1043-3155 Pediatr Neurol Briefs pedneurbriefs Pediatr Neurol Briefs Pediatric Neurology Briefs Pediatr Neurol Briefs 2166-6482 1043-3155 2166-3155 Pediatric Neurology Briefs Publishers Chicago, IL, USA PNB-2-96 10.15844/pedneurbriefs-2-12-12 Developmental Disorders and Learning Neurology Pediatrics Nervous System Diseases Child Development Brain Diseases Neurosurgery Child Infant Drugs in Treatment of Developmental Dyslexia http://orcid.org/0000-0002-0173-7931 Millichap J. Gordon MD 1 2 * Division of Neurology, Children's Memorial Hospital, Chicago, IL Departments of Pediatrics and Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL Correspondence: Dr. J. Gordon Millichap, E-mail: jgmillichap@northwestern.edu 12 1988 01 08 2016 2 12 96 96 Copyright: © 1988 The Author(s) 1988 This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The failure of antimotion sickness medication to improve reading in developmental dyslexia: results of a randomized trial

An acute 2 day trial of methylphenidate (10 mg) and of meclizine (12.5 mg) and a 6 month crossover placebo-controlled chronic trial of meclizine (12.5 mg) in children with developmental dyslexia are reported from the University of Calgary, Alberta, Canada.

 Methylphenidate Acute Trials Phonetic Analysis

An acute 2 day trial of methylphenidate (10 mg) and of meclizine (12.5 mg) and a 6 month crossover placebo-controlled chronic trial of meclizine (12.5 mg) in children with developmental dyslexia are reported from the University of Calgary, Alberta, Canada. Oral reading fluency, coordination, and motor accuracy improved on methylphenidate, and clinical improvements of eye fixation and tracking were found with meclizine, in acute trials. Three of 6 children showing benefit from acute doses of meclizine also showed significant improvements in eye fixation stability after 3 months chronic administration of the drug (12.5 mg BD), but measures of reading skills including comprehension, phonetic analysis, structural analysis, achievement, and oral and silent reading rates, were not benefitted. [1]

COMMENT. Levinson has proposed a theory of cerebellar-vestibular dysfunction as the etiology of dyslexia and has claimed that treatment with antimotion sickness medications may result in improvement in reading in 77% of cases of dyslexia. The present study fails to confirm these results and suggests that antimotion sickness drug treatment of dyslexia is unjustified. The relationship between fixation error and impaired reading is not completely understood, however. Geiger and Lettvin have found that dyslexics have poor foveal vision, but when the target is moved into the peripheral visual field, their ability to identify letters is better than control nondyslexic subjects. Imperfect oculomotor control in the dyslexic may be accompanied by abnormalities of visual processing and cognitive difficulties that impede the acquisition of reading skills. Further work on this aspect of dyslexia seems justified.

 Fagan JE Kaplan BJ Raymond JE Edgington ES The failure of antimotion sickness medication to improve reading in developmental dyslexia: results of a randomized trial J Dev Behav Pediatr 1988 Dec 9 6 359 66 10.1097/00004703-198812000-00008 3220956