Integrated Psychological Therapy (IPT) - For the Treatment of Neurocognition, Social Cognition, and Social Competency in Schizophrenia Patients

Dynamic imaging, such as PET and functional MRI, tends to indicate reduced metabolic activity in the frontal lobes of schizophrenia patients compared to controls. This pattern is generally termed hypofrontality (for reviews see Blakemore & Frith, 2000; Ragland, Minzenberg, & Carter, 2007). Metabolic hypofrontality appears to be associated with impairments in neuropsychological functions in the frontal cortex, for example, working memory and executive functioning (Fu et al., 2005; MacDonald et al., 2005). This could form a link between the biological and cognitive levels of a specific type of vulnerability.

Specific brain structures implicated in schizophrenia include the dorsolateral, prefrontal, and temporal cortex, the various limbic system structures, the basal ganglia, parts of the thalamus, and the cerebellum (Andreasen, Paradiso, & O’Leary, 1998; Camchong, Dyckman, Chapman, Yanasak, & McDowell, 2006; Lee et al., 2006; Rüsch et al., 2007). The diversity of findings has inspired a more integrative perspective on brain impairments. For example, the cortical dysconnectivity syndrome model hypothesizes that normal interaction between multiple brain areas is impaired by synaptic processes common to those areas (James, James, Smith, & Javaloyes, 2004; Vogeley & Falkai, 1998; Wobrock et al., 2008). The failure is not situated in a specific brain structure or area, but in the transmission of information between them. Similarly, there is empirical evidence for fronto-temporal dissociation, or impaired transmission between frontal and temporal areas, in schizophrenia patients (Murray et al., 2008; Woodruff et al., 1997).

Cognition

Cognitive abnormalities have long been seen as core features of schizophrenia, arguably since Kraepelin (Green, 1998). Systemic vulnerability models stimulated new hypotheses about the etiological roles of these abnormalities – as markers, endophenotypes, and expressions of the disease. Soon after the first vulnerability models had appeared, cognitive abnormalities were found in children at risk (e.g., Asarnow, Steffy, MacCrimmon, & Cleghorn, 1978; Erlenmeyer-Kimling & Cornblatt, 1978) and in unaffected first-degree relatives (DeAmicis & Cromwell, 1979; Sitskoorn, Aleman, Ebich, Appels, & Kahn, 2004). In longitudinal studies, in support of the vulnerability hypothesis, impaired attention, and related information processing in children at risk for schizophrenia is related to eventual onset (Erlenmeyer-Kimling et al., 2000). Such abnormalities are also associated with impairments in social functioning in adulthood (Cornblatt, Lenzenweger, Dworkin, & Erlenmeyer-Kimling, 1992), suggesting more than a mere marker role in etiology.

As the cognitive research progressed, it became important to distinguish between trait-like and state-like abnormalities (Nuechterlein & Dawson, 1984b; Nuechterlein & Subotnik, 1998; Özgürdal et al., 2009; Wang, Chan, Yu, Shi, & Deng, 2008; Wykes & van der Gaag, 2001). Vulnerability factors tend to be more trait-like, present before as well as after onset, and relatively stable in severity (e.g., Aleman, Hijman, deHaan, & Kahn, 1999; Kurtz, 2005; Woods, Twamley, Dawson, Narvaez, & Jeste, 2007); statelike abnormalities tend to be associated with the acute psychotic state (e.g., Baxter & Liddle, 1998; Filbey et al., 2008; Nopoulos, Flashman, Flaum, Arndt, & Andreasen, 1994). Some abnormalities show characteristics of both, present at low levels before onset and between episodes, and becoming more severe after onset and/or during acute psychotic episodes. Many cognitive impairments appear to exert their effects over the course of the illness, producing poorer treatment adherence (Jeste, Patterson, Palmer, Dolder, & Jeste, 2003), functional behavioral impairments (Frith, 1992), higher risk of relapse (Chen et al., 2005), and a poorer overall prognosis (Green, Kern, Braf, & Mintz, 2000; McEvoy, 2008; Milev, Ho, Arndt, & Andreasen, 2005).

Another distinction of increasing importance is that between neurocognition and social cognition (Corrigan & Penn, 2001; Green, Penn et al., 2008; Penn, Corrigan, Bentall, & Racenstein, 1997; Penn et al., 2005). Most of the cognitive processes of interest in vulnerability research are relatively elemental, for example, reaction time, attention, and memory, derived from the laboratory methods of experimental psychopathology and clinical neuropsychology. These cognitive processes were used in a nonsocial context as neurobiological correlates (neurocognition). More recently, however, more complex levels of cognition have attracted the interest of schizophrenia researchers. The terms neurocognition and social cognition came to distinguish between these subdomains, although they are not necessarily distinct or nonoverlapping. Social cognition refers to how people think about themselves and others in the social world; simply put, it is people’s thinking about people (Green, Olivier, Crawley, Penn, & Silverstein, 2005; Penn, Sanna, & Roberts, 2008). Interest in social cognition was inspired in part by the fact that, although more elemental measures appear linked to vulnerability factors, their actual mechanistic role in etiology has been difficult to establish. Green and Nuechterlein (1999) proposed a model including social cognition as a possible mediator between neurocognitive and behavioral functioning, and empirical evidence supports such a role (Addington, Saeedi, & Addington, 2006b; Bell, Tsang, Greig, & Bryson, 2008; Brekke & Nakagami, 2010; Brekke, Kay, Lee, & Green, 2005; Brüne, 2005; Pinkham & Penn, 2006; Pinkham, Penn, Perkins, & Lieberman, 2003; Roder & Schmidt, 2009; Schmidt, Mueller, & Roder, 2009; Sergi, Green et al., 2007; Sergi, Rassovsky, Nuechterlein, & Green, 2006; Sergi, Rassovsky et al., 2007; Vauth, Rüsch, Wirtz, & Corrigan, 2004). Also, since social cognition is more functionally proximal to the deficits in social behavior that are of primary clinical concern in schizophrenia, it is hoped that a better understanding of social cognition will lead more directly to improved clinical assessment and treatment methods (Addington et al., 2006b).

Specific social cognitive impairments under current study include theory of mind (a person’s ability to infer the cognitive and emotional states of other people), social schema, social attribution, and social perception (Bellack, Morrison, & Mueser, 1989; Corcoran, Mercer, & Frith, 1995; Frith, 2004; Nienow, Docherty, Cohen, & Dinzeo, 2006; Penn et al., 1999; Pinkham, Penn, Perkins, Graham, & Siegel, 2007; Toomey, Wallace, Corrigan, Schuldberg, & Green, 1997; Zanello, Perrig, & Huguelet, 2006). Our understanding of this level of organismic functioning will probably expand considerably over the next few years. Many aspects of social cognition pertinent to severe mental illness have likely not yet been identified or measured. Also, the relationship between social cognition and neurocognition may not be purely hierarchical: There are differences between processing of social versus nonsocial information at fairly elemental levels, for example, between visual processing of the physical features of alphanumeric characters versus human faces.

Environmental Factors

Studies of the stress side of the vulnerability hypothesis were influenced by two distinct research paradigms: life events and expressed emotion. Life-events research typically involves an enumeration of specific stressful events that may either accumulate over time to interact with vulnerabilities or precipitate onset in a single stroke (Bebbington et al., 1993; Day, 1989; Dohrenwend, Shrout, Link, Skodol, & Stueve, 1995; Phillips, Francey, Edwards, & McMurray, 2007; Tennant, 1985). Both types of mechanisms appear to operate in the etiology of schizophrenia. After onset, both major stressors and minor “daily hassles” may influence the course of the disorder. Recently, the disproportionate representation of persons with histories of major trauma, childhood abuse, and childhood neglect among those with serious mental illness has given life-events research a new focus (Bebbington et al., 2004; Janssen et al., 2004; Read, van Os, Morrison, & Ross, 2005; Spauwen, Krabbendam, Lieb, Wittchen, & van Os, 2006). As with other life events, trauma appears to influence the course of the disorder over time as well as to precipitate the onset (Schenkel, Spaulding, DiLillo, & Silverstein, 2005).

Expressed emotion research has evolved from early findings that the emotional climate in a family has an impact on the stability of family members with schizophrenia (Leff & Vaughn, 1985). Stress in a high-expressed emotion family may be produced by family members’ negative, critical attitudes – or by well-intended overinvolvement with the identified patient (Brown, Birley, & Wing, 1972; Butzlaff & Hooley, 1998; Hooley, 2007). Therapeutic techniques designed to reduce the expressed emotion in family networks demonstrated clear clinical efficacy in preventing relapse (Pilling et al., 2002).