Dyslexia Likely Not Caused by Ocular Motility Disorders

Medscape News
Lara C. Pullen, PhD
December 05, 2014

A functional MRI dyslexia study was recently reported 11/30/14 by Ibone Saralegui, MD and colleagues in Chicago at the Radiological Society of North America 100th Annual Meeting. Their results indicated that patterns of brain activation in readers with ocular motility disorders and normal individuals were similar but significantly different from dyslexics. (Children with motility disorders have impaired stereopsis [depth perception] and saccadic eye movements in binocular vision, but they have a normal ability to read.)

Dr. Saralegui’s team concluded that dyslexia stems from a deficit in the reading network rather than a deficit in the visual network.
As a result, they suggest that children with dyslexia would benefit most from phonologic treatment, not from special lenses and vision therapy.

According to Dr. Harold Levinson, the results of this important study were incorrectly interpreted due to an inadequate clinical understanding of dyslexia and its many symptoms and helpful therapies.

In addition, they relied on the phonological theory of dyslexia which fails to explain and encompass the well known visual symptoms and mechanisms (eg., visual reversals, impaired fixation and tracking, blurring, oscillopsia, double vision, etc.) characterizing the reading impairment in dyslexia. And this phonological theory also completely fails to explain all the many non-reading writing, math, memory, speech, spatial-temporal and balance/coordination symptoms invariably present in dyslexics.

Had they utilized Levinson’s cerebellar dyslexia theory and insights, the results would have been more realistically and scientifically interpreted. For example, Levinson had previously shown that a fine-tuning impairment within the cerebellum and inner-ear can readily explain the reading and related cognitive symptoms resulting when normal visual, auditory, phonetic and other brain centers fail to descramble them.

It also explains how these scrambled signals affect the motor system, resulting in the typically found dyslexic ocular-motor impairments, dysgraphia, dyspraxia or varied imbalance, dysrhythmic and dyscoordination symptoms.

As a result, impaired ocular fixation and sequential tracking secondarily adds more visual scrambling during reading. Although the latter does not cause dyslexia by itself, it certainly contributes to the impairment. Thus larger, bottom heavy, darker, tinted, glare free print often facilitates reading in dyslexics. And ocular-motor exercises may improve inner-ear mechanisms and so decrease signal-scrambling and resulting symptoms.

In addition, primary ocular motility and other visual acuity impairments may coexist in dyslexics, thus secondarily complicating reading. Needless to say, corresponding visual therapies are likely helpful.

About Dr. Harold Levinson
Formerly Clinical Associate Professor of Psychiatry at New York University Medical Center, Dr. Harold Levinson is currently Director of the Levinson Medical Center for Learning Disabilities in Long Island, New York. He is a well-known neuropsychiatrist, clinical researcher and author. For more information, call 1(800)334-7323 or visit: http://www.dyslexiaonline.com

SOURCE: http://www.medscape.com/viewarticle/836017

Radiological Society of North America (RSNA) 100th Annual Meeting: Abstract PDS213. Presented November 30, 2014.

Image Courtesy of Renjith Krishnan/FreeDigitalPhotos.net

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