Biofeedback Approach to Dyslexia
By Roslyn McCoy


Dyslexia is a form of learning disability that affects about 30 percent of the 
population (2002 LDA international conference -Denver Co.). For the last 50 
years a quest for the clear identification of causes and all of the symptoms have 
eluded scientists and educational specialists.  Only in the last few years have 
there been advancements in our understanding of the biological basis of 
developmental dyslexia through EEG, MRI, and autopsy on individuals who 
are known to have dyslexia (Grigorenko).
	
One of the first and dominant markers for dyslexia is a persistent difficulty in 
acquiring word-reading skills. (Grossniklaus).  "Many low level psychological 
processes such as phonemic awareness, phonological decoding, ability to 
process stimuli rapidly and automatize this process, memory, ability to 
recognize words" show impairment (Grigorenko).  Developmental dyslexia is 
known to affect the unimodal perception (visual, auditory, and tactile) and 
Crossmodal perception requiring two senses (Veijo). These weaknesses are a 
partly independent component that contributes to the act of reading, but does 
not fully explain this complex higher mental function.  

The identification of specific areas of the brain has been implicated in reading 
related processes by different laboratories and on different samples, but there 
has not been any unified brain mapping for reading-related cognitive processes 
(Grigorenko).   The identified neurobiological, cognitive, genetic, or 
developmental conditions have not conclusively accounted for the symptoms 
of developmental dyslexia.  The neurobiological evidence is found in autopsy 
brain specimens showing abnormal neuron migration of the cerebral cortex and 
injury of the cortical plate during development affecting both the low level and 
high level cortical processing, also a possible change in the thalamus 
(Grigorenko).  Crossmodal temporal processing activation is less in a dyslexia 
then non dyslexics this has led many to believe that this may be the cause 
rather than a symptom of dyslexia (Veijo). 
	
The underlying assumptions of learning disabled/dyslexia is that the frontal 
lobe is not stimulated enough, and that if you increase the experiential/sensory 
and motoric stimulation that an improvement in functional processing will 
happen. The cerebro-cortico-neural synaptic matrices increase the number of 
dendritic spines when an individual experiences an enriched environment, 
increasing the weight in those cortical areas that have received stimulation.  
Animal studies indicate experiential and functional stimulation can alter the 
brain's anatomical structure.
Through intervention procedure a positives, alteration of the brain structure 
and processing ability is hoped for. Most intervention programs present 
individual with high levels of external sensory barrage.  In comparison with 
EEG biofeedback training that can enables an individual with dyslexia to 
stimulate/exercise the sensorimotor cortex from an internal locus of control. 
	
In Tansey's study he hypothesized "that increased bilateral sensorimotor 
transactions can be facilitated via EEG biofeedback training of the 14 Hz 
neural discharge pattern (sensorimotor rhythm) over the Rolandic cortex of the 
brain. The effects, of such internal cerebral stimulation, are hypothesized to 
manifest as an increase in the amplitude of the sensorimotor rhythm, and a 
reduction in the learning disabilities of the recipients of such EEG biofeedback 
training".

Tansey designed a multisubject, A-B-A, experimental design to assess the 
impact of operant conditioning to increase the 14Hz neural discharge rhythm 
in the sensorimotor (Rolandic) cortex of the brain.  The active electrode was 
placed to pick up the maximal bilateral hemispheric transactions to 
demonstrate the correlation between cerebro-cortico-neural events and the 
documented behavior/learning patterns of each subject. The Wechsler 
Intelligence Scale for Children -- Revised (WISC-R) was administered to each 
individual before and after receiving the EEG training.  There weren't any 
other therapies provided for these individuals during the training of EEG 
sensorimotor rhythm biofeedback.

Method
The participants were six Caucasian boys, ranging in age from 10 years two 
months to 11 years 10 months, with a history of learning disabilities.  A 
weekly 30 min, EEG biofeedback training of the sensorimotor rhythm (SMR) 
was conducted for 9 to 24 months. "A single channel electroencephalograph 
was used to assist the subjects in emitting the 14±0.5 Hz neural discharge 
rhythm over the central Rolandic cortex".  The active electrode was placed over 
the Rolandic cortex and the reference and brown electrodes were placed on 
opposite years via ear clips.  The electroencephalograph received the signal to 
process and provide both amplitude and frequency modulation audio feedback.  
In a reclining position with their eyes closed the boys received instructions:" 
Now, let yourself become hollow and heavy. Just let yourself be a heavy, 
hollow rock; quiet, hollow, and heavy -- and let the beeps come out" Also 
positive reinforcements of verbal praise when beeps were produced by the EEG 
machine. At the end of the session, a tangible reinforcer of a Matchbox car was 
presented if the participants met a predetermined criterion.
	
Results
Case 1. 
 Male 10 years seven months; fourth grade with a one year discrepancy in his 
reading ability.  Verbal IQ 107 and a performance IQ of 82.  After his 24th 
EEG biofeedback training session he has increased his SMR from 300%, and 
reading recognition is at grade level.  Verbal IQ increased 10 points and 
performance IQ increased 16 points.

Case 2.
Male 11 years seven months attending third-grade.  Reading one year below 
expectancy.  Verbal IQ 97 and performance IQ 121.  By his 9th SMR, EEG 
biofeedback training he had a 50 percent increase in amplitude.  Verbal IQ 
increased 21 points and performance IQ increased 17 points.

Case 3.
Male 10 years eight months, second-grade placement.  Exceeded one year 
below expected language development with many other neurological 
impairments.  Verbal IQ 75 and performance IQ 81.  Increased SMR 
amplitude 42 percent over baseline.  Verbal IQ increased 13 points and 
performance IQ increased 15 points after 18th EEG sensorimotor rhythm 
training session.

Case 4.
Male 11 years 10 months.  Grade six.  Reading below grade level.  Testing after 
his 22nd session showed more than a year and half increase in reading ability.  
Verbal IQ increased 25 points, performance IQ increased seven points.


Case 5.
Male 11 years one month, grade six. Second-grade reading ability.  Verbal IQ 
101 and performance IQ 104.  By his 34th session he had a 279 percent 
increasing in his amplitude of sensorimotor rhythm, reading ability increased 
the fourth grade level.  Verbal IQ increased 19 points and performance IQ 
increased 14 points.

Case 6.
Male 10 years two months, grade five.  Reading ability at 3.6 grade level, 
verbal IQ 112 and performance IQ 91.  By his 19th EEG biofeedback training 
session he had a 120 percent increase in amplitude of SMR.  Reading ability 
has increased to 7.2-grade level, verbal IQ increased 13 points, and 
performance IQ had increased 24 points (Tansey).
 
Discussion
The results of this study replicate prior studies and have extended previous 
findings, showing that EEG biofeedback training procedures are affective 
intervention programs for individuals with learning disabilities/dyslexia. 
Intervention programs that address the challenges of dyslexia by external 
intervention are only able to stimulate the areas of the brain when it is 
discharging particular rhythms, so if the stimulation is unable to reach the 
sensorimotor cortex of the brain, then cerebro-cortico-neural synaptic matrices 
would not increase the number of dendritic spines. This would account for the 
biological difference in the structure of the brain of individuals with dyslexia.  

The accepted practice has been to provide a high level of stimulus, so over time 
enough stimuli would reach this part of the brain, so the individual could 
accommodate further disability.  When an individual is young, the synaptic 
matrix is very plastic, but after the individual matures the synaptic matrix 
stabilizes and is resistant to change.  Teaching a young individual to 
consciously increase the 14Hz neural discharge rhythm in the sensorimotor 
(Rolandic) cortex of the brain may allow more stimulation to reach 
sensorimotor cortex, which would increase the number of dendritic spines, 
increasing the weight and size of the brain. Only through more research will 
the older population of learning disabled/dyslexic show if there are benefits 
from EEG sensorimotor rhythm biofeedback training.


Reference

Galaburda, Albert M. 2001 " Models of temporal processing and language 
development" Clinical Neuroscience Research. Volume 1, Issue 3 Pg. 230-237

Grigorenko Elena L. 2001 "Developmental Dyslexia: An Update on Genes, 
Brains, and Environments" Journal of Child Psychology and Psychiatry. 42:91-
125 Cambridge University Press

Grossniklaus, Hans E. MD  2002,  "Dyslexia,-specific brain activation profile 
becomes  normal following successful remedial training" American journal of 
Ophthalmology Volume. 134, Issue 3, Page 477 

Tansey, Michael A. 1984,  "EEG sensorimotor rhythm biofeedback, training: 
Some effects on the neurologic precursors of learning disabilities" International 
Journal of Psychophysiology Volume 1, Issue 2, Pages 163-177

Virsu, Veijo, Pekka Lahti-Nuuttila and Maria Laasonen, 2003,  "Crossmodal 
temporal processing acuity impairment aggravates with age in developmental 
dyslexia" Neuroscience Letters, Volume 336, Issue. 3, 23 January Pages 151-
154

Copyright © 2003, Dr. John M. Morgan, All rights reserved - This page last edited May 13, 2003
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