This is in keeping with results suggesting that white matter lesion in humans are an important determinant of neglect (Thiebaut de Schotten et al., 2005), a view which, however, is not shared by other authors (Karnath et al., 2009). To our knowledge, constructional disorders have never been studied after parietal or cortical lesions in monkeys, probably because this species does not display constructive ability in the wild or, at least, this ability has never been tested in natural conditions. However, when forced in a laboratory setting, monkeys do show limited constructional abilities as a result of training. Under such conditions, certain properties of parietal neurons that

are of interest to pathology emerge, and their collapse could explain constructional disorders of the type observed in man, as documented in a previous section of this Saracatinib mouse manuscript. Although these properties are likely to be shaped as a result of extensive behavioural training, they could also be considered the substrate of an early form of spatial cognition encoded in parietal

cortex. Some forms of spontaneous spatial construction have been described in chimpanzees (Potì & Langer, 2001; Potì, 2005; Potìet al., 2009), although their constructive space is very primitive Ipatasertib order when compared to that of humans, especially when manipulating simultaneous spatial relationships between multiple objects is required, a task on which chimpanzees systematically fail. Why did elaborate constructional abilities emerge so late during primate evolution? The same question applies to hemispatial neglect, for which a full-blown syndrome closely resembling that observed in man has never been described in monkeys after parietal lesions, this in spite of the fact that parietal neurons encoding visual space in different reference frames have been described, the loss of which could very well explain different forms of neglect. An answer to this paradox can only by speculative. It is possible that, in spite of 30 million years of independent evolution, the basic parietal circuits that subserve attentional

and cognitive motor behaviour were preserved in the brains of humans and monkeys, as suggested Monoiodotyrosine by the similarities in parietofrontal connectivity of the two species. However, during human evolution an increase in the complexity of this elementary cortical circuit must have occurred. The specialization of this distributed system (Mountcastle, 1978a) has probably involved changes in the organization of parietal cortex and/or of its connections with other cortical areas. The former probably involved an expansion of the upper cortical layers (Marin Padilla, 1992) during human evolution, perhaps by extending the period of neurogenesis (Kornack & Rakic, 1998) when the neurons that eventually inhabit the upper cortical layers are born. The cell types involved would be likely to include both locally projecting intrinsic interneurons and neurons giving rise to corticocortical projections.