Pre-dispositional constitution and plastic disposition: toward a more adequate descriptive framework for the notions of habits, learning and plasticity

Behavioral studies and neurobiological models of mental illnesses can be used to inform theories of mind and action. In this paper I use specific aspects of some paradigmatic cases in order to establish what I consider to be a useful distinction for the analysis of human action and, more specifically, the delimitation of habitual action. Patient SM is a well-known case of Urbach-Wiethe disease—one of only 300 cases reported in the reference literature— that was submitted to a decade of investigations (Adolphs et al., 1994, 2005). This syndrome, also known as lipoid proteinosis, produces dermatological lesions as well as calcifications in regions of the brain, often affecting the amygdaloid region (Siebert et al., 2003; Bahadir et al., 2006). While her basic perception, memory, and language skills are essentially normal, SM has nearly complete bilateral destruction of the amygdala, and her social behavior is indiscriminately trusting and friendly (Adolphs et al., 1994). Ten years of research showed an intriguing impairment in her ability to recognize fear in facial expressions, due to a lack of spontaneous fixation on the eyes when viewing faces (Adolphs et al., 2005). The research showed that in control patients, spontaneous fixation is directed principally to the eyes and the mouth, tracking the regions of the face that allow one to distinguish facial expressions. However, patient SM spontaneously focused on the nose, thereby missing necessary information for judging emotions. What is so interesting to point out is that when given explicit instructions (“look at the eyes of this person”) SM had no problem focusing on the eyes and recognizing emotions but, surprisingly, after a decade of treatment, SM was not able to learn the habit of looking at the eyes of the face spontaneously. Another case of interest for action theory can be found in studies of subjects in the autistic spectrum (Klin et al., 2003; Boria et al., 2009; Gallese, 2009; Kana et al., 2014), particularly studies of deficits in the functioning of the “mirror mechanism” (Antonietti, 2013). This deficit appears related to other deficits such as atypical visual processing and encoding of social stimuli, as well as imitative behavior and the ability to share attention (for review, see Gallese et al., 2013). Atypical brain development has been identified in cases of autism; specifically, the neural organization in areas involved in social cognition, facial expression, and facial recognition, as well as in areas associated with the mirror mechanism, appears to be related to the functional architecture that characterizes the atypical development of the autistic spectrum (Cauda et al., 2011; Gallese et al., 2013). Another paradigmatic case that is informative for theories of mind-based action is schizophrenia (Synofzik et al., 2010; Leube et al., 2012; Mausbach et al., 2013). Multiple investigations suggest that schizophrenia and other neuropsychiatric disorders are associated with deficits in mirror neurons (Enticott et al., 2008; Mehta et al., 2013) and with interneuron dysfunction (Marin, 2012). For now, let us focus on the second dysfunction. Interneurons regulate the activity of pyramidal cells, largely through inhibitory mechanisms, and one of the functions of pyramidal cells is to maintain cerebral patterns associated with perception and memory. Migration of the interneurons during the development of the nervous system is fundamental to this function, as it determines the final positioning of the neurons, thereby establishing the basis for correct wiring of neural circuitry (Marín, 2013). It has been demonstrated that schizophrenics possess mutations in certain genes that affect the migration of the intercortical neurons during embryonic development (Valiente and Marin, 2010). In addition, for decades we have known that there is a correlation between schizophrenia and the alteration of visual perception and eye movements. In fact, just recently it has been shown that simple tests for the detection of abnormal eye movements can discriminate cases of schizophrenia from controls with exceptional accuracy (Benson et al., 2012). Of the genes that are involved in the disrupted tangential migration of cortical neurons, NRG1, ERBB4, GRIN1, DISC1, and DTNBP1 (Marin, 2012), four of them are involved in the expression of molecules related with visual structures, and one of them is related to early visual processing: NRG1 is expressed in the cornea (Brown et al., 2004) and one of its mutations (rs3924999) affects spatial accuracy on the anti-saccade (AS) task (Schmechtig et al., 2010) and is associated with auditory P300 in schizophrenia (Kang et al., 2012);