself and said: “Gotta sit still”. Now Timothy sits in the chair with no one holding him, wraps his legs around the technician whom he calls “Lady” and calls out the colors “red, yellow, blue” as he watches on the computer screen. After 3-months of LENS he is singing his ABCs and recently sang Twinkle Twinkle Little Star. His teacher is amazed at his progress. By 6 months Timothy now hugs his grandmother and says “I love you”. He has learned in school a song about “eyes, fingers noes and toes, eyes fingers, knees and toes, eyes, fingers ears and toes”. His teacher reports that he is reading.

Hannah W – Hannah is an 11-year-old girl whose parents, to no avail, have spent nearly a million dollars seeking brain therapy. Hannah was introduced to LENS and has made remarkable progress. Her prior diet consisted on only white rice, but now she is eating a variety of healthy foods. When she boards her school bus she says: “Love bus”, and proceeds to hug all the kids. Hanna’s father recently passed away. Her most astonishing behavior occurred when her mom took her to the cemetery, where she had never been, and she ran to her father’s grave and climbed up on the tombstone. How did she know?


Michael Beasley of Neuropaths of Austin Texas – Reported: I only worked with a few autistic clients, all of them young. One taught me a lot. Such a great kid. What his parents and I observed after each session was an increase in vocabulary. New words were added along with more social interaction, hugging and more eye contact. One day his uncle came to the family’s door and got a big hug along with a verbal greeting. Neither of these events ever happened previously. So naturally the Uncle was stunned and wanted to know what they were doing differently.

Other changes occurred; the child decided to rearrange his room because he was too old for it, whereas before no one could move or rearrange items without big emotional outbursts until the room was returned to “normal”.

One of the more interesting revelations about using the LENS with this autistic child was associated with the speed of recovery following strong immune system activity. During one session I was asked to smell his hair which had the aroma of bread dough. The mother explained that when he experienced a yeast bloom his hair smelled like bread. His progress would not only slow but travel backward in time until the yeast bloom stopped and then he would start the return progress. If the responses were sufficiently strong the ability to walk and/or talk stopped. Once the yeast situation was under control again the abilities to walk and talk returned, but it could take two or more months. His mother told me that since we started working with him, this took only a couple of weeks, not months. Somehow the therapy seems to shorten the recovery time in this situation.


Dallas Shepard of Harmonized Brain Centers of Colorado Springs, Colorado – Reported: A four year old autistic child with a lack of social skills, fine motor skills, low communication skills, attention deficit, hard time sitting still and was not potty trained. It took two sessions to complete a 21 site map as sensitivity was heightened. As shown on JH1 (Mean Total Amplitude) image the range in microvolts tops out at 110 microvolts (this range is quite common with young Autistic children). However, this is extremely high as up to 35 is more the norm. The more drastic display is in the JH1 bottom chart (Mean Dominant Frequency). This chart is measured in frequency (cycles per second) and as shown 19 of the 21 sights fall below 4 cycles per second meaning most of this brain is dominated with deep sleep delta waves. In essence most of his behavior seems to be related to his brain trying to sleep yet he was in an awake state.



Chart JH2 is after 12 sessions of LENS Neurofeedback and we saw great improvement in that the child would sit still in the chair, engage in brief conversation, was able to button his shirt, became potty trained, was a lot less restless and had better interaction at school. The JH2 chart (Mean Total Amplitude) is now 35 microvolts and below and the Mean Dominant Frequency only has 5 sites with deep sleep delta waves. Huge improvements in behavior and processing.


Evolving Innovations For Neurological DisordersNeurological disorders represent a great challenge and are the leading cause of death and disability globally. Although numerous complicated mechanisms are involved in the progressions of chronic and acute neurodegenerative disorders, most of the diseases share mutual pathogenic features such as oxidative stress, mitochondrial dysfunction, neuro-inflammation, protein misfolding, excitotoxicity, and neuronal damage, all of these are the common targets of nuclear factor erythroid 2 related factor 2 (Nrf2) signaling cascade. No cure has yet been discovered to tackle these disorders, so, intervention approaches targeting phytochemicals have been recommended as an alternative form of treatment. Sulforaphane is a sulfur-rich dietary phytochemical which has several activities such as antioxidant, anti-inflammatory, and anti-tumor via multiple targets and various mechanisms. Given its numerous actions, sulforaphane has drawn considerable attention for neurological disorders in recent years. Nrf2 is one of the most crucial targets of sulforaphane which has potential in regulating the series of cytoprotective enzyme expressions that have neuroprotective, antioxidative, and detoxification actions. Neurological disorders are auspicious candidates for Nrf2-targeted treatment strategy. Sulforaphane protects various neurological disorders by regulating the Nrf2 pathway (Ubin, 2020).


Nutrigenomics: The study of how nutrients and naturally occurring compounds effect our genes – Introducing the Protandim Tri-Synergizer products: NAD; NRF2, NRF1, Probio and Axio :

NAD – Recently, scientists have been sharing the importance of proteins called situins. Studies showing situin activity comes from a cascade of health benefits. Including supporting a healthy vascular system, maintaining cholesterol levels already in the health range, supporting the body’s healthy inflammation response, supporting joint health, heightening mental focus, improving mood, motivation, energy, and much more. Protandim NAD Synergizer was specifically formulated to target NAD, and has been shown to double situn activity in 24 hours, supporting increased health, focus, energy, mental clarity, and mood.


Benefits of Protandim NAD Synergizer

· Supports healthy longevity

· Supports autophagy (removal of cellular waste)

· Improves mental focus and concentration

· Supports positive mood and motivation

· Boosts mental and physical energy

· Supports body’s healthy inflammatory response

· Maintains cholesterol levels already in the healthy range

· Supports healthy vascular system


NRF2 – Protandim NRF2 Synergizer was sculpted to activate the Nrf@ pathway, a pathway responsible for antioxidant production. With peer-reviewed studies conducted by Harvard, Ohio State University, the American Journal of Physiology and many more, Protandim Nrf2 Synergizer has been shown to reduce oxidative stress by 40% in just 30 days.


Benefits of Protandim NRF2 Synergizer

· Helps the body detoxify genes, keeping the master blueprint of the cell’s function intact

· Reduce oxidative stress by 40% in just 30 days

· Significantly reduces cellular stress through Nrf2 activation

· Produces enzymes capable of neutralizing more than 1,000,000 free radicals

· Helps to regulate survival genes

· Supports the body’s natural ability to repair and rejuvenate its own cells.


NRF1 – Nrf1 is based on the fact that our mitochondria are literally powering everything in our bodies, from our heartbeat to or brain cells, and unfortunately, our mitochondria decline over time when stressed. The NRF1 pathway is responsible for mitochondrial health.


Benefits of Protandim NRF1 Synergizer

· Improves performance through energy function

· Enhances cellular health – cells function at peak performance

· Increases cellular energy (ATP)


PROBIO for Healthy Digestion – Probio is science’s answer to gastrointestinal health as it provides the right balance of probiotics and immune system to support and keep the body on track. It provides beneficial bacteria to maintain a healthy gut flora while enhancing the immune system. It features a unique controlled-release technology, delivering probiotics throughout the day and deep into the digestive system where they are needed most.


Benefits of PROBIO

· 6 billion CFU’s of healthy bacteria to support the digestive system

· Providing beneficial bacteria to maintain a healthy gut flora

· Safely enhancing the immune system

· Featuring a unique controlled-release technology, delivering probiotics throughout the day and deep into the digestive system – where they are needed most

· Helping to support tight junctions and the communication between brain and gut to help signal when full.


AXIO Start Energy – Axio is specifically formulated to give energy to the mind, not just the body. Engineered with Nrf2 ingredients, it’s designed to deliver mental clarity, focus, and concentration without the jitters of caffeine crash.


Benefits – The Brain-First Approach

· Supports mental endurance and mental activity

· Supports concentration and memory retention

· Supports physical and mental energy

· Supports positive mood

· Ore resiliency to everyday stress

· Enhanced information processing and attention

· Reduced mental fatigue and brain fog

· Clean formula – natural sweeteners (no addictive sugars), natural flavors, natural colors, non-gmo, gluten-free, low calories, low carbs, vegan, (BSCG approved)


* These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.


Applied Behavioral Analysis (ABA)The American Psychological Association (APA) embraces applied behavior analysis as “clearly within the scope of the discipline of psychology and … an integral part of the discipline of psychology” and affirms “that the practice and supervision of applied behavior analysis are well-grounded in psychological science and evidence-based practice.’

Evidence based” means that ABA has passed scientific tests of its usefulness, quality, and effectiveness. ABA therapy includes many different techniques. All of these techniques focus on antecedents (what happens before a behavior occurs) and on consequences (what happens after the behavior). While ABA is the most widely used therapy for autism, some people say its drills and routines are cruel, and its aims misguided.

Since ABA was began 50 decades ago (Baer, et al, 1987), more than 20 studies have established that intensive and long-term therapy using ABA principles improves outcomes for many but not all children with autism. “Intensive” and “long term” refer to programs that provide 25 to 40 hours a week of therapy for 1 to 3 years. These studies show gains in intellectual functioning, language development, daily living skills and social functioning. Studies with adults using ABA principles, though fewer in number, show similar benefits,


Combing LENS, Nutrigenomics and ABA for ASD Relief – It seems that ABA while proven to be an effective behavioral therapy, could be even more effective if LENS and Nutrigenomics were added to the treatment regime for ASD sufferers. The purpose of this paper is to provide science-based information for therapists and parents to consider the value of the science that suggests that this combination could actually be the best possible therapy for ASD.


REFERENCES

Adams, J. B., T. Audhya, S. McDonough-Means, R. A. Rubin, D. Quig, E. Geis, et al. (2011). Effect of a vitamin/mineral supplement on children and adults with autism. BMC Pediatrics 11:111. DOI: 10.1186/1471-2431-11-111.

Aman, M. G., & N. M. Singh (1994). Aberrant Behavior Checklist. Community. Supplementary Manual. Slosson Educational Publications, East Aurora, NY.

Asadabadi, M., M. R Mohammadi, A. Ghanizadeh, A. Modabbernia, M. Ashrafi, E. Hassanzadeh, et al. (2013). Celecoxib as adjunctive treatment to risperidone in children with autistic disorder: a randomized, double-blind, placebo-controlled trial. Psychopharmacology (Berl.) 225, 51–59. Doi: 10.1007/s00213-012-2796-8.

Baer, D. M., M. Montrose, & M. Wolf (1987). Some still-current dimensions of applied behavior analysis, Journal of Applied Behavior Analysis, 20(4):313-327.

Bishop-Fitzpatrick, L, N. J. Minshew, & S. M. Fack (2013). A Systematic review of psychosocial interventions for adults with autism spectrum disorders. Journal of Autism Developmental Disorder, 43(3):687-694. DOI: 10.1007/s10803-012-1615-8.

Buie, T., G. J. Fuchs, G. T. Furuta, K. Kooros, J. Levy, J. D. Lewis, & H. Winter, (2010). Recommendations for evaluation and treatment of common gastrointestinal problems in children with ASDs. Pediatrics, 125(Suppl 1), S19–S29.

Bodfish, J. W., F. J. Symons, & M. H. Lewi (1999). Repetitive behavior scale, Western Carolina Center Research Reports, Morgan, NC.

Boris, M., Kaiser, C. C., Goldblatt, A., Elice, M. W., Edelson, S. M., Adams, J. B., et al. (2007). Effect of pioglitazone treatment on behavioral symptoms in autistic children. J. Neuroinflammation 4:3. DOI: 10.1186/1742-2094-4-3.

Bradstreet, J. J., S. Smith, D. Granpeesheh, J. M. El-Dahr, & D. Rossignol (2007). Spironolactone might be a desirable immunologic and hormonal intervention in autism spectrum disorders. Med. Hypotheses 68, 979–987. DOI: 10.1016/j.mehy.2006.10.015.

Chauhan, A., & V. Chauhan, (2006). Oxidative stress in autism. Pathaophysiology; 13(3):171-181. DOI: 10.1016/j.pathophys.2006.05.007. Epub 2006 Jun 12.

Cassanova, M.F., I. van Kootcn, A. E. Switala, H. van England, H. Heinsen, H. W. Steinbuch, et al. (2006). Abnormalities of cortical minicolumnar organization in the prefrontal lobes of austic patients. Clinical Neuroscience Research. 6, 127-133.

Casanova, M. F., (2007). The neuropathology of autism. Brain Pathol. 17, 422-433.

Center for Disease Control and Prevention (CEC) (2012), Prevalence of Autism Disorders – Autism and Developmental Disabilities Monitoring network, 14 (SSO3), United States, 2008. Surveillance Summaries, 61 (SSO3), 1-19.

Chez, M. G., C. P. Buchanan, M.. C. Aimonovitch, M. Becker, K. Schaefer, C. Black, et al. (2002). Double-blind, placebo-controlled study of L-carnosine supplementation in children with autistic spectrum disorders. J. Child Neurololgy. 17, 833–837. DOI: 10.1177/08830738020170111501.

Coben, R. (2007). Connectivity-guided neurofeedback for autistic spectrum disorder. Biofeedback, 35(4), 131-135.

Coben, R., M. Linden, & T. E Meyers (2010). Nedurofeedback for autistic spectrum disorder: A review of the literature. Applied Psychophysiology & Biofeedback, 33, 83-105.

Coben, R., & L. Wagner (2011). Emerging empirical evidence supporting connectivity guided Neurofeedback for Autistic Disorders. In Coben & Evans (EDs.) Neurofeedback and Neuromodulation Techniques and Applications (152-182) Elsevier, London, UK.

Coben, R., & T. E. Meyers (2010). The relative effect of connectivity guided and symptom based EEG biofeedback for autistic disorders. Applied Psychophysiology & Biofeedback, 35(1):13-23.

Constantino, J.N., & C. P. Gruber (2005). The Social Responsiveness Scale (SRS) Manual. Western Psychological Services, Los Angeles, CA.

De Ridder, D. (2009). An evolutionary approach to brain rhythms and its clinical implications for brain modulation. Jounral of Neurotherapy (13)1:69-70.

Dolske, M. C., J. Spollen, S. McKay, E. Lancashire, & L. Tolbert(1993). A preliminary trial of ascorbic acid as supplemental therapy for autism. Prog. Neuropsychopharmacol. Biol. Psychiatry 17:765–774. DOI: 10.1016/0278-5846(93)90058-Z.

Fahmy, S. F., M. H. El-hamamsy, O. K. Zaki, & D. A. Badary (2013). l-Carnitine supplementation improves the behavioral symptoms in autistic children. Res. Autism Spectrum Disorder 7:159–166. DOI: 10.1016/j.rasd.2012.07.006.

Frye, R. E., R. Delatorre, H. Taylor, J. Slattery, S. Melnyk, N. Chowdhu et al. (2013a). Redox metabolism abnormalities in autistic children associated with mitochondrial disease. Transl. Psychiatry 3,:273. DOI: 10.1038/tp.2013.51.

Frye, R. E., & S. J. James (2014). Metabolic pathology of autism in relation to redox metabolism. Biomark. Med. 8:321–330. DOI: 10.2217/bmm.13.158.

Frye, R. E., S. Melny, & D. F. Macfabe (2013b). Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder. Transl. Psychiatry 3:e220. DOI: 10.1038/tp.2012.143.

Frye, R. E., & R. K. Naviauy (2011). Autistic disorder with complex IV overactivity: a new mitochondrial syndrome. J. Pediatr. Neurol. 9:427–434. DOI: 10.3233/JPN-2011-0507.

Frye, R. E., & D. A.Rossignol (2011). Mitochondrial dysfunction can connect the diverse medical symptoms associated with autism spectrum disorders. Pediatric Research. 69, 41R–47R. DOI: 10.1203/PDR.0b013e318212f16b.

Frye, R. E., & D. A. Rossignol (2012a). Mitochondrial and metabolic abnormalities in neurodevelopmental disorders. J. Ped. Biochem. 2, 177–180. DOI: 10.3233/JPB-120059.

Frye, R. E., & D. A. Rossignol (2012b). Treatments for mitochondrial dysfunction associated with autism spectrum disorders. J Ped Biochem 2, 241–249. DOI: 10.3233/JPB-120065.

Frye, R. E., & D. A. Rossignol (2013). Mitochondrial physiology and autism spectrum disorder. OA Autism 1, 5. DOI: 10.13172/2052-7810-1-1-433.

Frye, R. E., J. M. Sequeira, E. V. Quadros, S. J. James, & D. A. Rossignol (2013c). Cerebral folate receptor autoantibodies in autism spectrum disorder. Mol. Psychiatry 18, 369–381. DOI: 10.1038/mp.2011.17.

Gevirtz, R. (2010). Autonomic Nervous System Markers for Psychophysiological Anxiety, and Physical Disorder, Chaper 9 in Evian Gordan & Stephan H. Koslow, Eds). Integrative Neuroscience and Personalized Medicine, (Oxfort Press pp.164-181.

Green, V.A., K. A. Pituch, J. Itchon, A. Choi, M. O’Rielly, & J. Sigafoos (2006). Internal survey of treatments used by parents of children with autism. Research in Developmental Disabilities, 27, 70-84.

Geier, D. A., J. K. Kern, G. Davis, P. G. King, J. B. Adams, J. L. Young, et al. (2011). A prospective double-blind, randomized clinical trial of levocarnitine to treat autism spectrum disorders. Med. Sci. Monit. 17, PI15–23. DOI: 10.12659/MSM.881792.

Ghanizadeh, A., & E. Moghimi-Sarani (2013). A randomized double blind placebo controlled clinical trial of N-Acetylcysteine added to risperidone for treating autistic disorders. BMC Psychiatry 13:196. DOI: 10.1186/1471-244X-13-196.

Hammond, D. C. (2011). What is Neurofeedback: An Update. Journal of Neurotherapy 15:305.

Hardan, A. Y., L. K. Fung, R. A. Libove, T. V. Obukhanych, T. S. Nair, L. A. Herzenberg, et al. (2012). A randomized controlled pilot trial of oral N-acetylcysteine in children with autism. Biol. Psychiatry 71, 956–961. DOI: 10.1016/j.biopsych.2012.01.014336.

Hill, E L. (2004). Evaluating the theory of executive dysfunction in autism. Developmental Review, 24:189-233.

Jarusiewicz, G. (2007). Use of neurofeedback with autistic spectrum disorders. Chapter in J. R. Evans (Ed.), Handbook of Neurofeedback. Binghampton, NY: Haworth Medical Press, pp. 321-339.

James, S. J., S. Melnyk, S. Jernigan, M. A. Cleves, C. H. Halsted, D. H. Wong, et al. (2006). Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism. Am. J. Med. Genet. B Neuropsychiatr. Genet. 141B, 947–956. DOI: 10.1002/ajmg.b.30366.

Jarusiewicz, B. (2002). Efficacy of neurofeedback for children in the autistic spectrum: A pilot study. Journal of Neurotherapy, 6(4), 39-49.

Just, M. A., & T. Keller (2013). Is ‘underconnectivity’ in autism specific to frontal cortex? Spectrum, March: 1-6. https://spectrumnews.org/glopinion/viewpoint/s-underconnectivity-in-autism-specific-to-frontal-cortex.

Kanner L. (1943). Autistic disturbances of affective contact. Nervous Child; 2(3):217–250.

Keen, D., & S. Word (2004). Autistic spectrum disorder: A child population profile, Autism, 8, 39-58.

Kibby, J. (2011). The interface of psychotherapy and Autistic Spectrum Disorder. World Dreaming: World congress for Psychotherapy. 24-28 August 2011 Sydney Convention and Exhibition Centre Darling Harbour, Australia.

Knezevic, B., L. Thompson, & M. Thompson (2010). Pilot project to ascertain the utility of Tower of London Test to assess outcomes of neurofeedback in clients with Asperger’s Syndrome. Journal of Neurotherapy, 14(3), 3-19.

Kouijzer, M. E., J. M. H. de Moor, J. L. Gerrits, J. K. Buitelaar, & H. T. van Schie (2009). Long term effects of neurofeedback treatment in autism. Research in Autism Spectrum Disorders. 3,490-501.

Kouijzer, E. J., E. J. de Moor, J. L. Gerris, M. Congedo, & H. T. Schie (2009). Neurofeedback improves executive functioning in children with autism spectrum disorders. Research in Autism Spectrum Disorder, 3, 145-162.

Kouijzer, M., E. J., de Moor, J. M. H., Gerrits, B. J. L., Congedo, M., & van Schie, H. T.. (2009). Neurofeedback improves executive functioning in children with autisim spectrum disorder. Research in Autism Spectrum Disorders, 3, 145-162.

Kouijzer, M. E. J., H. T. van Schie, J. M. H. de Moor, B. J.L. Gerrits, & J. K. Buitelaar (2010) Neurofeedback treatment in autism. Preliminary findings in behavioral, cognitive, and neurophysiological functioning. Research in Autism Spectrum Disorders, 4:386-399.

Levy A, Perry A. (2011). Outcomes in adolescents and adults with autism: A review of the literature. Research in Autism Spectrum Disorders, 5(4):1271–1282.

McElhanon, B. O., C. McCracken, S. Karpen, & W. G. Sharp (2014). Gastrointestinal symptoms in autism spectrum disorder: A meta‐analysis. Pediatrics, 133:872–883.

Mostafa, G. A., El-Hadidi, E. S., Hewedi, D. H., and Abdou, M. M. (2010). Oxidative stress in Egyptian children with autism: relation to autoimmunity. J. Neuroimmunol. 219:114–118. doi: 10.1016/j.jneuroim.2009.12.003.

Napoli, E., S. Wong, & C. Giulivi (2013). Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism. Mol. Autism 4, 2. DOI: 10.1186/2040-2392-4-2

Neubrander, J., M. Linden, J. Gunkelman, & C. Kerson (2011) QEEG-Guided Neurofeedback: New Brain-Based Individualized Evaluation and Treatment for Autism.

Pineda, J. A., D. Brang, C. Futagaki, E. Hecht, M. Grichanik, L. Wood, & S. Carey (200). Effects of neurofeedback training on action comprehension and imitation learning. In H. L. Puckhaber (ed.), New research in biofeedback. (pp. 133-152. Hauppauge, NW: Nova Science Publishers.

Pineda, J. A., D. Brang, E. Hecht, L. Edwards, S. Carey, M. Bacon, & A. Rork (2008). Positive behavioral and electrophysiological changes following neurofeedback training in children with autism. Research in Autism Spectrum Disorders, 2, 557-581.

Porges, S. W., (20007). The Polyvagal Perspective, Biological Psychiatry, 74, 136-143.

Rossignol, D. A., & R. E. Frye (2014), Evidence linking oxidative stress, mitochondrial dysfunction, and inflammation in the brain of individuals with autism. Front Physiol. 2014; 5: 150. Published online 2014 Apr 22. DOI: 10.3389/fphys.2014.00150.

Rossignol, D. A., L. W. Rossignol, S. J. James, S. Melnyk, & E. Mumper (2007). The effects of hyperbaric oxygen therapy on oxidative stress, inflamationm, and symptoms in children with autism. An open-label pilot study, BMC Pediatrics, 7, 36-49.

Shenoy, S., S. Arnold, & T. Chatila (2000). Response to steroid therapy in autism secondary to autoimmune lymphoproliferative syndrome. J. Pediatr. 136: 682–687. DOI: 10.1067/mpd.2000.105355.

Sichel, A. G., L. G. Fehmi, & D. M. Goldstein (1995). Positive outcome with neurofeedback in a case of mild autism. Journal of Neurotherapy, 1(1):60-64.

Sokhadze, E., J. Baruth, A. El-Baz, T. Horrell, G. Sokhadze, T. Carroll, A. Tasman, L. Sears, & M. Casanova (2010).Impaired error monitoring and correction function in Autism. Journal of Neurotherapy 14(2):79-95.

Stefanatos, G. A., W. Grover, & E. Geller (1995). Case study: corticosteroid treatment of language regression in pervasive developmental disorder. J. Am. Acad. Child Adolesc. Psychiatry 34:1107–1111. DOI: 10.1097/00004583-199508000-00022

Taliou, A., E. Zintzaras, L. Lykouras, & K. Francis (2013). An open-label pilot study of a formulation containing the anti-inflammatory flavonoid luteolin and its effects on behavior in children with autism spectrum disorders. Clin. Ther. 35:592–602. DOI: 10.1016/j.clinthera.2013.04.006.

Theoharides, T. C., S. Asadi, S. Panagiotidou, & Z. Weng (2013). The “missing link” in autoimmunity and autism: extracellular mitochondrial components secreted from activated live mast cells. Autoimmun. Rev. 12:1136–1142. DOI: 10.1016/j.autrev.2013.06.018.

Thompson, L., M. Thompson, & A. Reid (2010). Neurofeedback outcomes in clients with Asperger’s syndrome. Applied Psychophysiologiy Biofeedback, 35(1):63-81.

Thompson, M. & L. Thompson (2010). Functional Neuroanatomy and the Rationale for Using EEG Biofeedback with Clients with Asperger’s Syndrome. Journal of Applied Psychoooophysiology and Biofeedback, (39) 1:39-61.

Thompson, M. & L. Thompson 2009). Systems Theory of Neural Synergy, Neuroanalogical Underpinings in Effective Intervention Using Neurofeedback plus Biofeedback, Journal of Neurotherapy, (13)1:72-74.

Thomospn, M., & L. Thompson (2007). Neurofeedback for Stress Management, Chapter in Paul M. Leher, Robert L. Wolfolk & Wesley E. Sims, (Eds). Principles and Practice of Stress Management, 3rd Edition, Guilford Publications, New York, NY.

Thompson, M., L. Thomppson, J. Thompson, & D. Hagedorn (2011). Networks: A Compelling Rational for Combining Neurofeedback, Biofeedback and Strategies. NeuroConnections, Summer.

Ubin S., et al (2020). Emerging promise of sulforaphane-mediated Nrf2 signaling cascade against neurological disorders. Scientific Total Environ; 10;707:135624. DOI: 10.1016/j-scitotenv.2019.135624. Epub 2019 Nov 21.

Uddin, L. Q., M. Jacobsoni, C. Lange, & J. P. Kennan (2007). The self and social cognition the role of cortical midline structures in micro neurons. Trends in Cognitive Science, (1)4:153-157.

Wing L, & J. Gould (1979). Severe impairments of social interaction and associated abnormalities in children: Epidemiology and classification. Journal of Autism and Developmental Disorders.;9(1):11–29.

Zhang, B., A. Angelidou, K. D.Alysandratos, M.Vasiad, K. Francis, S.Asadi, et al. (2010). Mitochondrial DNA and anti-mitochondrial antibodies in serum of autistic children. J. Neuroinflammation7:80. DOI: 10.1186/1742-2094-7-80.


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