Transcript MOOD DISORDERS

MOOD DISORDERS
ASSESSMENT & MANAGEMENT
‘SKETCH ARTIST’ MISTAKE:
TOO LITTLE INFORMATION
CASE EXAMPLE:
XYZ is a 44 yr old Caucasian female, currently in a relationship with a 37 yr old man on
Disability support pension, lives with her 9 yr old son, also has a 5 year old daughter who
doesn’t live with her. She has been on unemployment benefits for the last 2 years. She is
currently a voluntary in-patient on the ward. She gives a 2 year history of depressive
symptoms.
Establish broad spectrum
• –neurosis, depression or psychosis
• Once domain breached establish diagnosis according to
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DSM criteria.
Follow up immediately with most important co morbidities
and differentials.
Depression-bipolarity, anxiety, substance misuse and
personality dysfunction
Psychosis-depression, mania, substance misuse or
schizophrenia
Establish criteria for domains!!
Comorbidity
• Individuals with mood disorders
•  Risk of substance use disorders (especially alcohol)
•  Risk of anxiety disorders (e.g. OCD, panic disorder, social anxiety
disorder)
• Magnitude of risk:
• Bipolar disorders > MDD > general population
•  Risk of mood disorders in those with
• Substance use disorders
• Anxiety disorders
• Some personality disorders
• Medical co-morbididy
Depression
• Anxiety
• Bipolarity
• Substance misuse
• Personality disorder
DSM-IV-TR criteria for MDD
• At least 5 of the following occurring nearly every day (except for #9)
over at least 2 weeks, which are a change from previous functioning:
Depressed mood, most of the day*
Loss of interest or pleasure, most of the day*
Psychomotor agitation or retardation
 or  appetite, or significant weight loss or gain
Insomnia or hypersomnia
Loss of energy
 concentration or indecisiveness
Feelings of worthlessness or excessive/inappropriate guilt
Recurrent thoughts of death or suicide
*One of the symptoms must be either (1) or (2)
• Symptoms cause clinically significant distress or
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functional
impairment
• Excludes bereavement, substance, general medical condition and
mixed episode
MDE Subtypes
• With Catatonic Features
• rare
• With Melancholic Features
• older people
• no pre-morbid personality traits
• marked weight loss, early morning wakening, psychomotor
retardation/agitation, diurnal mood variation, anhedonia
• can present with delusions (psychotic depression)
• responds well to antidepressants and ECT
• responds less well to psychotherapies
• With Atypical Features
• With Postpartum Onset
Depression
• How are you feeling in yourself / in your spirits. On a scale of 1-10 if 10 was really down
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where would you put yourself. How long does it last for? (mood, clinical depression)
Have you been tearful lately? (mood)
When was the last time you smiled/cried? (mood)
What are the kinds of things you normally enjoy doing. / how do you spend your day?
(anhedonia)
If TV, mowing the lawn etc -have you been enjoying these things as much as you’ve done in
the past. (anhedonia)
When was the last time you played….(anhedonia)
What have your energy levels been like. / do your energy levels keep up with .e.g. physical
work (anergia)
What about your concentration/ how long can you read a book for/ do you find it difficult
taking things in when watching TV or reading a book .Has that affected your work? (anergia)
What are your plans for the future? /How do you see your future? (hopelessness)
Is there anything hurting your conscience? Have you been blaming yourself lately? (guilt)
Do you feel there is something wrong with functioning of your body? (hypochondriacal
ideation)
What about your confidence levels? (self esteem, self confidence)
Do you think other people would be better off without you? (worthlessness)
ANY SUGGESTIONS/ INSIGHTS INTO ASKING
THESE QUESTIONS OR STARTING THIS
CONVERSATION?
Listen to patients’ cues: use experience-near terms
(down not ‘depressed’)
# CLUB 2 OR 3 CRITERIA:
NEGATIVE THOUGHTS (GUILT, HOPELESS, HELPLESS,
WORTHLESS) OR
PHYSICAL EFFECTS (PANIC ATTACKS, FATIGUE,
MEMORY, CONCENTRATION, SLEEP, APPETITE
CHANGES ETC.) OR
EMOTIONS (SAD, DIURNAL VARIATION, ANHEDONIA,
CRYING) OR
BEHAVIOURS (AVOIDANCE, SOCIAL ISOLATION, POOR
FUNCTIONING, DRINKING)
-COGNITIVE MODEL (depression & mania)
Psychosis: positive, negative, cognitive domains & mood
Anxiety: …
STRESSORS & PRECIPITANT(S)
What does the ‘precipitant’ tell us?
Risk factors
Sociodemographic factors
Life stressors
Sociodemographic factors
• Largely weak correlation
• Marital status
• Separation/divorce: Bipolar >
MDD > Dysthymia
• Socioeconomic status
• Lower SES: MDD and BD
• Geography
• Distance from the Equator
• Distal from the Equator:
Depression
• Proximity to the Equator: Mania
• Western > Far Eastern countries
• Urbanicity
• Urban residence > Rural
residence
• Season
• Spring & Autumn: Depression
• Summer: Mania
• Diet
•  Folate
•  Omega-3-fatty-acids
• Western diet > Traditional diet
• Physical activity
•  with MDD
• Adiposity
•  with MDD
Life stressors
• Life stressors
• Stressors are not all the same in pertinence
• Less consistent association with bipolar disorder and
melancholic/psychotic MDD cf non-melancholic/non-psychotic MDD
• Association  with  number of episodes (“kindling”)
• For non-melancholic/non-psychotic MDD:
• Cumulative stress (series, chronic) more important than acute stressors
• Early life adversities: E.g. Poor parental relationship, prolonged separation
from parent, intrafamilial sexual abuse
• Early parental death (before adolescence)
• For bipolar disorder:
• Disruption in biorhythm
• Negative and positive “stress”
• Social support
• Social isolation: MDD
RISK ISSUES
CASE EXAMPLE:
XYZ is a 44 yr old Caucasian female, currently in a relationship with a 37 yr old
man on Disability support pension, lives with her 9 yr old son, also has a 5 year
old daughter who doesn’t live with her. She has been on unemployment
benefits for the last 2 years. She is currently a voluntary in-patient on the ward.
She gives a 2 year history of depressive symptoms.
Suicidal ideation
• Sometimes when people get depressed they may find life not
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worth living? Have you felt like this ….?
What thoughts have crossed your mind? (ideation)
How long have you been thinking about this? (intent/ideation)
What have you planned? (plans)
Have you made arrangements for after your death e.g. made a
will or written a note? (intent)
How close have you come to actually carrying out your plan?(
take patient through) (intent)
What stopped you/stops you? (protective factors)
Is there anything to live for at all? Mention friends , family
(protective factors)
Suicidal Attempt
• Go through detail of attempt
• Alcohol
• Seriousness
• Impulsivity-How long had you been planning this?
• Did you make any arrangements for your death e.g. note,
will , finances
• How do you feel now that you have survived?
• Do you really want to die/ have you actually imagined
yourself dead?
• Do you currently have any thoughts of suicide?
BIPOLAR DISORDER
DSM-IV-TR criteria for mania:
Distinct period of abnormally & persistently elevated,
expansive or irritable mood, lasting at least 1 week (or if
hospitalised)
Plus  3 of (4 if mood is only irritable):
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Inflated self-esteem or grandiosity
Decreased need for sleep
More talkative or pressure to keep talking
Flight of ideas or racing thoughts
Distractibility
Increase in goal-directed activity or psychomotor agitation
Excessive involvement in activities that have a high potential for
painful consequences
Severity: cause marked functional impairment, necessitate
hospitalisation, or if psychotic
Exclusion: direct physiological effects of a substance or general
medical condition
Hypomanic Episode
• A less severe form of mania
• DSM-IV-TR criteria is the same as Manic Episode, except:
• Duration: at least 4 days (rather than 1 week)
• No psychotic symptoms
• No hospitalisation
• Not severe enough to cause marked impairment in functioning
• Criticism
• Duration is too long
• Recognised brief hypomanic episodes (1-2 days) are common among those
with bipolar disorders
• Subthreshold symptoms still clinically and functionally significant
Mixed Episode
• Concurrent presence of both depressive & manic symptoms
• DSM-IV-TR criteria:
• Concurrent fulfilment of criteria for Major Depressive Episode and
Manic Episode for at least 1 week
• In broader terms, subthreshold “mixed states” refer to “non-
pure” depressive or manic states
• Intrusion of manic features in depression
or
• Intrusion of depressive features in mania
• Mixed Episode and subthreshold mixed states signal bipolarity
Longitudinal diagnosis: Mood Disorders
• History of a single MDE or recurrent MDEs
= Major Depressive Disorder
• History of a single or recurrent Manic or Mixed Episode(s)
+/- MDE(s)
= Bipolar I Disorder
• History of both MDE(s) + Hypomanic Episode(s)
= Bipolar II Disorder
• Schizophrenia + any mood episode
= Schizoaffective Disorder (MDD or Bipolar types)
Bipolar Illness (Mania)
• Have you ever had the opposite of depression when you have been extremely
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happy, over the top , doing things out of character for 2 weeks or more.? (mood)
If yes clarify again how long does it last for (DD borderline construct)
Had you/ have you taken on any new activities? (increased goal directed
activity)
What's your sleep been like. Do you feel like you can work all day without needing
rest/ do you feel like you don’t need much sleep ? (decreased need for sleep)
How do you see yourself in comparison to others./ do you consider yourself
special in any way? (grandiosity)
Do you think god has a special purpose for you here? (grandiosity/ delusions)
Do you find your thoughts racing? (increased psycho(motor) activity)
Have your friends commented on the way you talk/ too fast? (pressure of
speech)
Have you done any things that may be out of character for you like spending
excessive amounts of money, promiscuity ? (reckless behaviour)
Also ask for depressive symptoms to establish a mixed episode
Past History
• Previous admissions –diagnosis
• Trigger
• Medications- type, compliance and effectiveness
• Leading Q’s-Tegretol (Carbamazepine), Lithium, Valproate,
ECT , injections (Depots)
• Self harm
• Psychotherapy- type, compliance and effectiveness
Medical
• Have you had any significant medical illnesses such
as…………diabetes, high blood pressure, seizures/ a
significant head injury
• Diabetes, HT-vascular hypothesis
• Head injury and epilepsy ( composite neuropsychiatric
hypothesis)
• Investigations & treatment
ANY OTHER MEDICAL ISSUES
FOR MOOD DISORDERS
If there is: eg. my patient in the exam had an
anaphylactic reaction/ allergy (CL rotation)
Family History
• Is there anyone in your family that has a significant mental
health problem/issue / nervous breakdown such as
parents, uncles, cousins, grandparents….depression,
bipolar /manic depression, schizophrenia
• Has anyone in your family ever committed suicide?
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What about problems with drugs , or alcohol or
violence?
Family history
• Stronger family history in bipolar disorders and early onset
MDD
• For 1st degree relatives:
• Risk of BD with BD proband: 7x general population
• Risk of MDD with MDD proband:
2-3x general population
• Cross-over risk:
 risk of MDD (MDD>BD)
Minimally  risk of BD
• BP probands:
• UP probands:
• Twin concordance:
• BD:
• MDD:
MZ 40%
MZ 30%
DZ 10%
DZ 20%
• Overlap between bipolar disorder and schizophrenia
Genetic Counselling
• Yes, mood disorders are genetic.
• The risk to children and
grandchildren is the more difficult
question -The family data indicate
that if one parent has a mood
disorder, then a child will have a risk
for mood disorder of between 10
and 25 percent. If both parents are
affected, then this risk roughly
doubles.
• Greater risk :
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more members affected
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affected family members are
first-degree relatives
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A family history of bipolar
disorder (+specifically, a much
greater risk for bipolar disorder)
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presence of more severe illness
in the family
• Providing guidance in interpreting
and responding to that information.
• It is important to emphasize that
their child carries a risk or
predisposition to illness rather than
a certainty of illness. It is also useful
to emphasize the range of illness,
from mild to severe, that could
result and the availability and
efficacy of treatment.
• Ultimately, the use of such
information in family planning is a
highly personal decision.
Future Directions
• Though much is understood about the familiality and heritability of mood
disorders, the identification of specific genes has been challenging.
• Studies to date have reproducibly identified a number of genes, although
these genes together explain only a small portion of the genetic variance.
• It remains unclear how many genes are involved and how the illness is
transmitted.
CASE EXAMPLE:
XYZ is a 44 yr old Caucasian female, currently in a relationship with a 37 yr old man on Disability
support pension, lives with her 9 yr old son, also has a 5 year old daughter who doesn’t live with her.
She has been on unemployment benefits for the last 2 years. She is currently a voluntary in-patient on
the ward. She gives a 2 year history of depressive symptoms.
Background of 3 previous significant depressive episodes, post natal depression, significant self-harm
episode and treatment with ECT, several antidepressants, lithium and psychological treatments
And strong family history
Personal history
• Introduce this part clearly saying… I would now like to ask you some
questions about your childhood and your past to give me a better
understanding of the issue/ as the past often colors our present
• Where were you born? (migration hypothesis) Were there any
problems during your birth that you know of? (obstetric
complications)
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Were there any problems as a baby with illness or talking and
walking? (developmental delay-neurodevelopmental hypothesis)
Childhood memories
• How was discipline handled at home? Did that ever get
physical….such that you ended up with bruises or being hit? How did
that affect you? (attachment and unmet dependencies model)
• When you were a child, did anyone ever do something sexual that made you feel
uncomfortable ? (attachment and unmet dependencies model)
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Tell me about your relationship with mum and dad (harsh and critical –
psychodynamic and cognitive model)
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Was there ever any violence in the domestic household ?(male –identification
with aggressor , female-parallels in later life , self blame-cognitive model)
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How did you go at school? Did you have many friends? Were you bullied? Did
you wag/truant (peer group relationships-social and cognitive models)
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If suspicion of poor academics ask why. Difficulty concentrating? Did you often
get into trouble at school? Did you fight and break rules often? Ever damaged
property? Ever been cruel to animals ? (Conduct disorder)
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Did you find it difficult to sit down at one place for a long time (hyperactivity)
• Did you find it difficult organizing tasks at school, making
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careless mistakes? (inattention)
Did you find it difficult concentrating on subjects you did not
enjoy? What about the subjects you did enjoy? (inattention)
(DD depression)
Special education (developmental delay / learning
difficulties)
Relationships-how many significant relationships have you
had?
What sort of person are you in relationships? (hint towards
personality dysfunction)
When was the last time you worked? What was your longest
period of employment?
Forensic history
• Have you ever been in trouble with the police? yes•
Have you ever been charged or convicted? Ask for
charges
• Have you ever been in jail?-period
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If no-have you ever been violent towards others?
Personality
• Very important aspect often overlooked
• Main one is borderline personality disorder
• Do you often have mood swings/ do you find that your moods can shift from being happy to
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being sad in a matter of minutes or hours? (mood instability)
Are you generally a confident person or do you have difficulty knowing who……(use name)
is? (self identity disturbance)
Do you feel empty in yourself? (emptiness)
How often do you think about suicide? Why do you self harm/ how does it make you feel?
(chronic self harm ideation)
What sort of person are you in relationships? Are you particularly sensitive to rejection? Are
you often worried about being abandoned in relationships? Does that make you clingy?
(sensitive to rejection/fear of abandonment)
Are you the sort of person that would let other people know that he/she is angry or do you
bottle it up. Do you have difficulty controlling your anger? (impulse dyscontrol)
Would you call yourself an impulsive person?.... a person who does things on the spur of the
moment without thinking of the consequences (impulsivity)
Has that ever gotten you into trouble ? Like drugs, sex, reckless driving, spending and binge
eating etc (impulsivity displayed in at least two areas that are potentially damaging )
Transient stress related paranoid ideation and psychotic symptoms may occur
Relationship instability, job changes etc give a clue to the construct.
5 or more of the above are required
MENTAL STATE EXAMINATION
Marjorie
Insight
• Guides management
• What in your opinion is the issue/causing this distress?
• What do you think would help you?
• Do you think medication/talking therapy would help you?
• Ask about attitudes to medication?
• If I were to work with you what are the three most important
things you would like me to help you with currently?
Formulation
• Etiological
• Consequential
• Speculative
• Not mutually exclusive
• Most are a combination
• Biological
• Psychological
• Social
• Cultural
Biological
• Genetic predisposition
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Neurodevelopmental hypothesis (schizophrenia)
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Drugs and alcohol (schizophrenia)
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Head injury
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Epilepsy
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Other medical conditions
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Drugs causing psychiatric conditions
Models for Substance Use
• Self medication hypothesis (Khantzian, 1985, 1997)
• Reduction of negative symptoms, affective symptoms or
anxiety and depression. Reduction of side effects of
antipsychotics
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Affect regulation model (Blanchard, 2000)
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Motivational models of substance use (Cox and Kluges)
Coping motives , social motives and enhancement motives
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Simons (2000) showed that enhancement , coping and
conformity motives were common for drug and alcohol use
which inturn influenced affect regulation
• ?DISEASE MODEL
Psychological
• Attachment Model
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Cognitive models
Psychosocial development (Erikson’s)
Coping skills
Social Skills
Psychodynamic models
Attachment model
• Most applicable for personality disorders
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Interacts with the cognitive model
A good quality affect regulatory system, based on
secure attachment leads to optimal right hemisphere
maturation at a critical period during the 1st2-3 years of
life . Any experience (childhood sexual abuse, physical
trauma, losses) that disturbs this attachment will lead to
impaired development of neural pathways that subserve
emotional behaviours leading to impaired emotional
regulation that may persist throughout life affecting
interpersonal relationships.
Psychodynamic Aspects of Mood
Disorders
• Response to Loss/Anger Turned Inward: (Karl Abraham, Freud, and Sandor Rado)
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Depressed patients' reactions to object loss, in reality or in fantasy. Current loss invokes an
earlier, childhood loss, also either of a fantasy or a reality nature. Object attachments
characterized by excessive dependency, laced with an emphasis on need gratification in
emotionally charged relationships.
Guilt: Melanie Klein postulated that depressed patients fear that they cannot protect an
idealized, or good, internalized “other” from destructive, rageful impulses. As a result, the
depressed patient's characteristic guilt, inhibitions, and punitive superego develop.
Impairment in Self-Esteem Regulation: Edward Bibring viewed depression instead as
resulting from a sense of helplessness, impaired self-esteem, and self-directed anger
triggered by failures to live up to the narcissistic aspirations of any developmental phase.
Inadequacy of Early Caregivers: Hans Kohut described depression as connected to
experiences of profound emptiness in patients whose parents were unable to empathize with
their early affective experiences. Such is the case, as many parents of depressed patients
are themselves depressed. These patients crave compensatory relationships (“selfobject”
relationships, mirroring experiences, and idealizing relationships), leaving them vulnerable to
disappointment, as real relationships cannot live up to these compensatory fantasies.
Asch noted underlying masochistic pathology in dysthymic patients, a view that has been deemphasized by contemporary dysthymia researchers. Milton Horowitz emphasizes the
“pleasure of revenge” in the patient's defeating of all around him or her through failure,
hopelessness, and negativity. David Milrod describes both the rewarding and the punitive
aspects of superego function in response to narcissistic injury in patients with chronic
dysthymia and self-pity.
Synthesis: Dynamics of Depression
• FEELINGS OF EXQUISITE NARCISSISTIC VULNERABILITY (from early loss or
experiences with parents perceived as traumatically unempathic, frustrating, or rejecting.
A sense of helplessness or inadequacy with accompanying fantasies of damage or
castration; resulting impairment in self-esteem regulation prone to a self-image of being
unlovable, damaged, or inadequate.)
• FAILED TO LIVE UP TO THEIR AMBITIONS OR TO THEIR MORAL VALUES IN THE
EGO IDEAL, the intrapsychic mechanism that triggers guilt (the resulting aggression
toward a frustrating parent, or toward the self as damaged, contributes decisively to the
propensity toward depression. Aggression is largely self-directed. Guilt (conscious or
unconscious) or shame result from the patient's perceived sense of failure, with a
diminished sense of self. Difficulties in self-esteem regulation contribute to a selfrepresentation of being “bad”)
• AGGRESSION DIRECTED TOWARD THE SELF-REPRESENTATION, which proves
uncontainable and spreads to a mood state.
• By not living up to personal aspirations (giving rise to shame, rather than guilt);
• By not living up to the ego ideal (precipitating guilt);
• In an interpersonal depression, as described by Freud, in which a symbiotic bond to an
ambivalent object tie is shattered.
Psychoanalytic Formulations of Mania
• GLOBAL, MASSIVE REGRESSION THAT AFFECTS ALL THREE PSYCHIC
STRUCTURES: The id, the ego, and the superego. The regression leads to a
primitive mental state in which the pleasure principle is reinstated. In Group
Psychology and Analysis of the Ego, Freud described mania as a fusion of the
ego with its superego. Less cryptically, psychoanalysts have highlighted a
common organizing fantasy in manic patients of a fantasy incorporation, or
mystical union, of the patient with someone of great power, often an aristocrat, or
God, as in the story of St. Theresa's mystical union with God.
• Such organizing fantasies, couched in both sexual and “oral” terms, magically
impart a sense of omnipotence and specialness to the patient, highlighting one
aspect to the common phenomenology of mania.
• Defense mechanism of DENIAL, in which sad and negative aspects of reality are
entirely ignored. Mania could be considered a defensive reaction to depression.
Psychological theories: Psychodynamic
• Psychoanalytic
• Mood is an ego state that colours all ego functions
• Mood disorder involves denial (defence) of the opposite affect
• Examples
• Depression as response to loss; guilt; aggression turned inwards;
empathic failure of carer in early life; narcissistic injury
• Mania from denial, manic defence, mystical union with a greater other
• Attachment theory
• Insecure attachments predispose to subsequent psychopathology
Psychological theories: Cognitive
• Cognitive
• Triad of Affect, Behaviour, Cognition
• Negative cognitive schemata  negative automatic thoughts
(cognitive distortions)  depressed mood and behaviours
• Cognitive triad of negativity towards
self, environment &
future
• Foundation of CBT
Aaron Beck
Cognitive Theory of Depression
CONCEPTS
• A branch of behavioral psychology.
• Aaron Beck
• The cognitive model is based on the
recognition that an individual's
idiosyncratic perception of events
affects his or her emotions and
behaviors.
• Beck's initial observations about
major depression that depressed
patients tend to have
characteristically skewed and
negative thoughts about (1)
themselves, (2) their environment,
and (3) the future, a cluster he
termed the cognitive triad.
COGNITIVE ERRORS
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“all or nothing,” dichotomous
thinking: If things aren't entirely
one way, then they must be the
opposite.
arbitrary (negative) inferences
about events,
selectively abstract negative
details out of context,
overgeneralize (concluding
negative rules from single
instances),
magnify (the negative) and
minimize (the positive), and
take personally events that may
not be directly about them.
Cognitive Model: Bipolar Illness
• Based on Diathesis stress model
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Thus in combination with cognitive model for depression
patients with bipolar disorder also have an inherent
underlying biological vulnerability for instability of
circadian rhythms and motivational system controlling
reward and approach
• Thus with underlying striving for affection or
achievement, setting unrelenting standards of success
based on cognitive assumptions they predispose
themselves to disturbance in circadian rhythms which can
trigger a manic episode
Erikson’s Psychosocial Development
• Useful in certain cases
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Useful in old age and young adulthood particularly
• Young adulthood(intimacy vs. isolation)
• Old Age (ego-integrity vs. despair)
• E.g. increasing dependency in old age brings the
capacity for trust (trust vs. mistrust) to the fore. Thus, if
they did not develop trust early may present with
psychiatric distress which can be understood as a fear of
dependency (Martindale 1998)
Cognitive Theory of Depression
Interpersonal Theory of Depression
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Interpersonal theory dates back to the era after World War II, when it arose as a heretical response to the more intrapsychic emphasis of
psychoanalysis. Psychoanalytic theory emphasized the importance of early life experience, and many therapists at that time saw the
patient's psychic structure as essentially formed by the end of adolescence. Psychiatrists such as Adolf Meyer, Harry Stack Sullivan, Erich
Fromm, and Frieda Fromm-Reichmann challenged then current theory by emphasizing the influence of the real impact of current life events
on their patients' psychopathology, focusing on environmental and interpersonal encounters rather than underlying intrapsychic drives and
structures.
Sullivan coined the term “interpersonal” as a rubric for considering current life experience. He scrutinized communications in the social field,
a more “external” outlook than traditional psychoanalysis. The interpersonal theorists worked mainly with inpatients diagnosed with
schizophrenia in a prepharmacological era. Although their work stirred great controversy at the time and a Sullivanian school distinct from
the psychoanalysis of drives and ego psychology still exists, Sullivan was trained in psychoanalysis and did not entirely disagree with his
forebears. Over time, the rift between Sullivanians and other psychoanalysts has narrowed.
The consideration of current interpersonal factors gained currency over succeeding decades, and it is now mainstream clinical thinking that
current life events and interpersonal functioning affect and are affected by psychopathology. A school of interpersonal psychoanalysis—not
particularly focused on mood disorders—arose. Psychoanalytically trained therapists like Silvano Arieti and Jules Bemporad emphasized
interpersonal factors in the treatment of depressed patients. Jack Anchin and Donald Kiesler have reviewed other interpersonally based
psychotherapies. None of these theories has received empirical testing.
Researchers did develop a host of related data about interpersonal issues associated with depression. For example, research showed that
interpersonal support protects an individual against depression: Having a confidant to talk to reduces the risk of developing a depressive
episode. Major life stressors, including the death of a significant other, struggles in important relationships, and upheavals such as a change
in marital status, housing, job status, or physical health have been shown to increase the risk of depressive episodes in vulnerable
individuals. Moreover, the onset of depressive episodes leads to deterioration in relationships and social functioning.
John Bowlby postulated that people have an evolutionarily determined, instinctual drive to form emotional attachments. Animal evidence now
supports this theory. This basic component of human nature ensures infant survival: Children need to have parents nearby or available for
feeding and protection. As children develop, they begin to explore their environment, gradually moving out from the “secure base” of their
attachment figure. Disruptions in this early caregiving connection may lead to vulnerability of attachment style. For example, loss of one's
mother in the first decade of life has been shown to be a risk factor for subsequent depression. Children with insecure childhood attachments
may not learn to ask for help from others. When such vulnerable individuals face stressors or feel an absence or inadequacy of interpersonal
support during times of stress, they may be helpless to respond effectively and prone to developing symptoms. Furthermore, individuals with
insecure attachment styles may have difficulty in developing comfortable relationships on which they can rely for support in times of need.
In the 1970s, when Gerald L. Klerman, Myrna M. Weissman, and their colleagues were conducting a randomized controlled trial of
outpatients with major depressive episodes, they recognized that many such patients received psychotherapy in community treatment. They
sought accordingly to add a psychotherapy to their trial but realized that it was unclear then (as now) of what such community psychotherapy
consisted. They then developed IPT as a manualized, time-limited treatment for outpatients with major depressive disorder based on
interpersonal and attachment theories as well as empirical evidence of the psychosocial nature of depression. IPT is thus one specific
therapeutic application of more general interpersonal theory. IPT demonstrated efficacy for major depression in this and in subsequent
outcome trials.
•
In simplest terms, interpersonal theory as applied to IPT can be understood as a link between mood and
events. For all people, upsetting external events evoke a sad or demoralized mood: In lay terms, they are
“depressing.” For biologically or environmentally predisposed individuals, however, a sufficiently disturbing
life event can trigger an episode of major depression. Examples of such life events are the death of a
significant other (complicated bereavement), a problematic relationship (role dispute), or other major life
change (role transition). Once a depressive episode starts, its symptoms compromise functioning,
producing more negative life events in a vicious downward cycle. This formulation seems straightforward,
even commonsensical, but depressed patients have a peculiar amnesia for external events and tend to
blame themselves for how they feel or to see the depressed state as who they are. It can be helpful
clinically to remind them that they are ill, not defective, and that outside events may have contributed to
their distress.
• IPT therapists do not propose this as an etiological theory of depression, but as a pragmatic one: The
depressive mood episode can be linked either to a precipitating life event or to consequent life events that
become the focus for treatment. The IPT therapist defines major depression as a medical illness—a
treatable medical problem that is not the patient's fault—and links it to an interpersonal focus such as a role
dispute. The therapeutic contract for the patient is to solve the interpersonal focus within a time-limited
period. Solving the interpersonal problem is at once a realistic relief (e.g., improving a marriage), relieves
depressive symptoms, and builds interpersonal skills that may hopefully protect against future interpersonal
triggers and depressive episodes. Typical areas of interpersonal skill building are issues such as selfassertion, confrontation, effective expression of anger, and the taking of social risks.
• Clinicians armed with differing theories approach the same material in different ways. IPT seeks a life event
or interpersonal situation as a plausible and pragmatic fiction on which to focus a time-limited treatment in
which the patient can work on interpersonal skills. For example, the case of Ms. A might be conceptualized
as major depression arising in the context of a role dispute with her boyfriend, B. Had she been treated in
IPT, the focus might have been on recognition and appropriate expression of her own anger as part of
learning to renegotiate that relationship. Alternatively, or additionally, clinical judgment might have defined
the break up of that relationship as a role transition that Ms. A needed to mourn and accept in order to
move on to better relationships or activities. Ms. C's difficulty in tolerating her acceptance to graduate
school might similarly be considered a role transition, as might Mr. D's bout of renal stones. Medical
illnesses, even if transient, frequently provoke role transitions by shifting a patient's perception of his life
trajectory; Mr. D may have interpreted his hospitalization as evidence of his fading potency, aging, and
mortality. Ms. E's situation might conceivably be defined either as a role transition—adjusting to college life
away from her mother—or as a role dispute with her mother.
• Preliminary evidence supports the theory underlying IPT as a treatment. Patients in two IPT treatment trials
were asked to report the degree to which they had resolved the interpersonal crisis (e.g., role transition) on
which their treatment had focused. Subjects' report of making changes in this interpersonal focal area
correlated with symptomatic improvement during the trial.
Causes of poor mental health in
Aboriginal people
• Intergenerational transmission of trauma through
psychodynamic, sociocultural and genetic mechanisms
(Kellerman ,2001)
•
Grief, loss and trauma resulting from high mortality rates, loss
of land and culture and continuing impact of political policies
that result in sociocultural dislocation
•
Unresolved identity issues has been identified as source of
stressor when people had not dealt with or felt they had lost or
were uncertain about their aboriginal identity. (Swan P and
Raphael B, 1995)
•
Poor access to mental health services underpinned by
cultural disparities
DIFFERENTIAL DIAGNOSIS
Other disorders with mood features
• Adjustment Disorders
• An Adjustment Disorder is a psychological response to an identifiable
stressor that results in clinically significant symptoms.
• DSM-IV-TR criteria:
• Clinically significant emotional or behavioural symptoms in response to an
identifiable stressor(s), occurring within 3 months of its (their) onset & not
persisting beyond 6 months upon its (their) termination.
• Clinical significance is defined as either marked distress in excess of what
one would generally expect relative to the stressor(s), or significant
impairment in social or occupational functioning.
• Symptoms do not represent bereavement or meet the criteria for another
Axis I disorder.
• Mood Disorders due to Substances
• Mood Disorders due to a General Medical Condition
Depression vs. Grief
• Grief
• Response to loss, threatened or actual
• Kübler-Ross’ stages of anticipatory grief (1969)
• Denial, Anger, Bargaining, Depression, Acceptance
 Not chronological or “stage-wise” progression
 Not necessarily experience these
• Wide variations from person to person
• Influenced by many factors:
•
•
•
•
•
•
Personality, coping style, resilience
Past experience of losses & traumas
Nature & quality of relationship with lost object
Available supports
Culture
Spiritual beliefs
• Duration varies, can be ongoing
Depression vs. Grief
Grief
Depression
Symptoms occur in waves
Low mood is persistent
Reactivity preserved
Symptoms are pervasive
Yearning/longing a prominent
part of the affect
Apathy among range of
affects
Preserved hedonic capacity
Anhedonic
Preserved self-esteem
Worthlessness
Able to look forward to the
future
Hopelessness
MANAGEMENT OF MENTAL DISORDERS
4 Main Domains
•
Risk
• Clarification of Diagnosis
• Treatment of Psychiatric symptoms
• Long term Treatment : Relapse prevention , Social and
Vocational rehabilitation
Risk
• Physical risk-diabetes, medical complications in Anorexia
•
•
•
•
•
•
•
•
•
nervosa, other medical conditions
Suicide Risk/risk of self harm
Homicide Risk/harm to others-relevant in forensic case or
previous homicide .Remember HCR-20
Risk to reputation-Mania
Risk to finances-Mania
Risk of exploitation-Mania, Borderline personality structure
Risk of driving-Alcohol, dementia
Risk to children –in all case involving children this should be a
consideration
Corporate risk-employment that would put organisation and
public at risk
Mention management of safety e.g. MHA , Nursing
observations
HCR-20
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Historical factors:
•Previous violence
Young age at first violent incident
•Major mental illness
Psychopathy
•Early maladjustment
Personality disorder
•Earlier supervision failure
Employment problems
Clinical items:
•Lack of insight
Negative attitudes
•Active symptoms of mental illness
Impulsivity
•Unresponsive to treatment
Risk management items:
•Plans lack feasibility
•Exposure to destabilisers
•Lack of personal support
•Non compliance with remediation attempts
•Stress
CLARIFICATION
Example
Prognosis
Legal issues
• Testamentary capacity
•
•
•
•
•
•
•
Power of attorney
CTO
Protective estates order
Capacity to make decisions for medical issues
Reports for forensic patients
Driving
Legal IssuesCTF Course
Social/ Vocational Rehabilitation
• Accommodation –high level, low level supported
accommodation
• Supported employment/pre vocational training
• Education –TAFE
• Finances –carers allowance , benefits
•
Groups , day services/hospitals
Enhancing compliance
• Early relapse signature
•
•
•
•
•
•
•
•
•
•
•
Therapeutic alliance
Eliciting patient’s concerns
Uncovering non-adherence
Eliciting negative cognitions
Practical solutions: dosette box , beeping watches, mobiles,
notes on bathroom mirrors or refrigerators
Socratic questioning
Motivational enhancement therapy
Correction of misinformation
Framing medication trial as an experiment
Giving credit
Using legal framework
Treatment resistant depression
• Greater than or equal to 2 adequate monotherapy trials with
antidepressants of 2 different classes fail to elicit a therapeutic
response (APA DSM 2003)
• •Prevalence :10-30% (Joffe ,1996)
•
•
•
•
•
•
•
•
Diagnosis
•Non-Compliance
•Inadequate duration, dose
•Psychosocialfactors
•Medical condition –e.g. Hypothyroidism
•Drugs-B-Blockers, Methyldopa
DEPRESSION
Depression- Epidemiology
• Life time prevalence –20%
• •Co-morbidity is the rule
• •National Co morbidity survey and EpidemiologicalCatchment Area survey (ECA) -74% &
75% respectively with other lifetime diagnoses
• •Substance misuse , anxiety disorders and personality disorders commonest
• •Risk –ECA study-Lifetime risk of suicide 7.9% , 19.5% with concurrent alcohol and drug
misuse
• •Risk of suicide 21times that of normal population
• (Harris & Barraclough 1998)
• •Previous depressive episode increases risk of further depressive episodes through kindling
phenomenon (Post 1992)
• •Lower threshold of stress required to induce depression , ultimately episodes may occur
spontaneously (Post 1992)
• •Harris & Brown vulnerability factors
•
•
•
•
Loss of mother before age of 14
3 or more children under age of 11
Lack of confidant
Unemployed
Summary of STAR*D guidelines
• Number of patients that participated in medication trials
•
•
•
•
•
was 4 times that of Psychotherapy
•In primary switchany option is reasonable and no
statistical difference between different classes
•Cognitive therapy did as well as medication switching
and augmentation
•Overall 70% remission after 4 levels
•Not applicable for Psychotic depression
Psychotic Depression
• First line –TCA +antipsychotic
• ECT is effective treatment
• 2 metaanalyses (Spiker,1985 & Parker,1992): 80%
response rate to ECT
• 80% response rate to combination antidepressant and
antipsychotic
• 33% to antipsychotic alone
• 25% to antidepressant alone
ECT
• Uncertainty
• •Unilateral placement associated with less severe cognitive deficits
• •Case by case basis
• •Standard practice: D’Eliaposition(Non-Dominantunilateral ECT)
• •If no response after 4-6 sessions consider Bilateral
• •Stimulus dosing –titration method /fixed dose
• •RUL-2.5-3 times seizure threshold
• •BL-1.5 times seizure threshold
• •Other types: Bifrontal , Right frontotemporal and left frontalEEG
characteristics for response : short recruitment phase , high amplitude
slow waves, morphological regularity, bilateral synchronicity , post
seizure suppressionInadequate seizures –<20-30sec EEG evidence
•
ECT & medications
• Antidepressants –some evidenceof augmentationTCA’s –
seizuresSSRI’s-Prolonged seizures
• •Benzodiazepines-increase seizure threshold. Stop before
treatment
• •Mood Stabilisers-Consult neurologist if epileptic
• May need reduction of dose before treatment
• Stop 24-48hrs before ECT
• •Lithium –increases risk of post ECT delirium
• For certain patients on lithium careful risk-benefit analysis as
ECT induced mania is more significant than delirium.
ECT - 2
• Procedure
• General anaesthetic (pre-anaesthetic work up required)
• Frequency usually 3 times per week at the start, can be reduced as
clinically indicated
• Maintenance ECT can be an option
ECT - 3
• First session: “Titration” (determine seizure threshold)
• Paralysed (minimal motor activity)
• Adequacy of seizure as determined by EEG tracing
• Minimum duration: 20 seconds
• Response judged on clinical basis
• Total number of treatments depend on response & tolerability
ECT - 4
• Contraindication
• Raised intracranial pressure
• Relative contraindications:
•
•
•
•
Recent CVA
Cerebral aneurysm or vascular malformations
Unstable cardiovascular condition
High anaesthetic risk
• Risks & adverse effects
• General anaesthetic
• Post-ictal confusion
• Memory loss (anterograde & retrograde)
• Headache, aches and pains
• Chipped tooth, skin burns
ECT - 5
• Consent
• Informed consent from patient
or
• Guardianship Board consent
*Note: Detention is inadequate to give involuntary ECT
Novel treatments
• •Augmentation:Lithium (bauer,2000)T3 (Aronson,1996)Atypical
antipsychotics: Risperidone, Olanzapine, Ziprasidone,Quetiapine,
AripiprazoleAripiprazole was approved by the FDA as the first
augmenting therapy for treatment-resistant MDD in adults
• •Buspirone(5HT1A agonist)
• •Bupropion
•
•
•
•
•
•
•
•
•
Less evidence:
•Amantadine, riluzole,pramiprexole: not studied in RCT’s
•Modafinil
•Methyl folate-15-30mg/d
•SAMe: S-Adenosyl-L-Methionine:800-1600mg/d
•Lamotrigine :100-300 mg/d
•Gabapentin& Topiramate
•Omega-3 :1g/d not 2-3 mg/d
• •rTMS: Magnetic field produced over surface of head
depolarizes underlying superficial neuronsEffect size
:0.67(rTMS vs. Sham) –Pre FrontalResponse rates-2545%
• •Deep Brain Stimulation:Invasive procedureFDA approved
for treatment of Parkinsonism6 patients of refractory
depression –remission in 4/6Area stimulated is Subgenualanterior cingulate
• •Magnetic seizure therapy (Loo,2007)
• •FEAST –Focal electrically administered seizure therapy
(Loo,2007)
•
BIPOLAR DISORDER
Epidemiology
• 65% co morbidity
• High SMR´s: 15–20 times more likely to die by suicide
• High rates of cardiovascular disease
Signs of Bipolarity in Depressed patients
• WHIPLASHED
• W –Worse or wired when taking antidepressants
• H –Hypomania, hyperthymic temperament ,and mood swings
•
•
•
•
•
•
•
•
in history
I –Irritable hostile or mixed features
P –Psychomotor retardation
L –Loaded Family history : bipolar illness, affectivity and mood
swings
A –Abrupt onset and/ or termination of depressive episodes
less than 3 months
S –Seasonal or postpartum depression
H –Hyperphagia and Hypersomnia
E –Early age of onset
D –Delusions, Hallucinations and Psychotic features
Texas Implementation of Medication Algorithm -Bipolar
I Disorder (Suppes, 2005 )
TIMA guidelines –Maintenance
Treatment: Hypomania/Mania
TIMA Guidelines –Maintenance Treatment +
Most Recent Episode Depression
Prognosis
Models for Substance Use
• Self medication hypothesis (Khantzian, 1985, 1997)
• Reduction of negative symptoms, affective symptoms or
anxiety and depression. Reduction of side effects of
antipsychotics
•
Affect regulation model (Blanchard, 2000)
•
•
Motivational models of substance use (Cox and Kluges)
Coping motives , social motives and enhancement motives
•
Simons (2000) showed that enhancement , coping and
conformity motives were common for drug and alcohol use
which inturn influenced affect regulation
• ?DISEASE MODEL
Psychological
• Attachment Model
•
•
•
•
•
Cognitive models
Psychosocial development (Erikson’s)
Coping skills
Social Skills
Psychodynamic models
Attachment model
• Most applicable for personality disorders
•
•
Interacts with the cognitive model
A good quality affect regulatory system, based on
secure attachment leads to optimal right hemisphere
maturation at a critical period during the 1st2-3 years of
life . Any experience (childhood sexual abuse, physical
trauma, losses) that disturbs this attachment will lead to
impaired development of neural pathways that subserve
emotional behaviours leading to impaired emotional
regulation that may persist throughout life affecting
interpersonal relationships.
Psychodynamic Aspects of Mood
Disorders
• Response to Loss/Anger Turned Inward: (Karl Abraham, Freud, and Sandor Rado)
•
•
•
•
Depressed patients' reactions to object loss, in reality or in fantasy. Current loss invokes an
earlier, childhood loss, also either of a fantasy or a reality nature. Object attachments
characterized by excessive dependency, laced with an emphasis on need gratification in
emotionally charged relationships.
Guilt: Melanie Klein postulated that depressed patients fear that they cannot protect an
idealized, or good, internalized “other” from destructive, rageful impulses. As a result, the
depressed patient's characteristic guilt, inhibitions, and punitive superego develop.
Impairment in Self-Esteem Regulation: Edward Bibring viewed depression instead as
resulting from a sense of helplessness, impaired self-esteem, and self-directed anger
triggered by failures to live up to the narcissistic aspirations of any developmental phase.
Inadequacy of Early Caregivers: Hans Kohut described depression as connected to
experiences of profound emptiness in patients whose parents were unable to empathize with
their early affective experiences. Such is the case, as many parents of depressed patients
are themselves depressed. These patients crave compensatory relationships (“selfobject”
relationships, mirroring experiences, and idealizing relationships), leaving them vulnerable to
disappointment, as real relationships cannot live up to these compensatory fantasies.
Asch noted underlying masochistic pathology in dysthymic patients, a view that has been deemphasized by contemporary dysthymia researchers. Milton Horowitz emphasizes the
“pleasure of revenge” in the patient's defeating of all around him or her through failure,
hopelessness, and negativity. David Milrod describes both the rewarding and the punitive
aspects of superego function in response to narcissistic injury in patients with chronic
dysthymia and self-pity.
Synthesis: Dynamics of Depression
• FEELINGS OF EXQUISITE NARCISSISTIC
VULNERABILITY (from early loss or experiences with parents
•
•
•
•
•
perceived as traumatically unempathic, frustrating, or rejecting. A sense of
helplessness or inadequacy with accompanying fantasies of damage or
castration; resulting impairment in self-esteem regulation prone to a selfimage of being unlovable, damaged, or inadequate.)
FAILED TO LIVE UP TO THEIR AMBITIONS OR TO THEIR MORAL
VALUES IN THE EGO IDEAL, the intrapsychic mechanism that triggers
guilt (the resulting aggression toward a frustrating parent, or toward the
self as damaged, contributes decisively to the propensity toward
depression. Aggression is largely self-directed. Guilt (conscious or
unconscious) or shame result from the patient's perceived sense of failure,
with a diminished sense of self. Difficulties in self-esteem regulation
contribute to a self-representation of being “bad”)
AGGRESSION DIRECTED TOWARD THE SELF-REPRESENTATION,
which proves uncontainable and spreads to a mood state.
By not living up to personal aspirations (giving rise to shame, rather than
guilt);
By not living up to the ego ideal (precipitating guilt);
In an interpersonal depression, as described by Freud, in which a
symbiotic bond to an ambivalent object tie is shattered.
Psychoanalytic Formulations of Mania
• GLOBAL, MASSIVE REGRESSION THAT AFFECTS ALL THREE PSYCHIC
STRUCTURES: The id, the ego, and the superego. The regression leads to a
primitive mental state in which the pleasure principle is reinstated. In Group
Psychology and Analysis of the Ego, Freud described mania as a fusion of the
ego with its superego. Less cryptically, psychoanalysts have highlighted a
common organizing fantasy in manic patients of a fantasy incorporation, or
mystical union, of the patient with someone of great power, often an aristocrat, or
God, as in the story of St. Theresa's mystical union with God.
• Such organizing fantasies, couched in both sexual and “oral” terms, magically
impart a sense of omnipotence and specialness to the patient, highlighting one
aspect to the common phenomenology of mania.
• Defense mechanism of DENIAL, in which sad and negative aspects of reality are
entirely ignored. Mania could be considered a defensive reaction to depression.
Psychological theories: Psychodynamic
• Psychoanalytic
• Mood is an ego state that colours all ego functions
• Mood disorder involves denial (defence) of the opposite affect
• Examples
• Depression as response to loss; guilt; aggression turned inwards;
empathic failure of carer in early life; narcissistic injury
• Mania from denial, manic defence, mystical union with a greater other
• Attachment theory
• Insecure attachments predispose to subsequent psychopathology
Psychological theories: Cognitive
• Cognitive
• Triad of Affect, Behaviour, Cognition
• Negative cognitive schemata  negative automatic thoughts
(cognitive distortions)  depressed mood and behaviours
• Cognitive triad of negativity towards
self, environment &
future
• Foundation of CBT
Aaron Beck
Cognitive Theory of Depression
CONCEPTS
• A branch of behavioral psychology.
• Aaron Beck
• The cognitive model is based on the
recognition that an individual's
idiosyncratic perception of events
affects his or her emotions and
behaviors.
• Beck's initial observations about
major depression that depressed
patients tend to have
characteristically skewed and
negative thoughts about (1)
themselves, (2) their environment,
and (3) the future, a cluster he
termed the cognitive triad.
COGNITIVE ERRORS
1.
2.
3.
4.
5.
6.
“all or nothing,” dichotomous
thinking: If things aren't entirely
one way, then they must be the
opposite.
arbitrary (negative) inferences
about events,
selectively abstract negative
details out of context,
overgeneralize (concluding
negative rules from single
instances),
magnify (the negative) and
minimize (the positive), and
take personally events that may
not be directly about them.
Cognitive Theory of Depression
Erikson’s Psychosocial Development
• Useful in certain cases
•
Useful in old age and young adulthood particularly
• Young adulthood(intimacy vs. isolation)
• Old Age (ego-integrity vs. despair)
• E.g. increasing dependency in old age brings the
capacity for trust (trust vs. mistrust) to the fore. Thus, if
they did not develop trust early may present with
psychiatric distress which can be understood as a fear of
dependency (Martindale 1998)
Interpersonal Theory of Depression
•
•
•
•
•
•
Interpersonal theory dates back to the era after World War II, when it arose as a heretical response to the more intrapsychic emphasis of
psychoanalysis. Psychoanalytic theory emphasized the importance of early life experience, and many therapists at that time saw the
patient's psychic structure as essentially formed by the end of adolescence. Psychiatrists such as Adolf Meyer, Harry Stack Sullivan, Erich
Fromm, and Frieda Fromm-Reichmann challenged then current theory by emphasizing the influence of the real impact of current life events
on their patients' psychopathology, focusing on environmental and interpersonal encounters rather than underlying intrapsychic drives and
structures.
Sullivan coined the term “interpersonal” as a rubric for considering current life experience. He scrutinized communications in the social field,
a more “external” outlook than traditional psychoanalysis. The interpersonal theorists worked mainly with inpatients diagnosed with
schizophrenia in a prepharmacological era. Although their work stirred great controversy at the time and a Sullivanian school distinct from
the psychoanalysis of drives and ego psychology still exists, Sullivan was trained in psychoanalysis and did not entirely disagree with his
forebears. Over time, the rift between Sullivanians and other psychoanalysts has narrowed.
The consideration of current interpersonal factors gained currency over succeeding decades, and it is now mainstream clinical thinking that
current life events and interpersonal functioning affect and are affected by psychopathology. A school of interpersonal psychoanalysis—not
particularly focused on mood disorders—arose. Psychoanalytically trained therapists like Silvano Arieti and Jules Bemporad emphasized
interpersonal factors in the treatment of depressed patients. Jack Anchin and Donald Kiesler have reviewed other interpersonally based
psychotherapies. None of these theories has received empirical testing.
Researchers did develop a host of related data about interpersonal issues associated with depression. For example, research showed that
interpersonal support protects an individual against depression: Having a confidant to talk to reduces the risk of developing a depressive
episode. Major life stressors, including the death of a significant other, struggles in important relationships, and upheavals such as a change
in marital status, housing, job status, or physical health have been shown to increase the risk of depressive episodes in vulnerable
individuals. Moreover, the onset of depressive episodes leads to deterioration in relationships and social functioning.
John Bowlby postulated that people have an evolutionarily determined, instinctual drive to form emotional attachments. Animal evidence now
supports this theory. This basic component of human nature ensures infant survival: Children need to have parents nearby or available for
feeding and protection. As children develop, they begin to explore their environment, gradually moving out from the “secure base” of their
attachment figure. Disruptions in this early caregiving connection may lead to vulnerability of attachment style. For example, loss of one's
mother in the first decade of life has been shown to be a risk factor for subsequent depression. Children with insecure childhood attachments
may not learn to ask for help from others. When such vulnerable individuals face stressors or feel an absence or inadequacy of interpersonal
support during times of stress, they may be helpless to respond effectively and prone to developing symptoms. Furthermore, individuals with
insecure attachment styles may have difficulty in developing comfortable relationships on which they can rely for support in times of need.
In the 1970s, when Gerald L. Klerman, Myrna M. Weissman, and their colleagues were conducting a randomized controlled trial of
outpatients with major depressive episodes, they recognized that many such patients received psychotherapy in community treatment. They
sought accordingly to add a psychotherapy to their trial but realized that it was unclear then (as now) of what such community psychotherapy
consisted. They then developed IPT as a manualized, time-limited treatment for outpatients with major depressive disorder based on
interpersonal and attachment theories as well as empirical evidence of the psychosocial nature of depression. IPT is thus one specific
therapeutic application of more general interpersonal theory. IPT demonstrated efficacy for major depression in this and in subsequent
outcome trials.
•
In simplest terms, interpersonal theory as applied to IPT can be understood as a link between mood and
events. For all people, upsetting external events evoke a sad or demoralized mood: In lay terms, they are
“depressing.” For biologically or environmentally predisposed individuals, however, a sufficiently disturbing
life event can trigger an episode of major depression. Examples of such life events are the death of a
significant other (complicated bereavement), a problematic relationship (role dispute), or other major life
change (role transition). Once a depressive episode starts, its symptoms compromise functioning,
producing more negative life events in a vicious downward cycle. This formulation seems straightforward,
even commonsensical, but depressed patients have a peculiar amnesia for external events and tend to
blame themselves for how they feel or to see the depressed state as who they are. It can be helpful
clinically to remind them that they are ill, not defective, and that outside events may have contributed to
their distress.
• IPT therapists do not propose this as an etiological theory of depression, but as a pragmatic one: The
depressive mood episode can be linked either to a precipitating life event or to consequent life events that
become the focus for treatment. The IPT therapist defines major depression as a medical illness—a
treatable medical problem that is not the patient's fault—and links it to an interpersonal focus such as a role
dispute. The therapeutic contract for the patient is to solve the interpersonal focus within a time-limited
period. Solving the interpersonal problem is at once a realistic relief (e.g., improving a marriage), relieves
depressive symptoms, and builds interpersonal skills that may hopefully protect against future interpersonal
triggers and depressive episodes. Typical areas of interpersonal skill building are issues such as selfassertion, confrontation, effective expression of anger, and the taking of social risks.
• Clinicians armed with differing theories approach the same material in different ways. IPT seeks a life event
or interpersonal situation as a plausible and pragmatic fiction on which to focus a time-limited treatment in
which the patient can work on interpersonal skills. For example, the case of Ms. A might be conceptualized
as major depression arising in the context of a role dispute with her boyfriend, B. Had she been treated in
IPT, the focus might have been on recognition and appropriate expression of her own anger as part of
learning to renegotiate that relationship. Alternatively, or additionally, clinical judgment might have defined
the break up of that relationship as a role transition that Ms. A needed to mourn and accept in order to
move on to better relationships or activities. Ms. C's difficulty in tolerating her acceptance to graduate
school might similarly be considered a role transition, as might Mr. D's bout of renal stones. Medical
illnesses, even if transient, frequently provoke role transitions by shifting a patient's perception of his life
trajectory; Mr. D may have interpreted his hospitalization as evidence of his fading potency, aging, and
mortality. Ms. E's situation might conceivably be defined either as a role transition—adjusting to college life
away from her mother—or as a role dispute with her mother.
• Preliminary evidence supports the theory underlying IPT as a treatment. Patients in two IPT treatment trials
were asked to report the degree to which they had resolved the interpersonal crisis (e.g., role transition) on
which their treatment had focused. Subjects' report of making changes in this interpersonal focal area
correlated with symptomatic improvement during the trial.
4 Main Domains
• Risk
• Clarification of Diagnosis
• Treatment of Psychiatric symptoms
• Long term Treatment : Relapse prevention , Social and
Vocational rehabilitation
RISKS
Risk
• Physical risk-diabetes, medical complications in Anorexia
•
•
•
•
•
•
•
•
•
nervosa, other medical conditions
Suicide Risk/risk of self harm
Homicide Risk/harm to others-relevant in forensic case or
previous homicide .Remember HCR-20
Risk to reputation-Mania
Risk to finances-Mania
Risk of exploitation-Mania, Borderline personality structure
Risk of driving-Alcohol, dementia
Risk to children –in all case involving children this should be a
consideration
Corporate risk-employment that would put organisation and
public at risk
Mention management of safety e.g. MHA , Nursing
observations
HCR-20
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Historical factors:
•Previous violence
Young age at first violent incident
•Major mental illness
Psychopathy
•Early maladjustment
Personality disorder
•Earlier supervision failure
Employment problems
Clinical items:
•Lack of insight
Negative attitudes
•Active symptoms of mental illness
Impulsivity
•Unresponsive to treatment
Risk management items:
•Plans lack feasibility
•Exposure to destabilisers
•Lack of personal support
•Non compliance with remediation attempts
•Stress
Compliance
Enhancing compliance
• Early relapse signature
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Therapeutic alliance
Eliciting patient’s concerns
Uncovering non-adherence
Eliciting negative cognitions
Practical solutions: dosette box , beeping watches, mobiles,
notes on bathroom mirrors or refrigerators
Socratic questioning
Motivational enhancement therapy
Correction of misinformation
Framing medication trial as an experiment
Giving credit
Using legal framework
Legal issues
• Testamentary capacity
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Power of attorney
CTO
Protective estates order
Capacity to make decisions for medical issues
Reports for forensic patients
Driving
Legal Issues
Social/ Vocational Rehabilitation
• Accommodation –high level, low level supported
accommodation
• Supported employment/pre vocational training
• Education –TAFE
• Finances –carers allowance , benefits
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Groups , day services/hospitals
Depression- Epidemiology
• Life time prevalence –20%
• •Co-morbidity is the rule
• •National Co morbidity survey and EpidemiologicalCatchment Area survey (ECA) -74% &
75% respectively with other lifetime diagnoses
• •Substance misuse , anxiety disorders and personality disorders commonest
• •Risk –ECA study-Lifetime risk of suicide 7.9% , 19.5% with concurrent alcohol and drug
misuse
• •Risk of suicide 21times that of normal population
• (Harris & Barraclough 1998)
• •Previous depressive episode increases risk of further depressive episodes through kindling
phenomenon (Post 1992)
• •Lower threshold of stress required to induce depression , ultimately episodes may occur
spontaneously (Post 1992)
• •Harris & Brown vulnerability factors
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Loss of mother before age of 14
3 or more children under age of 11
Lack of confidant
Unemployed
ECT & medications
• Antidepressants –some evidenceof augmentationTCA’s –
seizuresSSRI’s-Prolonged seizures
• •Benzodiazepines-increase seizure threshold. Stop before
treatment
• •Mood Stabilisers-Consult neurologist if epileptic
• May need reduction of dose before treatment
• Stop 24-48hrs before ECT
• •Lithium –increases risk of post ECT delirium
• For certain patients on lithium careful risk-benefit analysis as
ECT induced mania is more significant than delirium.
Novel treatments
• •Augmentation:Lithium (bauer,2000)T3 (Aronson,1996)Atypical
antipsychotics: Risperidone, Olanzapine, Ziprasidone,Quetiapine,
AripiprazoleAripiprazole was approved by the FDA as the first
augmenting therapy for treatment-resistant MDD in adults
• •Buspirone(5HT1A agonist)
• •Bupropion
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Less evidence:
•Amantadine, riluzole,pramiprexole: not studied in RCT’s
•Modafinil
•Methyl folate-15-30mg/d
•SAMe: S-Adenosyl-L-Methionine:800-1600mg/d
•Lamotrigine :100-300 mg/d
•Gabapentin& Topiramate
•Omega-3 :1g/d not 2-3 mg/d
• •rTMS: Magnetic field produced over surface of head
depolarizes underlying superficial neuronsEffect size
:0.67(rTMS vs. Sham) –Pre FrontalResponse rates-2545%
• •Deep Brain Stimulation:Invasive procedureFDA approved
for treatment of Parkinsonism6 patients of refractory
depression –remission in 4/6Area stimulated is Subgenualanterior cingulate
• •Magnetic seizure therapy (Loo,2007)
• •FEAST –Focal electrically administered seizure therapy
(Loo,2007)
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Epidemiology
DEPRESSION
• Life time prevalence –20%
• Co-morbidity is the rule
• National Co morbidity survey
and Epidemiological
Catchment Area survey (ECA) 74% & 75% respectively with
other lifetime diagnoses
• Risk –ECA study-Lifetime risk
of suicide 7.9% , 19.5% with
concurrent alcohol and drug
misuse
• Risk of suicide 21times that of
normal population
BIPOLAR DISORDER
• 65% co morbidity
• High SMR´s: 15–20 times
more likely to die by
suicide
• High rates of
cardiovascular disease
Signs of Bipolarity in Depressed patients
• WHIPLASHED
• W –Worse or wired when taking antidepressants
• H –Hypomania, hyperthymic temperament ,and mood swings
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in history
I –Irritable hostile or mixed features
P –Psychomotor retardation
L –Loaded Family history : bipolar illness, affectivity and mood
swings
A –Abrupt onset and/ or termination of depressive episodes
less than 3 months
S –Seasonal or postpartum depression
H –Hyperphagia and Hypersomnia
E –Early age of onset
D –Delusions, Hallucinations and Psychotic features
Personal history
• I would now like to ask you some questions about your childhood and
your past to give me a better understanding/ as the past often colors
our present
• Where were you born? (migration hypothesis) Were there any
problems during your birth that you know of? (obstetric
complications)
• Were there any problems as a baby with illness or talking and
walking? (developmental delay-neurodevelopmental hypothesis)
• Childhood memories
• How was discipline handled at home? Did that ever get
physical….such that you ended up with bruises or being hit? How did
that affect you? (attachment and unmet dependencies model)
• When you were a child, did anyone ever do something sexual that made you
feel uncomfortable ? (attachment and unmet dependencies model)
• Tell me about your relationship with mum and dad (harsh and critical –
psychodynamic and cognitive model)
• Was there ever any violence in the domestic household ?(male –
identification with aggressor , female-parallels in later life , self blamecognitive model)
• How did you go at school? Did you have many friends? Were you bullied?
Did you wag/truant (peer group relationships-social and cognitive
models)
• If suspicion of poor academics ask why. Difficulty concentrating? Did you
often get into trouble at school? Did you fight and break rules often? Ever
damaged property? Ever been cruel to animals ? (Conduct disorder)
• Did you find it difficult to sit down at one place for a long time (hyperactivity)
• Did you find it difficult organizing tasks at school, making
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careless mistakes? (inattention)
Did you find it difficult concentrating on subjects you did not
enjoy? What about the subjects you did enjoy? (inattention)
(DD depression)
Special education (developmental delay / learning
difficulties)
Relationships-how many significant relationships have you
had?
What sort of person are you in relationships? (hint towards
personality dysfunction)
• When was the last time you worked? What was your longest
period of employment?
Personality
• Very important aspect often overlooked
• Do you often have mood swings/ do you find that your moods can shift from being happy to
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being sad in a matter of minutes or hours? (mood instability)
Are you generally a confident person or do you have difficulty knowing who……(use name)
is? (self identity disturbance)
Do you feel empty in yourself? (emptiness)
How often do you think about suicide? Why do you self harm/ how does it make you feel?
(chronic self harm ideation)
What sort of person are you in relationships? Are you particularly sensitive to rejection? Are
you often worried about being abandoned in relationships? Does that make you clingy?
(sensitive to rejection/fear of abandonment)
Are you the sort of person that would let other people know that he/she is angry or do you
bottle it up. Do you have difficulty controlling your anger? (impulse dyscontrol)
Would you call yourself an impulsive person?.... a person who does things on the spur of the
moment without thinking of the consequences (impulsivity)
Has that ever gotten you into trouble ? Like drugs, sex, reckless driving, spending and binge
eating etc (impulsivity displayed in at least two areas that are potentially damaging )
Transient stress related paranoid ideation and psychotic symptoms may occur
Relationship instability, job changes etc give a clue to the construct.
5 or more of the above are requiredCTF
Example XYZ
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An important theme that arises in her presentation is the presence of a strong biological predisposition to a depressive illness
with a family history in both her parents. Additionally her anxious temperament also predisposes to depression and anxiety.
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From a psychological point of view I wonder how growing up with two parents with depression impacted on her developing
sense of self and her self esteem due to attachment difficulties and parentification. It is possible that this may have led to
dysfunctional assumptions of self with a tendency to self blame and self criticality leading further to difficulties in negotiating the
early challenges of childhood and adolescence. This would have then impacted on forming peer group relationships.
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Her first episode of depression was at the age of 23 followed by 2 further episodes necessitating ECT. One of these led to a
possible manic episode. This in addition to the episode of postnatal depression raises the possibility of bipolarity which might
be contributing to the treatment resistance.
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Her current episode seems to be in the context of work stress further reinforces the sense of inadequacy and low self esteem
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I wonder how her depression has impacted on her being a mother, which parallels her early childhood.
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Perpetuating factors for her symptoms are social isolation, anxious temperament, self critical evaluation, un-supportive partner
and difficulty coping with the child. F
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Protective factors: she has positive prognostic factors which include compliance with medication, absence of drug and alcohol
misuse and absence of overt maladaptive personality traits
Formulation
• Etiological (genes; thyroid disorder)
• Consequential
• Speculative (childhood experiences): I wonder if…
• Most are a combination