Autism is a disorder of brain function that begins in early childhood and causes impairment in three crucial areas of development: communication, social interaction, and creative or imaginative play. In some cases, children with autism may never develop patterns of typical speech and social interaction. Their speech may be inflexible and unresponsive to context or limited to narrow topics of specialized knowledge or echolalia. Communication impairment includes nonverbal cues such as eye contact, facial expression, and gesture. Social behaviors are often characterized by a lack of interaction and cooperation. Play lacks cooperation and imagination and is often narrowly focused on repetitive activities.
Research shows that autism can be further categorized as part of a spectrum of heterogeneous disorders called Autistic Spectrum Disorders (ASD) characterized by a broad range of abilities and levels of severity but all showing the same triad of core symptoms involving impairments in communication, social interaction, and imagination. The Autistic Spectrum Disorders include: Autistic Disorder, Asperger's Disorder, Semantic Pragmatic Communication Disorder, Non-Verbal Learning Disabilities, High Functioning Autism, and Hyperlexia.
Autistic Disorder and Asperger's Disorder are also classified as forms of Pervasive Developmental Disorder (PDD)—a group of heterogeneous developmental disorders characterized by delays in the development of multiple basic functions including socialization, verbal and nonverbal communication, posture and movement, eating and drinking or sleeping patterns, and responses to sensory input. This group of disorders includes: Autistic Disorder, Asperger’s Disorder, Rett’s Disorder, and Childhood Disintegrative Disorder.
Children with ASD may have severe sensitivity to sounds, textures, tastes, and smells. Cognitive deficits are often associated with impaired communication skills. Repetitive stereotyped behaviors, perseveration, and obsessionality, common in ASD, are associated with executive deficits. Executive dysfunction in inhibitory control and set shiftng have been attributed to ASD but are also seen in ADHD.
ASD may be comorbid with sensory integration difficulties, mental retardation or seizure disorders. Seizure disorders occur in approximately one in four children with ASD; frequently beginning in early childhood or adolescence. There is also a significant symptom overlap between ASD and ADHD since both groups reveal executive dysfunction in inhibitory control, set shifting, and mediating frontostriatal neural pathways in the brain.
Most recent studies estimate a prevalence of 1-2 per 1000 for autism and close to 6 per 1000 for ASD more broadly. The prevalence of Asperger syndrome has been estimated at approximately 0.6 per 1000. PDD-NOS is estimated to have a prevalence of approximately 3-4 per 1000. For unknown reasons, the incidence of autistic spectrum disorders in the general population has increased more than ten-fold since the 1970s. According to Blaxill (2004) the rates of ASD in the United States rose from less than 3 in 10,000 in the 1970s to more than 30 in 10,000 by the mid-1990s.
A review of major textbooks and research articles on autism published since the early 1960s and the present yields convincing evidence for multiple interacting genetic factors as the major causative determinants of autism. Epidemiological studies indicate that environmental factors such as toxic exposures, teratogens, perinatal insults, and prenatal infections such as rubella and cytomegalo-virus account for only a few cases and the current research consensus fails to confirm a connection between immunization vaccine and autism. Autism is generally accepted as the most genetic of all the developmental neuropsychiatric syndromes. The broad variation in phenotypes and severities within the autism spectrum of disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients.
Many of the difficulties in functioning seen in ASD can be viewed from a neuropsychological systems perspective as involving dysfunction within arousal, attentional, sensory integration, and executive functions brain systems.
Current research suggests that ASD may be associated with functional disconnectivity between brain regions. There is evidence for anomalies in the functional connectivity of the medial temporal lobe. Abnormalities have been found specifically in the functional integration of the amygdala and parahippocampal gyrus. Such abnormalities in brain function point to the need for therapeutic interventions that address ASD as a neurodevelopmental and brain disorder.
Behavioural and social-educational treatments have been the traditional options for treatment. Dietary modification and food elimination interventions are becoming more common and appear to have positive impact in a minority of cases. Medication and OTC supplementation treatments have only been marginally effective. As yet, there is no treatment that can “cure” ASD. Current therapies focus on symptom reduction, behavioral and social skills training, and quality of life enhancements.
More recently EEG neurofeedback has shown itself to be a promising alternative treatment for the milder forms of autism and Asperger's. EEG neurofeedback is a non-invasive therapeutic intervention which has been shown to enhance neuroregulation and metabolic function in the brain. In contrast to behavior therapy, positive treatment outcomes as a result of neurofeedback training are achieved over the course of several months as opposed to a year or more of intensive behavioral training. EEG neurofeedback has no adverse side-effects while psychopharmacological interventions, as well as certain vitamin/mineral supplementation and secretin are associated with numerous side-effects. The therapeutic treatment outcomes of neurofeedback training are maintained over time and do not reverse after treatment has been withdrawn as in drug therapy, diet therapy, and supplementation with vitamins, minerals and enzymes.
For more information on autism, autism treatment and resources...
QEEG and Autistic Spectrum Disorders
A review of multiple studies suggests a mean incidence of 50% for abnormal EEG findings in autism with atypical EEGs often predicting poorer outcomes for intelligence, speech and educational achievement (Hughes & John, 1999). More recent neuroimaging research points to a theory of faulty neural connectivity as a mechanism underlying the symptoms of ASD. Connectivity can be defined as the extent to which any two or more neural locations within the brain are communicating with each other. Autistic symptoms appear to be associated with information integration deficits resulting from reduced or underconnectivity between specialized local neural networks and increased or overconnectivity between neurons within isolated neural assemblies in other brain locations, particularly the frontal lobes (Rippon, et al., 2007). Disordered connectivity may be associated with an increased ratio of excitation/inhibition in key neural systems. Anomalies in connectivity may be linked to abnormalities in information ntegration (Coben, Linden, & Meyers, 2010).
Pathologically, overconnectivity both within and between the frontal lobes has been found to be associated with autistic symptoms related to integration of information from emotional, language, behavioural, sensory, and autonomic regulation systems. Poor connectivity between frontal and posterior cortical areas and across other posterior to temporal cortical regions are associated with regional functional brain abnormalities. In particular, poor connectivity in the right frontal lobe in an area roughly corresponding to Broca's area on the left, may result in flat and/or inappropriate vocal tone. Poor connectivity in the right parietal-temporal junction has been shown to be associated with the inability to correctly interpret social innuendo, either verbal or non-verbal, and with difficulty copying emotional tones that express indifference, anger, sadness, or happiness. Furthermore, reducing such connectivity abnormalities is associated with the resolution of many autistic symptoms and improvements in attention, self-regulatory functions, social behaviour, and communication skills (Coben & Meyers, 2008; Coben & McKeon, 2009; Thompson, Thompson & Reid, 2009).
Dr. Robert Coben and colleagues have determined seven patterns of anomalous neural connectivity to be common in children with ASD...
- Frontotemporal Hyperconnectivity frequently found in posterior frontal to anterior temporal regions and associated with problems with attention, self-regulatory functions, social behavior, and communication skills.
- Frontal (Orbitofrontal) Hypoconnectivity often associated with problems involving social cognition and "theory of mind".
- Mu Rhythm Complex over the sensorimotor strip thought to be associated with reduced integrity of the mirror neuron system that is essential in observing others as a basis for proper responding.
- Posterior (occipital-parietal-temporal) Hypoconnectivity which is associated with excess theta activity with low conductivity in delta and theta and beta bands as well.
- Frontal-Posterior Hypoconnectivity which appears to represent the isolation of frontal lobe input from numerous posterior processing centers. Particularly significant is disconnection in the gamma frequency range between the primary visual cortex parietal integration areas and inferior frontal cortex containing mirror neurons.
- Left Hemisphere Intrahemispheric Hypoconnectivity is associated with problems in language processing tasks.
- Left Hemisphere Intrahemispheric Hyperconnectivity is associated increased connectivity in the delta frequency band in the frontotemporal regions and is suggestive of abnormal lateralization of language patterns.
The EEG connectivity (coherence) maps above show orbitofrontal hypoconnectivity pattern in ASD.
The EEG connectivity (coherence) maps above show the Mu rhythm complex pattern in ASD.
The EEG connectivity (coherence) maps above show the right posterior hypoconnectivity pattern in ASD.
Using QEEG brain mapping procedures to evaluate children diagnosed with autistic spectrum disorders, Dr. Michael Linden and colleagues at the Attention Learning Centers have identified four distinct patterns (phenotypes) of autism:
- Over Focused/Over Aroused Pattern (excessive High Beta activity); associated with obsessing, overfocusing, and anxiety.
- Abnormal EEG/Seizure Pattern.
- Excessive Delta/Theta Activity; associated with cortical slowing and inattention, impulsivity, and hyperactivity.
- Metabolic/Toxic Pattern of lower overall EEG activity; associated with low voltage EEG of less than 5 microvolts.
- Mu Activity Pattern; associated with social skills problems.
- Connectivity Abnormalities
The high Beta and connectivity abnormalities subtypes are the most commonly seen EEG; occurring in about 50-60% of in ASD children. The Excess Delta/Theta and Abnormal EEG/Seizure are the next most common at about 30-40% of ASD children. The MetabolicToxic Pattern of low EEG voltage accounts for about 10% of cases.
Dr. Linden and colleagues have also reported that children with Asperger's Syndrome frequently show a pattern of excessive Theta/Alpha slowing in the right temporal-parietal region and low connectivity between right temporal-parietal regions and other brain regions; especially with frontal lobes. Both of these patterns suggest a disconnection in the areas of the brain associated with recognizing facial gestures, emotions and expressing feeling. These EEG patterns may be the first biological markers available to diagnose Autism and Asperger’s.
QEEG Brain Mapping to Assess ASD
QEEG evaluation or mapping is an assessment technology designed to pinpoint anomalies in brain function. Qeeg analyses measure abnormalities, instabilities, or lack of proper communications pathways (connectivity) necessary for optimal brain functioning.
The QEEG is currently the best tool to assess dysfunctions related to neural connectivity due to its non-invasive nature, availability and relatively low-cost, and utility in detailing these types of difficulties. When an EEG recording is processed and analyzed with advanced quantitative techniques, it can be invaluable in evaluating autistic disorders, screening for possible seizures (a very common comorbidity with ASD), and assessing the underlying neurophysiological patterns related to the symptoms and challenges of children with ASD.
Assessment of regional brain dysfunction usually requires functional brain imaging techniques such as fMRI, PET, SPECT, MEG, or QEEG/LORETA, since static measures tend to miss most abnormalities in ASD. Unlike QEEG/LORETA techniques, these other imaging techniques require either sedation or injection of radioactive tracer materials or multi-million dollar scanning systems. QEEG is the safest, most available and most affordable method for the assessment of neural dysfunction in children and adults and has been shown to be able to distinquish typically developing children from children with ADHD or ASD with accuracy in excess of 90%.
Because ASD is actually a set of complex syndromes with associated neural connectivity anomalies and brain dysfunction involving numerous brain regions, a EEG recording and comprehensive evaluation using both visual and advanced quantitative techniques is essential before undertaking any EEG neurotherapy training. The application of connectivity-guided neurofeedback begins with a complex visual and quantitative analysis of EEG data.
Efficacy of EEG Neurofeedback for ASD
Basically, individuals who participate in EEG neurofeedback learn to inhibit brainwave frequencies that may produce negative symptoms and enhance specific frequencies that produce positive results. Through the process of operant conditioning and utilizing neurofeedback, individuals with poorly regulated cortical activity can learn to develop a fluid shift in brainwaves to better meet task demands; resulting in more normal brainwave patterns and improved behavior. These changes in EEG patterns have been shown to be associated with regulation of cerebral blood flow, metabolism, and neurotransmitter function.
Research into the efficacy of EEG neurofeedback for ASD is still somewhat limited but is growing year by year and it is encouraging to note that significant treatment effects have been reported in most of the studies published to-date.
Case studies of successful neurofeedback trials with clients diagnosed with autistic disorders have been reported as early as the mid-1990s (Cowan & Markham, 1994; Sichel, et al., 1995; Thompson & Thompson, 1995). These reports all suggested that EEG neuroffedback training to suppress excessive of low frequency Theta and Alpha while simultaneously augmenting SMR or low Beta frequencies in one or more areas of the cortex could improve attention, socialization, and academic behaviours.
Drs. Lynda and Micheal Thompson (Thompson & Thompson, 2003) of the ADDCentre in Missauga, Ontario presented a case series review of neurofeedback in 60 high functioning individuals with ASD aged 5 to 61 years. EEG neurofeedback training parameters varied as a function of each individuals QEEG findings, reported symptoms, and parent/teacher behaviour rating scales but the most common protocol involved suppression of dominant slow wave activity while augmenting SMR/low Beta frequencies at central and centre-right electrode placements. The number of neurofeedback sessions ranged from 40 to 100. Their results indicated improved EEG patterns, with decreased Theta/Beta Ratios and increases in SMR/low Beta amplitudes, IQ increases averaging 10 points, and significant improvements in parent/teacher reported social interactions. There was a positive relationship between amount of neurofeedback training received and behavioural improvements. The Thompsons continue to see hundreds of ADHD, learning disabled, and ASD children and adults in their clinic for EEG neurotherapy every year and continue to collect and report case data (Thompson & Thompson, 2007).
The first published group experimental study to evaluate EEG neurofeedback as an ASD intervention was authored by Jarusiewiscz less than ten years ago in 2002. In this study 12 autistic children who received an average of 36 EEG neurofeedback sessions each were compared to a matched group of 12 autistic children in a "wait list" control group. Jarusiewiscz found EEG neurofeedback to be effective in producing an average 26% reduction in austistic symptoms as compared to the 3% gains seen in the control group..
Robert Coben and Ilean Padolsky (2007) evaluated the efficacy of connectivity-guided EEG neurofeedback and reported obtaining at least 40% reduction in autistic symptoms in 89% of the children treated with just 10 weeks of treatment. In the largest case series of children with autism receiving EEG neurofeedback yet published, Robert Coben and his colleagues reported on the results of connectivity-guided EEG neurotherapy treatment with 85 children diagnosed with ASD. Based on pre versus posttreatment total scores on the Autism Treatment evaluation Checklist (ATEC), connectivity-guided EEG neurofeedback was effective in reducing autistic symptoms by an average of nearly 60%. As well, 94% of parents rated their children as having improved by at least 40% in terms of autistic behaviours and no parents reported their children getting worse.
An even more recent study with a smaller group of 14 ASD children by a Dutch group of researchers (Kouijzer, de Moor, Gerrits, Congedo, van Schie, 2009a) also showed EEG neurofeedback to be an effective treatment for children diagnosed with Pervasive Developmental Disoder-NOS. Compared to the 7 PDD-NOS children in a wait-list control group, the 7 children in the EEG neurofeedback training group realized statistically significant improvements in the following areas: sustained auditory selective attention (30%), inhibition of verbal responses (55%), inhibition of motor responses (15%), set shifting (57%), concept generalization (50%), and planning ability (37%). Significant improvements were also found in communication (17%), general communication (14%), social interaction (16%), and typical behavior (9%). Percentages reflect improvement in the experimental group at their post-assessment compared to their pre-assessment.
This Dutch group of researchers have now released one-year follow-up data on the 7 PDD-NOS children treated with 40 sessions of EEG neurofeedback in their 2009 study Kouijzer, et al, 2009b). After re-testing the children with the same pre-post measures used to determine treatment outcome in the original study, it was concluded that the EEG neurofeedback training resulted in lasting improvements in a variety of executive functions, social and communication skills, and positive behaviors.
In the five controlled group studies that have been completed to date by Robert Coben and his colleagues, a total of 180 individuals with autism have been sudied and positive results reported in each case (Coben & Wagner, 2011).
In a recent comprehensive review of the published literature on EEG neurofeedback for the treatment of autistic spectrum disorders (Coben, Linden, Meyers, 2010), the authors stated...
"With the possible exception of behavior modification interventions, there are few interventions for children with autism with proven efficacy. Pharmacologic interventions, hyperbaric oxygen and vitamin supplementation may have shown some promise. However, further research is necessary to demonstrate their efficacy. Based on... [our review] ...we consider neurofeedback to be in a similar position with respect to efficacy for ASD." "In sum, we view neurofeedback as an intervention that may prove to be efficacious in the treatment of symptoms of autism. Presently, it should be viewed as possibly efficacious with potential and would then be in the same category as most interventions used with this challenging population."
To see a YouTube video by Dr. Clare Albright on EEG neurofeedback training for autism, please click on this link... http://www.youtube.com/watch?v=KK_Fs9I0TG0&feature=BF&list=ULOy74rq6Q3WQ&index=2
References and Selected Readings
Coben, R., Hirshberg, L., Chabot, R. (in press). EEG discriminant power and subtypes in autistic spectrum disorder. International Journal of Psychophysiology.
Coben, R., Wagner, L. (2011). Emerging empirical evidence supporting connectivity-guided neurofeedback for autistic disorders. In R. Coben & J.R. Evans (eds)(2011). Neurofeedback and Neuromodulation Techniques and Applications. Chapter 6, pp. 153-182. New York, NY: Academic Press.
Assaf, M., Jagannathan, et al. (2010). Abnormal functional connectivity of default mode sub-networks in autism spectrum disorder patients. Neuroimage, 53(1): 247-256.
Coben, R., Linden, M., Myers, T. (2010). Neurofeedback for Autistic Spectrum Disorders: A review of the literature. Applied Psychophysiology & Biofeedback, 35(1): 83-105.
Coben, R. & Myers, T. (2010). The relative efficacy of connectivity guided and symptom based EEG biofeedback for Autistic Spectrum Disorders. Applied Psychophysiology & Biofeedback, 35(1):13-24.
Minshew, N., Keller, T. (2010). The nature of brain dysfunction in autism: Functional brain imaging studies. Current Opinion in Neurology, 23(2): 124-130.
Coben, R. (2009). Efficacy of connectivity-guided neurofeedback for autistic spectrum disorder. Controlled analysis of 75 cases with a 1-2 year follow-up. Journal of Neurotherapy, Vol. 13, No. 1, pp. 81.
Coben, R., McKeon, K. (2009). EEG assessment nd treatment of seizures in children with autistic spectrum disorder: A case example. NeuroConnections, Fall 2009, pp.17-22.
Coben, R., McKeon, K. (2009). EEG assessment and treatment for autism spectrum disorders. The Autism File, issue 32. www.autismfile.com
Kouijzer, M., de Moor, J., Gerrits, B., Buitelaar, J., & van Schie, H. (2009b). Long-term effects of neurofeedback treatment in autism. Research in Autism Spectrum Disorders, 3(2):496-501.
Kouijzer, M., de Moor, J., Gerrits, B., Congedo, M., van Schie, H. (2009a). Neurofeedback improves executive functioning in children with autism spectrum disorders. Research in Autism Spectrum Disorders, 3(1), 145-162.
Thompson, L., Thompson, M., Reid, A, (2009). Functional neuroantomy and the rationale for using EEG biofeedback for clients with Asperger's Syndrome. Applied Psychophysiology & Biofeedback,
Thompson, M., Thompson, L., Thompson, J., Reid, A. (2009). Biofeedback interventions for autistic spectrum disorders: An overview. NeuroConnections, Fall 2009, pp. 9-12 & 14.
Coben, R., Clarke, A., Hirshberg, W., Barry, R. (2008). EEG power and coherence in autistic spectrum disorder. Clinical Neurophysiology, Vol. 119, pp. 1002-1009.
Coben, R., Myers, T. (2008). Connectivity theory of autism: Use of connectivity measures in assessing and treating autistic disorders. Journal of Neurotherapy, Vol. 11, pp. 5-23.
Chan, A., Sze, S., Cheung, M. (2007). Quantitative electroencephalographic profiles for children with autistic spectrum disorder. Neurophysiology, Vol. 21, pp. 74-81.
Coben, R. & Padolsky, I. (2007). Assessment-guided neurofeedback for Autistic Disorders. Journal of Neurotherapy, Vol. 11, No. 1, pp.5-23.
Genardi, D. (2012). BrainAvatar-- A flexible individualization for treating autism, a complex disorder. NeuroConnections, Winter, 2012.
Rippon, G., Brock, J., Brown, C., Boucher, J. (2007). Disordered connectivity in the autistic brain: Challeges for the 'new psychophysiology'. International Journal of Psychophysiology, 63(2): 164-172.
Thompson, L., Thompson, M. (2007). Autistic Spectrum Disorders, especially Asperger's syndrome. Paper presented at the 38th Annual Meeting of the Association for Applied Psychophysiology & Biofeedback, Monterey, California.
Scolnick, B. (2005). Effects of electroencephalogram biofeedback with asperger’s syndrome. International Journal of Rehabilitation Research, Vol. 28, No. 2, pp. 159-163.
Linden, M. (2004). Case studies of QEEG mapping and neurofeedback with autism. Presented at the 12th Annual Conference of the International Society for Neuronal Regulation, Fort Lauderdale, Florida.
Ross, J. & Caunt, J. (2003). A comparison of QEEG characteristics in pediatric Asperger's syndrome and attention deficit disorder. Paper presented at the 11th Annual Conference of the International Society for Neuronal Regulation, Houston, Texas.
Jarusiewicz, B. (2002). Efficacy of neurofeedback for children in the autistic spectrum: A pilot study. Journal of Neurotherapy, Vol. 6, No. 4, pp. 39-44.
Sichel, A., Fehmi, L., Goldstein, D. (1995). Positive outcome with neurofeedback treatment in a case of mild autism. Journal of Neurotherapy, Vol. 1, No. 1, pp. 60-64.
Thompson, L., Thompson, M. (1995). Autism/Asperger's/obnoxious child, 3 case histories: How we get positive results with complex ADD clients. Paper presented at the Annual Conference of the Society for Neuronal Regulation, Scottsdale, Arizona.
Cowan, J. & Markham, L. (1994). EEG Biofeedback for the attention problems of autism: A case study. Presented at the Annual Meeting of the Association for Applied Psychophysiology and Biofeedback. March 1994.
HEG Neurofeedback for the Treatment of Autism
Among other brain abnormalities that have been identified, numerous studies using positron emission tomography (PET) and single-photon emission computerized tomography (SPECT) have shown cerebral hypoperfusion in autism, leading to the hypothesis that increasing the flow of oxygenated blood within the cortex may be beneficial in autism.
One approach to increasing oxygenation of cerebral cortex in autism is the use hyperbaric air pressure chambers for hyperbaric oxygen therapy (HBOT). This therapy involves the inhalation of 100% pure oxygen in a pressurized chamber, usually above one atmosphere absolute. It has been shown in a number of clinical and research studies that HBOT can lead to improved functioing in various neurological populations that show cerebral hypoperfusion including stroke, cerebral palsy, brain injury, and fetal alcohol syndrome. With respect to autism, Rossignol and Rossignol (2006) have suggested that the increased oxygen delivered by HBOT could counteract the hypoxia caused by hypoperfusion, and lead to a reduction in symptoms of autism. A clinical case series of 40 ASD children treated with 40 sessions of HBOT published by Rossignol, et al. in 2007 in BMC Pediiatrics suggests that HBOT may indeed improve symptoms in autistic children with safety and no adverse events. However, access to hyperbaric chambers is quite limited in Canada and very expensive; making this form of treatment impractical. A much less complex and more accessible method of safely and noninvasively increasing cerebral blood flow is hemoencephalographic neurofeedback.
Hemoencephalography (HEG) is a form of neurofeedback that focuses on intentionally increasing cerebral blood flow within the prefrontal cortex (PFC) of the brain. Prefrontal and frontal lobe hypoperfusion (reduced blood flow) has been shown to be a factor in ADHD as well as autism.
Called the "executive brain" for good reason, the prefrontal cortex has neural connections to, and exerts some control over, all other parts of the brain. It plays a central role in controlling attention, blocking distractions in the environment, formulating and carrying out plans and intentions, controlling physical and emotional impulses, and helping to access memory. By increasing blood flow within the prefrontal cortex, HEG neurofeedback can improve the functioning of this critical area of the brain and improve self-control.
Whereas the goal of EEG neurofeedback is to train the individual to produce and/or inhibit certain brainwaves, the goal of HEG is to increase blood flow to targeted areas of the cortex. Increasing the amount of oxygenated blood perfusing a region of the cortex will result in increased metabolism and allow the targeted brain area to function more optimally.
Edmonton Neurotherapy uses a near-infrared HEG (nirHEG) system originally developed by Dr. Hershel Toomin in 1997. This system uses a spectrophotometer to measure the oxygenated blood flow inside the skull, which is semi-translucent and lets light in. The HEG Instrument measures the amount of blood that is carrying oxygen. This is similar to the "pulse-oximeter" that is used as a finger clip in the hospital, and shines a red light through your skin to measure the blood oxygen level. Similar to EEG neurofeedback, HEG neurofeedback is completely non-invasive, very safe and drugless.
HEG neurofeedback may be an effective adjunct to EEG neurofeedback training. Unlike EEG neurofeedback, HEG is not affected by eye blinks or facial movement which typically cause signal distortion when using EEG neurofeedback to train frontal locations. EEG neurofeedback focuses on activating neurons and changing neural connectivity whereas HEG neurofeedback increases the supply of oxygen and nutrients necessary to support neural activity.
xxxxxx vvvAutism spectrum disorders (ASD) are associated with dysfunction in multiple areas of the brain that not only involve abnormal patterns of neural activation and interconnectivity but also abnormal blood flow dynamics and cellular metabolism. Findings of significantly reduced blood perfusion (hypoperfusion) within the prefrontal lobes is a finding common to both ADD and ASD.
Although there is still very little published research on the use of HEG neurofeedback to treat such brain disorders as ADHD and ASD, over 2000 clinicians internationally have been using HEG neurofeedback for over a decade to improve brain functioning by increasing vascularity and the flow of oxygenated blood to specific regions of the cortex.
In research conducted in Thailand by a student of Dr. Hershel Toomin in 2003, a series of 181 students with ASD were given 20 treatment sessions of HEG neurofeedback focused on increasing blood flow within the prefrontal cortex (Limsila, et al., 2004). The result was that 86% of the students showed significant improvements in cognitive functioning. These improvements resulted in an average increase of 0.94 GPA points in a 4-point Grade Point Average scale. HEG training was also associated with an average 53% increase in cerebral blood flow within the prefrontal cortex.
More recently, Robert Coben (2006) presented the results of a controlled group study in which 40 patients with autism were non-randomly assigned to treatment with hemoencephalographic (HEG) neurofeedback or a "wait-list" control group. The groups were matched for gender, age, race, handed-ness, and previous treatments. All patients had previously recieved 20 sessions of EEG neurofeedback and were identified as having frontal lobe executive system dysfunction. Compared to the "wait-list" control group, the HEG neurofeedback group showed an average 42% reduction in overall autistic symptoms and social interaction deficits decreased by 55%. In addition, there were statistically significant improvements in neurobehavioral and neuropsychological functioning.
Coben, R. (2006). Hemoencephalography for Autistic Spectrum Disorder. Presented at the 14th Annual Conference of the International Society for Neuronal Regulation, Atlanta, Georgia.
Limsila, P., Toomin, H., Kijvithee, J.et al. (2004). Hemoencephalography (HEG): An additional treatment for autism and ADD. SAMITIVAJ Proceedings 2004.