%0 Journal Article
%T Saccadic Alterations in Severe Developmental Dyslexia
%A Stefano Pensiero
%A Agostino Accardo
%A Paola Michieletto
%A Paolo Brambilla
%J Case Reports in Neurological Medicine
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/406861
%X 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 ˇ°magnocellular theoryˇ± postulates a deficit in the magnocellular neuroanatomy and neurophysiology [6, 7] that leads to deficits in fixation and eye movements [8¨C10], but some authors do not agree with this hypothesis [11]. The ˇ°fast temporal deficit hypothesisˇ± 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 ˇ°cerebellar-deficit hypothesisˇ± 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
%U http://www.hindawi.com/journals/crinm/2013/406861/