An evolutionary account of impairment of self in cognitive disorders.

Atypical functioning of cortico-striatal brain networks that support cross-modality—a key human cognitive ability—may underlie altered processing of the self in schizophrenia, autism spectrum disorders, and synesthesia. This disruption affects both the minimal self and the narrative self. The authors link these cognitive conditions to an atypical presentation of human self-domestication features, building on prior work connecting cognitive disorders and language evolution. This framework unifies linguistic and non-linguistic symptoms through deficits in the notion of self, supports the hypothesis that schizophrenia and autism are diametrically opposed conditions, and suggests that their origins are tied to recent human evolution, offering cues for earlier and more accurate diagnosis.

Study at a glance

Abstract

Recent research has proposed that certain aspects of psychosis, as experienced in, e.g., schizophrenia (SCZ), but also aspects of other cognitive conditions, such as autism spectrum disorders (ASD) and synesthesia, can be related to a shattered sense of the notion of self. In this paper, our goal is to show that altered processing of self can be attributed to an abnormal functioning of cortico-striatal brain networks supporting, among other, one key human distinctive cognitive ability, namely cross-modality, which plays multiple roles in human cognition and language. Specifically, our hypothesis is that this cognitive mechanism sheds light both on some basic aspects of the minimal self and on some aspects related to higher forms of self, such as the narrative self. We further link the atypical functioning in these conditions to some recent evolutionary changes in our species, specifically, an atypical presentation of human self-domestication (HSD) features. In doing so, we also lean on previous work concerning the link between cognitive disorders and language evolution under the effects of HSD. We further show that this approach can unify both linguistic and non-linguistic symptoms of these conditions through deficits in the notion of self. Our considerations provide further support for the hypothesis that SCZ and ASD are diametrically opposed cognitive conditions, as well for the hypothesis that their etiology is associated with recent human evolution, leading to a deeper understanding of the causes and symptoms of these disorders, and providing new cues, which can be used for an earlier and more accurate diagnostics.