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MOOD DISORDERS - PPT Presentation

ASSESSMENT amp 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 ID: 534245

risk depression mood interpersonal depression risk interpersonal mood life treatment patients depressive relationships cognitive symptoms episode amp disorder patient

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Slide1

MOOD DISORDERS

ASSESSMENT & MANAGEMENTSlide2

‘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.Slide3

Establish broad spectrum

neurosis, depression or psychosis

Once

domain breached establish diagnosis according to 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!!Slide4

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 disordersAnxiety disordersSome personality disordersMedical co-morbididy

ComorbiditySlide5

Depression

Anxiety

Bipolarity

Substance

misuse

Personality disorderSlide6

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 s

ignificant weight loss or gainInsomnia or hypersomniaLoss of energy concentration or indecisivenessFeelings of worthlessness or excessive/inappropriate guiltRecurrent thoughts of death or suicide*One of the symptoms must be either (1) or (2)Symptoms cause clinically significant distress or functional impairmentExcludes bereavement, substance, general medical condition and mixed episode

DSM-IV-TR criteria for

MDDSlide7

With Catatonic Features

r

are

With Melancholic Features

older people

no pre-morbid personality traits

marked weight loss, early morning wakening, psychomotor retardation/agitation, diurnal mood variation, anhedoniacan present with delusions (psychotic depression) responds well to antidepressants and ECTresponds less well to psychotherapiesWith Atypical FeaturesWith Postpartum Onset

MDE SubtypesSlide8

Depression

How are you feeling in yourself / in your spirits. On a scale of 1-10 if 10 was really down 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)Slide9

Any suggestions/ insights into asking these questions or starting this conversation?

Listen to patients’ cues: use experience-near terms (down not ‘depressed’)Slide10

# 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 &

moodAnxiety: …Slide11

STRESSORS &

PRECIPITANT(S)

What does the ‘precipitant’ tell us?Slide12

Risk factors

Sociodemographic

factors

Life stressorsSlide13

Sociodemographic factors

Largely weak correlation

Marital status

Separation/divorce: Bipolar > MDD >

Dysthymia

Socioeconomic status

Lower SES: MDD and BDGeography Distance from the Equator Distal from the Equator: Depression

Proximity to the Equator: Mania

Western > Far Eastern countries

Urbanicity

Urban residence > Rural residenceSeasonSpring & Autumn: DepressionSummer: ManiaDiet Folate Omega-3-fatty-acidsWestern diet > Traditional dietPhysical activity with MDDAdiposity with MDDSlide14

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 stressorsEarly life adversities: E.g. Poor parental relationship, prolonged separation from parent,

intrafamilial

sexual abuse

Early parental death (before adolescence)

For bipolar disorder:Disruption in biorhythmNegative and positive “stress”Social supportSocial isolation: MDDSlide15

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.Slide16

Suicidal ideation

Sometimes when people get depressed they may find life not 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)Slide17

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 , financesHow 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?Slide18

BIPOLAR DISORDERSlide19

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):Inflated self-esteem or grandiosityDecreased need for sleep

More talkative or pressure to keep talking

Flight of ideas or racing thoughts

Distractibility

Increase in goal-directed activity or psychomotor agitationExcessive involvement in activities that have a high potential for painful consequencesSeverity: cause marked functional impairment, necessitate hospitalisation, or if psychoticExclusion: direct physiological effects of a substance or general medical conditionSlide20

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 hospitalisationNot severe enough to cause marked impairment in functioningCriticismDuration is too longRecognised brief hypomanic episodes (1-2 days) are common among those with bipolar disordersSubthreshold symptoms still clinically and functionally significant

Hypomanic

EpisodeSlide21

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 weekIn broader terms, subthreshold “mixed states” refer to “non-pure” depressive or manic statesIntrusion of manic features in depressionorIntrusion of depressive features in maniaMixed Episode and subthreshold mixed states signal bipolarity

Mixed EpisodeSlide22

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 DisorderSchizophrenia + any mood episode = Schizoaffective Disorder (MDD or Bipolar types)Longitudinal diagnosis: Mood Disorders Slide23
Slide24

Bipolar Illness (Mania)

Have you ever had the opposite of depression when you have been extremely 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 Slide25

Past History

Previous admissions –diagnosis

Trigger

Medications-

type

, compliance

and effectivenessLeading Q’s-Tegretol (Carbamazepine), Lithium, Valproate, ECT , injections (Depots)Self harmPsychotherapy- type, compliance

and

effectivenessSlide26

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 & treatmentSlide27

Any other medical issues for mood disorders

If there is

:

eg

.

my patient in the exam had an anaphylactic reaction/

allergy (CL rotation)Slide28

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?

What about problems with drugs , or alcohol or violence?Slide29

Family history

Stronger family history in bipolar disorders and early onset MDD

For 1

st

degree relatives:

Risk of BD with BD

proband: 7x general populationRisk of MDD with MDD proband: 2-3x general populationCross-over risk:BP probands: 

risk of MDD (MDD>BD)

UP

probands

: Minimally  risk of BDTwin concordance: BD: MZ 40% DZ 10%MDD: MZ 30% DZ 20%Overlap between bipolar disorder and schizophreniaSlide30

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 : more members affectedaffected family members are first-degree relatives A family history of bipolar disorder (+specifically, a much greater risk for bipolar disorder)

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. Slide31

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.Slide32

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 treatmentsAnd strong family historySlide33

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)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)Slide34

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 blame-cognitive 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)Slide35

Did you find it difficult organizing tasks at school, making 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?Slide36

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

If no-have you ever been violent towards

others?

Slide37

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 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 occurRelationship instability, job changes etc give a clue to the construct.5 or more of the above are required Slide38

Mental state examinationSlide39

Marjorie Slide40

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?Slide41
Slide42

Formulation

Etiological

Consequential

Speculative

Not

mutually exclusive

Most are a combinationSlide43

Biological

Psychological

Social

CulturalSlide44

Biological

Genetic predisposition

Neurodevelopmental hypothesis (schizophrenia)

Drugs and alcohol (schizophrenia)

Head injury

Epilepsy

Other medical conditionsDrugs causing psychiatric conditionsSlide45

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 MODELSlide46

Psychological

Attachment Model

Cognitive models

Psychosocial development (Erikson’s)

Coping skills

Social Skills

Psychodynamic modelsSlide47

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.Slide48

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 de-emphasized 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.Slide49

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 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. Slide50

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.Slide51

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 theoryInsecure attachments predispose to subsequent psychopathologyPsychological theories: PsychodynamicSlide52

Psychological theories: Cognitive

Cognitive

Triad of Affect, Behaviour, Cognition

Negative cognitive schemata

 negative automatic thoughts (

cognitive distortions)

 depressed mood and behavioursCognitive triad of negativity towards self, environment & futureFoundation of CBT

Aaron Beck Slide53

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

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. Slide54
Slide55

Cognitive Model: Bipolar Illness

Based on Diathesis stress model

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

episodeSlide56

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)Slide57

Cognitive Theory of DepressionSlide58

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.Slide59

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 self-assertion, 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.Slide60

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 disparitiesSlide61

Differential DiagnosisSlide62

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

Other disorders with mood featuresSlide63

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” progressionNot necessarily experience theseWide variations from person to personInfluenced by many factors:Personality, coping style, resiliencePast experience of losses & traumas

Nature & quality of relationship with lost object

Available supports

Culture

Spiritual beliefsDuration varies, can be ongoingSlide64

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 affectApathy among range of affectsPreserved hedonic capacityAnhedonicPreserved self-esteemWorthlessnessAble

to look forward to the future

HopelessnessSlide65

Management of Mental

Disorders

Slide66

4 Main Domains

Risk

Clarification of Diagnosis

Treatment

of Psychiatric symptoms

Long term Treatment : Relapse prevention , Social and Vocational rehabilitationSlide67

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-ManiaRisk to finances-ManiaRisk of exploitation-Mania, Borderline personality structureRisk of driving-Alcohol, dementiaRisk to children –in all case involving children this should be a considerationCorporate risk-employment that would put organisation and public at riskMention management of safety e.g. MHA , Nursing observationsSlide68

HCR-20

Historical

factors:

•Previous violence

Young

age at first violent incident

•Major mental illness Psychopathy•Early maladjustment Personality disorder•Earlier supervision failure Employment problemsClinical 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•StressSlide69

CLARIFICATIONSlide70

Example Slide71

PrognosisSlide72

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 Slide73

Social/ Vocational Rehabilitation

Accommodation –high level, low level supported accommodation

Supported employment/pre vocational training

Education –TAFE

Finances –carers allowance , benefits

Groups , day services/hospitalsSlide74

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 frameworkSlide75

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 Slide76

depressionSlide77

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 Slide78

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 Slide79

Psychotic Depression

First line –TCA +antipsychotic

ECT is effective treatment

2

metaanalyses

(Spiker,1985 & Parker,1992): 80% response rate to ECT80% response rate to combination antidepressant and antipsychotic33% to antipsychotic alone25% to antidepressant alone Slide80

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

Slide81

ECT & medications

Antidepressants –some

evidenceof

augmentationTCA’s

seizuresSSRI’s-Prolonged seizures•Benzodiazepines-increase seizure threshold. Stop before treatment•Mood Stabilisers-Consult neurologist if epilepticMay need reduction of dose before treatmentStop 24-48hrs before ECT•Lithium –increases risk of post ECT deliriumFor certain patients on lithium careful risk-benefit analysis as ECT induced mania is more significant than delirium. Slide82

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 - 2Slide83

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 & tolerabilitySlide84

Contraindication

Raised intracranial pressure

Relative contraindications:

Recent CVA

Cerebral aneurysm or vascular malformations

Unstable cardiovascular condition

High anaesthetic riskRisks & adverse effectsGeneral anaestheticPost-ictal confusionMemory loss (anterograde & retrograde)Headache, aches and painsChipped tooth, skin burns

ECT - 4Slide85

Consent

Informed consent from patient

or

Guardianship Board consent

*Note: Detention is inadequate to give involuntary ECT

ECT - 5Slide86

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)•BupropionLess 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

Novel treatmentsSlide87

rTMS

: Magnetic field produced over surface of head depolarizes underlying superficial

neuronsEffect

size :0.67(

rTMS

vs. Sham) –Pre FrontalResponse rates-25-45%•Deep Brain Stimulation:Invasive procedureFDA approved for treatment of Parkinsonism6 patients of refractory depression –remission in 4/6Area stimulated is Sub-genualanterior cingulate•Magnetic seizure therapy (Loo,2007)•FEAST –Focal electrically administered seizure therapy (Loo,2007) Slide88

Bipolar disorderSlide89

Epidemiology

65% co morbidity

High SMR´s: 15–20 times more likely to die by suicide

High rates of cardiovascular disease Slide90

Signs of Bipolarity in Depressed patients

WHIPLASHED

W –Worse or wired when taking antidepressants

H –Hypomania,

hyperthymic

temperament ,and mood swings in historyI –Irritable hostile or mixed featuresP –Psychomotor retardationL –Loaded Family history : bipolar illness, affectivity and mood swingsA –Abrupt onset and/ or termination of depressive episodes less than 3 monthsS –Seasonal or postpartum depressionH –Hyperphagia and HypersomniaE –Early age of onsetD –Delusions, Hallucinations and Psychotic features Slide91

Texas Implementation of Medication Algorithm -Bipolar I Disorder (

Suppes

, 2005 )Slide92
Slide93

TIMA guidelines –Maintenance Treatment: Hypomania/ManiaSlide94

TIMA Guidelines –Maintenance Treatment + Most Recent Episode DepressionSlide95

PrognosisSlide96

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 MODELSlide97

Psychological

Attachment Model

Cognitive models

Psychosocial development (Erikson’s)

Coping skills

Social Skills

Psychodynamic modelsSlide98

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.Slide99

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 de-emphasized 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.Slide100

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 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. Slide101

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.Slide102

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 theoryInsecure attachments predispose to subsequent psychopathologyPsychological theories: PsychodynamicSlide103

Psychological theories: Cognitive

Cognitive

Triad of Affect, Behaviour, Cognition

Negative cognitive schemata

 negative automatic thoughts (

cognitive distortions)

 depressed mood and behavioursCognitive triad of negativity towards self, environment & futureFoundation of CBT

Aaron Beck Slide104

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

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. Slide105

Cognitive Theory of DepressionSlide106

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)Slide107

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.Slide108

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 self-assertion, 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.Slide109

4 Main Domains

Risk

Clarification

of Diagnosis

Treatment

of Psychiatric symptoms

Long term Treatment : Relapse prevention , Social and Vocational rehabilitationSlide110

risksSlide111

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-ManiaRisk to finances-ManiaRisk of exploitation-Mania, Borderline personality structureRisk of driving-Alcohol, dementiaRisk to children –in all case involving children this should be a considerationCorporate risk-employment that would put organisation and public at riskMention management of safety e.g. MHA , Nursing observationsSlide112

HCR-20

Historical

factors:

•Previous violence

Young

age at first violent incident

•Major mental illness Psychopathy•Early maladjustment Personality disorder•Earlier supervision failure Employment problemsClinical 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•StressSlide113

ComplianceSlide114

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 frameworkSlide115

Legal issues

Testamentary capacity

Power of attorney

CTO

Protective estates order

Capacity to make decisions for medical issues

Reports for forensic patientsDriving Legal Issues Slide116

Social/ Vocational Rehabilitation

Accommodation –high level, low level supported accommodation

Supported employment/pre vocational training

Education –TAFE

Finances –carers allowance , benefits

Groups , day services/hospitalsSlide117

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 Slide118

ECT & medications

Antidepressants –some

evidenceof

augmentationTCA’s

seizuresSSRI’s-Prolonged seizures•Benzodiazepines-increase seizure threshold. Stop before treatment•Mood Stabilisers-Consult neurologist if epilepticMay need reduction of dose before treatmentStop 24-48hrs before ECT•Lithium –increases risk of post ECT deliriumFor certain patients on lithium careful risk-benefit analysis as ECT induced mania is more significant than delirium. Slide119

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)•BupropionLess 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

Novel treatmentsSlide120

rTMS

: Magnetic field produced over surface of head depolarizes underlying superficial

neuronsEffect

size :0.67(

rTMS

vs. Sham) –Pre FrontalResponse rates-25-45%•Deep Brain Stimulation:Invasive procedureFDA approved for treatment of Parkinsonism6 patients of refractory depression –remission in 4/6Area stimulated is Sub-genualanterior cingulate•Magnetic seizure therapy (Loo,2007)•FEAST –Focal electrically administered seizure therapy (Loo,2007) Slide121

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 populationBIPOLAR DISORDER65% co morbidity

High

SMR´s

: 15–20 times more likely to die by suicide

High rates of cardiovascular disease Slide122

Signs of Bipolarity in Depressed patients

WHIPLASHED

W –Worse or wired when taking antidepressants

H –Hypomania,

hyperthymic

temperament ,and mood swings in historyI –Irritable hostile or mixed featuresP –Psychomotor retardationL –Loaded Family history : bipolar illness, affectivity and mood swingsA –Abrupt onset and/ or termination of depressive episodes less than 3 monthsS –Seasonal or postpartum depressionH –Hyperphagia and HypersomniaE –Early age of onsetD –Delusions, Hallucinations and Psychotic features Slide123

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 presentWhere 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)Slide124

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 blame-cognitive 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)Slide125

Did you find it difficult organizing tasks at school, making 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?Slide126

Personality

Very important aspect often overlooked

Do

you often have mood swings/ do you find that your moods can shift from being happy to 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 occurRelationship instability, job changes etc give a clue to the construct.5 or more of the above are requiredCTF Slide127

Example XYZ

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.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.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.Her current episode seems to be in the context of work stress further reinforces the sense of inadequacy and low self esteemI wonder how her depression has impacted on her being a mother, which parallels her early childhood. Perpetuating factors for her symptoms are social isolation, anxious temperament, self critical evaluation, un-supportive partner and difficulty coping with the child. FProtective factors: she has positive prognostic factors which include compliance with medication, absence of drug and alcohol misuse and absence of overt maladaptive personality traitsSlide128

Formulation

Etiological (genes; thyroid disorder)

Consequential

Speculative (childhood experiences): I wonder if…

Most

are a combination