Neurofeedback Treatment for Autistic Spectrum Disorders:  
Review of 60 Cases - Principles and Outcome

Dr. L. Thompson, Ph.D.

Introduction

Autistic spectrum disorders have characteristic EEG signatures (Thompson, 2002) and respond to neurofeedback intervention (Thompson, 1995, 1998, 2002). These disorders have core symptoms characterized by the triad of impairments of social interaction, communication, and imagination associated with a narrow range of repetitive activities (Wing, 2001, p. xiv, Attwood, 1999). Relevant DSM-IV diagnostic codes are Pervasive Developmental Disorder (PDD) and Aspergers Syndrome (AS).

Those clients who are diagnosed as autistic have severe deficiencies and delays in language development that are not found in clients with Aspergers Syndrome. Both the autistic and the Aspergers syndrome clients demonstrate primary deficits in their ability to interpret non-verbal social communications (innuendo, abstract meaning), appropriately initiate and maintain social interactions, handle anxiety, shift mental set, and sustain external attention span and response control. Their symptoms overlap with those of Attention Deficit Disorder.

They may demonstrate islands of very high intelligence that correspond to a singular (obsessive) area of interest (Thompson & Havelkova, 1983). They often present like little professors with extensive knowledge in this one area. AS clients want to have social interactions but lack the innate ability to understand social innuendo and appropriately communicate emotions.

Incidence is on the rise and currently 1 child in 150 is affected. Brain differences include: smaller cells in the limbic system (Bauman, 2001); abnormal interaction between frontal and parietal brain areas (Pavlakis, 2001), larger brains due to more growth in grey and white matter during the first three years of life (Courchesne, 2001); fewer Purkinje cells in the cerebellum (Courchesne, 2001); different activation of the fusiform gyrus for facial recognition (Pierce, 2001);. EEG brain maps show less activation in the areas of the right hemisphere that process emotional information (unpublished data from Gunkleman).

Method

The charts for more than 60 clients with autistic spectrum disorders, age five to fifty-one, and seen over the last ten years, have been reviewed to check EEG patterns and to determine if these clients have benefited from neurofeedback training. Information includes EEG assessments, medication status, parent questionnaires, clinical observations, IQ testing, continuous performance tests and academic measures.

Full testing was not possible with all clients but EEG data was always obtained at intake (CZ placement, eyes open), artifacted and analyzed using Lubars protocol with the Autogen A620. Training parameters were based on client’s symptom picture, EEG pattern, and knowledge of cortical functions.

The most frequent intervention was to decrease the client’s dominant slow wave frequencies while enhancing 13-15 Hz activity with placement at CZ or C4 referenced to the right or the left ear respectively. When full cap assessments showed excessive slow wave activity at other locations (PZ, P4, T6, F4, FZ, F3, Fp1) these sites were also used. Coaching in metacognitive strategies was done as appropriate for academic levels. A follow-up of earlier clients is in process and these findings will be shared.

Results

EEG patterns at FZ and CZ resembled ADD patterns but amplitudes tended to be more extreme. Excess slow wave activity in either the delta through theta range, or excess alpha (7-10 Hz) activity was found. Peaks at 7 Hz had the morphology of pediatric alpha. However, in the autistic spectrum disorders, full cap assessments showed slowing (excessive 5 Hz activity) and / or excessive low alpha (7 to 10 Hz.) in the right parietal region (P4), and some slowing at T6. There was high amplitude delta and theta at FP1, F3, FZ and CZ. There were also differences in coherence and co-modulation.

Sufficient training (sometimes more than 100 sessions) consistently produced a decrease in theta/beta ratio with the clearest change being an increase in SMR. In those clients where pre-testing of the IQ was possible, increases of about 10 points were found. TOVA data were inconsistent: autistic children could not complete the test, and Asperger’s children often scored well even prior to training.

Parents noted remarkable improvement in social interactions: children went from having no friends to initiating and maintaining some peer friendships. The largest improvements were in those who received > 80 sessions. Autistic clients were initially more difficult to work with. Those with AS were easy to work with once they knew the routines.

Discussion

EEG differences observed in autistic spectrum disorders provide a rationale for using neurofeedback. Excess slow wave activity corresponds to being more in their own internal world; low SMR is consistent with fidgety and impulsive behavior, anxiety, and also with the tactile sensitivity exhibited by many; high left prefrontal and frontal slow wave activity is consistent with lack of appropriate inhibition; high slow wave activity in right parietal-temporal area is consistent with inability to interpret social cues and emotions; high slow wave activity at or near F4 may correspond to difficulties with appropriately communicating socially.

Improved social interaction found in conjunction with EEG shifts makes sense when these areas are more active: more activation also means more alert to the outside world and thus better able to benefit from socialization efforts. The positive results support neurofeedback as an intervention in autistic spectrum disorders, particularly Asperger’s syndrome and high functioning autism. Further research could build on these observational data.

References:

Attwood, Tony (1997) Asperger’s Syndrome: A Guide for Parents and Professionals. London: Jessica Kingsley Publications.

Bauman, Margaret (2001) Neurobiology of the Limbic System in Autism. Boston University, MA. Current ATP Brain Research Projects (2000-2002)

Courchesne, Eric., Karnes, C.M., Davis, H.R., Ziccardi, R., Carper, R.A., Tigue, A.D., Chisum, H.J., Moses, P., Pierce, K., Lord, D., Lincoln, A.J., Pizzo, S., Schreiban, L., Haas, R.H., Akshoomoff, N.A., Courchesne, R.Y., (2001). Unusual brain growth patterns in early life in patients with autistic disorder: an MRI study. Neurology, 57(2):245-54, July 24.

Pavlakis, Frank Y. (2001) Brain imaging in neurobehavioral disorders. Review, Paediatric Neurology. 25(4): 278-287, Oct.

Pierce, Karen, Muller, R.-A., Ambrose, G., Allen, G., Courchesne, E., (2001). Face processing occurs outside the fusiform face area in autism: evidence from functional MRI. Brain. 124, 2059-2073.
Thompson L., Exceptional Results with Exceptional Children. Proceedings, SSNR Annual Conference, Scotsdale, Arizona, 1995

Thompson L., Helping Autistic Spectrum Disorders. Proceedings SNR Annual Conference, Scottsdale Arizona, 2002

Thompson L.(1998), Neurofeedback Combined with Training in Metacognitive Strategies: Effectiveness in Students with ADD, Applied Psychophysiology and Biofeedback, Vol. 23, No. 4
Thompson, M.G.G.; Havelkova, M., (1983) "Childhood Psychosis" in Psychological Problems of the Child, Paul Steinhauer (Editor).

Wing, Lorna (2001) The Autistic Spectrum. Berkeley, CA: Ulysses Press

(*NOTE: Using EEG Biofeedback, Sensory Integration Training, Auditory Integration Training, and Sound Therapy treatment plans that are customized for each patient's individual needs, The Attention & Achievement Center has produced significant improvements in the lives of patients with autism and autistic spectrum disorders, including PDD.)

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