Many authors have argued that there is a marked lack of a coherent psychological model of bipolar disorder (e.g., Jones, 2001; Scott, 2001a). Recent research, however, highlights the role of cognitive and psychosocial factors in the development and course of bipolar disorder, and the first treatment manuals were published in recent years, delineating the application of CBT principles to bipolar disorders (Basco & Rush, 1996; Lam et al., 1999; Newman et al., 2002; Scott, 2001b). A body of research focused on cognitive factors such as attributional styles (Alloy et al., 1999); perfectionism, deficits in problem-solving skills, and elevated scores of sociotropy and autonomy (Lam et al., 2000); and maladaptive schemata (Young, 1999). These factors appear to play a significant role in the interaction of severe changes in behaviour, reactions to and the creation of significant psychosocial stressors, disruptions in chronobiological functioning and varied responsiveness to psychotropic medications. One of the reasons for the complex pattern of factors influencing each individual's phenomenology and course of the disorder is the huge variability in the spectrum of bipolar disorders, ranging from chronic cyclothymic presentations to episodic manifestations of severe depression and mania with psychotic features.
Overall, the cognitive behavioural model aids our clinical understanding of the psy-chopathology of bipolar disorder and the ways in which specific problems and interactions can be targeted, rather than offering aetiological clarification of this disorder. Researchers have suggested that similar cognitive structures and biases underlie both unipolar and bipolar depression (Alloy et al., 1999; Lam et al., 2000; Reilly-Harrington et al., 1999), particularly in terms of systematic attributional errors and sensitivity to failure or interpersonal rejection. Specific to individuals suffering from bipolar disorder, however, is the extreme valence shift in the content of their thinking. A cognitive model of bipolar disorder needs to integrate the variability in the stress responses of individuals. In other words, some individuals with bipolar disorder respond to stress by developing depressive symptoms, and others with the development of manic responses. The model also needs to take into account that bipolar individuals display trait-like thought processes in the form of long-standing predispositions and state-like responses to environmental triggers and physiological activation. Furthermore, it needs to take into account the specific effects of significant life events and environmental stressors on individuals' affect regulation, in line with a diathesis-stress model of mood disorders (Lam et al., 1999); in particular, the fact that only certain life events appear to be able to predict mania, while others do not (Johnson et al., 1999). Therefore, a clinical working model of bipolar disorder needs to encompass biology, individual beliefs and behavioural reactions, interpersonal functioning, environmental triggers and life events, and the individual's idiosyncratic conceptualisation of these events.
Beck's (1979) cognitive behavioural model suggests that depressed mood is mediated by particular patterns of thinking that accentuate mood shifts. Individuals who are depressed become more negative in how they perceive themselves, others, and the world in general; as a result, they are prone to systematic cognitive distortions in that they tend to overgeneralise, self-blame, jump to negative conclusions, and view things in black- and-white terms. The avoidance of social contacts and other safety behaviours often result as an interaction of mood shifts and negative thinking patterns. These cognitive styles of depression are thought to arise out of early learning experiences. Beck suggested in his cognitive model that mania is a mirror image of depression, as determined by a hyperpositive triad of self, others, and the future. Scott and colleagues (2000) found that individuals with bipolar disorder demonstrated lower levels of self-esteem, over-general memory, poorer problem-solving skills, and higher levels of dysfunctional attitudes, particularly those related to need for social approval and perfectionism. They further found that these vulnerabilities persisted between episodes in patients who were adherent to prophylactic treatment. Beck and colleagues worked on a reformulation of the original linear cognitive model for bipolar disorders (Beck, 1996; Newman et al., 2002). This recent reconceptualisation includes the notion of "modes". Modes are understood as integrated "cognitive affective behavioural networks" of powerful combinations of schemata, overlearned behaviour patterns, and intense, difficult-to-modulate emotions. When schemata and modes are activated by specific life events, chronobiological disruption, or other such triggers, the bipolar individuals' predispositional reactions become expressed by extremities in emotional and behavioural functioning. The authors argue that individuals' belief systems interact with their inherent perception of current stressors and events. This activation of long-standing beliefs and schemata determines their affect and behaviour, and influences their information processing by directing the individual towards information consistent with the schema. In this way, a negatively valenced schema is activated during a depressed phase, directing memory retrieval towards events of loss and rejection, and focusing current attention on the possibility of failure. In a manic phase, a positively valenced schema is activated, and is likely to lead to problematic decision making by selectively ignoring the need for adaptive caution and inhibition.
Clinically, a reliable understanding of the individual's cognitive assumptions and core beliefs, encompassing self-perception and perception of the world and the future, helps the therapist to demonstrate an accurate understanding of the individual's experiences and to focus on the assumptions and beliefs that cause most distress and dysfunction. It is therefore important to assess individuals' core beliefs independently of their presenting symptom pattern. A grandiose and manic individual might have the same core schema of "unlov-ability" and "incompetence" as a depressed patient. Bipolar individuals appear to maintain consistent, maladaptive core beliefs and schemata that shift polarity in their manifestations. The successful modification of these beliefs through cognitive therapy should result in the reduced amplification of the dysfunctional mood swings of the bipolar client.
Apart from the reformulation of the cognitive model for bipolar disorder by Beck and his colleagues, other alternatives have been formulated to capture the complex interactions between thoughts and emotions. Teasdale and Barnard (1993) differentiate between propo-sitional and implicational "schematic" levels of information processing. They argue that propositional-level cognitions, or direct appraisals of any given information, do not directly activate emotional reactions, but are mediated on a level of implicational meaning by a process of schematic appraisal, in the context of present and past propositional information. Power and Dalgleish (1997, 1999) support this model and add an additional direct or associative route to emotions. This model has several clinical implications in disentangling the rational or schematic processes of change that appear to be primarily focused on by classical cognitive therapy approaches from the associative or direct associations of certain cues and emotional reactions. Jones (2001) utilised this multilevel approach to emotion and cognition to investigate the vulnerability of bipolar individuals to mood changes following disruptions in their circadian rhythms. Applying this model in individuals with bipolar disorder schema change is achieved by associative links through behaviour modification and corrective experiences, rather than rational cognitive techniques such as the challenging of automatic thoughts and restructuring. Patients should therefore be encouraged to experience subsyndromal mood changes and stimulation through adaptive coping strategies with the subsequent absence of prodromal symptoms.
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