Anti-Motion Sickness Medications in Dyslexia
The experimental attempt to treat dyslexic individuals with anti-motion sickness medications was based on the following reasoning: (1) If, indeed, the sensory-motor dysmetria underlying dyslexia is of a primary c-v origin; and (2) if the cerebellum modulates the motion input in a manner analogous to its demonstrated role in modulating the visual, acoustic, proprioceptive and tactile input; and (3) if the anti-motion sickness medications improve the functional capacity of the cerebellum (and vestibular circuits) to process and modulate motion input and autonomic motion-sickness reflexes; then perhaps these very same “motion” medications may similarly improve the cerebellum’s capacity to modulate and harmonize the non-motion sensory-motor organismic dysmetria characterizing and underlying dyslexia. Furthermore, if these hypotheses are correct, any and all pharmacologically induced therapeutic responses in dyslexia may be viewed as neurophysiologic indicators suggesting that subclinically impaired c-v functional patterns were being compensated for by chemically improved c-v modulating and sensory-motor processing capacity. In addition, the chemically triggered and clinically observed conversion of “dyslexic” to improved or “normal” functioning may be utilized to highlight, and thus explore, the specific c-v neurodynamic role in dyslexic functioning, and to test the c-v potency of specific chemical agents.
KeywordsPlacebo Fatigue Librium Lost Ritalin
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