The Relationship Between GoalOriented Motivation and Mood
Variability: Implications for
Bipolar Disorder
PhD (Clinical) Research Project
Student Investigator: James Collett
Primary Supervisor: Greg Murray
Secondary Supervisor: Conrad Perry
Classified as an affective disorder.
 Can consist of:
- Manic episodes
- Depressive episodes
- Mixed episodes
- Occurrence of hypomania
- Returns to euthymic mood
 Unipolar mania considered to be
spurious.
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Piquer (1759), Falret (1854), Baillarger
(1854), Kraepelin (1899): Dual-form insanity
and manic-depressive illness.
Kraepelin (1899): Cyclicity and recurrence
originally prioritised.
Leonhard (1957): Term “bipolar” applied,
bipolar depression differentiated from
unipolar depression.
Idea of reactive versus recurrent
depression.
American Psychiatric Association (2000):
DSM approach emphasises component
episodes.
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The DSM-5 contains several categories of
recurrent affective disorder:
Bipolar I Disorder
Bipolar II Disorder
Major Depressive Disorder
Cyclothymia
Persistent Depressive Disorder
(Dysthymia)
Disruptive Mood Dysregulation Disorder
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Several factors have been suggested
as being involved in the causation and
exacerbation of bipolar disorder:
Evolutionary theories
Manic defence versus primacy-ofmania hypotheses
Genetic linkage
Monoamine hypothesis
Circadian rhythm hypothesis
Social rhythm hypothesis
Behavioural activation system (BAS)
hypersensitivity model
Like most mental disorders, bipolar disorder
can be conceptualised under a diathesisstress (vulnerability-trigger) model.
 Can think of disorders as differing in their
balance of diathesis versus stress.
 Bipolar disorder appears to be weighted
more towards diathesis, but episodic nature
often keyed to exogenous environmental
stressors.
 Kindling effect observed where occurrence
of mood episodes may become more
endogenous over time.
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As with many disorders, bipolar disorder can
be thought of as occurring on a
quantitative spectrum with normal mood.
 Vulnerability trait of emotion dysregulation.
 Difference between being sad versus being
depressed, and between being energised
and being manic.
 Extremes of vulnerability trait more likely to
be defined as being of clinical severity.
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It is useful to separate mania and
depression as distinct vulnerability traits:
Concordant with factor analytic evidence
Allows ranking of affective diagnoses based
on severity
Facilitates explanation of reactive and
recurrent unipolar depressions
Enhances sensibility of mixed episodes
Provides more complex diagnostic groups
(Md, MD, Dm, md)
Mania
Mania
versus
Depression
&
Depression
versus
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If bipolar disorder involves extreme mood
states, this raises question of how traits
(dispositional) and states (transient) interact.
Can view traits as underlying predispositions
towards certain states.
Can also view traits as signifying that baseline
personality is likely to be characterised by
state attributes.
Research attempting complex state-trait
models of affective disorder is still in its
infancy.
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There are several reasons why examining bipolar
disorder vulnerability as a personality trait can be
useful:
Supports evolutionary retention of disorder traits as
adaptive
Matches multifactorial nature of genetic transmission
Permits much larger sample sizes
Allows for research that avoids prodomal and
residual state effects and pharmacological
“scarring” effects
Avoids over-stigmatising bipolar disorder and
conceptualising it as wholly alien to “normal” human
experience
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While the trait approach is useful, it is important to
keep in mind the following caveats:
The treatment model for bipolar disorder is
dominantly medical, possibly implying a biologically
distinct disorder
Interaction between both quantitative and
qualitative factors
Research does not always replicate findings between
clinical and non-clinical samples
Trait content is usually developed from a top-down
clinic perspective, and hence may be out of touch
with non-clinical trait expressions (resulting in
pronounced positive skew).
Attempts to establish and explain the
relationship between trait bipolar disorder
and reward sensitivity using Reinforcement
Sensitivity Theory (RST).
 Examines correlations between bipolar
disorder traits and RST traits.
 Assesses how traits influence behavioural
task performance.
 Explores how mood state manipulation
interacts with traits to alter behavioural task
performance.
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By definition, mania is a state of almost pure BAS.
Similar physiological systems (largely
dopaminergic) have been implicated.
BAS sensitivity has been observed in euthymic
bipolar disorder.
Elevated BAS scores predictive of bipolar disorder
onset and of greater frequency of mania once
diagnosed.
Individuals with bipolar disorder experience
greater mobilization in response to goal progress
(whereas non-psychiatric controls more likely to
decrease effort if goal progress is going well).
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Many scales available assessing depression
(e.g., BDI, DASS, HAMDS).
Scales also available to measure mania
(e.g., YMRS).
Few scales conceptualise both.
General Behavior Inventory (GBI) provides
valid measure of depression and
(hypo)mania.
Also allows separation of biphasic
symptoms.
BIS/BAS Scales (BBS) measure BAS and
behavioural inhibition system (BIS).
 Validated on Australian sample.
 Divide BAS into statistically-identified
subscales (Drive, Fun-Seeking, Reward
Responsiveness).
 Alternate measures (SPSRQ, GRAPES, AGQ)
either more simplistic in structure, measure
subtly different content, or are simply
redundant.
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Do mood variability traits correlate with RST
traits?
How is risky decision-making influenced by
mood variability and RST traits?
Does mood variability impair cognitive
flexibility, and if so, does this occur
generally or only during tasks that engage
reward sensitivity processes?
Are individuals more or less likely to engage
in riskier decision-making dependent on
their mood state?
How is the effect of mood state modulated
by underlying personality traits?
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Study 1 (N = 760): Self-report trait investigation
examining the structure of mood variability and
RST using exploratory and confirmatory factor
analysis.
Study 2 (N = 118): Behavioural investigation
examining performance on a range of
cognitive-affective tasks assessing risky
decision-making and set-shifting.
Study 3 (Positive n = 53, Negative n = 68): Mood
induction experiment examining how state
manipulations interact with underlying traits to
influence performance on a risky decisionmaking task.
GBI
BIS/BAS Scales
BAS-D
Depression
BAS-FS
Hypomania
and Biphasic
Symptoms
BIS
BAS-RR
Note. These results were not replicated in the smaller Study 2 sample.
WCST
BART
SS-IGT
GDT
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Systematic exploration at level of (i) bivariate
correlations, (ii) hierarchical regression
controlling for affect, (iii) structural regression
models testing for mediation.
No consistent pattern of correlation present
across tasks at any level of analysis, despite
task outcomes and self-report traits purporting
to measure similar constructs.
This finding conflicts with previous research and
the theory that BAS dysregulation is of key
importance to phenomena characteristic of
bipolar disorder.
Positive Mood
Induction Group
Negative Mood
Induction Group
Neutral False Feedback
Neutral False Feedback
BART (Baseline Mood)
BART (Baseline Mood)
Positive False Feedback
Negative False Feedback
BART (Positive Mood)
BART (Negative Mood)
Mood induction appeared to function as
expected.
 Although significant differences were found
between and within BART trials, these
appeared to be artefacts of fatigue and
baseline variance.
 Underlying traits did not predict behaviour
change on the BART.
 Underlying traits did not predict mood
induction susceptibility in a consistent
manner.
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Despite the range of evidence linking BAS
dysregulation to bipolar disorder, this was not evident
in the present study.
Rigorously tested observationally and experimentally
across range of studies.
Potential explanations for lack of significance:
Possible that BAS is important to individual clinical
phenomenology but this is obscured at more general
trait level.
Possible that BAS dysregulation is only a significant
influence upon clinically severe cases (implying a
qualitative difference).
Possible that what has been labelled as euthymic
BAS dysregulation is in fact prodromal or residual
symptom of manic or hypomanic state.
I hope that you enjoyed the
presentation.
 Does anyone have any questions?
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