We start by review the evolution of Bálint syndrome, covering the various interpretations of it over time. We then develop a novel integrative view in which we propose that the various symptoms, historically reported and labelled by various authors, result from a core mislocalization deficit. This idea is in accordance with our previous proposal that the core deficit of Bálint syndrome is attentional (Pisella et al. 2009, 2013, 2017) since covert attention improves spatial resolution in visual periphery (Yeshurun and Carrasco 1998); a deficit of covert attention would thus increase spatial uncertainty and thereby impair both visual object identification and visuo-motor accuracy. In peripheral vision, we perceive the intrinsic characteristics of the perceptual elements surrounding us, but not their precise localization (Rosenholtz et al. 2012a,b), such that without covert attention we cannot organize them to their respective and recognizable objects; this explains why perceptual symptoms (simultanagnosia, neglect) could result from visual mislocalisation. The visuo-motor symptoms (optic ataxia) can be accounted for by both visual and proprioceptive mislocalisations in an oculocentric reference frame, leading to field and hand effects, respectively. This new pathophysiological account is presented along with a model of posterior parietal cortex organisation in which the superior part is devoted to covert attention while the right inferior part is involved in visual remapping. When the right inferior parietal cortex is damaged, additional representational mislocalisations across saccades worsen the clinical picture of peripheral mislocalisations due to an impairment of covert attention.