Theory of Mind in Schizophrenia: Damaged Module or Deficit in Cognitive Coordination?
A Commentary on:Phillips and Silverstein: Convergence of biological and psychological perspectives on cognitive coordination in schizophrenia. (appeared in Brain and Behavior Science, 26(1), 94-95, 2003)
David Leiser* & Udi Bonshtein
Dept of Behavioral SciencesBen-Gurion UniversityPOB 653IL 84105 BeershevaIsrael
Schizophrenics exhibit a deficit in theory of mind (ToM), but an intact theory of biology (ToB). One explanation is that ToM relies on an independent module that is selectively damaged. Philips and Silverstein analyses suggest an alternative: ToM requires the type of coordination that is impaired in schizophrenia, whereas ToB is spared because this type of coordination is not involved.
P and S document how schizophrenic patients exhibit deficits that may be explained by impaired cognitive coordination. The specific phenomena they discuss involve paradigms that engage perceptual and low-level semantic processes. Can this line of analysis also account for specific deficit patterns in higher cognitive and social-cognitive functioning in schizophrenia?
We summarize here work of our own and by others on the abilities of schizophrenic patients to handle "naïve theories" in two contrasting domains: Theory of Mind (ToM) and biology (ToB). ToM is defined as the ability to attribute mental states to the self and to others, to predict and explain their behavior with reference to mental states (Premack & Wooduff, 1978). Several recent studies examined ToM in schizophrenia, and all indicate that ToM is damaged in the acute phase (eg, Frith and Corcoran, 1996; Doody, Goetz, Johnson, Frith, & Cunnigham-Owens, 1998), but return to normal in periods of remission (Drury, Robinson, & Birchwood, 1998). This is a specific deficit that cannot be accounted for by IQ or memory. As is well-know, a similar specific deficit is found in the case of autism, where it is also permanent (Baron-Cohen, 1995). The relation between schizophrenia and autism was pointed out by Frith (1992), who speculated that there is a common cognitive failing in these two conditions: autists never developed a ToM, whereas schizophrenics attempt to exercise a lost capability.
One way to test ToM in schizophrenia uses a non-verbal paradigm, where subjects are presented with cartoons (Sarfati et al. 1997). Each cartoon strip contains three pictures, which depicts a character performing some activity. Understanding these strips requires deriving the mental state and goals of the character. After studying the cartoon strip, subjects are presented with three additional pictures, one of which provides a suitable ending to the story. One filler depicts a common everyday activity, performed by the character, while and the other is very similar to the last picture in the strip. Neither of them is related to the context of the mental states of the character as established by the strip. In a variant of the task which involved an absurd filler (Sarfati et al., 1999) virtually no patients selected that option. This indicates that the patients do attempt to make sense of the task, and the paradigm makes it possible to identify the compensatory strategy used by schizophrenic patients. Lacking understanding of what the character is up to, schizophrenic patients who are not disorganized tended to select the picture that is visually similar to the last picture. Disorganized patients and manic patients tend to select familiar everyday activities, regardless of its resemblance to the preceding pictures.
We replicated these findings, and complemented them with the more common set of stories used to test ToM (Frith & Corcoran, 1996). These stories involve understanding cheating and false beliefs, either "first-order beliefs" requiring distinguishing the beliefs of characters from the true state of affaires, or "second-order beliefs" about others' beliefs. These stories are read aloud, and simple drawings help the subjects follow and remember the plots. Schizophrenic performed significantly worse than the control groups (both normals, and affective disorders hospitalized patients).
We tested the same subjects for ToB, adapting the battery designed by Johnson and Carey (1998). This battery relies on two levels of understanding biology, known to discriminate young from older children. The lower level relies on acquired information about living beings. The higher level marks accession to the understanding of living beings as functional systems, which gives meaning to biological functions. (For instance, since all organisms expand energy, they all must eat somehow, even if they have no apparent food ingesting organs.) In their study of Williams Syndrome patients, Johnson and Carey found that for all their verbal fluency, WS patients remain at the lower, childlike level of understanding.
Schizophrenic patients test normal on ToB, even during acute episode. One explanation for this difference between ToM and ToB would be to posit a "module" or cerebral specialization for ToM (Povinelli& Preuss, 1995). The alternative, "theory-theory" view, maintains that ToM is acquired like any other naïve theory (Gopnik & Wellman, 1992). On that view, it would seem difficult to account for the dissociation of ToB and ToM.
We suggest that the challenge of ToM may be different from that encountered in other naïve theories (Leiser, 2001) The tasks used to test for ToM require coordination of several pieces of information. Integration of multiple relations is a specific source of cognitive complexity (Halford et al, 1998; Waltz et al, 1999, Astington, Pelletier & Homer, 2002). In the false beliefs tasks, subjects must hold separate and coordinate the actual state of affairs, the first character's beliefs about them, and the second's character's beliefs about the first one's. This coordination is evidently beyond them. In Sarfati’s paradigm tasks, selecting the right answer implies building a context for his actions, and this requires coordination of the successive steps. Failing this complex contextual disambiguation, subjects fall back on either familiar actions to provide meaning, or use a much reduced context, consisting of the last picture only. If this line of reasoning is correct, we would have in ToM a symptom that arises, not from a module, but from the vulnerability of ToM to a deficit in coordination. Preservation of ToB, in contrast, can be explained by the absence of such coordination once the higher level of understanding is achieved.
This conclusion remains tentative as an account of deficits specific to schizophrenia. The authors's description of the effects of "schizomimetic" drugs fit psychotic-like state in general, yet non-schizophrenic psychoses (eg affective psychosis) do not damage ToM to the same extent as schizophrenic psychosis (,Sarfati et al., 1997; Bonshtein and Leiser, unpublished data). Equally, Sarfati et al. (1997) reported that a breakdown of schizophrenia into sub-types is unrelated to the severity of deficit in ToM, except for disorganized schizophrenia, which is associated with severe deficit in ToM. But this condition is characterized by a breakdown of personality and further traits that render cognitive collapse almost self-evident.
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