Artigo Revisado por pares

An intersubjective perspective on negative symptoms of schizophrenia: Implications of simulation theory

2007; Taylor & Francis; Volume: 12; Issue: 2 Linguagem: Inglês

10.1080/13546800600819921

ISSN

1464-0619

Autores

Giampaolo Salvatore, Giancarlo Dimaggio, Paul H. Lysaker,

Tópico(s)

Schizophrenia research and treatment

Resumo

Abstract The majority of neurocognitive models of negative symptoms in schizophrenia focus on failures to construct and sustain accurate representations of others and the world. Rarely considered are the intersubjective dimensions of negative symptoms as well as the mechanisms that sustain such symptoms. This paper critically analyses neurocognitive models of schizophrenia based on Theory of Mind (TOM) deficits and describes an alternative model of negative symptoms of schizophrenia based on Simulation Theory. We assert that several forms of negative symptoms of schizophrenia can be explained by an inability to express oneself, participate in, or be attuned to the context of social interactions. We label this deficit disadherence and suggest it may result from dysfunctions in "mirror" neurons. In particular, we suggest that patients with schizophrenia are unable to construct an inner model of the mind of another person and "select", from among various hypotheses, the one most suited to immediately understand the meanings and goals of interpersonal interactions. Moreover dysfunction in both "canonical" and "mirror" neurons, situated for the most part in the premotor and parietal cortex, could cause psychomotor negative symptoms. These hypotheses are explored in the context of a single case study. Notes 1Fictitious name. 2Rizzolatti and Fadiga (1998) discovered neurons with such characteristics recording single-neuron electrical activity in the monkey's rostroventral premotor cortex. The same kinds of neurons were observed in humans on the basis of brain imaging evidences (see Rizzolatti, Fogassi, & Gallese, 2002). 3Gallese, Fadiga, Fogassi, and Rizzolatti (Citation1996) described neurons with such characteristics recording single-neuron electrical activity in the monkey's rostroventral premotor cortex. The same kind of neurons were observed in humans on the basis of brain imaging evidences (Rizzolatti et al., Citation1996). 4One of the areas presenting the most relevant signal increase was the pars opercularis of the inferior frontal gyrus. 5Bilateral anterior insula, rostral anterior cingulated cortex, brainstem, and cerebellum. 6In the case of linguistic understanding, this theoretical position seems incompatible with the distinction between semantic and pragmatic understanding, i.e., it is in contrast with several neurocognitive models of semantic processing, postulating that syntactic, semantic, and pragmatic processing depend on the activation of mutually independent neural models (Frazier, Citation1987; Frazier & Rayner, Citation1987; Friederici, Citation2002). 7The difference we briefly describe here between the individualist "classical cognitive science" and the intersubjectivist "second generation cognitive science" reflects the "second cognitive revolution", namely, the paradigm shift that occurred in cognitive science in the last decade of the twentieth century (see Harrè & Gillet, Citation1994; Sinha, 2001). 8This perspective is consistent with Husserl (1989), in the sense that what makes the other understandable to us at a basic level is just that we do not experience other's body as a material object (Körper), but as something alive and acting (Leib), just like our own body. 9In this perspective, the TOM theorists (including Frith), do not show an entirely coherent approach to the problem: Some of them, though postulating that schizophrenia patients suffer from a deficit in TOM module, show that they do not fail at all in tasks testing that capacity (Frith, 1994; Frith & Corcoran, Citation1996). 10Also, in his more recent work, Frith (Citation2005) continues on the track of his neuropsychological model of schizophrenic symptoms: He investigates the neural basis of symptoms in the field of "alien control", in which the patient attributes his own actions to another agent. This may be based on a failure to integrate information generated in frontal cortex (goal-oriented action) with information generated in posterior cortical regions (sensory processing). Thus, Frith does not investigate the neural basis of the relationship between goal-oriented action and more complex and intersubjective psychological dimensions that concern us.

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