Research has shown an association between functioning of the visual magnocellular system and dyslexia. While many studies have provided evidence supporting the magnocellular deficit, some studies have failed to replicate these findings. The main aim of the current study was to examine different theoretical explanations of reduced motion sensitivity in dyslexia. These included: (1) a sensory deficit caused by a structural abnormality in the magnocellular system affecting the processing of sparse motion signals (Talcott et al., 1998), (2) a deficit in temporal integration (Raymond & Sorensen, 1998), (3) a deficit at extrastriate visual areas only (e.g., Hill & Raymond, 2002), and (4) a deficit in noise exclusion (Sperling, Lu, Manis, & Seidenberg, 2005, 2006b). Three global motion experiments were conducted to investigate motion extraction, motion integration, and simultaneous motion processing. A local motion control task was also administered. Participants were two groups of high functioning adults with and without dyslexia. The dyslexia group were significantly less sensitive than the skilled reader group on each of the global motion processing tasks, but not on the local motion processing task. Manipulations of dot density, the number of animation frames presented in the random dot kinematogram (RDK), and signal dot lifetime affected motion sensitivity in the dyslexia and skilled reader groups similarly. A combination of high dot density and presentation of an increased number of animation frames in the global motion stimulus increased sensitivity for both reader groups. These results suggest that the global motion deficit found in dyslexia can partially be explained by sensory and perceptual motion processing deficits mediated by visual area V5.