Vous êtes sur la page 1sur 7

CanJPsychiatry 2013;58(6):319325

In Review

Cognitive Remediation Therapy for Mood Disorders:

Rationale, Early Evidence, and Future Directions
Christopher R Bowie, PhD1; Maya Gupta, MSc (PhD Candidate)2;
Katherine Holshausen, MSc (PhD Candidate)2

Associate Professor, Department of Psychology and Department of Psychiatry, Queens University, Kingston, Ontario.
Correspondence: 356 Humphrey Hall, Psychology Department, Queens University, Kingston, ON K7L 3N6; bowiec@queensu.ca.

Clinical Psychology Student, Queens University, Kingston, Ontario.

Key Words: cognitive

remediation, mood disorders,
depression, bipolar disorder,
cognition, functional outcome,
psychosocial treatment,
cognitive-behavioural therapy
Received May 2012, revised,
and accepted August 2012.

People with mood disorders experience cognitive impairments that are predictive of
functional disability. Cognitive remediation (CR) is an empirically validated intervention that
is designed to remediate neurocognitive deficits and improve functioning. Although much of
the focus of this treatment during the last decade has centred on attention deficit disorders,
brain injury, and schizophrenia spectrum disorders, emerging evidence suggests that CR
is an effective intervention for mood disorders and that these treatment effects translate
into improvements in cognitive performance and possibly functioning. Our review aims to
examine the profile and magnitude of cognitive impairments in mood disorders, review the
evidence in support of CR for this population, and discuss future research directions in CR.

Thrapie de rducation cognitive pour les troubles de lhumeur :

raison dtre, nouvelles donnes probantes, et futures orientations
Les personnes souffrant de troubles de lhumeur connaissent des dficits cognitifs qui
sont prdicteurs dune incapacit fonctionnelle. La rducation cognitive (RC) est une
intervention empiriquement valide qui est destine remdier aux dficits neurocognitifs
et amliorer le fonctionnement. Bien que durant la dernire dcennie, ce traitement ait
surtout t ax sur les troubles de dficit de lattention, les traumatismes crniens, et les
troubles du spectre de la schizophrnie, de nouvelles donnes probantes suggrent que
la RC est une intervention efficace pour les troubles de lhumeur et que les effets de ces
traitements se traduisent par des amliorations du rendement cognitif et possiblement du
fonctionnement. Notre tude vise examiner le profil et lampleur des dficits cognitifs dans
les troubles de lhumeur, examiner les donnes probantes lappui de la RC pour cette
population, et prsenter les orientations futures de la recherche en matire de RC.

n recent years, the barometer for treatment success in

chronic mental disorders has expanded from symptom
reduction to include recovery of functioning in everyday
contexts, such as work, independent living, and community
activities. Accordingly, treatment strategies have evolved to
target the factors associated with functioning, which are often
not the diagnostic symptoms that are a focus of traditional
pharmacological and psychological treatments. Impaired
neurocognitive functioning is increasingly recognized as
a persistent and functionally relevant problem in chronic
mental disorders. Treatment of cognition in schizophrenia
spectrum conditions is well established, but only recently
have these cognitive enhancing techniques been examined
in mood disorders. In our paper, we present an argument
for the importance of considering cognitive-enhancing
treatments for mood disorders by reviewing the prevalence
and functional meaningfulness of deficits and preliminary
evidence of efficacy of these treatments.

Neurocognitive Dysfunction in Mood

Disorders: Prevalence and Profile
Major Depressive Disorder

MDD is characterized by feelings of sadness or emptiness

and diminished interest or pleasure in activities. These
symptoms are accompanied by numerous concomitant
features, including physiological and affective symptoms.
In addition to these debilitating clinical symptoms, MDD
is associated with deficits in multiple cognitive domains
that tend to be mild to moderately severeabout 0.5 to
1.0 standard deviation below population mean. A metaanalysis by Veiel1 estimated prevalence rates for specific
neurocognitive deficits in people with MDD. The study
classified severe impairment (that is, 2 standard deviation
units below the mean), for about 11% of people with MDD
on verbal fluency, 18.2% on scanning and visual-motor
tracking, 15% on visual-spatial skills, 14.5% on verbal
The Canadian Journal of Psychiatry, Vol 58, No 6, June 2013 W 319

In Review

learning, and 50% on executive functions, such as mental

flexibility and control. It is important to bear in mind the
considerable variability between studies in the severity of
symptoms of the patients and in the neurocognitive test
batteries used across samples.
A recent meta-analysis evaluating cognitive functioning
over the lifespan in MDD found that some impairments,
including the domains of executive functioning and
attention, may be more trait-like, while others, such as verbal
learning and memory, verbal fluency, and psychomotor
speed, tend to fluctuate in relation to mood state.2
Neurocognitive impairments are most severe when people
are in an MDE; specific deficits, most notably in executive
functioning, episodic memory, and processing speed, are
most strongly associated with the severity of depressive
symptoms.3 Despite the variability in the magnitude of
deficits, neurocognitive impairments persist, even during
states of euthymia for many people with MDD.4
Thus the profile of cognitive impairment in MDD is likely
one of mild-to-moderate impairment in several domains.
Patients who are more likely to have severe neurocognitive
deficits are those with a younger age of illness onset,5
repeated MDEs,6 a history of depression with psychotic
features,7 poor response to pharmacological intervention,8
and more severe residual symptoms.9

Bipolar Disorder

The BDs are characterized by recurrent MDEs and (or)

mania. It is estimated that at least 60% of people with a
BD have some degree of clinically meaningful cognitive
impairment, even during symptom remission.10 Interestingly,
the profile of impairment tends to follow that observed
in schizophrenia, with the most severe impairments in
executive functions and verbal memory,11,12 although they
are considerably less severe in magnitude. This diagnostic
difference in the magnitude of impairment is minimized
when people with BD are experiencing psychosis.13
Several neuropsychological studies have demonstrated that
patients with BD have persistent cognitive impairments,
even during states of euthymia, including difficulties in
processing speed, attention, working memory, verbal
and visual memory, and executive functioning.14,15 These
impairments tend to be between 0.5 and 1.5 standard

bipolar disorder


cognitive-behavioural therapy


cognitive remediation


effect size


major depressive disorder


major depressive episode


Neuropsychological Educational Approach to



prefrontal cortex

320 W La Revue canadienne de psychiatrie, vol 58, no 6, juin 2013


CR is a validated treatment in psychotic disorders.

Emerging evidence suggests that this treatment is

efficacious for mood disorders, where deficits are linked
to functional impairments.


Early studies were not rigorously controlled.

Transfer of cognitive gains to everyday functioning

improvements has been small, although there remain
challenges to assessing functional outcomes in mood

deviations worse than general population mean performance,

and, as a group, are broader and more severe than those we
observe in MDD. Cognitive difficulties, often self-reported
by people with BD, include sluggish thinking, difficulty
focusing, getting started on tasks, and multi-tasking, as
well as difficulties with memory and becoming easily
overwhelmed.16,17 See Table 1 for a qualitative description
of impairments in mood disorders by cognitive domains
based on a summary of the literature.

The Importance of Treating Cognition in

Mood Disorders

Functional disability is a major problem for many people

with mood disorders, during both euthymic and symptomatic
states. People with mood disorders experience impairment
in many areas of psychosocial functioning; common areas
of underperformance include academic and occupational
achievement, interpersonal relationships, independent
living, and community participation. Interestingly,
diagnostic symptoms account for surprisingly little variance
in everyday functional behaviours and contribute poorly to
the prediction of the breadth and persistence of impairment
experienced by people with these disorders.11,18,19 With most
treatments focused on these salient symptoms, it is thus
not surprising that restoration of everyday living skills and
functioning is often missing from treatment strategies and
Neurocognitive impairments are strong predictors of
outcomes in mood disorders. Long-term clinical recovery
is predicted by baseline executive functioning,20 and
improvements in everyday functional behaviours are
predicted by baseline performance on tests of attention.21 At
1-year follow-up, baseline22 and change scores23 in verbal
memory, attention, and executive functions explain more
than one-quarter of the variance in functioning, even after
considering clinical symptoms.
Given the high rates of persistent cognitive deficits in mood
disorders and their relevance to functional outcomes, these
deficits should be considered among the primary targets for
treatment. With validated success in other chronic mental
disorders, CR is poised to enter the armamentarium of
treatment options for CR and the BDs. Below, we review

Cognitive Remediation Therapy for Mood Disorders: Rationale, Early Evidence, and Future Directions

Table 1 Magnitude of cognitive impairmenta by domain in groups of people

with mood disorders, compared with schizophrenia




Sensory motor




Processing speed








Visual processing




Language skills




Working memory




Verbal memory




Visual memory




Executive functions




Impairment classification defined by standard deviation unit impairment relative to

control subjects, where intact is more than 0.5, mild is 0.5 to 1.0, moderate is less
than 1.0 to 1.5, severe is less than 1.5 to 2.0, and profound is less than 2.0
standard units.

some promising preliminary evidence to support further

research and dissemination to clinical environments.

CR for Mood Disorders

Major Depressive Disorder

A proof of principle study by Siegle et al24 found evidence

for the malleability of cognitive impairments in depression
using a drill-and-practice intervention that targeted working
memory via a serial addition task, and honed attention
with a task that required focus on selected sounds. In that
study, treatment was designed to increase PFC activation,
which was proposed to regulate amygdala functioning
and consequent emotional dysfunction. The authors
administered a 2-week cognitive training program, 3-times
weekly, to 19 people with MDD, while another 10 were
randomized to a treatment-as-usual condition. Compared
with the wait-list group, people in the cognitive training
group improved in executive functioning and demonstrated
normalization of neurobiological functions indexed by
imaging and pupil dilation. Further, depressive symptoms
and ruminative tendencies improved more during this
targeted intervention. This abbreviated treatment suggests
that the neurophysiological mechanisms proposed to
underlie depressive symptoms are malleable with efforts to
improve cognitive control.
To date, only a few studies have structured CR in MDD,
with duration and techniques similar to those used in studies
with schizophrenia patients. For example, Elgamal et al25
administered a 10-week computerized cognitive training
package to 12 people with MDD and a group of healthy
control participants. The cognitive training package (PSS
CogReHab, Psychological Software Services, Indianapolis,
IN) involved drill-and-practice repetition in multiple areas
of cognition. Patients who received cognitive training
improved on a range of neuropsychological tests targeting
attention, verbal learning and memory, psychomotor speed,
and executive function. This improvement exceeded that

observed during the same time period in a wait-list control

group. There was no change in depressive symptom scores
over the course of the trial, suggesting improvement in
cognitive performance occurred independently of other
illness variables.
Naismith and colleagues conducted 2 studies (see Naismith
et al26,27) evaluating the efficacy of the NEAR28 in MDD.
Treatment was delivered twice weekly for 10-weeks in a
group format and used commercially available computer
exercises that are tailored to a persons strengths and
weaknesses. NEAR uses learning strategies to enhance
intrinsic motivation; techniques include shaping and
errorless learning to enhance competency. Patients maintain
choice of tasks to help foster a sense of control and tasks
are personalized to address individual needs. Participants
in both studies26,27 were allocated to a treatment or waitlist control condition and were assessed on a standardized
battery of neuropsychological tests by administrators who
were blind to the treatment condition of the participants. In
the first study (published in 2010, after the second study),26
participants in the treatment condition (n = 8) showed
greater improvements on test of memory encoding and
memory retention than their peers in the wait-list control
group (n = 8). There were no between-group differences in
psychomotor speed, executive functioning, or self-reported
level of disability. Study limitations included a small
sample of participants who were not randomly assigned to
a condition. The second study (published in 2008)27 focused
on enhancing memory in elderly people (n = 41) with a
lifetime history of depression.27 The treatment consisted of
a combination of NEAR and psychoeducation for which
some of the topics included diet and exercise, depression
in older adults, and pharmacological treatments, anxiety,
and sleep hygiene. Participants in the treatment condition
demonstrated gains in visual and verbal memory in the
medium-to-large ES range. However, there was very limited
transfer to change in self-reported functional disability.
The Canadian Journal of Psychiatry, Vol 58, No 6, June 2013 W 321

In Review

In her thesis, Meusel29 evaluated the efficacy of a

computer-assisted CR program in promoting gains in
neuropsychological and psychosocial functioning among
people with MDD and BD. Participants improved on
measures of delayed recall and working memory following
completion of the treatment. It was observed that gains
in cognitive functioning were positively correlated with
psychosocial functioning, suggesting partial generalization
of improvements in neurocognition to functioning.
Interestingly, depressive symptom severity and engagement
in treatmentbut neither medication burden nor degree of
baseline impairmentspredicted magnitude of treatment
response. These performance-based measures of cognitive
functioning coalesce with functional magnetic resonance
imaging results demonstrating increased activation in
the lateral and medial PFC, dorsal cingulate, and right
hippocampus following completion of remediation. Taken
together, these findings suggest that engagement in CR can
induce improvement in cognitive functioning evidenced
through performance-based measures of neurocognition
and neuroplastic change in brain regions that govern
working and recollection memory.
Bowie et al examined the efficacy and effectiveness
of CR for treatment-resistant depression, which is
characterized by persistent depressive symptoms,31
severe cognitive and functional deficits,32 and little or no
response to pharmacological treatment.33,34 Participants
were randomized to a CR or wait-list control group, with
treatment involving 1 weekly session for 10 weeks and
an additional component of online exercises completed
at home. Treatment effects were large for verbal memory
and medium for verbal fluency, processing speed,
and sustained attention. There was a trend, but not a
significant improvement, on a composite measure of realworld functioning. However, the magnitude of cognitive
improvement was significantly associated with the degree
of improvement in functioning. Moderate correlations were
observed between the amount of homework completed
and improvement in cognition, which may be an exciting
avenue for future work in people who may have a difficult
time being a participant in high-intensity treatments, such
as those in rural areas or those working. Thus CR appears
effective, even for people with severe and recalcitrant
symptoms, although the mechanisms for improving transfer
of cognitive gains to everyday functional improvements
need to be explored.

Bipolar Disorder

Despite the well-documented evidence for considerable

cognitive impairments that are robustly associated with
functional disability, there is very little research reporting
on CR strategies with BD. Deckersbach et al35 conducted
an open-trial study that sequentially delivered 3 treatment
strategies: principles of CBT, such as activity monitoring,
awareness of automatic thoughts, and cognitive restructuring;
compensatory approaches to assist with organization,
planning, and time management; and finally, behavioural
322 W La Revue canadienne de psychiatrie, vol 58, no 6, juin 2013

strategies to enhance attention and memory strategy.

Eighteen people with BD who were employed and had only
residual symptoms engaged in 14 treatment sessions during
the course of 4 months. Following treatment, depressive
symptoms improved, and better occupational and overall
psychosocial functioning was reported. Improvements were
found in executive functioning, which were associated with
improvements in occupational functioning. Interestingly,
pretreatment cognitive functioning predicted treatment
response, such that people with more severe deficits
benefited less. These findings suggest that systematically
targeting residual depressive symptoms and top-down
training prior to attention and memory training may be an
avenue to improving occupational and overall functioning
for people with BD. However, given the heterogeneity in
cognitive functions in BD, individually tailored treatment
approaches remain sensible while specific strategies are
being explored. Future research that examines other models
of CR, and with diverse samples of people with BD, is
needed to understand what treatment techniques may be
efficacious and effective in this condition.
Martinez-Aran et al36 described a novel CR approach
for BD, which they have coined functional remediation.
Although this study is still under way, the authors describe
functional remediation as a treatment that integrates
psychoeducation about cognitive deficits, CR strategies to
improve attention, memory, and executive function, and
problem solving within an ecological framework (that is,
a focus on daily life examples, group tasks, role plays,
and practical take-home assignments). The treatment also
incorporates communication, interpersonal relationships,
and stress management strategies. Treatment consists of
21 weekly sessions of 90 minutes, and families are often
involved in treatment. The authors suggest that functional
remediation may be an important avenue for increasing the
transference of skills to daily functioning in people with

Clinical Meaningfulness of CR for Chronic

Mental Disorders

The CR story in schizophrenia has more recently graduated

from one of efficacy to improve neurocognition to one of
effectiveness in improving functioning. Meta-analyses of
CR in schizophrenia from the past 5 years demonstrate that
CR is associated with small-to-moderate ESs in cognitive
performance and psychosocial functioning, and a small ES
for symptoms.37,38 The strength of these findings fluctuate
depending on whether CR was embedded into existing
rehabilitative programs, the type of strategic approach
employed, and the homogeneity of the sample in terms
of stringency in diagnostic criteria for inclusion.38 In
schizophrenia, CR appears to potentiate the effects of skills
training programs on real-world functioning, but as a standalone treatment without opportunities to gain skills, its
generalization to everyday behaviours is less substantial.39
With proof of principle studies supporting efficacy of CR in
mood disorders, it is sensible to avoid the same criticism that

Cognitive Remediation Therapy for Mood Disorders: Rationale, Early Evidence, and Future Directions

plagued schizophrenia research for years and immediately

incorporate an evaluation of whether and how cognitive
gains can transfer to positive changes in everyday social
and adaptive outcomes.
There are several reasons to believe that the factors
associated with transfer of cognitive skills to everyday
behaviours may differ in mood disorders. First, unlike
schizophrenia spectrum conditions, where we observe
the insidious neurodevelopmental problems and longstanding premorbid cognitive deficits that may preclude
the acquisition of everyday living skills, people with
mood disorders typically have a more acute onset, with
little evidence for premorbid disruption to everyday
living skills. Second, the magnitude of cognitive and
functional impairment is substantially less severe in mood
disorders11,12; therefore, a similar size treatment effect
would bring functioning closer to the normal range. In
contrast to these potential arguments in favour of a more
clinically meaningful effect in mood disorders, we must
also be mindful of the likelihood that mood symptoms and
dysfunctional attitudes may be more common, broad, and
severe, and could thus exert more potent moderating effects
on transfer of cognitive improvements. Third, with as many
as 24% to 56%4042 of people with MDD or BD carrying
a comorbid anxiety disorder, it is imperative to be aware
of how concurrent anxiety symptomatology may affect
both cognitive functioning and gains acquired through
engagement in CR. Cognitive inflexibility, a core feature
of some anxiety disorders,43 may pose as a rate limiter of
gains borne out of engagement in CR, particularly designs
that explicitly incorporate the practice of developing new
strategies to solve cognitive tasks and discussion of how one
can extend these cognitive strategies to real-world problem
solving. Finally, the ability of people with mood disorders
to put skills into action in the community is often restricted
by low motivation and anhedonia. Motivation differentiates
people with schizophrenia who demonstrate cognitive
improvement following CR.44 Given our understanding of
the mechanistic, reward-related dysfunctions that underlie
anhedonia45anticipatory (wanting) and consummatory
pleasure (liking)measurement of these constructs may
help us understand variability in treatment engagement and
response. Thus in mood disorders, symptoms that disrupt
motivation or confidence may restrict generalization despite
ability to do a task. This has important implications for how
CR may need to be packaged with different supplemental
treatments in a comprehensive recovery program across

Conclusions and Future Directions

CR for mood disorders is emerging as an effective

nonpharmacological treatment option for improving
cognitive performance in people with MDD and BD.
Cognitive improvements may help to improve psychosocial
functioning and reduce disability, although more research
in this area is required to evaluate what mechanisms may

be responsible for the generalization of CR to everyday

behaviour change.
There are important methodological considerations we
have learned from schizophrenia research that can be
applied to cognitive enhancing studies for mood disorders.
Challenges with the reliable assessment of cognitive change
in BD have been carefully considered elsewhere. A recent
consensus panel recommended considering what particular
cognitive tests may be useful to detect changes in BD.15
Future studies may consider focusing on targeting specific
cognitive deficits, rather than global impairment. For
example, executive functioning and attention are reliable
predictors of clinical and functional recovery; coupled with
their seemingly trait-like relation with depression, these 2
domains may be considered as possible primary treatment
We face unique challenges regarding pseudospecificity
of cognitive change in mood disorders, which refers to
the degree to which cognitive improvements truly reflect
cognitive gains and are not artifacts of spurious changes
associated with mood state. Specific mood episodes and
euthymia are at least moderately associated with degree of
impairment, if not even categorically associated with their
presence in some patients. Thus it will be a methodological
and statistical chore to examine the degree to which
cognitive change is independent of mood change, or the
direction of causality where change does occur. Recruitment
of patients who are stable and euthymic, face long-standing
recalcitrant symptoms, or have a history of long mood
episodes may make sense from the perspective of statistical
delineation of treatment, compared with mood effects, but
certainly limits the degree to which any findings would be
widely applicable. Use of statistical models, such as linear
mixed models, that account for baseline and dynamic
mood symptoms can be useful to address the challenges of
mood state and provide useful information regarding the
moderators of change scores.
It is also important to consider the unique characteristics of
mood disorders that not only distinguish the cognitive profile
from schizophrenia but also have implications for how and
for whom transfer of effects can occur in the everyday
environment. Functioning in occupational, interpersonal,
and community activities is often impaired in mood
disorders, but not as prevalent, pervasive, or disabling as in
psychotic disorders. We need to consider the challenges in
measurement that we will face with the possibility of ceiling
effects on typical assessments of functioning, the likelihood
that mood symptoms will restrict gains in functional skills
from transferring to behaviour change in the real world,
and the problematic issues of relying on self-reports.46
Following recent work in schizophrenia,47 the development
of a gold-standard method of examining functional change
is needed in mood disorders.
The mechanisms of treatment are an additional, important
consideration in mood disorders that will likely require
empirical testing rather than direct translation of techniques
developed and refined for psychotic disorders. Many of
The Canadian Journal of Psychiatry, Vol 58, No 6, June 2013 W 323

In Review

Table 2 Common cognitive distortions48,49 and their relation to CR

Potential manifestations during cognitive
remediation exercises

Anecdotes during cognitive remediation for

treatment-resistant depression

Black or white thinking

Believing errors on a single task are

representative of ones entire existence

If I cant do it perfectly, Im a failure.

Emotional reasoning

A tendency for emotions to dominate the

engagement with, or completion of, tasks

I feel like Im bad at this, therefore this

treatment wont work for me.


Attaching a negative label to oneself and using

global descriptions of ones cognitive abilities

Im a loser; Im slow; Im too dumb.

Should statements

Failure to recognize the importance of errors

for identifying new strategies and problem
solving approaches

I should pay more attention; I should

remember things better; I should be getting

Catastrophizing and (or)


Extending the difficulties that one faces on a

cognitive exercise to all other exercises and to
other aspects of ones life

I cant do any of these games. If I cannot do

this exercise, how can I ever return to work?


A tendency to ignore progress and frequently

recall perceived failures during other exercises
or during attempts to use skills in everyday life

I had a lucky streak, but Im back to not

being able to do it! I just cant do it right.

Mind reading

Embarrassment about the perceived judgment

made by therapists or other group members
resulting in excessive reassurance from others

You must think Im so stupid.


Anticipation of failure or poor performance that

may disrupt focus and motivation

Im going to fail this one.


Blaming oneself for poor performance without

considering possible extraneous factors, such
as an adjusted difficulty level of the exercise

That is just what I always do: I get one right

and then I just mess it up.

Cognitive distortion

the manualized approaches for improving the severe and

long-standing impairments in schizophrenia, whether
drill-and-practice or compensatory, may be considered too
monotonous or too facile for those with mood disorders.
A greater range of exercises and discussion topics that
are more in line with the specificity and magnitude of
impairment in mood disorders may be especially important
during refinement of treatment techniques. Relative to
schizophrenia, the more discreet impairments in mood
disorders and spared sensory functions may suggest that
bottom-up, sensory training approaches that have been
gaining popularity in schizophrenia would be less effective
than top-down treatments that focus on executive functions
and cognitive control.
We have observed frequent instances of cognitive distortions
while people with mood disorders perform cognitive
exercises (see Table 2 for exemplars), which suggests that
borrowing principles of cognitive restructuring from CBT is
a potential avenue for increasing the retention of participants
and improving outcomes. Incorporating principles of CBT
to address nascent attitudes related to cognitive challenges
may foster greater transfer of skills, just as skills training
has done for schizophrenia.


The authors are supported by an Early Researcher Award

to Dr. Bowie from the Ontario Ministry of Research and
Innovation. The Canadian Psychiatric Association proudly
324 W La Revue canadienne de psychiatrie, vol 58, no 6, juin 2013

supports the In Review series by providing an honorarium

to the authors.


1. Veiel HOF. A preliminary profile of neuropsychological deficits

associated with major depression. J Clin Exp Neuropsychol.
2. Douglas KM, Porter RJ. Longitudinal assessment of
neuropsychological function in major depression. Aust N Z J
Psychiatry. 2009;43(12):11051117.
3. McDermott LM, Ebmeier KP. A meta-analysis of depression severity
and cognitive function. J Affect Disord. 2009;119(13):18.
4. Harvey PD. Mood symptoms, cognition, and everyday functioning
in major depression, bipolar disorder, and schizophrenia. Innov Clin
Neurosci. 2011;8(10):1418.
5. Burt DB, Zembar MJ, Niederehe G. Depression and memory
impairment: a meta-analysis of the association, its pattern, and
specificity. Psychol Bull. 1995;117(2):285305.
6. Basso MR, Bornstein RA. Relative memory deficits in recurrent
vs first-episode major depression on a word-list learning task.
Neuropsychology. 1999;13(4):557563.
7. Andreasen NC. Linking mind and brain in the study of mental
illnesses: a project for a scientific psychopathology. Science.
8. Dunkin JJ, Leuchter AF, Cook IA, et al. Executive dysfunction
predicts nonresponse to fluoxetine in major depression. J Affect
Disord. 2000;60(1):1323.
9. Williams RA, Hagerty BM, Cimprich B, et al. Changes in directed
attention and short-term memory in depression. J Psychiatr Res.
10. Martino DJ, Strejilevich SA, Scpola M, et al. Heterogeneity in
cognitive functioning among patients with bipolar disorder. J Affect
Disord. 2008;109(1):149156.
11. Bowie CR, Depp C, McGrath JA, et al. Prediction of real-world
functional disability in chronic mental disorders: a comparison
of schizophrenia and bipolar disorder. Am J Psychiatry.

Cognitive Remediation Therapy for Mood Disorders: Rationale, Early Evidence, and Future Directions
12. Reichenberg A, Harvey PD, Bowie CR, et al. Neuropsychological
function and dysfunction in schizophrenia and psychotic affective
disorders. Schizophr Bull. 2009;35:10221029.
13. Glahn DC, Bearden CE, Barguil M, et al. The neurocognitive
signature of psychotic bipolar disorder. Biol Psychiatry.
14. Burdick KE, Goldberg JF, Harrow M, et al. Neurocognition as
a stable endophenotypes in bipolar disorder. J Nerv Ment Dis.
15. Yatham LN, Torres I, Malhi GS, et al. The International Society
for Bipolar DisordersBattery for Assessment of Neurocognition
(ISBD-BANC). Bipolar Disord. 2010;12(4):351363.
16. Deckersbach T, Armistead M, Otto MW. Cognitive rehabilitation
for bipolar disorder. Annual Meeting of the Association for
the Advancement of Behavior and Cognitive Therapies; 2007;
Philedelphia (PA).
17. Deckersbach T, Lund H, Ametrano R, et al. Cognitive-behavioral
approaches for improving inter-episode functioning in bipolar
disorder. Annual Meeting of the Association for the Advancement of
Behavior and Cognitive Therapies; 2008; Orlando (FL).
18. Jaeger J, Berns S, Uzelac S, et al. Neurocognitive deficits
and disability in major depressive disorder. Psychiatr Res.
19. Sanchez-Moreno J, Martinez-Aran A, Tabares-Seisdedos R, et al.
Functioning and disability in bipolar disorder: an extensive review.
Psychother Psychosom. 2009;78:285297.
20. Gruber SA, Rosso IM, Yugelun-Todd D. Neuropsychological
performance predicts clinical recovery in bipolar patients. J Affect
Disord. 2008;105(13):253260.
21. Jaeger J, Berns S, Loftus S, et al. Neurocognitive test performance
predicts functional recovery from acute exacerbation leading to
hospitalization in bipolar disorder. 2007;9(12):93102.
22. Martino DJ, Marengo E, Igoa A, et al. Neurocognitive and
symptomatic predictors of functional outcome in bipolar
disorders: a prospective 1 year follow-up study. J Affect Disord.
23. Tabares-Seisdedos R, Balanza-Martinez V, Sanchez-Moreno J, et
al. Neurocognitive and clinical predictors of functional outcome
in patients with schizophrenia and bipolar I disorder at one-year
follow-up. J Affect Disord. 2008;109(3):286299.
24. Siegle GJ, Ghinassi F, Thase ME. Neurobehavioral therapies in
the 21st century: summary of an emerging field and an extended
example of cognitive control training for depression. Cogn Ther
Res. 2007;31(2):235262.
25. Elgamal S, McKinnon MC, Ramakrishnan K, et al. Successful
computer-assisted cognitive remediation therapy in patients with
unipolar depression: a proof of principle study. Psychol Med.
26. Naismith SL, Redoblago-Hodge MA, Lewis SJG, et al. Cognitive
training in affective disorders improves memory: a preliminary study
using the NEAR approach. J Affect Disord. 2010;121(3):258262.
27. Naismith SL, Diamond K, Carter PE, et al. Enhancing memory
in late-life depression: the effects of a combined psychoeducation
and cognitive training program. Am J Geriatr Psychiatry.
28. Medalia A, Revheim N, Herlands T. Cognitive remediation for
psychological disorders, therapist guide. New York (NY): Oxford
University Press; New York.
29. Meusel L-AC. 2011 Aug. Cognitive remediation in patients
with mood disorders: behavioural and neural correlates [thesis].
[Hamilton (ON)]: McMaster University. Open Access Dissertations
and Theses, 2012, Paper 6580.
30. Bowie CR, Gupta M, Holshausen K, et al. Cognitive remediation for
treatment resistant depression: effects on cognition and functioning
and the role of supplemental homework exercises. J Nerv Ment Dis.
Forthcoming 2013.


31. Kornstein SG, Schneider RK. Clinical features of treatment resistant

depression. J Clin Psychiatry. 2001;62(16):1825.
32. Harvey PD. Update on cognition: cognitive impairments in
major depression and bipolar disorders. Psychiatry (Edgmont).
33. Thase ME, Rush AJ. Treatment resistant depression. In: Bloom FE,
Kupfer DJ, editors. Psychopharmacology: the fourth generation of
progress. New York (NY): Raven Press; 1995. p 10811097.
34. Fava M. Diagnosis and definition of treatment-resistant depression.
Biol Psychiatry. 2003;53(8):649659.
35. Deckersbach T, Nierenberg AA, Kessler R, et al. Cognitive
rehabilitation for bipolar disorder: an open trial for employed
patients with residual depressive symptoms. CNS Neurosci Ther.
36. Martinez-Aran A, Torrent C, Sole B, et al. Functional remediation
for bipolar disorder. Clin Pract Epidemiol Ment Health.
37. McGurk SR, Twamley EW, Sitzer DI, et al. A meta-analysis
of cognitive remediation in schizophrenia. Am J Psychiatry.
38. Wykes T, Huddy V, Cellard C, et al. A meta-analysis of cognitive
remediation for schizophrenia: methodology and effect size. Am J
Psychiatry. 2011;168(5):474485.
39. Bowie CR, McGurk SR, Mausbach B, et al. Combined cognitive
remediation and functional skills training for schizophrenia: effects
on cognition, functional competence, and real-world behavior. Am J
Psychiatry. 2012;169(7):710718.
40. Henry C, Van den Bulke D, Bellivier F, et al. Anxiety disorders
in 381 bipolar individuals: prevalence and impact on illness
severity and response to mood stabilizer. J Clin Psychiatry.
41. Boylan KR, Bieling PJ, Marriott M, et al. Impact of comorbid
anxiety disorders on outcome in a cohort of patients with bipolar
disorder. J Clin Psychiatry. 2004;65(8):11061113.
42. Mantere O, Melartin TK, Suominen K, et al. Differences in Axis
I and II comorbidity between bipolar I and II disorders and major
depressive disorder. J Clin Psychiatry. 2006;67(4):584593.
43. Bradbury C, Cassin SE, Rector NA. Obsessive beliefs and
neurcognitive flexibility in obsessive-compulsive disorder. Psychiatr
Res. 2011;187(12):160165.
44. Medalia A, Richardson R. What predicts a good response
to cognitive remediation interventions? Schizophr Bull.
45. Sherdell L, Waugh CE, Gotlib IH. Anticipatory pleasure predicts
motivation for reward in major depression. J Abnorm Psychol.
46. Burdick KE, Endick CJ, Goldberg JF. Assessing cognitive
deficits in bipolar disorder: are self-reports valid? Psychiatr Res.
47. Leifker FR, Patterson TL, Heaton RK, et al. Validating measures of
real-world outcome: the results of the VALERO expert survey and
RAND panel. Schizophr Bull. 2011;37(2):334343.
48. Beck AT. Depression: clinical, experimental, and theoretical aspects.
New York (NY): Harper and Row; 1967.
49. Beck AT. Cognitive therapy and the emotional disorders. New York
(NY): Meridian; 1976.

The Canadian Journal of Psychiatry, Vol 58, No 6, June 2013 W 325