As a consequence, the study of AHP and related disorders got a ‘c

As a consequence, the study of AHP and related disorders got a ‘cognitive neuroscience’ make over. This can be detected in at least

four different developments: (a) new theoretical hypotheses were put forward, stemming from philosophical or computational approaches on motor and embodied cognition, that view AHP as a specific disorder of motor awareness rather than a secondary consequence of deficits in other domains (e.g., Berti et al., 2005; Frith, Blakemore & Wolpert, 2000; Heilman, Barret & Adair, 1998); (b) improvements in structural neuroimaging methods, software and statistics allowed lesion mapping studies LY2835219 to identify brain lesions selectively associated with AHP (Berti et al., 2005; Karnath, Baier & Nägele, 2005); (c) new diagnostic tests and meta-analysis of diagnostic criteria allowed group studies and statistical data about the prevalence of AHP (for reviews see Orfei, Caltagirone & Spalletta, 2009; Jenkinson, Preston & Ellis, 2011); and finally (d) well-controlled, psychophysical experiments FG-4592 clinical trial began to supplement clinical descriptions and neuropsychological assessments of patients (see Jenkinson & Fotopoulou, 2010 for review). These developments have undoubtedly advanced our understanding of

AHP. Yet, as aforementioned, it would be a mistake to assume that

the epistemological premises of cognitive neuroscience are free from all the epistemological errors of cognitive neuropsychology. In the case of the study of AHP, contemporary studies seem to have inherited several epistemological premises from cognitive neuropsychology, most notably its strong emphasis on functional Urease segregation and modularity. Simultaneously, and perhaps most unfortunately, some new studies of AHP portray some older limitations of traditional neuropsychology that cognitive neuropsychology had attempted to avoid, namely naive localizationism and reductionism. For example, while progress in lesion mapping methods has allowed for a more precise identification of the lesion sites selectively associated with AHP, the results of such studies and their interpretations portray a return to strict modularity and a novel reductionism in the field. The labs of Berti (Berti et al., 2005) and Karnath (Baier & Karnath, 2008; Karnath et al., 2005) pioneered studies in which the anatomical extent of brain damage in groups with AHP was compared with that of matched control groups with hemiplegia and neglect. These studies offer minimal details of their patients’ unawareness symptoms, or of the subjective experience of their deficits.

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