PAPER Electrophysiological evidence for the magnocellular-dorsal pathway deficit in dyslexia Katarzyna Jednoróg, 1,2 Artur Marchewka, 1,3 Pawel Tacikowski, 1 Stefan Heim 4 and Anna Grabowska 1,5 1. Nencki Institute of Experimental Biology, Department of Neurophysiology, Warsaw, Poland 2. Laboratoire de Sciences Cognitives et Psycholinguistique (CNRS ⁄ DEC-ENS), Paris, France 3.Laboratoire de recherche en neuroimagerie, UNIL, Lausanne, Switzerland 4.Department of Psychiatry and Psychotherapy, RWTH Aachen University, Germany; JARA-BRAIN, Jülich and Aachen, Germany; Research Centre Jülich, Institute of Neurosciences and Medicine (INM-1), Jülich, Germany 5.Warsaw School of Social Sciences and Humanities, Poland Abstract In adults, the onset of coherent motion compared to random motion in a random dot kinematogram leads to a right hemispheric amplitude advantage of the N2 response. The source of this asymmetry is believed to lie in the motion selective MT+ cortex. Here, we tested whether the right tempo-parietal N2 component shows a similar regularity in children. In particular, we were interested in whether coherent vs. incoherent motion modulates the amplitude of N2 similarly in dyslexic and control children. We found higher N2 amplitude for coherent compared to random motion in the right hemisphere for controls but not for dyslexics. This effect was related to topographical differences of N2 amplitude for random motion between the studied groups and was accompanied by longer reaction times to random motion in dyslexic compared to control children. Furthermore, a negative correlation between the amplitude of N2 for random motion and spellingerrors was observed in both groups, which is consistent with previous findings linking the magnocellular-dorsal (MD) pathway with orthographic skills. These data support the hypothesis of subtle deficiencies in the MD pathway in dyslexia. Introduction One causal hypothesis of developmental dyslexia sug- gests a specific deficit in the magnocellular-dorsal (MD) pathway responsible for visual and auditory processing. In vision, the magnocellular-dorsal pathway projects from the inferior layers of the lateral geniculate nucleus, to layer IVCa in the primary visual cortex, and domi- nates the response of neurons in motion selective cortex, MT (Maunsell, Nealey & DePriest, 1990; Wandell, 1995). In support of this hypothesis, a number of investigators have found deficiencies in a psychophysical test often used to assess MD pathway (visual coherent motion detection) among dyslexic readers (e.g. Cornelissen, Richardson, Mason, Fowler & Stein, 1995; Talcott, Witton, Hebb, Stoodley, Westwood, France, Hansen & Stein, 2002). However, there are also studies that failed to show such differences between dyslexic and control groups (e.g. Edwards, Giaschi, Dougherty, Edgell, Bjornson, Lyons & Douglas, 2004; White, Milne, Rosen, Hansen, Swetten- ham, Frith & Ramus, 2006). The majority of the mea- surements testing the MD hypothesis (e.g. coherent motion, contrast sensitivity, velocity discrimination) are behavioral, with no direct relation to the underlying neurophysiological mechanisms in the MD pathway. These behavioral measurements might not be sensitive enough to assess the hypothesized MD deficit in dyslexia and it is impossible to confidently determine that a particular behavioral task is limited entirely by the signals within the MD pathway (Ben-Shachar, Dougherty, Deutsch & Wandell, 2007; Skottun & Skoyles, 2008). Hence, physiological measurements that reliably probe the magnocellular pathway are necessary in order to obtain a more brain-based account of the deficit. So far only a few studies have been carried out to elucidate the neural basis of the MD pathway deficit in dyslexia. Anatomical evidence from post-mortem examinations has described a significant difference in the size of magnocellular neurons in the lateral geniculate nucleus (LGN) (Galaburda & Livingstone, 1993; Livingstone, Rosen, Drislane & Galaburda, 1991). fMRI studies have indicated abnormal responses in dyslexics to motion in the MT ⁄ V5 complex (Ben-Shachar et al., 2007; Demb, Boynton & Heeger, 1997, 1998; Eden, VanMeter, Rumsey, Maisog, Woods & Zeffiro, 1996). Eden et al. Address for correspondence: Katarzyna Jednoróg, Laboratoire de Sciences Cognitives et Psycholinguistique (CNRS ⁄ DEC-ENS), 29 Rue d’Ulm, 75002 Paris, France; e-mail: k.jednorog@nencki.gov.pl Ó 2011 Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA. Developmental Science 14:4 (2011), pp 873–880 DOI: 10.1111/j.1467-7687.2011.01037.x