WHICH DYSLEXIC SUBTYPES DEMONSTRATE A MAGNOCELLULAR PATHWAY DEFECT?

Title WHICH DYSLEXIC SUBTYPES DEMONSTRATE A MAGNOCELLULAR PATHWAY DEFECT?
Author, Co-Author WH III, E Borsting, M Cooper, B McNeel
Topic
Year
1994
Day
Tuesday
Program Number
1:40 pm
Room
San Diego Ballroom C
Affiliation
Abstract A review of the literature reveals that approximately 75% of dyslexics have a processing deficit in the magnocellular pathway (Lovegrove et al., 1990). In addition, a recent report demonstrated that the dyseidetic dyslexic subtype, which comprises 10 to 30% of the dyslexic population, does not have an abnormal magnocellular pathway (Ridder et al., 1993). These results suggest that the other two subtypes of dyslexia (dysphonetic and dysphoneidetic) should have a magnocellular pathway deficit. The purpose of this study was to determine if the dysphonetic and dysphoneidetic dyslexics exhibit a magnoceullar pathway defect. Four dyseidetic, 4 dysphonetic and 5 dysphoneidetic dyslexics were compared with 13 age and sex matched, normal controls. All subjects had normal intelligence and educational opportunities, no ocular disease, sensory impairments, overt psychological problems, or systemic pathology. The presence of dyslexia was determined with the Adult Dyslexia Test or the Dyslexia Determination Test. Temporal contrast sensitivity functions were determined with a full field flickering stimulus (5, 10, 15, 20 and 25 Hz) by employing a temporal, 2 alternative, forced-choice technique. A t-test demonstrated significant differences existed between the dysphoneidetic dyslexics and the normal controls for the data obtained at high temporal frequencies. Similar results were obtained for the dysphonetic dyslexics but not the dyseidetic dyslexics. These results suggest that the dysphonetic and dysphoneidetic dyslexics have a magnocellular pathway defect.
Affiliation of Co-Authors
Outline