It is not sure if persons with dyslexia have ocular motor deficits in addition to their deficits in rapid visual information processing. A 15-year-old boy afflicted by severe dyslexia was submitted to saccadic eye movement recording. Neurological and ophthalmic examinations were normal apart from the presence of an esophoria for near and slightly longer latencies of pattern visual evoked potentials. Subclinical saccadic alterations were present, which could be at the basis of the reading pathology: (1) low velocities (and larger durations) of the adducting saccades of the left eye with undershooting and long-lasting postsaccadic onward drift, typical of the internuclear ophthalmoplegia; (2) saccades interrupted in mid-flight and fixation instability, which are present in cases of brainstem premotor disturbances. 1. Introduction Dyslexia refers to the inability to develop the capability to read, at an expected level, despite an otherwise normal intellect. The definitive cause is unknown, and the clinical spectrum is quite variable. A wide variety of intracranial abnormalities have been described on both structural and functional magnetic resonance imaging, including increased or decreased frontal lobe activity and size differences in frontal gyri, cerebella, temporal lobes, and thalamic nuclei. Various forms of ocular disturbances have been associated with reading disabilities. These disorders include exophoria, esophoria, amblyopia, and binocular dysfunctions [1]. Many pieces of evidence show that deficits in the perception of rapid visual information impact on reaction times (been longer) for eye movements [2, 3], hand movements, and vocal responses [4] in persons with dyslexia. Various hypotheses have been suggested to explain the presence of sensorimotor disorders in dyslexia [5]. The “magnocellular theory” postulates a deficit in the magnocellular neuroanatomy and neurophysiology [6, 7] that leads to deficits in fixation and eye movements [8–10], but some authors do not agree with this hypothesis [11]. The “fast temporal deficit hypothesis” focuses on the limited ability of persons with dyslexia to process rapid sequential auditory and visual stimuli. This could be related to the magnocellular theory [8] or to a basic sequential sensory processing deficit, unrelated to dysfunction of the magno cells [12, 13]. The “cerebellar-deficit hypothesis” suggests that many deficits associated with dyslexia, such as automatization [14], time estimation [15], and speeded performance [16], are caused by abnormalities within the lateral parts of the posterior
References
[1]
H. D. Simons and J. D. Grisham, “Binocular anomalies and reading problems,” Journal of the American Optometric Association, vol. 58, no. 7, pp. 578–587, 1987.
[2]
G. F. Eden, J. F. Stein, H. M. Wood, and F. B. Wood, “Differences in eye movements and reading problems in dyslexic and normal children,” Vision Research, vol. 34, no. 10, pp. 1345–1358, 1994.
[3]
M. Biscaldi, S. Gezeck, and V. Stuhr, “Poor saccadic control correlates with dyslexia,” Neuropsychologia, vol. 36, no. 11, pp. 1189–1202, 1998.
[4]
H. Sigmundsson, “Do visual processing deficits cause problem on response time task for dyslexics?” Brain and Cognition, vol. 58, no. 2, pp. 213–216, 2005.
[5]
R. Ram-Tsur, M. Faust, A. Caspi, C. R. Gordon, and A. Z. Zivotofsky, “Evidence for ocular motor deficits in developmental dyslexia: application of the double-step paradigm,” Investigative Ophthalmology and Visual Science, vol. 47, no. 10, pp. 4401–4409, 2006.
[6]
A. Galaburda and M. Livingstone, “Evidence for a magnocellular defect in developmental dyslexia,” Annals of the New York Academy of Sciences, vol. 682, pp. 70–82, 1993.
[7]
J. Stein and J. Talcott, “Impaired neuronal timing in developmental dyslexia—the magnocellular hypothesis,” Dyslexia, vol. 5, no. 2, pp. 59–77, 1999.
[8]
J. Stein, “The magnocellular theory of developmental dyslexia,” Dyslexia, vol. 7, no. 1, pp. 12–36, 2001.
[9]
P. G. Overton, “Collicular dysfunction in attention deficit hyperactivity disorder,” Medical Hypotheses, vol. 70, no. 6, pp. 1121–1127, 2008.
[10]
M. P. Bucci, N. Nassibi, C. Gerard, E. Bui-Quoc, and M. Seassau, “Immaturity of the oculomotor saccade and vergence interaction in dyslexic children: evidence from a reading and visual search study,” PLoS One, vol. 7, no. 3, Article ID e33458, 2012.
[11]
F. Hutzler, M. Kronbichler, A. M. Jacobs, and H. Wimmer, “Perhaps correlational but not causal: no effect of dyslexic readers' magnocellular system on their eye movements during reading,” Neuropsychologia, vol. 44, no. 4, pp. 637–648, 2006.
[12]
S. Amitay, G. Ben-Yehudah, K. Banai, and M. Ahissar, “Disabled readers suffer from visual and auditory impairments but not from a specific magnocellular deficit,” Brain, vol. 125, no. 10, pp. 2272–2285, 2002.
[13]
G. Ben-Yehudah and M. Ahissar, “Sequential spatial frequency discrimination is consistently impaired among adult dyslexics,” Vision Research, vol. 44, no. 10, pp. 1047–1063, 2004.
[14]
A. van der Leij and V. H. P. van Daal, “Automatization aspects of dyslexia: speed limitations in word identification, sensitivity to increasing task demands, and orthographic compensation,” Journal of Learning Disabilities, vol. 32, no. 5, pp. 417–428, 1999.
[15]
R. I. Nicolson, A. J. Fawcett, and P. Dean, “Time estimation deficits in developmental dyslexia: evidence of cerebellar involvement,” Proceedings of the Royal Society B, vol. 259, no. 1354, pp. 43–47, 1995.
[16]
D. L. Compton, J. C. DeFries, and R. K. Olson, “Are RAN- and phonological awareness-deficits additive in children with reading disabilities?” Dyslexia, vol. 7, no. 3, pp. 125–149, 2001.
[17]
A. Fawcett and R. Nicolson, Dyslexia: The Role of the Cerebellum, Whurr, London, UK, 2001.
[18]
G. T. Pavlidis, “Eye movements in dyslexia: their diagnostic significance,” Journal of Learning Disabilities, vol. 18, no. 1, pp. 42–50, 1985.
[19]
G. Stanley, G. A. Smith, and E. A. Howell, “Eye-movements and sequential tracking in dyslexic and control children,” The British Journal of Psychology, vol. 74, no. 2, pp. 181–187, 1983.
[20]
B. Brown, G. Haegerstrom Portnoy, A. J. Adams, et al., “Predictive eye movements do not discriminate between dyslexic and control children,” Neuropsychologia, vol. 21, no. 2, pp. 121–128, 1983.
[21]
R. K. Olson, B. W. Wise, F. Conners, J. P. Rack, and D. Fulker, “Specific deficits in component reading and language skills: genetic and environmental influences,” Journal of Learning Disabilities, vol. 22, no. 6, pp. 339–348, 1989.
[22]
J. Judge, M. Caravolas, and P. C. Knox, “Visual attention in adults with developmental dyslexia: evidence from manual reaction time and saccade latency,” Cognitive Neuropsychology, vol. 24, no. 3, pp. 260–278, 2007.
[23]
M. P. Bucci, D. Brémond-Gignac, and Z. Kapoula, “Latency of saccades and vergence eye movements in dyslexic children,” Experimental Brain Research, vol. 188, no. 1, pp. 1–12, 2008.
[24]
J. E. Raymond, N. A. Ogden, J. E. Fagan, and B. J. Kaplan, “Fixational instability and saccadic eye movements of dyslexic children with subtle cerebellar dysfunction,” American Journal of Optometry and Physiological Optics, vol. 65, no. 3, pp. 174–181, 1988.
[25]
P. C. Pierrot-Deseilligny, F. Gray, and P. Brunet, “Infarcts of both inferior parietal lobules with impairment of visually guided eye movements, peripheral visual inattention and optic ataxia,” Brain, vol. 109, no. 1, pp. 81–97, 1986.
[26]
G. C. Baylis, J. Driver, L. L. Baylis, and R. D. Rafal, “Reading of letters and words in a patient with Balint's syndrome,” Neuropsychologia, vol. 32, no. 10, pp. 1273–1286, 1994.
[27]
D. I. Friedman, J. Jankovic, and J. A. McCrary III, “Neuro-ophthalmic findings in progressive supranuclear palsy,” Journal of Clinical Neuro-Ophthalmology, vol. 12, no. 2, pp. 104–109, 1992.
[28]
M. P. Bucci, D. Brémond-Gignac, and Z. Kapoula, “Poor binocular coordination of saccades in dyslexic children,” Graefe's Archive for Clinical and Experimental Ophthalmology, vol. 246, no. 3, pp. 417–428, 2008.
[29]
R. J. Leigh and D. S. Zee, The Neurology of Eye Movements, University Press, Oxford, UK, 4th edition, 2006.
