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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 • • • • 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 1) 2) 3) 4) 5) 6) 7) 8) 9) 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 • • • • • • • • • • • • 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 • • • • • • • 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): 1) 2) 3) 4) 5) 6) 7) 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 • • • • • • • • • 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? • 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 : 1. more members affected 2. affected family members are first-degree relatives 3. A family history of bipolar disorder (+specifically, a much greater risk for bipolar disorder) 4. 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) • • 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 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) • 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? 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? 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 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 • Neurodevelopmental hypothesis (schizophrenia) • Drugs and alcohol (schizophrenia) • Head injury • Epilepsy • Other medical conditions • 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 • 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 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 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 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 episode 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) Cognitive Theory of Depression 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. 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 • • • • • • • • • • • 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 • • • • • • • 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 • 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 • • • • 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 • • • • • • • • • 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) • 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 • • • • • • • • 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 • • • • 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 • • • • • • • • • • 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 • 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 esteem • I 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. F • 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