Impaired visual word processing in dyslexia revealed with magnetoencephalography

Abstract

Dyslexia is most often attributed to phonological impairments, manifested in abnormal activation of the left temporal and temporoparietal cortex in response to auditorily presented language and possibly associated with anomalies in the cytoarchitecture and hemispheric symmetry of the plana temporale. The immediate cortical correlate of the severely impaired reading process has, however, remained obscure. Here we report on the distinct time courses of cortical activation in dyslexic and control subjects during passive viewing of single words, tracked with whole-head magnetoencephalography. A striking difference was found in the left inferior temporo-occipital region where intracranial recordings have recently identified word-specific responses within 200 msec after stimulus onset: controls showed a sharp activation at about 180 msec after word presentation, whereas dyslexics failed to activate this area entirely, or showed a slowly increasing late response. Perception of words as specific units thus seems to be impaired in dyslexics.

The left occipitotemporal system in reading: Disruption of focal fMRI connectivity to left inferior frontal and inferior parietal language areas in children with dyslexia

“…This deficit has been associated with a dysfunction of the left ventral occipitotemporal cortex in adolescents and adults (e.g., (Brunswick et al, 1999;Helenius et al, 1999;Horwitz et al, 1998; Kronbichler et al, 2006; McCrory et al, 2005; Paulesu et al, 2001;Rumsey et al, 1997a;Rumsey et al, 1997b;Salmelin et al, 1996;Shaywitz et al, 2003; In our previous fMRI study, we specifically investigated print processing in the VWF-System in children with and without dyslexia while they indicated if visual stimuli (real words, pseudohomophones, pseudowords and false-fonts) sounded like a real word (Van der Mark et al, 2009). We found that a posterior-anterior gradient of print specificity (higher anterior activity to letter strings but higher posterior activity to false-fonts) as well as a constant sensitivity to orthographic familiarity (higher activity for unfamiliar than familiar word-forms) along the VWF-System could only be detected in controls.…”

“…This deficit has been associated with a dysfunction of the left ventral occipitotemporal cortex in adolescents and adults (e.g., (Brunswick et al, 1999;Helenius et al, 1999;Horwitz et al, 1998;Kronbichler et al, 2006;McCrory et al, 2005;Paulesu et al, 2001;Rumsey et al, 1997a;Rumsey et al, 1997b;Salmelin et al, 1996;Shaywitz et al, 2003; as well as in children with dyslexia (e.g. (Cao et al, 2006;Hoeft et al, 2007;Maurer et al, 2007;Shaywitz et al, 2002;Shaywitz et al, 2007;van der Mark et al, 2009) for a large number of languages using a wide range of functional imaging methods.…”

Specialization within the ventral stream: the case for the visual word form area

“…Activation in this region can be identified merely by contrasting word reading relative to rest, either with PET or with fMRI (Beauregard et al, 1997;Brunswick et al, 1999;Fiez et al, 1999;Paulesu et al, 2000;Wagner et al, 1998). This region appears as a likely source of electrical and magnetic fields that are recorded over the left ventral occipitotemporal region, with a latency of about 150 -200 ms, whenever subjects see words Cohen et al, 2000;Nobre et al, 1994;Salmelin et al, 1996;Simos et al, 2002;Tarkiainen et al, 1999). When word reading is contrasted to a resting period, the active regions obviously comprise a large unspecific component of visual activity.…”

Cerebral cortical dysfunction in patients with temporomandibular disorders in association with jaw movement observation

“…The next ECD was identified by removing the effect of the previous sources from the magnetic signal pattern (signal space projection method; Uusitalo and Ilmoniemi, 1997) and then searching for additional sources in the response of the residual waveforms. This surveillance was discontinued when the strength of new ECDs could not exceed 5 nAm (Salmelin et al, 1996). Note that the source which could not be detected at a particular brain area was assumed to be 0 nAm in source strength.…”