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Edmonton Neurotherapy
Treatment of Learning Disabilities
EEG Neurofeedback for Connectivity Problems

 

 

 

A "learning disability" may be defined as a disorder in basic psychoneurological processes involved in understanding or using language, spoken or written, that may manifest itself in an imperfect ability to listen, think, speak, read, write, spell or use mathematical calculations. The term includes conditions such as perceptual disability, brain injury, minimal brain dysfunction, dyslexia, and developmental aphasia. Learning disabilities may be developmental or acquired but are always defined within the context of the individual's general level of intelligence. That is, extreme difficulty in learning a specific mental skill which is inconsistent with the person's overall intelligence.

It has been variouly estimated that as many as 8% - 15% of the school population has a learning disability (LD) and about two-thirds of learning disabled children have a reading disability. Every year another 10 to 20 thousand Canadian children are diagnosed with learning disabilities.  

The considerable heterogeneity of the LD population has lead to a general consensus among professionals that many subtypes exist within the broad category of learning disabilities, and that the boundaries between the subtypes often overlap.

About one-half of the elementary school-aged children (ages 6-11) diagnosed with attention-deficit/hyperactivity disorder (ADHD), will also have a learning disability (LD) of some kind. For example, Gerhardstein et al., (2001) reported an overlap of 50% between reading disabilities and ADHD.

Recent research has tended to divide students with LD into two main groups-- verbal learning disabilities and nonverbal learning disabilities. Individuals in the verbal disability group have verbal/language deficits or specific phonological processing deficits as well as impaired reading, written language and/or spelling skills deficits, while those in the nonverbal group may have problems in visual-spatial-organizational, tactile-perceptual, psychomotor, and/or nonverbal problem solving skills. In addition, the nonverbal LD student may have problems in computational mathematics and/or writing skills, and is at an increased risk for social and behavioral problems. The math disability situation has received very little research attention in comparison to the reading disability situation. 

The advent of modern neurodiagnostic brain imaging technologies has given us new methods to distinguish among the LD subtypes and new ways of understanding learning disabilities in terms of actual brain functioning. Those seeking to understand the neural correlates of learning disability can now draw on various functional brain imaging technologies such as functional magnetic resonance imaging (fMRI), positron emission tomography (PET), single-positron emission tomography (SPECT), diffusion tensor imaging (DTI), and quantitative EEG (QEEG) to more precisely differentiate between the different types of learning disability and to better understand what functional brain abnormalities may be associated with specific problems. 

Dyslexia

Developmental dyslexia is characterized by difficulties with accurate and/or fluent word recognition and by poor spelling and decoding abilities. These difficulties typically result from a deficit in the phonological component of language that is often unrelated to other cognitive abilities. Dyslexia is probably the most common neurobiological learning disorder affecting children, with prevalence rates ranging from 5 to 10 percent. It is a persistent, chronic condition.

Dyslexia is a term primarily used by neurologists; educators describe reading difficulty instead. Traditional tests for dylexia include psychometric testing or computerized testing.

 A number of fMRI neuroimaging studies have compared cortical activation patterns in adults with dyslexia to that of non-impaired readers while engaged in reading tasks. These studies have shown that non-impaired readers increased their activation in the posterior superior temporal gyrus (T5), angular gyrus (P3), and just above P3 in the supramarginal gyrus as the task demands increased from orthographic comparisons to phonological comparisons. In contrast, dyslexic adults showed over-activation in response to increasing task demands in anterior regions including the inferior frontal gyrus (F7). While the nonimpaired readers showed activation of a widely distributed system for reading, the dyslexic readers had disrupted activity in the posterior cortex that involves traditional attentional, visual and language areas.

The anatomic correlates of the reduced function in left temporoparietal regions can also be visualized by diffusion tensor imaging (DTI), which identifies the white matter tracts between brain regions. Using DTI, Klingberg et al., (2000) showed that reading ability is directly related to the degree of connection between the left temporparietal areas designated as superior temporal gyrus (T3) and inferior parietal cortex (T5 and P3) for both dyslexic and non-impaired readers.

Another important study (Ramsey, et al., 1999) also points to the left angular gyrus (between T5 and P3) as the most likely site of functional impairments in dyslexic adults. This study found higher blood flow (increased perfusion) associated with better reading skill in control subjects and lower blood perfusion associated with poor reading in dyslexics.

In conclusion, modern neuroimaging techniques have provided the beginning of a physical definition for reading disability by identifying the left temporal and left posterior regions of the cortex as critical areas of neural deficits.

QEEG Findings in Dyslexia

QEEG studies have generally failed to show any consistent difference between dylexics and normal readers in the standard "eyes-closed, resting state" as may be expected, but some changes have been seen when the EEG is recorded during reading. Walker and Norman (2004) reported finding increasing neural activation (as indicated by the presence of 15-18 Hz Beta activity) in normal readers from recording electrodes placed at T3 (over the left superior temporal gyrus) when challenged with increasingly difficult reading material. They suggested that this Beta2 activity was an indicator that the area was engaged in the reading process and as the reading task becomes more difficult there will be an increase in the amplitude of Beta2 from this area. But as the reading task becomes too difficult, it was noted that the area would disengage and stop generating Beta2 activity. Based on these findings, Walker and Norman suggested that EEG neurofeedback training to quiet the left superior temporal gyrus at rest but produce more Beta2 activity with reading may improve reading ability. They also suggested that even higher frequency 21-30 Hz Beta activity might be dysfunctional during reading and an indicator of anxiety.

Interestingly, Walker and Norman's findings are quite congruent with earlier fMRI studies done by Shaywitz (1996) that showed underactivity in the left middle temporal and supramarginal areas associated with phonological processing during reading in dyslexics as well as overactivity in the left lateral frontal area that is associated with expressive speech. Shaywitz argued that the overactivity in the frontal regions was a sign of an inefficient compensatory mechanism in action.

Studies examining EEG coherence (a measure of functional connectivity) between different brain areas in dyslexics have been more consistently fruitful and suggest that developmental dyslexia may represent a neural disconnection syndrome. In this regard, Evans (1996) reported finding significantly decreased coherence between multiple left posterior hemisphere sites (i.e., T3, T5, P3, O1) in 70 percent of dyslexic subjects. In a similar vein, Pugh et al. (2000) reported finding a disruption in functional connectivity between the left angular gyrus and related occipital and temporal sites, but only on tasks requiring phonologic assembly....  

More recently, Leisman (2002) reported finding that normal readers have significantly greater coherence in the 1-30 Hz frequency range between the two hemispheres at homologous sites such as T5 vs T6, T3 vs T4, P3 vs P4 than do dyslexics; while dyslexics demonstrated significantly greater 1-30 Hz coherence within hemispheres.

Most QEEG studies hQA recent study by Martijn Arns and colleagues in Holland (Arns, Peters, Breteler, Verhoeven, 2007) used QEEG and various neuropsychological tests to investigate the underlying neural processes in dyslexia. This study focused on the question of whether QEEG could identify different brain activation patterns in children with dyslexia and to what extent correlations between reading and spelling abilities and specific tasks for rapid naming and phonological awareness address the "double-deficit theory" of dyslexia.

Note: The "double-deficit theory" of dyslexia is based on the observation that most dyslexics perform poorly on tasks of processing and remembering symbols and some also perform poorly on visual processing tasks.

Compared to normal controls, the dyslexic group showed increased slow activity (slow 1-4 Hz Delta and 4-8 Hz Theta EEG) in the frontal and right temporal regions of the brain. Beta-1 (15-20 Hz) was specifically increased at F7. EEG coherence was increased in the frontal, central and temporal regions for all frequency bands. There was a symmetric increase in coherence for the lower frequency bands (Delta and Theta) and a specific right-temporocentral increase in coherence for the higher frequency bands (Alpha and Beta).

High coherence between two EEG signals means high cooperation and synchronization between underlying brain regions within a certain frequency band. Increased coherence can thus be interpreted as increased functional connectivity. This could implicate that dyslexic children have more activated frontal, central and temporal networks. Significant correlations were observed between subtests such as Rapid Naming Letters, Articulation, Spelling and Phoneme Deletion and QEEG coherence profiles.

These results support the double-deficit theory of dyslexia and demonstrate that the differences between the dyslexia and control group might reflect compensatory mechanisms of brain function in dyslexia. They help to separate real dysfunction in dyslexia from acquired compensatory mechanisms. 

Walker and Norman (2006) presented preliminary data from their treatment clinic on results of EEG neurofeedback training with 12 dyslexic children aged 7-12 years. They reported that an individualized treatment protocol that combined both amplitude and coherence training was successful in gaining an average of two grade levels in reading skill with an average of 30-35 sessions. 

EEG Neurofeedback for Learning Disorders

Relatively few full-scale studies on neurofeedback and learning disorders have been conducted, but in several case studies, children have shown remarkable improvement after neurofeedback therapy. 

 

To see a YouTube video by Dr. Clare Albright on EEG Neurofeedback training for learning disabilities, please click on this link... 
http://www.youtube.com/watchv=P8XgOi7HnOg&feature=BF&list=ULOy74rq6Q3WQ&index=7 

 

References:

Arns, M., Peters, S. Beteler, R. Verhoeven, L. (2007). Different brain activation patterns in dyslexic children: Evidence from EEG power and coherence patterns for the double-deficit theory of dyslexia. Journal of Integrative Neuroscience, 6(1): 175-190.

Coben, R .(2007).  Learning Disability: A controlled study of EEG Coherence Training.  Presented at the 15th Annual Conference of the International Society for Neurofeedback and Research, San Diago, California, September 2007.

Fonseca, L., Tedrus, G., Chiodi, M., Cerqueira, J., Tonelotto, J. (2006). Quantitative EEG in children with learning disabilities: Analysis of band power.

Lowes, J., Hammond, B., Blake-Hammond, L. ( ). Effects of brainwave training on cognitive abilities in pupils with learning disablities.

Walker, J. & Norman, C. (2004). Normal adult readers recruit increasing beta power at T3 as reading difficulty increases. Paper presented at the 12th Annual Scientific Conference of the International Society for Neuronal Regulation, Fort Lauderdale, Florida.

Walker, J., & Norman, C.  (2006).  The neurophysiology of dyslexia:  A selective review with implications for neurofeedback remediation and results of treatment in twelve consecutive patients.  Journal of Neurotherapy, 10(1), 45-55. 

 

To view a brief YouTube video of Barbara Arrowsmith-Young "The Woman Who Changed Her Brain" speak on brain plasticity and learning disability, please click on this link...
http://www.youtube.com/watch?v=o0td5aw1KXA

To learn more about the Arrowsmith Academy program for children and adults with learning disabilities, please click on the following link...
http://www.arrowsmithschool.org/arrowsmithprogram-background/intro-video.html

 

 

 

 

 

 

    

 




 


Edmonton Neurotherapy.  Dr. Horst H. Mueller, RPsych, CRHSP, BCN, ICPP.

Information contained on this website is intended for educational and informational purposes only and does not constitute medical advice or diagnosis. Nothing on this site is intended nor should be taken as a substitute for the advice provided by your physician or other qualified healthcare professional. You should not use the information on this website for self-diagnosing or self-treating any health problem or disease, or self-prescribing any medication or other treatment.