Longitudinal Predictors of Bipolar Spectrum …...LONGITUDINAL PREDICTORS OF BIPOLAR DISORDER • ALLOY ET AL. 207 Sahakian, 2006), there is a recognition that genetic and neurobiological

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LONGITUDINAL PREDICTORS OF BIPOLAR DISORDER • ALLOY ET AL.CLINICAL PSYCHOLOGY: SCIENCE AND PRACTICE • V16 N2, MARCH 2009

Longitudinal Predictors of Bipolar Spectrum Disorders: A Behavioral Approach System Perspective

Lauren B. Alloy, Temple University Lyn Y. Abramson and Snezana Urosevic, University of Wisconsin–MadisonRachel E. Bender and Clara A. Wagner, Temple University

We review longitudinal predictors, primarily psychosocial,

of the onset, course, and expression of bipolar spectrum

disorders. We organize our review along a proximal–

distal continuum, discussing the most proximal (i.e.,

prodromes) predictors of bipolar episodes first, then

recent environmental (i.e., life events) predictors of

bipolar symptoms and episodes next, followed by more

distal psychological (i.e., cognitive styles) predictors,

and ending with the most distal temperament (i.e.,

Behavioral Approach System [BAS] sensitivity) predictors.

We then present a theoretical model, the BAS dysregula-

tion model, for understanding and integrating the

role of these predictors of bipolar spectrum disorders.

Finally, we consider the implications of the reviewed

longitudinal predictors for future research and psychosocial

treatments of bipolar disorders.

Key words:

behavioral approach system dysregulation,

bipolar disorder, cognitive styles, life events, longitudinal

predictors, prodromes, temperament.

[Clin Psychol Sci

Prac 16: 206–226, 2009]

Bipolar disorder is at the same time puzzling andfascinating to researchers and laypeople alike becauseextreme contrasts in mood (hypomanic/manic euphoriaand irritability vs. depressive sadness) and behavior(supercharged energy and excessive goal-striving vs.extreme lethargy and hopelessness) occur within the

same individual. Indeed, bipolar disorder has been associatedboth with high achievement and artistic creativity on theone hand (e.g., Andreasen, 1987; Kutcher, Robertson, &Bird, 1998), and serious functional impairment includinglower academic achievement, erratic work history, divorce,substance abuse, and increased suicide on the other (e.g.,Angst, Stassen, Clayton, & Angst, 2002; Conway, Compton,Stinson, & Grant, 2006; Goodwin & Jamison, 2007; Lagace& Kutcher, 2005; Nusslock, Alloy, Abramson, Harmon-Jones, & Hogan, 2008; Strakowski, DelBello, Fleck, &Arndt, 2000). Bipolar disorder has been ranked as thesixth leading cause of disability among both physical andpsychiatric disorders worldwide (Murray & Lopez, 1996).Despite being quite prevalent (4.4% of a nationallyrepresentative U.S. sample were affected by a bipolarspectrum disorder; Merikangas et al., 2007) and sometimesdisabling, bipolar disorder has been understudied relativeto other mental health disorders (Hyman, 2000).

Bipolar disorders appear to form a continuum orspectrum of severity from the milder subsyndromalcyclothymia, to bipolar II disorder, to full-blown bipolarI disorder (Akiskal, Djenderedijian, Rosenthal, & Khani,1977; Akiskal, Khani, & Scott-Strauss, 1979; Cassanoet al., 1999; Depue et al., 1981; Goodwin & Jamison,2007). Moreover, milder forms of bipolar disorder oftenprogress to the more severe forms (e.g., Akiskal et al.,1977, 1979; Shen, Alloy, Abramson, & Sylvia, 2008),providing support for the spectrum concept of bipolardisorder. Thus, we consider the full range of bipolarspectrum disorders in this article.

Although bipolar disorder has a strong genetic predis-position (McGuffin et al., 2003; Merikangas et al., 2002)and important neurobiological underpinnings (Clark &

Address correspondence to Lauren B. Alloy, Department ofPsychology, Temple University, 1701 N. 13th Street, Philadelphia,PA 19122. E-mail: [email protected].

LONGITUDINAL PREDICTORS OF BIPOLAR DISORDER • ALLOY ET AL. 207

Sahakian, 2006), there is a recognition that genetic andneurobiological factors cannot fully account for thetiming, expression, and polarity of symptoms. Thus, inthe past two decades, there has been increasing interestin the role of psychosocial processes in the onset, course,and treatment of bipolar spectrum disorders (see Alloyet al., 2005, 2006a, 2006b, 2006d, 2006e, 2006f, forreviews). In this article, we review empirical research onlongitudinal predictors, primarily psychosocial in nature,of the onset, course, and expression of bipolar spectrumdisorders. We organize our review of these longitudinalpredictors along a proximal–distal continuum (Abram-son, Metalsky, & Alloy, 1989), considering the mostproximal or immediate (i.e., prodromes) predictors ofbipolar episodes first, then recent environmental (i.e.,life events) predictors of bipolar symptoms and episodesnext, followed by more distal psychological (i.e.,cognitive styles) predictors, and ending with the most distaltemperamental (i.e., Behavioral Approach System [BAS]sensitivity) predictors. We then present a theoretical

model, the BAS dysregulation model (e.g., Depue & Iacono,1989; Depue, Krauss, & Spoont, 1987; Johnson, 2005;Urosevic, Abramson, Harmon-Jones, & Alloy, 2008),for understanding and integrating the role of theselongitudinal predictors of bipolar spectrum disorders (seeFigure 1). Finally, we end with a consideration of theimplications of the reviewed longitudinal predictorsfor psychosocial treatments of bipolar disorders anddirections for future research.

We note that there are other potential longitudinalpredictors of bipolar disorder that we do not cover inthis review, either because of lack of longitudinal data onthese predictors or due to other reviews providing extensivesummaries of them. For example, the role of supportiveand nonsupportive interpersonal relationships in bipolardisorder are covered in the Miklowitz and Johnson (2009)article in this special issue and in Alloy et al. (2005), butare not addressed in this review. Similarly, impairedexecutive functions (e.g., attention, working memory,cognitive perseveration) have been associated with bipolar

Figure 1. Longitudinal predictors of bipolar episodes.

CLINICAL PSYCHOLOGY: SCIENCE AND PRACTICE • V16 N2, JUNE 2009 208

disorder, have been found to be stable across mood states(see Alloy et al., 2006d; Walshaw & Alloy, 2009, forreviews), and may influence the longitudinal course ofthe disorder. These are not addressed in this review asneurocognitive functioning in bipolar disorder is coveredin the Henin et al. (2009) article in this special issue. Earlydevelopmental experiences (e.g., parenting styles, familyfunctioning, maltreatment history) have been associatedwith bipolar disorder, but these studies almost exclusivelyuse retrospective or cross-sectional designs, rather thanlongitudinal ones, and, therefore, we do not review themhere (but see Alloy et al., 2005, 2006a, 2006b, 2006d,for reviews). The present review is unique in its focus onthe temporal sequence of predictors of bipolar episodes,its integration of this set of predictors, and its provisionof a theoretical model that may explain this temporalsequence. To this end, we highlight longitudinal andhigh-risk design studies and outline future directionsthat would further elucidate this temporal sequence.

GENERAL METHODOLOGICAL ISSUES AND CHALLENGES

In reviewing the literature on prodromes, recentenvironmental factors, and more distal cognitive andtemperamental predictors of the onset, course, andexpression of bipolar spectrum disorders, we chose tofocus on the longitudinal and prospective studies.Longitudinal and prospective studies are better able toestablish the potential predictor as independent ofbipolar symptoms and to determine its temporal distancefrom the bipolar mood episodes or symptoms it ishypothesized to predict (Alloy et al., 2005). However,we also reviewed cross-sectional studies that comparebipolar individuals in a euthymic or remitted state tonormal controls on potential psychosocial predictors. Wedid so because such studies serve to demonstrate that thepotential predictor under examination is independent ofthe symptoms of bipolar disorder, although they cannotestablish that the psychosocial variable is a risk factorfor bipolar disorder, rather than its consequence ( Just,Abramson, & Alloy, 2001). Naturalistic longitudinal orprospective studies of psychosocial predictors of bipolardisorder are not without methodological limitations,such as potential third-variable explanations (in particular,the effects of genetic predisposition; Alloy et al., 2005).Few studies try to control for genetic vulnerability bycontrolling for family history of bipolar disorder (which,

of course, also controls for family environment associatedwith having a relative with bipolar disorder). The verynature of bipolar spectrum disorders also presents amethodological challenge in that these disorders arerecurrent with significant interepisode symptoms.Studies wishing to establish predictor status for psychosocialvariables need to ensure that potential predictors areindependent of bipolar symptoms by controlling formood and symptoms at the time the psychosocial variableunder examination is assessed.

We also include in our review studies with high-riskresearch designs, in which the offspring of bipolar parentsare compared to offspring of normal control parents (genetichigh-risk design) or individuals at high versus low riskfor bipolar disorder based on a behavioral characteristic(behavioral high-risk design) are compared. We includeeven those high-risk study designs that are actually cross-sectional. Given that offspring of parents with bipolardisorder are at significantly higher risk for bipolardisorder themselves ( Jones & Bentall, 2008), any psycho-social factors they experience at higher rates than theoffspring of controls are potential predictors of bipolardisorder, even if not established longitudinally. Similarly,if the behavioral characteristic leading to designation ofindividuals as “high risk” in behavioral high-risk studieshas been shown to be a longitudinal predictor of bipolarmood episodes or symptoms in other studies, then bythe same logic, any psychosocial factor these behavioralhigh-risk individuals show at higher levels than low-riskindividuals can be considered a potential predictor ofbipolar disorder. We turn now to our review of psycho-social predictors of bipolar spectrum disorders.

IMMEDIATE PREDICTORS: PRODROMES

A “prodrome,” from the Greek word

prodromos

, meaningforerunner of an event, is defined as the early symptomsand signs that precede the acute clinical phase of anillness (Fava & Kellner, 1991). Thus, by definition,prodromes precede episodes of disorder and are short-term longitudinal predictors of those episodes. However,there are methodological difficulties involved in studyingprodromes of bipolar disorders. First, it is difficult toidentify prodromes for mental disorders in generalbecause there can be disagreement about what constitutesthe acute phase of a psychological disorder. Second,although prodromes precede acute mood episodes in


bipolar disorder by definition, most studies of bipolardisorder prodromes involve retrospective reporting ofprodromes, increasing the possibility of questionableaccuracy of the reports. Finally, a balance is neededbetween sensitivity and specificity in assessing pro-dromes. The assessment instruments need to be sensitiveenough to identify small changes in signs and symptomscharacteristic of the prodromal period, but not so sensitiveas to identify normative mood and behavioral fluctu-ations as prodromal symptoms (Fava & Kellner, 1991).With these methodological caveats in mind, we reviewstudies of the prodromes of bipolar hypomanic/manicand depressive episodes.

Research suggests that both bipolar individuals andtheir relatives are able to report prodromes reliably(Keitner et al., 1996; Lam, Wong, & Sham, 2001). Fourstudies examined the prodromes of manic episodes. Lamand Wong (1997; Wong & Lam, 1999) found thatreduced sleep (58.3%) and increased goal-directed activity(55.5%) were the most frequently reported prodromalsymptoms of an impending manic episode among indi-viduals with bipolar I disorder (Figure 1). In addition,compared to bipolar I individuals with poor copingskills, those with good coping strategies for prodromesdecreased their goal-directed activity (e.g., took extratime to rest, restrained themselves, engaged in calmingactivities) in order to deal with hypomania/mania. And,this behavioral deactivation coping strategy was successful.In a prospective study, Lam et al. (2001) found that over18 months, bipolar I individuals who actively decreasedtheir goal-directed activity in response to manic pro-dromes were less likely to have a manic relapse (12.5%)than those who did not cope in this manner (45.5%).Based on these findings, Lam et al. (2003) modifiedtraditional cognitive therapy to target excessive goalstriving and found that this led to significantly reducedrelapse and hospitalization rates for bipolar episodes overone year.

Seven studies (Altman et al., 1992; Bauer et al., 2006;Keitner et al., 1996; Lam & Wong, 1997; Molnar,Feeney, & Fava, 1988; Smith & Tarrier, 1992; Wong &Lam, 1999) have examined prodromes of bipolar depressiveepisodes. Across these studies, decreased pleasure oranhedonia (45–82%), decreased motivation and goal-directed activity (82%), decreased energy (71–86%), sadmood (21–86%), and decreased self-confidence (88%)

were the most commonly reported prodromal symptomsfor bipolar depression (Figure 1). In addition, Bauer et al.(2006) found that hypersomnia predicted depressed moodthe next day; but they did not investigate prodromalsymptoms other than sleep disturbances. Similar to theirfindings for coping strategies for manic prodromes, Lamet al. (2001) found that bipolar I individuals who copedwith depressive prodromes by increasing their goal-directed activity (e.g., keeping busy and getting organized,becoming more social) were less likely to experiencedepressive relapses (8.3%) over an 18-month follow-upthan those who did not increase their behavioral activity(46.2%). Thus, studies of prodromes in bipolar disordersuggest that increased goal striving and decreased pleasure/goal-directed activity are important immediate harbingersof impending manic and depressive episodes, respectively.

RECENT ENVIRONMENTAL PREDICTORS: LIFE EVENTS

Much evidence suggests that aspects of a person’s currentenvironment influence the onset, course, and expressionof bipolar spectrum disorders (Alloy et al., 2005, 2006a,2006d). Specifically, we review the role of recentlyexperienced life events as longitudinal predictors ofbipolar disorder mood episodes and symptoms. Asdiscussed in detail by Alloy et al. (2005), there are avariety of methodological limitations in many of the lifeevents studies in bipolar disorder. The most problematiclimitation of longitudinal studies of environmentalpredictors of bipolar disorder is failure to control forbipolar individuals’ mood state at the time they reporton life events and, thus, for mood-associated reportbiases. Second, some studies rely on self-report measuresof life events, which can produce different interpreta-tions across participants of what experiences count asan instance of a particular life event category. Suchdifferences in self-reported life events could potentiallyintroduce systematic differences in reporting as afunction of symptoms or vulnerability factors. Thus,studies that employ structured interviewer assessmentsof life events should be given greater weight. Third,many studies do not examine life event predictors ofhypomanic/manic and depressive episodes separately todetermine if there are polarity-specific relationships.Finally, some studies define mood episode onset usingmarkers that frequently do not correspond to the actualtime of episode onset, such as admission to the hospital


or start of treatment. With these caveats in mind, wereview work on life events and bipolar disorder.

Recent Life Events as Predictors of Bipolar Symptoms/Episodes

Recent reviews of the association between life events andbipolar disorder (Alloy et al., 2005, 2006a, 2006d, 2006e;Johnson, 2005; Johnson & Kizer, 2002) indicate thatindividuals with bipolar spectrum disorders experienceincreased life events prior to first onsets and recurrencesof mood episodes. Whereas negative life events precedethe depressive episodes of bipolar individuals, bothnegative and positive life events precede hypomanic/manic episodes. We briefly discuss the more methodo-logically limited retrospective studies first, followed by amore detailed review of the stronger longitudinal andprospective studies. We then examine whether specifictypes of life events are particularly likely to triggerhypomanic/manic and depressive mood episodes andwhether bipolar mood episodes and symptoms, in turn,lead to the generation of specific types of life events aswell.

Retrospective studies of life events have found thatbipolar individuals’ first and subsequent episodes arepreceded by the occurrence of negative events, includingevents rated as independent of their behavior (see Alloyet al., 2005, 2006a, 2006d, 2006e, for detailed reviews).The three retrospective studies of adolescent offspring ofbipolar parents (Hillegers et al., 2004; Petti et al., 2004;Wals et al., 2005) found that affected offspring experiencedsignificantly higher levels of negative life events thanunaffected offspring. Wals et al. (2005) observed that itwas only life events dependent on a participant’s behaviorthat were related to increased risk of a mood episode(39% vs. 10%) in the offspring of the bipolar parents.This difference was no longer significant when prioranxious or depressive symptoms in the offspring werecontrolled. None of the retrospective studies investigatedwhether particular types of negative events are morerelevant as triggers of manic versus depressive episodes.

A smaller number of prospective, longitudinal studiesof life events in bipolar disorder have been conducted todate. Three of these studies used questionnaire assessmentsof life events in bipolar samples. In an early study, Hall,Dunner, Zeller, and Fieve (1977) reported that bipolarpatients with a hypomanic relapse had greater numbersof work-related stressors than did nonrelapsers, although

the overall number of events did not differ betweenbipolar patients who relapsed and nonrelapsers. Christensenet al. (2003) assessed life events every three months forthree years via questionnaire and found that bipolarwomen, but not men, had a greater number of events inthe three months prior to a depressive episode comparedto a control period. However, they failed to trackrelapses between the three-month assessments. Lovejoyand Steuerwald (1997) tracked stressful events for21 days in a small sample of cyclothymic, intermittentdepressive, and control undergraduates and found thatthe cyclothymic group experienced more stressful eventsthan the intermittent depressive group, which, in turn,had more events than the controls.

There are six prospective studies of bipolar samplesthat used interview assessments of life events. Most ofthese studies did not include a control group. Ellicott,Hammen, Gitlin, Brown, and Jamison (1990) observedthat bipolar outpatients with high levels of stressfulevents had a 4.5-fold greater relapse rate over a two-yearfollow-up period than those with lower stress. Thesefindings could not be explained by differences intreatment adherence or medication levels. Similarly,Hammen and Gitlin (1997) found that bipolar patientswho relapsed during a two-year follow-up had moretotal stress and more severe events during the precedingsix months than those who did not relapse. Hunt,Bruce-Jones, and Silverstone (1992) found that 19% of52 relapses among bipolar patients were preceded by asevere event in the previous month compared to 5% ofpatients with a severe event at other times; manic anddepressive relapses did not differ in the rate of priorsevere events. Another study followed recovered bipolarpatients, unipolar depressed patients, and normalcontrols for one year with interview assessments of lifeevents and symptoms every two months (Pardoen et al.,1996). Pardoen et al. reported that bipolar patients witha hypomanic/manic relapse had more marital stressorsprior to the relapse than other bipolar patients, althoughbipolar and unipolar patients who relapsed did notexperience more life events overall in the two monthsprior to the relapse than patients who did not relapse.McPherson, Herbison, and Romans (1993) also did notfind a significant difference in moderately severe,independent events in the month prior to relapse ascompared to control periods among bipolar patients.


However, these findings’ interpretation is limited by ahigh attrition rate and the absence of a required wellperiod prior to study entry. Finally, Johnson and Miller(1997) found that bipolar inpatients who reported asevere, independent event during the index episode tookthree times longer to recover from that episode thanthose who did not have a severe independent event. Thiseffect was not mediated by medication compliance.

In a “kindling” model, Post (1992) hypothesized thatmood episodes become more autonomous with eachrecurrence such that life events are less likely to precipitatelater than earlier episodes of mood disorder. Monroe andHarkness (2005) hypothesized two distinct, alternatemodels that might explain Post’s kindling effect. The“stress sensitization” model postulates that major lifestress is important in initiating first episodes, butdecreases in unique importance for subsequent episodes.Although major life stress continues to be capable oftriggering an episode, stress sensitization implies thatlower and lower levels of stress may trigger episodes withsubsequent recurrences, so that events that would nothave been sufficient to trigger an initial episode acquirethe power to precipitate recurrent episodes. Thus, theimpact of major life events should increase with eachepisode as the individual becomes increasingly sensitizedto stress. However, the relative frequency of major lifeevents should decrease over time, as episode recurrencesare increasingly triggered by more commonly occurringminor stressors. The impact and relative frequency of minorlife events becomes stronger with episode recurrences.In contrast, the “stress autonomy” model postulatesthat major life stressors are important in initiating thefirst episode, but that later episodes are increasinglyindependent of psychosocial factors to the point whererecurrences eventually take place fully independently ofpsychosocial triggers. This model postulates that theassociation between major life stress and initial moodepisodes contributes to the development of another(potentially neurobiological) process that eventually takesover and fully accounts for episode recurrences. Accordingto the stress autonomy model, the impact and frequencyof both major and minor life events should decrease witheach episode, as processes other than life stress increasinglytrigger episode recurrences.

Although five retrospective studies (see Alloy et al.,2005, 2006a, for reviews) claimed to support the kindling

effect, these studies did not distinguish between the stresssensitization and stress autonomy models of kindling.They did not examine major and minor events separatelyor the impact versus frequency of these events relative to theonset of bipolar mood episodes. Furthermore, Hlastalaet al. (2000) found that age, rather than the number ofprevious mood episodes, predicted higher levels ofstressful events in pre-onset than control periods. Also, theone prospective study that examined the kindling effectin bipolar disorder (Hammen & Gitlin, 1997) foundthat contrary to the hypothesis, a greater proportion ofbipolar patients with multiple lifetime mood episodes,rather than patients with few mood episodes, experienceda severe negative event prior to relapse. Thus, the evi-dence for a greater triggering effect of stressful events onearlier than later mood episodes in bipolar disorder is notstrong at present. More longitudinal studies are neededthat examine major and minor events, and the impactand frequency of these events, separately.

Role of Specific Types of Life Events

Recent evidence suggests that hypomanic/manic anddepressive episodes of bipolar spectrum disorders may betriggered by specific types of life events, i.e., socialrhythm disruption and BAS-relevant events

1

(see Figure 1).Four prospective, longitudinal studies found that lifeevents involving goal striving or goal attainment thatactivate the BAS specifically trigger hypomanic/manicsymptoms and episodes among bipolar individuals.In two separate studies, Johnson et al. (2008; Johnson,Sandrow, et al., 2000) reported that events involvingattainment of goals predicted increases in manic, but notdepressive, symptoms among bipolar I patients over prospec-tive follow-up, whereas general positive life events did not.Similarly, Nusslock, Abramson, Harmon-Jones, Alloy, andHogan (2007) found that students with bipolar spectrumdisorders (bipolar II, cyclothymia) were significantly morelikely to develop a new onset of hypomania, but notdepression, following a goal-striving life event (studyingfor and taking final exams) compared to other bipolarparticipants without this event (42% vs. 4%). Finally,Alloy et al. (2009) found that BAS activation-relevantevents (e.g., goal-striving and attainment events) andBAS deactivation-relevant events (e.g., failures and losses)prospectively predicted increases in hypomanic anddepressive symptoms, respectively, among bipolar spectrum


participants over a one-year follow-up. Some studieshave also found that negative life events can triggerhypomanic or manic episodes (e.g., work-related stressorsin Hall et al., 1977), but it is not known whether it isparticular kinds of negative events that are relevant topredicting hypomania/mania. Given that hypomania/mania sometimes presents with irritable mood, it is ofinterest that anger-inducing events that also are BAS-activating (e.g., goal obstacles, insults) have been associatedwith increased hypomanic symptoms (Carver, 2004;Harmon-Jones et al., 2002). However, prospective,longitudinal studies have not yet examined whetheranger-provoking events predict onset of hypomanic/manic episodes in bipolar individuals.

Just as BAS-relevant events may trigger mood episodesin bipolar individuals, bipolar mood episodes and prodromesmay also increase the likelihood of experiencing such eventsthrough processes of stress generation (Hammen, 1991; seeFigure 1). In a prospective study, Urosevic, Abramson, Alloy,et al. (2009) found that bipolar spectrum individualsgenerated both BAS-activating and deactivating eventsat significantly greater rates than normal controls. Similarly,in another prospective study, Bender, Alloy, Abramson,Sylvia, and Urosevic (2009) reported that hypomanicsymptoms predicted greater subsequent occurrence ofBAS-related positive and negative achievement events inmales, whereas depressive symptoms predicted greateroccurrence of positive and negative interpersonal eventsin females.

Another specific type of life event that has beenfound to trigger bipolar mood episodes in five of sevenstudies is events that disrupt daily social rhythms (e.g., meal-times, sleep-wake times). Such events are hypothesizedto trigger bipolar mood episodes through their effects ondestabilizing circadian rhythms (see Ehlers, Frank, &Kupfer, 1988; Grandin, Alloy, & Abramson, 2006; Healy& Williams, 1988, for reviews). Two studies (Ashmanet al., 1999; Jones, Hare, & Evershed, 2005) found thatbipolar patients had lower social rhythm scores than age-and sex-matched controls, but the relationship betweendaily social rhythms and mood was not significant.However, the Ashman et al. study was underpowereddue to small sample size. In two retrospective studieswith structured interview assessments of life events inbipolar I patients, Malkoff-Schwartz et al. (1998, 2000)found that manic episodes were significantly more likely

to be preceded by social rhythm disruption (SRD)events than depressive episodes. Kadri, Mouchtaq,Hakkou, and Moussaoui (2000) found that 45% of 20Muslim bipolar patients relapsed during Ramadan (afasting month with no meals and, thus, involving socialrhythm disruption), and 71.4% of those relapses weremanic episodes. In a prospective study of 206 bipolarspectrum individuals and 206 matched normal controls,Shen et al. (2008) reported that bipolar individuals hadless regular social rhythms than the controls at Time 1.Moreover, lower Time 1 social rhythm regularity pre-dicted a shorter time to onset of hypomanic/manic anddepressive episodes during an average of 33 months offollow-up. Finally, in another one-year prospective studyof 101 bipolar spectrum participants and 100 matchednormal controls, with structured interview assessmentsof life events and bipolar symptoms every four months,Sylvia et al. (in press) found that SRD events at eachassessment predicted increased depressive symptoms atthe next assessment. In addition, bipolar participantsexperienced more depressive symptoms after rather thanbefore an SRD event occurred, and they were morelikely to experience an SRD event prior to a depressiveepisode than during a control period. Thus, SRD eventsappear to increase the likelihood of both hypomanic/manic and depressive episodes.

PSYCHOLOGICAL PREDICTORS: COGNITIVE STYLES

Given the success of cognitive models of unipolardepression (e.g., Abramson et al., 1989; Beck, 1987), thelogic of these theories has been extended to bipolardisorders. Maladaptive cognitive styles (e.g., negativeinferential styles, dysfunctional attitudes) found to increasevulnerability to unipolar depression also may contributeto the onset and course of bipolar mood episodes. Cog-nitive styles may be defined as people’s typical patterns ofperceiving, interpreting, and reacting to events in theirlives. Negative inferential styles consist of the tendencyto infer stable (enduring) and global (widespread) causes,negative consequences, and negative self-characteristicsin response to a negative life event (Abramson et al.,1989). Dysfunctional attitudes involve maladaptivebeliefs that one’s self-worth depends on being perfect oron others’ approval (Beck, 1987). In this section, wereview the literature on cognitive styles alone and incombination with life events as predictors of the course


of bipolar disorders, with specific emphasis on identifyingcognitive styles uniquely characteristic of and importantto bipolar disorders (Figure 1).

A central methodological issue in this literature is theneed to establish cognitive predictors of bipolar moodepisodes independent of potential mood state biases onthe assessment of cognition. Studies have addressed thisissue in several ways by (a) controlling statistically formood and symptoms at the time of cognitive measure-ment; (b) examining cognitions in remitted or euthymicbipolar individuals; (c) comparing bipolar individuals indepressive versus manic episodes; or (d) conducting within-subject longitudinal studies of the same bipolar individualsin different mood states. Other study limitations in thisliterature include failure to take treatment status intoaccount, absence of control groups, unvalidated cognitive-style measures, undiagnosed samples, and small samplesizes (see Alloy et al., 2005, 2006a, 2006d, 2006e, 2006f ).

Cognitive Styles as Predictors of Bipolar Symptoms/Episodes

We briefly review the more limited cross-sectional studiesof cognitive styles first, followed by a more detailedreview of longitudinal studies. Cross-sectional studies ofbipolar individuals in a depressed state find that theircognitive styles are as negative as those of unipolardepressed individuals and more negative than those ofnormal comparison groups. Also, in cross-sectionalstudies, current hypomania is associated with positivecognitive styles on explicit (direct) measures of cognition,but with negative cognitive styles on implicit (indirect)measures. Cross-sectional studies that compared bipolarindividuals in different mood states found more positivecognitive styles in manic than depressed bipolar individualswith explicit measures, but more negative cognitive stylesin hypomanic/manic than remitted bipolar individuals (seeAlloy et al., 2005, 2006a, 2006d, 2006e, 2006f, for moredetailed reviews).

Studies of bipolar individuals in a remitted oreuthymic state, although also cross-sectional, are at leastable to assess cognition independent of potentialmood state–related biases. The results of 14 such studiesof cognitive styles have been mixed. Six studies (Hollon,Kendall, & Lumry, 1986; Lex, Meyer, Marquart, &Thau, 2008; MacVane, Lange, Brown, & Zayat, 1978;Pardoen, Bauwens, Tracy, Martin, & Mendlewicz, 1993;Reilly-Harrington, Alloy, Fresco, & Whitehouse, 1999;

Tracy, Bauwens, Martin, Pardoen, & Mendlewicz, 1992)using primarily explicit measures obtained little evidenceof negative cognitive styles in the euthymic state.However, Lex et al. (2008) did find a trend (

p

= .06) forremitted bipolar individuals to have more negativedysfunctional attitudes than normal controls. In contrast,eight other studies (Alloy et al., 1999, in press; Goldberg,Gerstein, Wenze, Welker, & Beck, 2008; Knowles et al.,2007; Lam, Wright, & Smith, 2004; Rosenfarb, Becker,Khan, & Mintz, 1998; Scott, Stanton, Garland, & Ferrier,2000; Winters & Neale, 1985), also using mostly explicitmeasures, did find negative cognitive styles amongeuthymic bipolar individuals.

Cross-sectional studies of individuals at genetic orbehavioral risk for bipolar disorder have also obtainedevidence for maladaptive cognitive and coping styles. Ina genetic high-risk study, adolescent offspring of bipolarparents exhibited greater ruminative response styles fornegative affect, but not greater dysfunctional attitudes,than offspring of control parents ( Jones, Tai, Evershed,Knowles, & Bentall, 2006). In addition, three studies ofindividuals at behavioral high risk for bipolar disorderfound that high-risk participants exhibited both a greaterruminative style in response to negative and/or positiveaffect and more dysfunctional attitudes than low-riskparticipants (Carver & Johnson, in press; Knowles, Tai,Christensen, & Bentall, 2005; Thomas & Bentall, 2002).

Two types of longitudinal studies have examinedcognitive styles in bipolar individuals. The first typeinvestigated the stability of cognitive styles across dif-ferent mood states within the same bipolar individualsover time. Two studies found that inferential styles anddysfunctional attitudes were stable and relatively negativeover time and across untreated bipolar spectrum par-ticipants’ different mood swings (Alloy et al., 1999;Gerstein, Alloy, & Abramson, 2008). In contrast, Ashworthet al. (1985) found that explicit self-esteem reverted tonormal levels when previously manic or depressedbipolar patients recovered. Thus, there is some evidenceof stable cognitive styles in bipolar individuals acrossmood states, but further longitudinal studies of this kindare needed. In particular, it is important for such studiesto control for treatment status, because treatment couldremediate bipolar individuals’ cognitive styles.

The second kind of longitudinal study examinedgeneral cognitive styles as predictors of the course of


bipolar disorder. Scott and Pope (2003) found that lowself-esteem was the most robust predictor of relapse at12-month follow-up among hypomanic bipolar patients.Two other studies found that negative automatic thoughts( Johnson & Fingerhut, 2004) and low self-esteem( Johnson, Meyer, Winett, & Small, 2000) predicteddepressive, but not manic, symptoms over prospectivefollow-up.

Bipolar Disorder–Specific Cognitive Styles

Recent evidence suggests that particular types of cog-nitive styles may be especially relevant to bipolar disorderand prediction of bipolar mood episodes and symptoms.Five remitted design studies found that euthymic bipolarindividuals exhibited a unique profile of maladaptivecognitive styles characterized by perfectionism, autonomy,self-criticism, and goal striving and not by maladaptivedependency, approval-seeking, or attachment attitudestypically observed among unipolar depressed individuals(Alloy et al., in press; Goldberg et al., 2008; Lam et al.,2004; Rosenfarb et al., 1998; Scott et al., 2000). The bipolarindividuals’ types of maladaptive cognitive styles areconsistent with the high drive and incentive motivationassociated with high BAS sensitivity

2

(Figure 1). Inaddition, seven behavioral high-risk studies found thatindividuals at increased risk for bipolar disorder exhibitedspecific cognitive styles with high BAS relevance. Inparticular, individuals prone to hypomania/maniaexhibited overly ambitious goal striving and goal setting,even controlling for current hypomanic and depressivesymptoms (Carver & Johnson, in press; Gruber & Johnson,in press; Johnson & Carver, 2006; Johnson, Ruggero, &Carver, 2005; Meyer & Krumm-Merabet, 2003) andmore positive appraisals of major personal goals (Meyer,Beevers, & Johnson, 2004). They also showed greatercognitive reactivity and positive generalization in responseto success experiences (Carver & Johnson, in press;Eisner, Johnson, & Carver, 2008, Study 2; Johnson et al.,2005).

Finally, two longitudinal studies specifically examinedwhether BAS-relevant cognitive styles predicted bipolarmood symptoms or episodes over time. Lozano andJohnson (2001) reported that the BAS-relevant style ofhigh achievement-striving predicted increases in manicsymptoms over six months in a bipolar I sample. Similarly,Alloy et al. (in press) reported that BAS-relevant cognitive

styles of self-criticism and autonomy, but not cognitivestyles involving approval seeking, dependency, andattachment, predicted prospective onsets of hypomanic/manic and depressive episodes among individuals withbipolar spectrum disorders.

Cognitive Styles X Life Event Interactions as Predictors of Bipolar

Symptoms/Episodes

Six longitudinal studies tested the cognitive vulnerability-stress hypothesis for prediction of bipolar mood symptomsand episodes. Swendsen, Hammen, Heller, and Gitlin(1995) found that stressful events interacted with obses-sionality and extraversion to predict relapse amongremitted bipolar patients. Alloy et al. (1999) reportedthat among individuals with cyclothymic and hypomanicdisorders, Time 1 (euthymic state) negative attributionalstyle for negative events interacted with negative eventsto predict subsequent increases in depressive symptoms,and Time 1 positive attributional style for positive eventscombined with positive events to predict later increasesin hypomanic symptoms. The interaction of dysfunc-tional attitudes and life events did not predict subsequentsymptoms. In a unipolar and bipolar I and II sample,Reilly-Harrington et al. (1999) found that controllingfor initial symptoms, Time 1 negative attributionalstyles, dysfunctional attitudes, and negative informationprocessing about oneself each interacted significantlywith negative life events to predict subsequent increasesin depressive symptoms and, among the bipolar par-ticipants, manic symptoms as well. Note that in the Alloyet al. (1999) study, hypomanic symptoms were predictedby positive life events combined with positive attributionalstyles, whereas in Reilly-Harrington et al. (1999), manicsymptoms were predicted by negative events combinedwith negative cognitive styles. Given that bipolar I and IIindividuals (in the study of Reilly-Harrington et al.)have a course of disorder that includes major depressiveepisodes, they may be more responsive to negative lifeevents than the bipolar individuals without major depressionin the study of Alloy et al. (1999). It is also possible thatthe particular types of negative events (e.g., BAS activation-relevant anger-inducing events) experienced by partici-pants in the two studies may determine whether suchevents would precipitate hypomanic/manic symptoms.

Longitudinal studies have also investigated sociotropic(i.e., dependent) and autonomous cognitive styles in


interaction with congruent life events (interpersonalevents for sociotropic/dependent individuals and achieve-ment events for autonomous individuals) as predictors ofbipolar symptoms. Hammen et al. (1989, 1992) foundthat sociotropy and negative interpersonal eventsinteracted to predict symptom severity, but not symptomonset, in bipolar individuals (although only a trend inHammen et al., 1989). Autonomy combined with achieve-ment events did not predict symptom severity. However,Hammen et al. (1989, 1992) did not examine predictionof depressive and hypomanic/manic symptoms sepa-rately. Finally, controlling for initial symptoms and thetotal events experienced, Francis-Raniere, Alloy, andAbramson (2006) reported that a BAS-relevant self-critical, perfectionistic cognitive style interacted withstyle-congruent negative or positive events to predictprospective increases in depressive and hypomanic symp-toms, respectively, among bipolar spectrum individuals.

PSYCHOBIOLOGICAL PREDICTORS: TEMPERAMENT/

PERSONALITY

Given that bipolar disorder has a strong genetic pre-disposition (McGuffin et al., 2003; Merikangas et al., 2002),and temperament is considered to be genetically influenced,researchers have become interested in temperamentalfactors involved in bipolar spectrum disorders. Onetemperamental characteristic that has figured prominentlyin theorizing and research about bipolar disorder is BASsensitivity (approach motivation and reward responsiveness).We review its role as a predictor of bipolar mood episodesand symptoms here. Only some of the studies in this areacontrol for mood symptoms at the time of assessment ofBAS sensitivity, and none control for genetic predisposi-tion itself.

BAS Sensitivity as a Predictor of Bipolar Symptoms/Episodes

Investigators suggest that two fundamental psychobiologicalsystems are critical in regulating behavior (Davidson,1999; Gray, 1981, 1982), the BAS and the BehavioralInhibition System (BIS). The BAS regulates approachbehavior to attain rewards and goals, whereas the BISregulates inhibition of behavior in response to threat andpunishment.

3

We focus on the BAS because theory andrecent research underscore its importance in bipolardisorder. Activation of the BAS by signals of rewardcauses a person to increase approach motivation and

movement toward attainment of goals, as well as cog-nitive processes (e.g., hope, self-efficacy, planning) aimedat promoting goal attainment. BAS activation is alsohypothesized to be associated with happiness and elation(Depue & Iacono, 1989; Gray, 1994). Recent work alsodocuments a link between anger and BAS activation(Carver, 2004; Harmon-Jones & Allen, 1998; Harmon-Jones & Sigelman, 2001), especially when people have ahigh expectancy of success for rectifying the anger-provoking situation (Harmon-Jones, Sigelman, Bohlig, &Harmon-Jones, 2003). BAS sensitivity and state activationlevels have been assessed in three main ways: (a) withself-report questionnaires (e.g., BIS/BAS Scales [Carver& White, 1994] and Sensitivity to Punishment Sensitivityto Reward Questionnaire [SPSRQ; Torrubia, Avila,Molto, & Caseras, 2001]); (b) with behavioral tasksinvolving rewards (e.g., Card Arranging RewardResponsivity Objective Test [CARROT; Powell, Al-Adawi, Morgan, & Greenwood, 1996]); and (c) withrelative left versus right prefrontal cortical activationas measured with EEG, both in the resting state and inresponse to rewards. Greater relative left frontal corticalactivation on EEG has been found to reflect higher BASsensitivity and activation (e.g., Coan & Allen, 2004;Davidson, Jackson, & Kalin, 2000; Harmon-Jones &Allen, 1997; Sobotka, Davidson, & Senulis, 1992; Sutton& Davidson, 1997).

4

Cross-sectional studies have found that even con-trolling for bipolar mood symptoms, individuals withbipolar spectrum disorders exhibit higher levels ofself-reported BAS sensitivity, as well as greater rewardresponsiveness on behavioral tasks and greater relativeleft frontal cortical activity on EEG than relevantcontrols. Studies of bipolar individuals in a remittedor euthymic state, although also cross-sectional, are ofinterest because they assess BAS sensitivity or responsive-ness independent of potential mood state–related biases.Salavert et al. (2007) found that controlling for concurrentdepressive and hypomanic/manic symptoms, euthymicbipolar I patients exhibited higher BAS sensitivity on theSPSRQ than normal controls. Hayden et al. (2008)reported that euthymic bipolar I patients exhibitedhigher reward responsivity on the CARROT card-sortingtask than normal controls, but they did not exhibithigher self-reported BAS sensitivity on the BIS/BAS Scalesor greater relative left frontal cortical activation on EEG


in the resting state. In a 28-day daily diary study, Wright,Lam, and Brown (2008) found that euthymic bipolar Iindividuals and controls did not differ on recovery ofbehavioral activation to baseline following rewardingor frustrating life events. However, time taken forbehavioral activation to recover from rewarding eventsincreased with increasing numbers of previous manicepisodes, and time taken to recover following frustratingevents increased with increasing numbers of bothprevious manic and depressive episodes. Moreover, bothBAS sensitivity and BAS-related dysfunctional attitudesremain stable across fluctuations in clinical symptomsand despite positive mood induction (Meyer, Johnson, &Winters, 2001; Urosevic, Abramson, Harmon-Jones,et al., 2009; Wright, Lam, & Newsom-Davis, 2005).

With one exception, individuals at genetic orbehavioral risk for bipolar disorder have shown higherBAS sensitivity than controls. Although Jones et al. (2006)did not observe higher self-reported BAS sensitivity inoffspring of bipolar parents than offspring of controlparents, Chang, Blasey, Ketter, and Steiner (2003) didfind that children of bipolar parents displayed a greatertendency to approach novel, potentially rewardingsituations on a temperament scale than controls. Inaddition, Nurnberger et al. (1988) reported greaterself-reported sensation-seeking in offspring of bipolarparents than controls. In behavioral high-risk studies,high BAS sensitivity has also been associated with riskfor bipolar disorder. Individuals prone to hypomanicsymptoms exhibited higher self-reported BAS sensitivitythan controls (Carver & Johnson, in press; Meyer, Johnson,& Carver, 1999) and greater relative left frontal corticalactivation on EEG in response to a BAS-activating event(an anger-provocation scenario; Harmon-Jones et al., 2002).Finally, Alloy et al. (2006c) selected participants withhigh versus moderate levels of BAS sensitivity on boththe BIS/BAS Scales and the SPSRQ and administeredstructured diagnostic interviews. They found thatindividuals with high BAS sensitivity were six timesmore likely to meet diagnostic criteria for a lifetimebipolar spectrum disorder than those with moderateBAS sensitivity.

Four longitudinal studies have examined BASsensitivity as a predictor of subsequent bipolar symptomsor episodes. Meyer et al. (2001) found that higher self-reported BAS sensitivity at recovery predicted greater

manic symptoms over time in bipolar I patients. Similarly,controlling for initial depressive and manic symptoms,Salavert et al. (2007) found that over an 18-month follow-up, bipolar I patients who relapsed with a hypomanic/manic episode had higher, and those who relapsed witha depressive episode had lower, BAS sensitivity at Time 1than patients who remained asymptomatic. Also con-trolling for initial depressive and hypomanic symptoms,Alloy et al. (2008) found that higher Time 1 self-reportedBAS sensitivity predicted a shorter time to onset ofhypomanic/manic episodes among individuals withbipolar spectrum disorders over a three-year follow-up.In addition, higher BAS Reward Responsiveness pre-dicted shorter time to onset of major depressive episodes(with marginal significance). Finally, among bipolarspectrum individuals, Nusslock et al. (2009) found thatgreater relative left frontal cortical activity on EEG in theresting state predicted shorter time to onset of hypomanic/manic episodes, whereas decreased relative left frontalcortical activation in response to reward incentivespredicted an increase in the number of major depressiveepisodes over follow-up.

A BAS DYSREGULATION PERSPECTIVE ON LONGITUDINAL

PREDICTORS

How can we understand the evidence regarding theprodromal, environmental, cognitive, and temperamentalpredictors of the course and expression of bipolardisorders? A BAS dysregulation perspective on bipolardisorders may allow us to integrate these predictors ofbipolar disorder into a more comprehensive, explanatorymodel (Figure 1). According to the BAS dysregulationmodel of bipolar disorder (Depue & Iacono, 1989;Depue et al., 1987; Johnson, 2005; Urosevic et al., 2008),individuals vulnerable to bipolar spectrum disordersexhibit an overly sensitive BAS that is hyperreactive torelevant cues and, thus, becomes dysregulated easily.Such BAS hypersensitivity may lead individuals toexperience great variability in their state levels of BASactivation over time and across situations in responseto BAS activating and deactivating stimuli. Thus, ahyperresponsive BAS can lead to excessive BAS activityin response to BAS activation-relevant events involvinggoal striving and attainment, reward incentive, and angerevocation. In vulnerable individuals, this excessive BASactivation is hypothesized to lead to hypomanic/manic


symptoms, such as elation, excessive goal-seeking behavior,decreased need for sleep, irritability, distractibility,excessive self-confidence, and optimism (Figure 1, top). Incontrast, in response to BAS deactivation-relevant eventsinvolving definite failure and nonattainment of goals,excessive BAS deactivation or shutdown of behavioralapproach should occur, leading to depressive symptoms ofsadness, low energy, anhedonia, motor retardation,hopelessness, and low self-confidence (Figure 1, bottom).In essence, individuals vulnerable to bipolar disorderare unable to effectively regulate their emotions andbehavior because their proneness to BAS dysregulationrenders them excessively responsive to BAS-relevantevents. Indeed, even quite minor BAS-relevant eventsmay be sufficient to trigger bipolar mood episodes inindividuals with highly sensitive BAS temperaments

5

(i.e.,stress sensitization as a function of higher vulnerability).Such BAS hypersensitivity and vulnerability to dysregula-tion may be an endophenotype that mediates the effectsof the genetic predisposition to bipolar disorder.

This BAS dysregulation model provides an integrativebiopsychosocial perspective for understanding the effectsof the predictors of bipolar disorder reviewed here(Figure 1). As reviewed in the section on prodromes, andconsistent with the BAS dysregulation model, the mostfrequent prodromal signs of impending hypomanic/manicepisodes are reduced sleep and increased goal-directedactivity, both indicators of increased approach motivationmediated by BAS activation. Similarly, decreased motiva-tion, goal-directed activity, and pleasure, indicators ofBAS deactivation, are frequent prodromal signs ofimpending depressive episodes. Moreover, strategies forcoping with prodromes involving decreasing goal-directedactivity when it starts to increase, or increasing suchactivity when it begins to decrease, were found toreduce the likelihood of manic and depressive relapses,respectively.

Our review of the life events literature indicated thatnegative events precipitate bipolar depressive episodesand both negative and positive events precipitatehypomanic/manic episodes. However, consistent withthe BAS model, studies that investigated specific types ofevents that trigger bipolar mood episodes found thatgoal-striving and goal attainment events that activate theBAS precipitate hypomania/mania, whereas failures andlosses that deactivate the BAS precipitate bipolar

depression. Some evidence suggests that negative eventsinvolving anger provocation also trigger hypomania/mania, consistent with the BAS model. Thus, the BASmodel provides a plausible explanation for the seeminglyinconsistent findings of negative life events sometimespredicting onset of hypomania/mania as well as depres-sion, because certain types of negatively valenced events(e.g., goal obstructions, insults) should activate the BASrather than deactivate it. Finally, our review indicatedthat events that disrupt daily social rhythms (SRDevents) also precipitate both hypomanic/manic anddepressive episodes in bipolar individuals. It is possiblethat SRD events exert their effect on bipolar symptomsthrough their BAS-relevant characteristics. For example,events involving goal striving may trigger a dysregulatedBAS response with social rhythm disruption as onecomponent of this dysregulated response (e.g., a bipolarindividual starts a new job, becomes overinvolved inprojects, and as a result, loses hours of sleep). Futurestudies assessing both the BAS relevance of events (e.g.,the extent of goal striving) and the events’ SRDcharacteristics are needed to determine whether SRD isrelated to and mediates dysregulated BAS response inpredicting bipolar mood symptoms.

The evidence regarding cognitive styles and bipolardisorder, although mixed, indicated that individuals withbipolar spectrum disorders frequently exhibit maladaptivecognitive styles, even in the euthymic state, as negative asthose seen in unipolar depressed persons. Moreover,these cognitive styles predict subsequent bipolar moodsymptoms and episodes alone or in interaction with lifeevents. However, a growing number of studies suggestthat it is cognitive styles involving perfectionism,excessive goal striving, self-criticism, and autonomy (i.e.,styles that are relevant to the high drive and incentivemotivation associated with high BAS sensitivity) that areuniquely characteristic of risk for bipolar disorder andpredictive of bipolar mood symptoms and episodes.Finally, research on BAS sensitivity itself indicated thatindividuals with or at increased risk for bipolar disordersexhibit high BAS sensitivity assessed via self-report,behavioral tasks, and neurophysiology, and that highBAS sensitivity predicts bipolar mood symptoms andepisodes longitudinally. Consequently, the BAS dysregula-tion theory of bipolar disorders, a model that integratespsychosocial and neurobiological (e.g., reward system


circuitry) underpinnings of bipolar disorder, may pro-vide a useful conceptual framework for understanding adiverse set of empirical findings regarding longitudinalpredictors of bipolar disorder.

The BAS model suggests novel predictions about thecourse of bipolar spectrum disorders (see Urosevic et al.,2008). According to a BAS dysregulation perspective,both a hypersensitive BAS temperament and BAS-relevant life events should interact to predict the courseand prognosis of bipolar disorders, yet no studies haveexamined this prediction to date. The frequency of BASactivation-relevant and deactivation-relevant events alsoshould predict the relative predominance of hypomania/mania versus depression, respectively, in the course ofbipolar disorder. Moreover, an individual’s level of BASactivation prior to the occurrence of a BAS-relevant lifeevent, along with their general degree of BAS sensitivity,should influence the magnitude of their dysregulatedresponse to that event and, thus, the severity and durationof bipolar symptoms.

CLINICAL IMPLICATIONS

The BAS dysregulation model also suggests newdirections for improving treatment for bipolar disorders(see Nusslock, Abramson, Harmon-Jones, & Alloy, in press).Given the evidence that environmental factors (e.g., lifeevents) play an important role in the onset and course ofbipolar disorders and the limitations of pharmacotherapyalone in treating these conditions (Prien & Rush, 1996),promising psychosocial therapies have been developed asadjuncts to medication (e.g., cognitive behavioral therapy[CBT] and Interpersonal Social Rhythm Therapy[IPSRT]) in an attempt to reduce the likelihood ofrelapse of mood episodes. The evidence reviewed hereon longitudinal predictors of bipolar disorder and theBAS dysregulation perspective for integrating these pre-dictors have implications for increasing the effectivenessof these psychosocial interventions (see Nusslock et al.,in press, for a detailed explication of the therapeuticimplications of the BAS model).

As an adjunctive intervention for bipolar disorder,CBT teaches bipolar individuals to recognize prodromesfor depressive and manic episodes and then modifytheir cognitions and behavior to prevent the onset offull-blown episodes (Lam et al., 2003; Newman et al.,2002). Thus, CBT focuses on recognizing proximal

predictors of impending episodes (i.e., prodromes) andmodifying more distal cognitive styles to prevent moodepisodes. Overall, the small outcome literature on CBTfor bipolar disorder suggests that it has a positive pro-phylactic effect (see Alloy et al., 2005; Nusslock et al.,in press, for reviews). Based on the evidence that thecognitive styles of bipolar individuals are characterizedby perfectionism and extreme goal-striving tendenciesand the prodromes of manic and depressive episodesinvolve increased and decreased goal-directed activity,respectively, CBT based on a BAS dysregulation perspectiveshould aid bipolar clients in recognizing the relationshipbetween ambitious goal setting and onset of manic episodesand giving up on goals and onset of depressive episodes.In addition, CBT cognitive techniques in which surgesof confidence and ambitious goal striving on the onehand, or reduced efficacy and decreased goal striving onthe other hand, are challenged and reframed as earlyharbingers of impending episodes should be beneficial.Furthermore, behavioral strategies designed to reducegoal-directed activity when the client recognizes a surgein success expectancies and goal striving, and to increasegoal-oriented behaviors when the client notes a decreasein confidence and goal striving, should reduce thelikelihood of manic and depressive episodes, respectively,as found by Lam et al. (2001, 2003).

Based on the social/circadian rhythms theory ofbipolar disorder and supporting evidence, IPSRT wasalso designed as an adjunct to pharmacotherapy forbipolar disorder (Frank, Swartz, & Kupfer, 2000). IPSRTencourages bipolar patients to notice the associationbetween life events and their moods, the importance ofmaintaining regular daily schedules, and to manageinterpersonal stressors that may precipitate SRD, andthus, mood episodes. Thus, IPSRT focuses almost entirelyon recent environmental triggers of mood episodes. Thesmall outcome literature on IPSRT finds that it may alsohave promise for improving the course of bipolar disorder(e.g., Frank et al., 2005; see Alloy et al., 2005; Nusslocket al., in press, for reviews). To date, IPSRT has focusedon the disruptive effects that interpersonal events canhave on social and circadian rhythms. However, the BASmodel and supportive evidence reviewed here suggestthat BAS-relevant events in the achievement domain arealso likely to precipitate social and circadian rhythmdisruption in bipolar individuals, because work, school,


and goal striving are also important social zeitgebers(“time-givers”). For example, when working on aproject or faced with a deadline, many people lose sleep,miss meals, and significantly alter their usual daily routine.BAS deactivation events may also precipitate SRD.Therapeutic strategies designed to address the effect ofinterpersonal events on SRD could be applied to BAS-relevant events as well. For example, the therapist andclient could identify the extent to which various BAS-relevant events are likely to induce social and circadianrhythm disruption and develop strategies for regulatingrhythms when these events occur. Thus, added therapeuticbenefit might result from an expansion of IPSRT’sfocus to strategies for coping with the effects of bothindependent and self-generated BAS-relevant events onsocial and circadian rhythms (see Nusslock et al., in press,for details).

No psychosocial interventions have been developedyet designed to modify or decrease the likelihood ofactivation of a hypersensitive BAS temperament, theproposed distal vulnerability for bipolar spectrum dis-orders. Recent evidence suggests that it is possible tomanipulate neurophysiological indicators of BAS activa-tion in the laboratory (Harmon-Jones, 2006; Peterson,Schackman, & Harmon-Jones, 2008). Thus, future workon the therapeutic implications of the BAS dysregulationmodel might also address the development of strategiesfor more directly reducing BAS hyperresponsivity.

CONCLUSIONS

More prospective, longitudinal studies are needed withadequately sized samples, controls for initial mood stateand symptoms, separate examination of depressive andhypomanic/manic episodes, standardized and well-validated measures of psychosocial and neurobiologicalvariables, and controls for genetic predisposition orgenetically informative designs (e.g., longitudinal twinstudies) to further our understanding of important predic-tors of bipolar disorders. Despite these methodologicalcaveats and the long-standing assumption that bipolardisorders are primarily caused by genetic predispositionand resulting neurobiological dysfunction, the evidencereviewed here indicates that psychosocial factors alsoserve as distal and proximal predictors of the onset,course, and expression of bipolar disorders. Specifically, atemperament involving high BAS sensitivity and related

cognitive styles characterized by perfectionism, self-criticism, autonomy, and excessive goal striving predictrisk for bipolar symptoms and episodes. In addition, lifeevents that activate and deactivate the BAS, as well asevents likely to disrupt daily social rhythms, predictsubsequent mood episodes, and prodromes involvingchanges in goal-directed activity, sleep, and self-confidenceserve as immediate harbingers of the impending moodepisodes. Future studies are needed to further delineatethe temporal relationships of these psychosocial predictorsand bipolar symptoms (e.g., as seen in Figure 1). Finally,a BAS dysregulation perspective on bipolar disorder mayprovide a comprehensive and integrative psychobiologicalmodel for understanding the role of these empiricallyidentified predictors of bipolar course and expression. AsAkiskal (1986, p. 671) speculated, “. . . what is transmittedare these affectively dysregulated temperaments and thatthe progression to full-blown bipolar illness is due toenvironment.”

NOTES

1. BAS activation-relevant events have been defined toinvolve approach to (i.e., goal striving) or attainment ofrewards/goals, whereas BAS deactivation-relevant eventsinvolve failure to obtain or loss of pertinent rewards/goals andcessation of approach (see Urosevic et al., 2008). Certain typesof negative events (e.g., anger-inducing events, such asobstacles to goals and insults) have also been defined as BASactivation-relevant, because such events tend to elicit approachemotions and behaviors (Carver, 2004; Harmon-Jones &Allen, 1998; Harmon-Jones et al., 2002, 2003; Harmon-Jones& Sigelman, 2001). BIS-relevant events, or events that involvethreats without definitive failure or loss, have not been specifi-cally studied in relation to bipolar disorders and are notreviewed here.

2. As our review shows, the maladaptive cognitive stylescharacteristic of bipolar disorder, BAS-relevant cognitive styles,are a subset of those found to provide vulnerability to unipolardepression. But, they are unique in exhibiting a combination ofcharacteristics involving high drive and incentive motivation(e.g., perfectionism, goal striving,, autonomy, and self-criticism),but not the approval seeking and dependency typicallyobserved in unipolar depression. Consequently, cognitivestyles in unipolar depression and bipolar disorder can beassessed using the same instruments, and although there wouldbe overlap in endorsed items, a combination of items endorsedconsistent with BAS-relevant cognitive styles wouldemerge for bipolar disorders. For example, this has been shown


in factor analysis of the Dysfunctional Attitudes Scale (Lam,Wright, & Smith, 2004).

3. Whereas BIS activation involves inhibition of behaviorsin order to avoid threats and punishments, BAS deactivationinvolves an extreme reduction in goal-directed activity followinginability to obtain a reward (as signaled by unequivocal failure orloss). Someone with high BIS activation would be quicker thanmost to withdraw/inhibit behavior in response to the threat of anegative consequence. BIS activation has been associated withboth anxiety and depression. Instead, someone with BASdeactivation would show a reduction in approach behaviorfollowing an actual, irrevocable failure or loss. Thus, BASdeactivation is associated only with depression (Kasch,Rottenberg, Arnow, & Gotlib, 2002; McFarland, Shankman,Tenke, Bruder, & Klein, 2006; Pinto-Meza et al., 2006). Typically,the correlation between BAS and BIS sensitivities on self-reportquestionnaires is quite low (e.g., Alloy et al., 2008; Carver &White, 1994).

4. Although self-report, behavioral task, and EEG measuresof BAS sensitivity and activation have been found to correlatewith each other, in some studies their convergence is relativelyweak. One possible reason for this is that BAS sensitivity mayinclude three components, supported by factor analyses ofthe BIS/BAS scales (e.g., Carver & White, 1994): BAS Drive(persistence in pursuit of reward), BAS Fun-seeking (willingnessto approach novel and rewarding stimuli), and BAS RewardResponsiveness (positive reactivity to rewards). Some of theseBAS components may relate to behavioral and EEG measuresof BAS activation more strongly than others; this has not beeninvestigated well to date. Similarly, across studies, there areinconsistent findings with respect to which of these BASsubscales are related more strongly to bipolar disorder. Thus,although it is important to continue to explore potentialdifferential effects of these BAS components, at present, thereis insufficient evidence to determine which are more implicatedin BAS dysregulation and bipolar disorder.

5. From a BAS dysregulation model perspective, at leastsome cases of bipolar mood episodes that appear to arise “outof the blue” may actually have environmental triggers—relativelyminor BAS-relevant events that are overreacted to by individualswith a hypersensitive BAS. The stronger an individual’s BASsensitivity, the less environmental input would be required totrigger a bipolar mood episode. However, it is also possible thatsome subtypes of bipolar disorder represent a more pure expressionof the high BAS temperament (e.g., hyperthymic personality).

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Longitudinal Predictors of Bipolar Spectrum …...LONGITUDINAL PREDICTORS OF BIPOLAR DISORDER • ALLOY ET AL. 207 Sahakian, 2006), there is a recognition that genetic and neurobiological