Mood Disorders: Depression and Bipolar

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MOOD DISORDERS Dale Metcalfe t…BUT it’s n lo t o f conte looks at IS a s a s it There sl id e many not as ance! first gl  TODAY’S AIM 01 02 03 04 Understand the Gain knowledge Have an Have an overview link between of the symptoms understanding of of the different ‘depression’ and of mood different mood causes of mood ‘bipolar’ disorders disorders, their disorders and similarities and treatment their differences approaches  MOOD DISORDERS: DSM-5 CATEGORIES Two broad types: Only depressive symptoms (unipolar disorders) Manic and depressive symptoms (bipolar disorders) DSM-5 Depressive disorders: Major depressive disorder Persistent Depressive Disorder (Dysthymia) Mixed anxiety/depressive disorder Premenstrual dysphoric disorder Disruptive mood dysregulation disorder DSM-5 Bipolar Disorders: Bipolar I disorder Bipolar II disorder Cyclothymia  MOOD DISORDERS Two key emotions: Depression Dysphoria: Low, sad state, excessive unhappiness Anhedonia: Loss of interest in activities Mania Euphoria: State of euphoria or excess high elation Mania: Expansive mood  Major depressive disorder (MDD) Episodic, recurrent episodes Average episode is 8 months, average of 4 DEPRESSION episodes per person TYPES Chance of recurrence is 25% within 1 year, 40% in 2, 70% in 5 Dysthymia Symptoms that persist through time (e.g. 20+ years) Symptoms not as strong as MDD Early onset (pre-21) greater chronicity / poorer Double depression prognosis MDD on top of dysthymia 95% of patients with dysthymia develop MDD within 10 years (Klein et al., 2006) Associated with problematic future course & severe psychopathology Lots of others in workshop handout, even more in DSM5!  SIGNS AND SYMPTOMS OF BIPOL AR DISORDER Used to be called manic-depressive disorder Characterised by Episodes of unusually high and low levels of: Mood, energy, and activity Periods of relatively stable mood between ‘episodes’ (euthymia) Defining feature is high mood Must have at least 1 manic or hypomanic episode Persistent low mood – depression Mixed states  KEY STATES IN BIPOLAR Depression Mania Hypomania Distinct period of: Distinct period of: Characterised by the same symptoms as mania Low and sad state Elevated, expansive or irritable mood e.g. over-confidence, sociability, Excessive unhappiness (dysphoria) Increased goal-directed behavior or energy and risky behaviour. Loss of interest in activities (anhedonia) Mania is the defining feature of bipolar Changes are not as severe & no spectrum disorders psychotic features Mania is not just about euphoria  WHAT ARE PSYCHOTIC SYMPTOMS? Psychosis is sometimes experienced as part of an episode of mania or depression in Bipolar I disorder Psychotic experiences include: Hallucinations, where the individual can see, hear, taste, smell or touch something that is not actually there Delusions, which are strong yet untrue beliefs the individual has Disturbed or confused thoughts and speech Unusual behaviour A lack of self-awareness  Concurrent symptoms of a manic or depressive episode Significant impairment on social and occupational functioning WHAT IS A May be psychotic features MIXED STATE? Most of the day, nearly every day, for at least one week Mania not polar opposite of depression  Bipolar I Alternations between full manic episodes and depressive episodes At least one episode of mania With or without depression or mixed episode Bipolar II Alternations between major depressive episodes and BIPOLAR hypomanic episodes SUBTYPES At least one episode of hypomania At least one episode of depression Cyclothymia Persistent, fluctuating course of hypomania and depressive symptoms, that do not meet criteria for a manic, mixed, or major depressive episode More chronic: Going on for at least 2 years and not symptom free > 2 months Also - Bipolar disorder not otherwise specified Also, people are subsyndromal 50% of the time Without treatment episodes become more frequent  In any given year ~8% of adults will suffer UNIPOL AR from severe unipolar depression DEPRESSION EPIDEMIOLOGY Women more likely than men (6.0% vs 9.6%) Adults more common than children Around 40% do not respond favourably to treatment e.g. will experience another episode later Onset might be gradual or sudden but usually history of milder episodes that do not reach criteria  Age and Gender Peak age of onset 16-25 years (approx. 60% have a first episode prior to 19) Rate increases after puberty (pre-10 is rare) BIPOLAR Equally common in women and men EPIDEMIOLOGY Women may experience more depressive episodes and fewer manic episodes and rapid cycling is more common Bipolar 1 Can begin in childhood: average age on onset is 18 More common among people years with low incomes, compared Tends to be chronic and suicide is common to those with high incomes Bipolar 2 About 1/3 of people develop Can begin in childhood: average age on onset is 22 bipolar within 5 years of MDD years diagnosis Tends to be chronic Only 10 to 13% of cases progress to full bipolar I Cyclothymia disorder Average age on onset is 12 to 14 High risk for developing bipolar I or II disorder Most are female  QUESTION TIME 1 https://forms.office.com/Pages/ResponsePage.as px?id=3c9X5zUfV0Svj3ycaxQ34xQGvmjdZ2lLm PofE4hzdp9UNk5DUUxWNEVFWUdIQ1M4SUhH WFVUTkI5Ry4u  UNIPOLAR DEPRESSION BIO-CAUSES: GENETICS A predisposition is inheritable Heritability estimates 20-45% / 37% MDD (Sullivan et al., 2000) Severe mood disorders have a stronger genetic contribution Twin studies Concordance rates for mood disorders are higher in identical twins Concordance rates for identical (MZ) twins = 46% Concordance rates for fraternal (DZ) twins = 20% Adoption studies also have implicated a genetic factor in cases of severe unipolar depression Research has not conclusively identified 1 specific gene But DRD4.2 gene, which influences dopamine function, appears to be related to MDD (Lopez, Leon et al., 2005)  FA M I LY S TU D I E S Closer genetic link = Greater the likelihood of developing the disorder Rate of mood disorders is higher in relatives of probands 20% of relatives of someone with depression are themselves depressed, Compared with fewer than 10% of the general population Children of parents with depression have about 3x the risk of depression Heritability rates are higher for females compared to males What is inherited is likely a vulnerability to depression With certain environmental stressors needed for these disorders to be expressed…families can bring those common environments out  BIPOLAR BIO-CAUSES : GENETIC Genetic linkage studies to identify possible patterns of inheritance High heritability 0.80 Family studies support this theory: Genetic patterns run in families Identical (MZ) twins = 40% likelihood Fraternal (DZ) twins and siblings = 5% to 10% likelihood General population = 1 to 2.6% likelihood Not the whole story! Not all family members of an individual with bipolar disorder develop the condition Mechanism through which BD is ‘transmitted’ remains unclear People may inherit a biological predisposition (genetic vulnerability) to develop bipolar disorders No single gene: Multiple genes may be involved + Overlap with other conditions  BIPOLAR BIO-CAUSES : GENETIC Genetic linkage studies to identify possible patterns of inheritance High heritability 0.80 Family studies support this theory: Genetic patterns run in families Identical (MZ) twins = 40% likelihood Fraternal (DZ) twins and siblings = 5% to 10% likelihood General population = 1 to 2.6% likelihood Not the whole story! Not all family members of an individual with bipolar disorder develop the condition Mechanism through which BD is ‘transmitted’ remains unclear People may inherit a biological predisposition (genetic vulnerability) to develop bipolar disorders No single gene: Multiple genes may be involved + Overlap with other conditions  UNIPOLAR DEPRESSION BIO-CAUSES: BIOCHEMICAL FACTORS Neurotransmitter Endocrine s (NTs): Noradrenaline, system/CORTISO Melatonin Dopamine, Serotonin L Original models focused People with depression Melatonin increase = on absolute levels of NTs have been found to have Sleep ‘Dracula Hormone’ (E.g. MDD = Low levels) abnormal elevated levels of cortisol People with depression, But medication alters abnormal melatonin levels immediately - Released by the adrenal secretion Relief takes 2-3 weeks, glands during times of neurogenesis stress Too much = damaged sleep and circadian A complicated interaction Overactivity of HPA axis rhythms is at work: other NTs may which triggers release of Hallmark of most mood be involved cortisol, stress hormone disorders  BIPOLAR BIO -CAUSES: BIOCHEMICAL FACTORS Neurotransmitters: Noradrenaline, dopamine, Mania Ion activity serotonin Low levels in depression… Noradrenaline and Ions send incoming so high levels in mania? dopamine high; serotonin messages to nerve low endings Overactivity of noradrenaline is Permissive Theory These may be improperly supported in research addresses this transported via neurons contradiction: in bipolar disorder But relationship with Low serotonin opens the door to serotonin is the opposite mood disorders Irregularities in transport (low levels too) Low serotonin + Low noradrenaline = of ions may cause Contradictory? Depression neurons to fire too easily Low serotonin + High noradrenaline = (mania) or resist firing Mania (depression)  BIPOLAR BIO -CAUSES: STR UCTURAL FACTORS Imaging studies - smaller brain areas? Prefrontal cortex, Basal ganglia, Cerebellum (and others) It is not clear what role such structural abnormalities play Potentially cause or effect of Neurotransmitter & ion activity, or medication? Imaging studies link mood fluctuations to abnormalities in activity in areas related to emotion regulation prefrontal and anterior cingulate cortex hippocampus, amygdala, thalamus, and basal ganglia Some structural points linked to unipolar depression too, slide at end – check textbooks for more!  UNIPOLAR DEPRESSION PSYCH-CAUSES: THEORIES Psychodynamic Behavioural Cognitive Link between depression Depression results from Focus on relationship and grief/loss changes in rewards and between negative punishments people thinking and mood Actual or receive in their lives symbolic/imagined loss of Emphasize Lewinsohn suggests that: “depressogenic” a love object The positive rewards in life Depression is viewed as the cognitions dwindle for some people, conversion of aggressive instinct Negative thoughts and beliefs leading them to perform fewer into depressive affect and fewer constructive associated with depressive behaviors, and they spiral symptoms Newer psychoanalysts toward depression (object relations theorists) Hopelessness theory Propose comes from feeling Social rewards are Depression-prone individuals unsafe and insecure in especially important have a negative attributional relationships style (blame themselves for negative events in their lives)  COGNITIVE THEORIES Cognitive Triad Covered in the workshop! Learned Helplessness: Hopelessness Theory Covered in the workshop! Theories also cover bipolar, check your textbooks  Consistent finding: Depression repeatedly tied to unavailability of social support Vulnerability + Provoking agent + UNIPOLAR D E P RE SS I O N S O C I O C U LT U RA L M O D E L : T H E FA M I LY S O C I AL Absence of protective factors PE R S PE C T I VE (e.g. social support) = depression. Additional slides on this at the end!  BIPOLAR SOCIAL AND PSYCHOLOGICAL TRIGGERS Trigger of depressive episodes Triggers of Mania (similar to major depressive episodes) Negative life events Stress Negative cognitions, Sleep disruption/deprivation (e.g. late night Lack of social support partying, jet lag) Recreational stimulant use Goal/achievement-oriented activity – reward sensitivity INTEGRATIVE MODEL OF MOOD DISORDERS  PHARMACOLOGICAL: MOOD STABILIZERS Most common prescribed medications for treating unipolar depression: Selective Serotonin Reuptake Inhibitors (SSRIs) E.g., Fluoxetine (Prozac), Zoloft Also used for depressive symptoms of bipolar  BIPOLAR MEDICATION Lithium Carbonate (a Common Salt) Primary drug of choice for bipolar disorders 40% - 80% receive at least some relief with this mood stabilizer Potentially serious side effects Lithium toxicity Dosage must be carefully monitored Kidney & thyroid function Better at blunting mania than alleviating depression episodes Reduces its recurrence.  MEDICATION: NEGATIVE SIDE EFFECTS Side effects are common SSRI: Suicidal thoughts and self-harm Warnings out for use with children and adolescents (FDA hearings) – “Black Box” Warning on prescriptions. With that said Medication is one of (if not the most) broadly effective treatment. Whilst there are issues, this should not discourage their use where medical professionals see them as beneficial!  Cognitive-behavioural therapy (CBT) Most common form of psychosocial intervention Behavior therapy: Focuses on increasing pleasurable activities & events Cognitive therapy: Identify, challenge, and modify negative thoughts Effective at detecting warning signs and approaches for preventing P S YC H O S O C I A L relapse I N T E RV E N T I O NS Psychoeducation Provide information about symptoms, course, triggers, and treatments Family-focused treatment (FFT) Educate family about disorder, enhance family communication, improve problem solving  PSYCHOLOGICAL INTERVENTIONS Interpersonal Psychotherapy IPT (Adolescent version: IPT-A) Focuses on problematic interpersonal relationships and social context in which they occur Mindfulness-based cognitive therapy (MBCT) Strategies, including meditation, to prevent relapse  DEPRESSION SHORT FILM https://www.youtube.com/watch?v=qap-E8oqSnk 7 WAYS TO MAXIMIZE MISERY https://www.youtube.com/watch?v=LO1mTELoj6o  TASK FOR THE WEEK I have uploaded two articles that relate to bipolar disorder. One about Bipolar and ADHD, and another about various conditions and how the NHS have become better at diagnosing them Read these and think about A) Why might the NHS have become better at detecting various conditions? B) What does the intersection tell us about comorbidity of conditions in the DSM-5/ICD-10? C) Design a study building on the information provided in either (or both) of these articles. Write down some bullet points that could be used in a rationale for this study, (there's lots of articles linked above too, this should help you plan something out) This is excellent practice for labs/your dissertation. If you would like me to look at your rationale, email it over to me (in the body of the email, not as an attachment please) and I'll happily give you some feedback. There is also the 2-part documentary on Stephen Fry linked on the reading list too ADDITIONAL SLIDES  SYMPTOMS Emotional Depressed mood is the most central symptom and a prerequisite for diagnosis Feelings of hopelessness and dejection Anxiety (panic symptoms), irritability, low self-esteem. Loss of interest and pleasure in usual activities  SYMPTOMS Motivational Excessive tiredness Lack of energy Lethargic Don’t dress, go to work, university Slowness in thinking and (in more severe cases) in movement Thoughts of suicide and suicide attempts Avoid other people SYMPTOMS Behavioural Look and behave sad Speak and move slowly  SYMPTOMS Cognitive Holding negative views on everything Self-critical and low self-esteem Difficulty in concentrating, easily confused. Fear of losing one's mind or going mad. Blame self for every negative event Feelings of hopelessness and helplessness Feelings of self-condemnation and guilt.  SYMPTOMS Physical Sleep disturbance Appetite disturbance Headaches Indigestion Dizzy spells Pain Decrease in sexual interest  MANIA IN THE DSM- V Activation/energy now as important as elevated/expansive mood Distinct period of persistently elevated/irritable mood AND Persistent goal-directed behaviour or energy PLUS three (four is irritable mood) or more of: Inflated self-esteem/grandiosity Decreased need for sleep Pressure of speech Flight of ideas/racing thoughts Distractibility Goal-directed activity/psychomotor agitation Activities with high potential for painful consequences  HYPOMANIA Characterised by the same symptoms as mania, E.g. over-confidence, sociability, and risky behaviour. Changes are not as severe, No psychotic features Close friends and family would notice a change in the person Must last for 4 or more days  CAUS ES ( AET I OLOGY ) OF MOOD DI SORDER S What factors contribute to onset of mood disorders? Neurobiological factors Psychosocial factors  U N I POL A R DE P R E SSIO N OT H E R C A US E S Brain Anatomy and Circuits Brain circuits = Networks of brain structures which work together These trigger each other into action Can produce emotions Emotional reactions are tied to brain circuits Abnormality in structure/function of multiple emotion regulating regions = A circuit responsible for depression https://www.youtube.com/watch?v=2rxeFgKIS9s Likely brain areas in the circuit include: Prefrontal cortex, Hippocampus and Amygdala https://www.youtube.com/watch?v=CplGWHEX6cA  U N I PO LA R DE P R E SSIO N OT H E R C A US E S Immune system The body's network of activities/cells that fight off bacteria/other foreign invaders When stressed: The immune system may become dysregulated Some believe may help produce depression Support for this explanation is circumstantial but compelling  U N I P O LA R D E P R E SS I O N S O C I O C U LT U RA L M O D EL : TH E FA M I LY S O C I A L P E R S P E CT I V E Sociocultural theorists propose that unipolar depression is greatly influenced by the social context that surrounds people Belief is supported by depression is often being triggered by outside stressors Life events: 42-67% report a stressful life event in year prior to depression Loss: Romantic breakup, loss of job, death of loved one, loss of health, income; life changes; daily hassles Lack of social support may be one reason a stressor triggers depression Interpersonal Difficulties U N I P O L A R DE P R E SS I O N Marital conflict/dissatisfaction also predicts T H E FA M I LY S O C I A L depression. P E R S P E CT I V E Particularly strong in males Behaviour of depressed people often makes other people uncomfortable May cause them to avoid them Excessive reassurance seeking Few positive facial expressions Negative self disclosures Slow speech and long silences Leads to decreased social contact and further deterioration of social skills  BIOLOGICAL/GENETIC VULNERABILITY Stressors such as Poor social routine life events or highly Sleep deprivation Biological/genetic driven behaviour factors in combination with environmental factors (e.g. life stress Biological and family Stigma/ vulnerability Relationship problems disturbances) Poor coping Prodromal Episode stage strategies  UNIPOLAR DEPRESSION TREATMENT OF DEPRESSION  OTHER TREATMENTS FOR DEPRESSION Vitamin B12 Omega acids Exercise: 30 mins a day can reduce symptoms by 50% Can be as effective as antidepressants for mild and moderate depression Sleep hygiene https://www.youtube.com/watch?v=xUt3RiQyx- c Inflammation? Tentative but well worth a listen https://www.artofmanliness.com/articles/podca st-585-inflammation-saunas-and-the-new-scien  PROGNOSIS FOR UNIPOL AR DEPRESSION Effectiveness of Psychological Treatments comparable to medications Prognosis: Typically ~60% respond  IMPACT OF DEPRESSION Some difficulties may affect intellectual and academic functioning, for example: Concentrating Loss of interest Slowness of thought and movement May lead to Lower scores on tests Poor teacher ratings Lower levels of grade attainment May have problems on tasks requiring attention, coordination, and speed  IMPACT OF DEPRESSION Cost of lost days working Other mental and physical health issues (and associated costs) Together, depression and anxiety disorders are estimated to reduce England’s national income by over 4% (approximately £80 billion). Reduction in economic output results from: Increased unemployment Absenteeism (a higher number of sick days) Reduced productivity Accompanied by increased welfare expenditure.  CONTINUED: SES AND LOCATION The rate of depression is 3x higher among poor people than wealthier people Prevalence varies across world/country/region  IMPACT OF DEPRESSION Social and peer problems Few close friendships, feelings of loneliness, and isolation Social withdrawal and ineffective coping styles in social situations Can result in the maintenance of difficulties Relationship breakdown Family problems May have less supportive and more conflicted relationships with parents and siblings May be socially isolated from families and prefer to be alone  T R E AT ME NT O F M O O D D I S O R DE R S : E LE CT R O CO NV U L S IV E T H E RAPY (EC T ) ECT is effective for Cases of Severe Depression Involves applying brief electrical current to the temples (brain) Results in temporary seizures Usually, 6 to 10 outpatient treatments are required Side effects e.g. Short-term memory loss Uncertain why ECT works PHARMACOLOGICAL TREATMENTS: DEPRESSIVE SYMPTOMS  FURTHER MEDICATIONS FOR BIPOL AR DISORDER Anticonvulsants Antipsychotics/Neuroleptic Valproate Olanzapine Carbamazepine Risperidone Lamotrigine Quetiapine Anti-depressants Clozapine With caution – not on its own! Can help initially to reduce high levels of mania Long-term mood stabiliser Serious side effects Managed person by person basis  POLYPHARMACY More than half of patients receive polypharmacy - mood stabilisation via anti- epileptics and atypical anti-psychotics  DEPRESSION COMORBIDITY Up to 90% of young people with depression have one or more other disorders; 50% have two or more Most common comorbid disorders include: Anxiety disorders (especially GAD) Specific phobias Separation anxiety disorders Dysthymia Conduct problems ADHD Substance-use disorder 60% of adolescents with MDD have comorbid personality disorders Especially borderline personality disorder  High rates of co-occurring disorders BIPOL AR COMORBIDITY are extremely common Most typical are: Separation anxiety disorders Generalized anxiety disorders ADHD Oppositional and conduct disorders Also - Substance use disorders Co-occurring medical problems Cardiovascular and metabolic disorders Epilepsy Migraine headaches