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Asperger's & ADD; Differences and Similarities - Preliminary Observations
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Futurehealth WinterBrain Workshop by Michael & Lynda Thompson
  • neurofeedback
  • aspergers
  • ADD
  • autism


Asperger’s Syndrome lies along the autistic spectrum but does not have the language delays that are characteristic of autism (pervasive developmental disorder, PDD). Core symptoms are “characterized by the triad of impairments of social interaction, communication, and imagination associated with a narrow range of repetitive activities.” (Wing, 2001). Delayed language is characteristic of the autistic child (pervasive developmental disorder, PDD) but is not characteristic of AS. They want to have social interactions but lack the social graces to do it appropriately. The Asperger’s child will often present like a little professor with extensive knowledge in their area of interest. These children also often exhibit all the classic symptoms of Attention Deficit Disorder including inattention and distractibility when asked to do tasks that they find boring or irrelevant.

Preliminary observations concerning the EEG in Asperger’s appears to be showing slowing (theta and alpha) in the right parietal and temporal areas (P4, T6) and, at times, frontally at F3 and F4. There are also findings of comodulation (spectral correlation) differences including hyper-comodulation between P4, C4 and F4 and a comodulation ‘disconnect’ between the right cerebral hemisphere sites and the left frontal area. However, these children also show the characteristic patterns seen in ADD with slowing at C3, Cz and C4, and/or at F3 and Fz with a ‘dip’ in 13-15 Hz (SMR) across the central region (C3, Cz and C4).

Clinically the children with ADD appear to have somewhat different patterns on intellectual and academic testing. While the Asperger’s group often show excellent verbal and reading capacities (left hemisphere strengths), they tend to have symptoms of non-verbal learning disabilities (right hemisphere problems). The ADD children, on the other hand, may perform well on non-verbal performance tasks but demonstrate increased incidence of preschool speech disorders (Love & Thompson) and reading difficulties in the early school years.

The amygdala, orbital and medial prefrontal cortex, medial and temporal areas and the thalamus are all involved in the process of attaching emotional significance to stimuli and are most likely of central importance in understanding the autistic spectrum disorders (Schulz, 2000). Temporal lobe dysfunction has been found (Boddaert, 2002). Neurophysiologically the medial and basal zones of the cerebral hemispheres are critical in the emotional aspects of social interactions; the ventromedial prefrontal region is important in learning concerning social interactions and the lateral nucleus of the amygdala is critical in assigning emotional valance to events. The central nuclei of the amygdala are more involved in emotional expressions including flight or fight responses. Dysfunction in the interconnections between the orbital and medial wall of the prefrontal cortex and the amygdala, and/or dysfunction in the lateral and central nuclei of the amygdala, may therefore lie at the root of some of the difficulties encountered in the autistic spectrum disorders. Of importance to NFB practitioners, however, are the aprosodia symptoms and their correspondence to EEG patterns seen on assessment. High right frontal slow wave activity is consistent with flat, monotone speech and inappropriate intonation (motor aprosodia – note correspondence to Broca’s aphasia with damage to this area in the left hemisphere.)

High slow wave activity in right parietal-temporal area is consistent with inability to interpret social cues, inuendo and emotions (sensory aprosodia – note correspondence to Wernicke’s aphasia with damage to this area in the left hemisphere).

It is postulated that in ADD there is reduced dopamine in the fronto-mesolimbic system in the left hemisphere. The type of cognitive processing which is affected and deficient is that which requires slow, serial effort. In the right hemisphere differences from normal may relate to excessive locus coeruleus norepinephrine production and thus excess noradrenergic stimulation to the right cerebral hemisphere. This may in part account for people with ADD seeming to have automatic processing which is fast and simultaneous. This style of attention is biased towards novelty and change. (Note that persons with AS, in contrast to AD, dislike novelty and change.) Overactivation of the noradrenergic system in the right hemisphere is also associcated with extroversion and impulsivity (Tucker, 1984).

Both Asperger’s and ADD may be associated with anxiety. In Asperger’s, however, anxiety in social situations where they are unsure of how to behave appears to be at the core of their difficulties. In ADD, on the other hand, mild to moderate anxiety may be a protective factor that can result in the child doing well academically and not acting out in an oppositional and defiant manner.


Chart reviews on more than 100 clients with ADD have been reported by the authors previously (Thompson, 1998) The charts for more than 50 clients with AS, age five to fifty-one, are being reviewed to check EEG patterns and to determine if these clients have benefited from neurofeedback training to the same extent as ADD clients did. Information on all clients includes EEG assessments, medication status, parent questionnaires, clinical observations, IQ testing, continuous performance tests and academic measures. Training parameters were based on client’s symptom picture, EEG pattern, and knowledge of cortical functions. The most frequent intervention for both groups of clients was to decrease the client’s dominant slow wave frequencies while enhancing 12-15 Hz or 13-15 Hz activity with placement at Cz or C4 referenced to the right or the left ear respectively. With the Asperger’s group, when full cap assessments showed excessive slow wave activity at other locations (P4, T6, FZ, F3, Fp1) these sites were also used. Coaching in metacognitive strategies was done as appropriate for academic levels.


EEG patterns of the Asperger’s group resembled ADD patterns in the central areas but amplitudes tended to be more extreme. Excess slow wave activity in either the delta through theta range or excess alpha activity were found in both groups. In the Asperger’s group the peaks at 7 Hz had the morphology of paediatric alpha. Full cap assessments showed slowing (excessive low alpha, 8 to 10 Hz.) in the right parietal region (P4) and some slowing at T6. There was high amplitude theta at FP1, F3, Fz and Cz. There were also differences in coherence and comodulation.

ADD training usually took between 40 and 60 sessions. In the Asperger’s group, sometimes more than 100 sessions was necessary. In both groups NFB training consistently produced a decrease in theta/beta ratio with the clearest change being an increase in SMR. IQ increases of about 10 points were found. TOVA data were inconsistent with the Asperger’s children. This may be due to their anxiety and willingness to follow instructions precisely resulting in them often scoring well even prior to training. In both groups social interactions improved. In the Asperger’s group the children went from having no friends to initiating and maintaining some peer friendships. The largest improvements were in those who received > 80 sessions.


There is overlap in symptoms and overlap in EEG differences observed in clients with ADD and AS. These findings provide a rationale for using neurofeedback. In both groups excess slow wave activity corresponds to being more in their own world; low SMR is consistent with fidgety and impulsive behaviour and also with the tactile sensitivity exhibited by many; high left prefrontal and frontal slow wave activity is consistent with lack of appropriate inhibition. In AS high slow wave activity in right parietal-temporal area is consistent with inability to interpret social cues and emotions. Improved social interaction found in conjunction with EEG shifts makes sense: more activation 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 Asperger’s syndrome. In future we may find ways to make the training in AS more efficient perhaps through the application of comodulation training.


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

Boddaert, N., Chabane, N., (2002) Temporal Lobe dysfunction in childhood autism: J. Radiol Dec. 83 1829-33

Love, A.J.; Thompson, M.G.G.; Language Disorders and Attention Deficit Disorders in a Child Psychiatric Outpatient Population, American Journal of Orthopsychiatry, 58(1), January 1988.

Malone, M.A., Kershner, J.R., Swanson J.M. (1994). Hemispheric Processing and Methylphenidate Effects in Attention-Deficit Hyperactivity Disorder. Journal of Child Neurology, 9( 2), 181-189.

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

Schultz, Robert T., Romanski, Lizabeth M., Tsatsanis, Katherine D. (2000) Neurofunctional Models of Autistic Disorder and Asperger Syndrome, Clues from Neuroimaging. In Asperger Syndrome edited by Ami Klin, Fred R. Volkmar, Sara S. Sparrow. New York: Guilford Press.
Thompson L., Thompson M., (1998), Neurofeedback Combined with Training in Metacognitive Strategies: Effectiveness in Students with ADD. Applied Psychophysiology and Biofeedback, 23, ( 4), 243-263.


Author: Michael & Lynda Thompson

Other Products by Michael & Lynda Thompson

1) Setting up for Clinical Success Suite
2) Using Neurofeedback for Autistic Disorders
3) Asperger's, ADHD, or Seizure Disorder? Differential Diagnosis and Intervention
4) BioGraph Infiniti Software Tutorial
5) The Neurofeedback Book
6) ADD Workshop

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