Download Depression-Bio-Psycho-Social Management and EBT

Depression-Bio-Psycho-Social
Management and EBT
Dr Sumanta Gupta
Consultant Psychiatrist
Oldham
Outline
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NICE guideline
Antidepressant Treatments
Treatment Resistant Depression
CBT & MCBT
IPT
Evidence Base for the above treatments
NICE Guideline-Principles for assessment
• When assessing a person who may have depression, conduct
a comprehensive assessment that does not rely simply on a
symptom count.
• Take into account:
– the degree of functional impairment and/or disability
associated with the possible depression and
– the duration of the episode.
Effective delivery of interventions for
depression (1)
• All interventions should be delivered by competent
practitioners.
• Psychological and psychosocial interventions should be
based on the relevant treatment manual(s).
• Practitioners should consider using competence
frameworks.
Effective delivery of interventions for
depression (2)
For all interventions, practitioners should:
• receive regular high-quality supervision
• use routine outcome measures
• ensure the patient with depression is involved in reviewing
treatment efficacy
• engage in monitoring and evaluation of:
– treatment adherence
– practitioner competence.
NICE-The stepped-care model
Focus of the
intervention
STEP 4: Severe and complex1
depression; risk to life; severe selfneglect
STEP 3: Persistent subthreshold depressive
symptoms or mild to moderate depression with
inadequate response to initial interventions;
moderate and severe depression
STEP 2: Persistent subthreshold depressive
symptoms; mild to moderate depression
STEP 1: All known and suspected presentations of
depression
1,2
see slide notes
Nature of the
intervention
Medication, high-intensity psychological
interventions, electroconvulsive therapy,
crisis service, combined treatments,
multiprofessional and inpatient care
Medication, high-intensity psychological
interventions, combined treatments, collaborative
care2, and referral for further assessment and
interventions
Low-intensity psychosocial interventions, psychological
interventions, medication and referral for further
assessment and interventions
Assessment, support, psycho-education, active monitoring
and referral for further assessment and interventions
Low-intensity psychosocial
interventions
• For people with persistent subthreshold depressive
symptoms or mild to moderate depression, consider
offering one or more of the following interventions,
guided by the person’s preference:
– individual guided self-help based
on the principles of cognitive
behavioural therapy (CBT)
– computerised cognitive
behavioural therapy (CCBT)
– a structured group physical
activity programme.
Drug treatment –NICE guideline
• Do not use antidepressants routinely to treat persistent
subthreshold depressive symptoms or mild depression
because the risk–benefit ratio is poor
• Consider antidepressants for people with:
– a past history of moderate or severe depression or
– subthreshold depressive symptoms present for a long time or
– subthreshold depressive symptoms or mild depression that persist(s)
after other interventions.
Treatment for moderate or severe
depression
• For people with moderate or severe depression, provide
a combination of antidepressant medication and a highintensity psychological intervention (cognitive
behavioural therapy [CBT] or interpersonal therapy [IPT]).
Psychological interventions
for relapse prevention
People with depression who are considered to be at significant
risk of relapse or who have residual symptoms, should be
offered one of the following psychological interventions:
• individual CBT:
– for people who have relapsed despite antidepressant medication
– for people with a significant history of depression and residual symptoms
despite treatment.
• mindfulness-based cognitive therapy:
– for people who are currently well but have experienced three
or more previous episodes of depression.
Antidepressants
Few Dates
 1958
 1958
 1982
 1988
 1989
 1994
 1994
 1996
Monoamine oxidase inhibitors (MAOIs)
Tricyclics (TCA’s)
Trazodone (Molipaxin)
Fluoxetine (Prozac)
Bupropion (Zyban)
Nefazodone (Serzone)
Venlafaxine (Effexor)
Mirtazapine (Zispin)
Treatment Response Categories
PREVALENCE
IN RCTS
STATE
OBJECTIVE
CRITERION
CLINICAL
STATUS
Remission
HAM-D ≤ 7
No residual
psychopathology
~ 40%
Response
≥ 50% decrease in
HAM-D without
remission
Substantially improved,
but with residual sxs
~ 25%
Partial
response
25%-50% decrease Mild-moderate
in HAM-D
improvement
~ 10%
Nonresponse
< 25% decrease
in HAM-D
~ 25%
No clinically
meaningful response
Fig. 1. Survival analysis of weeks to major depressive episode relapse (MDE):
comparing patients with unipolar major depressive disorder who recovered from
intake MDE with residual subsyndromal depressive symptoms vs.
asymptomatic status. Wilcoxon Chi Square Test of Difference=47.96; P<0.0001.
Why Is Achieving Remission
Important?
• Residual symptoms put patients at high risk of relapse
and recurrence
– Patients with residual symptoms after medication
treatment are 3.5 times more likely to relapse
compared to those fully recovered (Judd et al,
1998)
– This risk is greater than the risk associated with
having ≥ 3 prior depressive episodes
– Similar finding exists after response to cognitive
therapy
Why a temporal delay for maximal
therapeutic benefit
-adrenergic receptor downregulation
5-HT2 receptor down-regulation
Antidepressant
medications have
essentially equivalent
efficacy
Tricyclic Antidepressants (TCAs)
 Characteristic three-ring nucleus
 Clinical effects
 Normalization of mood and resolution of
neurovegetative symptoms
 Biochemical effects
 Inhibit monoamine uptake at nerve terminals
 May potentiate action of drugs that cause
neurotransmitter release
 Temporal delay of weeks for clinical effects, although
biochemical effects are immediate
Mechanism of action of TCAs
“Tertiary” TCAs
imipramine
amitriptyline
clomipramine
“Secondary” TCAs
desipramine
nortriptyline


Inhibit 5-HT uptake
(weaker inhibition of NE uptake)
Inhibit NE uptake
(weaker inhibition of 5-HT uptake)
In vivo action of TCAs
If one administers a tertiary TCA

If one administers a secondary TCA 
there is always both the tertiary
and the secondary amine in the
circulation
there is only the secondary
amine in the circulation.
Neuropharmacology of TCAs
Inhibit monoamine uptake (NE and 5-HT)
Muscarinic cholinergic antagonism
H1 histamine antagonism
1-adrenergic antagonism
Tricyclics-Contraindications
• QTc greater than 450 msec
• Conditions worsened by muscarinic blockade
(eg myasthenia gravis, BPH)
• pre-existing orthostatic hypotension
• Seizure disorder
Side effect profile of TCAs
Dry mouth
Constipation
Dizziness
Tachycardia
Urinary retention
Impaired sexual funtion
Orthostatic hypotension
Low therapeutic index of TCAs
 Cardiotoxicity: resulting from combination of:
 Conduction defects, arrhythmias
 Delirium
Potentiation of effects of other sedating drugs
 Consequences
 Suicide
 requires care in prescribing
 monitoring drugs that might have synergistic effects on
monoamine function
Monoamine Oxidase Inhibitors
(MAOIs)
Irreversibly inhibit monoamine oxidase
enzymes
Effective for major depression, panic
disorder, social phobia
Drug interactions and dietary restrictions
limit use
Biochemistry of MAO
Occurs as two isoenzymes
 MAO-A –
•Oxidizes norepinephrine, serotonin,
tyramine
 MAO-B
• selective for dopamine metabolism
Dietary and Drug Interactions
 Increased stores of catecholamines sensitize patients to
effects of sympathomimetics
 Accumulation of tyramine (sympathomimetic) = high risk
of hypertensive reactions to dietary tyramine
 requires dietary restrictions
 Interactions with other sympathomimetic drugs
 Antidepressants
 OTC cold remedies
• phenylpropanolamine
 Meperidine
 L-dopa
Examples of MAOIs
 Irreversible, non-selective MAOIs
 phenelzine
 isocarboxazid
 tranylcypromine
 Selective MAO-B inhibitors
 deprenyl (selegiline)
 loses its specificity for MAO-B in antidepressant doses
 Reversible monoamine oxidase inhibitors (RIMAs)
 Moclobemide
 Appears to be relatively free of food/drug interactions
Selective Serotonin Uptake Inhibitors
(SSRIs)
 Currently marketed medications
 Fluoxetine (Prozac).
 Sertraline (Lustral).
 Paroxetine (Seroxat)
 Fluvoxamine (Luvox)
 Citalopram (Cipramil)
 Escitalopram (Cipralex)
 Selectively inhibit 5-HT (not NE) uptake
 Differ from TCAs by having little affinity for muscarinic, as well
as many other neuroreceptors
Selective Serotonin Reuptake Inhibitors
(SSRIs)
 Much higher therapeutic index than TCAs or
MAO-I’s
 Much better tolerated in early therapy
 Equal or almost equal in efficacy to TCAs
Side effects associated with SSRIs
Nausea
Sexual dysfunction
 Delayed ejaculation/anorgasmia
Anxiety
Insomnia
Hyponatremia
Serotonin syndrome
 Evoked by interaction between serotonergic agents
 e.g., SSRIs and MAOIs
 Combination of increased stores plus inhibition of
reuptake after release
 Symptoms
 Hyperthermia
 Muscle rigidity
 Myoclonus
 Rapid changes in mental status and vital signs
 Can be lethal
Selective Norepinephrine-Serotonin
Reuptake Inhibitors
 Venlafaxine (Effexor), Duloxetine (Cymbalta),
 relatively devoid of antihistaminergic,
anticholinergic, and antiadrenergic properties
 nonselective inhibitor of both NE and 5-HT uptake.
Adverse effects: GI , Sexual dysfunction,
hypertension (venlafaxine), hyponatremia
Other antidepressants
 Trazodone
 mixed 5-HT agonist/antagonist
• 1 antagonist
• H1 antagonist
 Nefazodone (Serzone)
 5 HT2 antagonist
 Bupropion (Wellbutrin; Zyban)
 Inhibits uptake of DA and NE
 antismoking properties probably involves parent
molecule
 Lacks sexual side effects
 Seizure risk
Mirtazapine
 2 antagonist
 5H2 and 5HT3 antagonist
 Net effect selective increase in 5HT1A
function
 H1 antagonist
advantages: sedation, no adverse sexual
effects
Antidepressants and drug interactions
 Pharmacodynamic
– Additive effects with alcohol and other sedating drugs
– MAOI interactions
 Pharmakokinetic
– Cytochrome P450-2D6 inhibition
• Fluoxetine and paroxetine
• Increased levels of TCAs, antipsychotics, warfarin
– Cytochrome P450-3A4 inhibition
• Nefazodone and fluvoxamine
• Increased levels of terfenadine, astemizole, cisapride – can cause
fatal arrhythmias
Treatment Resistant Depression(TRD)
• When Do You Characterize a Response As
Treatment Resistant?
• After a patient has been on an antidepressant at for a reasonable amount
of time at an adequate dose
• No commonly accepted time point
– Most drug trial data comes from 8 week long studies
– If no onset of response by weeks 4 or 6, there is a 73-88% chance of
not having onset of response by end of 8 week trial (Nierenberg et al,
2000), so 4 weeks is a reasonable point to increase dose
– An 8-12 week course is consistent with acute treatment framework
and allows patients 8 weeks at a dose expected to produce response
A Working Definition of
Treatment Resistant Depression
6-8 weeks of at least a middle range dose
without remission
What Are the Clinical Features
Associated With TRD(1)
• Incorrect primary diagnosis
– Is there a secondary cause of the depressive
symptoms (e.g., substance-induced mood
disorder from prescription meds or ethanol,
hypothyroidism, hypercalcemia )
– Is their primary psychiatric diagnosis wrong
(?bipolar, schizoaffective, cluster B personality
DO)?
– Is there an unrecognized depressive subtype?
• Psychotic depression
What Are the Clinical Features
Associated With TRD (2)
• Patient factors
-acceptance of diagnosis
-compliance
• Physician factors
-Underdosing
-Inadequate length of treatment
TRD-Strategies
• Level 1
– Initial Treatment: Citalopram
• Level 2
– Switch To:
• bupropion
• sertraline
• Venlafaxine
– Augment With:
• bupropion
• buspirone
• Level 3
– Switch To:
• mirtazapine or nortriptyline
– Augment With:
• Lithium or T3
• Level 4
– Switch To:
• Tranylcypromine or mirtazapine combined with
venlafaxine
ECT should be considered at all stages if indicated.
How Effective is an SSRI in Real World
Practice?
• ~1/3 met criteria for remission (HAM-D ≤ 7)
• ~ 1/2 met criteria for response (≥ 50% decrease
in depressive severity)
(Trivedi et al, Am J Psychiatry, 2006)
TREATMENT OUTCOMES
L-3 Switch
• Mirtazapine
• Nortriptyline
Remission (HAM-D)
12.3%
19.8%
TREATMENT OUTCOMES
L-3 Augmentation
• Lithium
• T3
Remission (HAM-D)
15.9%
24.7%
TREATMENT OUTCOMES
L-4 Switch
Remission (HAM-D)
• Tranylcypromine
6.9%
• mirtazapine + venlafaxine
13.7%
• Electroconvulsive Therapy
– Response rate in patients with
• inadequate medication trials: 86%
• adequate trials: 50%
– Probably treatment of choice for catatonic
states
SUMMARY of Drug treatments of
Depression
• Patients suffering from major depression (primarily with
chronic disease and multiple recurrences) in Primary and
Specialty Care settings have a 30% chance of achieving full
remission with an adequate dose of Citalopram
• Patients who did not remit with citalopram had a 1 in 4
chance of achieving remission by switching to bupropion,
sertraline or venlafaxine and a 1 in 3 chance of responding to
augmentation of the citalopram with bupropion or buspirone
• There was no clear advantage in switching antidepressant
class although its often the only option.
SUMMARY-2
• Depressed patients who fail to respond to two antidepressant
trials are have a 12-20% remission rate with another single
antidepressant agent and a 16-25% remission rate with T3 or
lithium augmentation
• While there is indisputable evidence for real world
effectiveness of available antidepressant medications, many
patients do not achieve remission.
• There is a pressing need to develop more effective treatments
for depression and also to elucidate factors that may help us
choose from our currently available treatments
Cognitive Behavioural Therapy (CBT)
One of the most extensively researched forms of
psychotherapy with over 325 outcome studies looking at CBT
effectiveness published in 2006 (Butler et al., 2006).
CBT encompasses a number of therapeutic cognitive and
behavioural approaches. The compelling evidence base for
CBT lead to an announcement in 2007 that there would be
£173 million into an Improving Access to Psychological
Therapies Program (IAPT) based on the finding that CBTs
were more efficient than pharmacotherapy or other
interventions (Rachman & Wilson, 2008).
Depression-Recap
Minor depression: Rumination on negative themes: Resentful,
irritable, or angry
Major depression: 5 or more symptoms in the last 2 weeks (Diagnostic
Criteria (DSM IV) Major Depressive Episode)
 Emotional changes: feelings of sadness and hopelessness.
 Cognitive changes: low self esteem, guilt, concentration difficulties.
 Behavioural and motivational difficulties: feeling slowed down,
reduced interest in social activities.
 Bodily changes: sleep, eating, loss of energy.
Chronic depression occurs in 15-39% of cases with individuals still
experiencing major depression one year after symptom onset (Berti,
Ceroni, et al., 1984).
Early experience
• e.g. rejection
and criticism
from parents
Negative core
beliefs/schemas
Beck’s cognitive model
- Recap.
From Dozois & Beck (2008)
• I am
incompetent
Negative life event
Activation of
schema
Cognitive biases
• Nothing ever goes
right for me
Negative automatic
thoughts
Depression
Structured:
• Time limited
• Problem orientated
Role of therapist:
• As a guide
• As a scientist
practitioner
• Socratic method
CBT STRUCTURE
Cognitive techniques:
• Hot cognitions
Recording cognitions
(mood diaries)
• Identifying
cognitive biases
Behavioural techniques:
• Behavioural
experiments
• Experiments with
therapist
• Experiments alone
From: Westbrook, Kennerley, & Kirk (2007)
Cognitive techniques
Cognition: “either a thought or a visual image that you may not be very
aware of unless you focus your attention on it” (Beck et al., 1979, p. 147)
The C in CBT
Help clients observe and record thoughts and images that
run through their minds and help them to distinguish
between thoughts and feelings.
For example
• Identifying ‘hot cognitions’: Rapid automated decisions
based on significant emotions.
• Identifying: ‘cognitive biases/ thinking errors’
Extreme thinking : Dichotomous thinking or unrealistic
biases.
Selective attention: Overgeneralization or disqualifying the
positive.
Example of techniques used to help people understand the
link between thoughts and emotions
Daily Thought Record
Date &
time
Situation
What mood
were you in?
How intense was the
mood?
0
10
Not at all
Very
Thoughts
Behavioural techniques/experiments
The B in CBT
Planned experimental activities, performed in or between
cognitive therapy sessions. (Bennett-Levy et al., 2004)
Their design is derived from a cognitive formulation of the problem
and their primary aims are:
1. Test validity of clients existing beliefs about themselves, others,
world.
2. Construct new, more adaptive beliefs.
3. Contribute to the development of the cognitive formulation.
(Bennett-Levy et al., 2004)
In depression, behavioural experiments may be used to test
negative automatic thoughts and to re-evaluate underlying
beliefs and assumptions.
Behavioural experiments
One example: Emma became depressed in University and dropped out when the
pressure of exams became too much. She moved back to her parents’ house and
felt too depressed to contact her friends.
Hypothesis testing
Theory A: Client’s initial belief: ‘My friends will think I am thoughtless and selfish
and won’t want to know me’ - 80% belief.
Theory B: Alternative belief: ‘One or two of my friends may be missing me, a
couple have tried to contact me’ – 20% belief.
Prediction: My best friend won’t want to know me any more. Even if we do meet I
will probably feel foolish and cry all night.
Outcome: After two more sessions working on the idea that the alternative belief
may be true, Emma picked up the phone and rang her friend. Her friend was
pleased to hear from her, they arranged to go out and Emma was surprised to find
that she had fun and did not cry.
Emma’s belief that her friend’s wouldn’t want to know her dropped to 10%.
Common CBT goals
1.The client needs to counteract negative cognitive
biases and develop a more balanced view of
him/herself, the world, and the future.
2. Restore activity levels, especially of activities that
bring a sense of pleasure and achievement.
3. Increase active engagement with problem
solving.
Efficacy of CBT for depression
• Based on clinical trials evidence – NICE recommends CBT for depression
http://www.nice.org.uk/cg90
• Important questions to consider when thinking about efficacy:
1. What is CBT compared to? Drug treatments, other therapeutic approaches,
nothing?
2. Long term outcomes: Are treatment gains maintained over time?
• CBT is more effective than no intervention
– Based on meta-analysis of 97 studies, d = 0.67, Cuijpers et
al., 2011
• Is equally effective as other types of psychological therapy
– Based on meta-analysis of 56 studies, d = 0.03, Cuijpers et
al., 2011
• CBT is equally effective to antidepressant medication, and may
be more effective at preventing relapse (De Rubeis et al., 2005)
Efficacy of CBT for depression
De Rubeis et al (2005) Study comparing cognitive therapy with antidepressant
medication in adults
No difference in outcomes at 16 weeks
Cognitive Therapy was associated with lower
rates of relapse
Mindfulness Based Cognitive Therapy
(MBCT)
MBCT aims to prevent depressive relapse by developing
awareness of and changing the relationship with unwanted
negative thoughts, feelings and bodily sensations.
In this way previously depressed individuals respond to negative
thoughts not in an automatic way, but in a skilful intentional
way.
Ma & Teasdale (2004)
Mindfulness
“Paying attention in a particular way: on purpose, in the present
moment , and nonjudgmentally ” Kabat-Zinn (1990)
Core assumptions of MBCT
MBCT assumes that once in a mode of recovery from depression, previously
depressed individuals will still be vulnerable to experiencing low mood and
patterns of negative thinking.
Reactivation of depression related thoughts, feelings, and physical sensations
is often automatic – and can trigger relapse.
Model underlying development of MBCT for depressive relapse
Negative
thinking:
Depressive
episode
Nonnegative
thinking:
Remission
Potential
RELAPSE
Negative thinking
patterns “nipped in the
bud ”
Negative thinking patterns
re-established.
From: Segal, Williams, & Teasdale (2002), p. 37
LOW MOOD
Reactivation of
negative thinking
How does it work?
“The aim of the program is freedom, not happiness”
(Segal, Williams, & Teasdale, 2002, p.91)
8 week manualised course : Mindfulness practices and traditional cognitive therapy
techniques
AIM: To prevent re-establishment of patterns of negative thinking
Core themes
• Recognition of patterns of negative thinking e.g. ‘automatic pilot’ &
‘attachment to achieving happiness’.
• How to step out of old cognitive routines e.g. ‘decentring & ‘mindful
awareness’.
• Experiential learning e.g. engaging in ‘being’ not ‘doing’ mode (in class
and through homework.
• Empowerment and acceptance/kindly awareness.
Comparing MBCT and CBT
Practical differences:
MBCT delivered in a group format whereas CBT is often 1:1
MBCT is based on an 8 week program
Theoretical differences:
CBT encourages individuals to identify and change maladaptive thoughts
by challenging the accuracy of their beliefs.
MBCT teaches individuals to recognise the occurrence of depressive
thoughts without emotionally responding to them.
(Manicavasgar, Parker, & Perich, 2011)
MBCT includes techniques and exercises from cognitive behavioural
therapy with additional meditation components.
(Segal, Williams, & Teasdale, 2002)
Both MBCT and CBT include didactic elements, which provides the
participants with information about depression to facilitate them in
recognising and dealing with their relapse signatures.
Is it effective?
• NICE recommends MBCT for depressive relapse:
http://www.nice.org.uk/cg90
• In individuals who had > 3 episodes of depression relapse
was reduced when compared to TAU. (Ma & Teasdale, 2000, 2004)
• MBCT shown to be more effective than m-ADM at
preventing relapse. (Kuyken, 2008)
• MBCT has shown promise for those still currently
depressed or experiencing chronic depression. (Kenny &
Williams, 2007; Kingston et al., 2007)
Summary
• A range of cognitive approaches are available in the UK
• CBT has one of the largest evidence bases
Both cognitive and behavioural techniques help the individual
to develop strategies for managing problems and guide the
development of more adaptive perspective on the world.
• MBCT has been developed to break the cycle of relapse
common to depression
Techniques teach individuals to be present, in the moment,
to recognise negative thinking and decentre from it.
Compassion and kindness to the self are fostered.
Interpersonal Psychotherapy
Historical Influences of IPT
•
•
•
•
Psychoanalysis
Harry Stack Sullivan
Object Relations Therapy
Interpersonal Theory (Leary, Kiesler)
IPT: Roots in Psychodynamic Theory
• Primary instincts of sex and aggression involve relating to
others
• Relationships with others contribute to personality
development
• Psychological Problems due to deficits in early relations
 Transference and counter-transference are interpersonal
Outline of IPT Intervention
Initial Sessions (Overview)
• Assess Depressive symptoms
• Complete Interpersonal Assessment
• Identify Major Interpersonal Problem Area
• Explain IPT and make treatment contract
Prominent Features of IPT
• IPT designed for symptom reduction and
improved interpersonal relationships
• Focus on current disputes, frustrations,
anxieties in the interpersonal context which
impact mood and self esteem
IPT Compared to CBT
• Focus on affect and expression of emotions
• Explores avoidance and resistance behavior
• Identification of patterns in client’s behavior,
thinking, feeling and relationships
• Attention to past experiences
• Focus on interpersonal experience
• Emphasis on the therapeutic relationship
• Exploration of client’s wishes, dreams,
fantasies
Blagys & Hilsenroth, 2000
Role of IPT Therapist
• Therapist is patient advocate, not neutral
• Expresses unconditional positive regard
• Intentionally cultivates positive expectations
of treatment
– Optimistic, positive, reassuring
• Therapist is active in keeping interpersonal
problem areas to focus
Setting Treatment Contract
• Set 2 –3 treatment goals with client related to
problem area focus
• Ask client what would be the:
– Best possible outcome
– Most expectable outcome
– Worst possible outcome
• Describe expected Duration and Frequency of
treatment (12-16 weeks)
Relate Depression to Interpersonal Context
What interpersonal events related to depression?
Review current & past interpersonal relationships
• Who does client interact with?
• Frequency of contact, activities shared?
• Assess quality and themes of relationships
• Assess expectations of client (and other) in
relationships
• Assess satisfying and unsatisfying aspects of
relationships
• Discuss changes client wants in relationships
Identification of Major Problem Area
Assess interpersonal experience and depression to
identify of one of Four Problem Areas:
• Interpersonal Role Dispute: with spouse, lover,
family member, friends, co-worker
• Role Transition: e.g. new job, relocation, divorce
• Interpersonal Deficits: evidenced by social
impoverishment, loneliness, isolation
• Grief: following death if abnormally severe,
protracted or impairing
Evidence for IPT Efficacy
•
•
•
•
•
•
Boston-New Haven Study (1979)
4 Tx Groups (16 wks & 1yr follow-up):
IPT, amitriptyline, both combined, control
IPT and amitriptyline equally effective
Combination IPT & amitrip. most effective
IPT grp. Sustained improved psychosocial
functioning 1 yr later (not amitrip. Grp)
NIMH Tx Depression Research (1989)
• 4 Tx grps (16 wks, multi-site, N=250)
• IPT, CBT, Imipramine & clinical management
(CM), placebo & CM
• IPT comparable to Imipramine & CM
• CBT showed somewhat less improvement
• IPT grp. had lowest attrition rate
• Results for mod.-severe depression
Brain Activity Changes with either IPT
or Antidepressant Tx
• PET scans showed higher prefrontal and less
temporal activity in depressed vs controls
• Both IPT and Paroxetine resulted in
normalized PET scan activity and improved
Depressive symptoms.
Brody (2001); Martin (2001)
References
• NICE guideline CG 90-2009(Review March 2015)
• Rush AJ, Trivedi MH, Wisniewski SR, et al. Bupropion-SR, sertraline, or
venlafaxine-XR after failure of SSRIs for depression. N Engl J Med. Mar
23 2006;354(12):1231-1242.
• Trivedi MH, Fava M, Wisniewski SR, et al. Medication augmentation
after the failure of SSRIs for depression. N Engl J Med. Mar 23
2006;354(12):1243-1252.
• Fava M, Rush AJ, Wisniewski SR, et al. A Comparison of Mirtazapine and
Nortriptyline Following Two Consecutive Failed Medication Treatments
for Depressed Outpatients: A STAR*D Report. Am J Psychiatry 2006;
163:1161-1172.
• Nierenberg AA, Fava M, Trivedi MH, et al. A Comparison of Lithium and
T3 Augmentation Following Two Failed Medication Treatments for
Depression: A STAR*D Report. Am J Psychiatry 2006; 163:1519-1530.
• www.ids-qids.org
References
CBT
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Bennett-Levy, J., Butler, G., Fennell, M., Hackmann, A., Mueller, M. & Westbrook, D.
(2004) The Oxford guide to behavioural experiments in cognitive therapy. Oxford:
Oxford University Press.
Butler, A. C. Chapman, J. E. Forman, E. M. & Beck, A. T. (2006). The empirical status of cognitive-behavioral therapy: a review of metaanalyses. Clinical Psychology Review, 26, 17-31).
Cuijpers P, Clignet F, van Meijel B, van Straten A, et al. (2011). Psychological treatment of depression in inpatients: a systematic review
and meta-analysis. Clinical Psychology Review 31(3):353-60.
DeRubeis, R. J., Hollon, S. D., Amsterdam, J.D., Shelton, R. C., Young, P. R., Salomon, R.
M., et al. (2005). Cognitive therapy vs. medications in the treatment of
moderate to severe depression. Archives of General Psychiatry, 62, 409-416.
Dozois, D.J.A. & Beck, A.T. (2008). Cognitive schemas, beliefs, and assumptions. In K.S. Dobson & D.J.A. Dozois (Eds.), Risk factors in
depression. London Academic Press. (Available online via ScienceDirect).(Nice explanations of main factors of cognitive model of
depression)
Rachman S, Wilson GT. (2008). Expansion in the provision of psychological treatment in the United Kingdom. Behaviour Research &
Therapy, 46(3), 293-5.
Westbrook, D. Kennerley, H. & Kirk, J. (2007). An introduction to Cognitive Behaviour Therapy: Skills and application. Sage. London
MBCT
Kenny, M. A., & Williams, J. M. G. (2007). Treatment-resistant depressed patients show a good response to mindfulness-based Cognitive
Therapy. Behaviour Research and Therapy, 45, 617-625.
Kingston, T., Dooley, B., Bates, A., Lawlor, E., & Malone, K. (2007). Mindfulness-based cognitive therapy for residual depressive
symptoms. Psychology and Psychotherapy, 80 (2), 193- 203.
Kuyken, W., Byford, S., Taylor, R.S., Watkins, E.R., Holden, E.R., White, K., Barrett, B., Byng, R., Evans, A., Mullan, E. & Teasdale,
J.D. (2008). Mindfulness-based cognitive therapy to prevent relapse in recurrent depression. Journal of Consulting and Clinical Psychology
76(6), 966-978.
Ma, S.H., & Teasdale, J.D. (2004). Mindfulness-based cognitive therapy for depression: Replication and exploration of differential relapse.
Journal of Consulting and Clinical Psychology, 72, 31-40.
Manicavasgar, V. Parker, G. & Perich, T. (2011). Mindfulness-based cognitive therapy vs cognitive behaviour therapy as a
treatment for non-melancholic depression. Journal of Affective Disorders, 130, 138–144.
Segal, Z.V., Williams, J.M.G., & Teasdale, J.D. (2002). Mindfulness-based cognitive therapy for depression: A New Approach to Preventing
Relapse. New York: Guilford.
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