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Dyslexia is not just a severe reading disorder characterized by reversals. And it is not due to brain damage as traditionally thought for the past century. It is a syndrome of many and varied symptoms affecting over 40 million American children and adults.
Ever since the early 1970's, Dr. Harold Levinson's groundbreaking research has continued to demonstrate that the symptoms of dyslexia or Learning Disabilities (LD), Attention Deficit Disorder (ADD), and related Phobic symptoms are due to a simple signal-scrambling disturbance of inner-ear (cerebellar-vestibular) origin.
In other words, the inner-ear acts as a "fine-tuner" for all motor (balance/coordination/rhythm) signals leaving the brain and all sensory and related cognitive signals entering it. As a result, normal thinking brains will have difficulty processing the scrambled or distorted signals received. And the final symptoms will depend on: (1) the degree of signal-scrambling, (2) the location and function of the varied normal brain centers receiving and having to process these scrambled signals, as well as (3) the brain's compensatory ability for de-scrambling.
By contrast, the brain-damage theorists mistakenly believe that vital processing cells scattered throughout the thinking brains of dyslexics are severely impaired. And thus normally-received signals can't be properly interpreted. Were this brain-damage theory true, then the IQ's of dyslexics would be severely impaired and their prognosis or outcome would remain hopeless — despite all efforts and therapies — since abnormal processing cells within the thinking brain can't be significantly compensated for. And as might have been expected, despite escalating research efforts by gifted scientists, this flawed 100-year-old brain-damage theory has led absolutely nowhere in so far as medical ways of diagnosing, treating, and explaining the dyslexic syndrome.
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