Mood Disorders Lecture Notes PDF

PS2008- INTRODUCTION TO CLINICAL PSYCHOLOGY M o o d D is or d e r s D r C r i s ti n a M ar t in e l li Outline Symptoms and clinical features Epidemiology and stats Aetiology and risk factors Treatments  Mood Disorders Unipolar...

PS2008- INTRODUCTION TO CLINICAL PSYCHOLOGY M o o d D is or d e r s D r C r i s ti n a M ar t in e l li Outline Symptoms and clinical features Epidemiology and stats Aetiology and risk factors Treatments  Mood Disorders Unipolar Bipolar Premenstr Disruptive Major Persistent Mood Bipolar Bipolar Cyclothymia Depressive Depressive ual II Dysregula I Disorder Disorder Depressive Disorder tion Disorder ------------------------Marked by depression------------------------ -----Marked by mania----- TRISH Trish was a 51-year-old woman who was brought to the emergency room by her husband. She said, “I feel like killing myself.” She had lost her interest in life about four months before. During that time, she reported depression every day for most of the day. Symptoms had been getting worse for months. She had lost 14 pounds because she did not feel like eating. She had trouble falling asleep almost every night and woke at 3:00 a.m. several mornings a week (she normally woke at 6:30 a.m.). She had low energy, trouble staying focused and less ability to do her office job at a dog food- processing plant. She was convinced that she had made a mistake that would lead to the deaths of thousands of dogs. She expected that she would soon be arrested and would rather kill herself than go to prison. Trish experienced these symptoms for at least two weeks.  MD Episode and MDD Fiv e + of following during sa me 2 week s At l east one i s 1 o r 2 : ne arly eve ry d ay 1. De pr ess ed m ood m os t of da y 2. Diminis he d inte res t/pleas ur e in most activities most of day Sig nifica nt w eig ht l oss whe n not die ti ng, or wei ght gai n Insomn ia/hyp ersomn ia Psycho motor agi ta ti on/retard ation Fatigu e/loss of ene rgy Feel ing s o f wo rth lessn ess/excessi ve/ina ppro pria te g uil t, dimi nish ed ab ili ty to thin k o r co ncen tra te o r i nde cisive ness Re curren t thou ghts of d eath, suici dal i dea ti on or sui cide a ttemp t  MDD Diagnosis One MD episode not attributable to ’expected’ reactions to experiences (e.g., bereavement) Symptoms cause significant distress, social/occupational dysfunction Not due to: substance /general medical condition Another disorder (e.g., schizoaffective disorder) Never experienced a manic episode Mahli et al. 2018 Lancet Psychosis in MDD Sometimes depression can include delusions and hallucinations. Typically, the content of psychosis is syntonic with depression. For examp le, th e patie nt b eli eves that he is go ing to di e beca use he is in p ain a s a re sult of d epre ssion o r h e bel ieve s tha t he i s pe rsecuted be cause h e is a sinn er. Persistent Depressive Disorder De pr ess ed m ood m os t of da y, more days than not, 2 y ear s + Di spla ys 2 +: Poo r a ppe ti te o r o verea ti ng Sle ep di stu rban ce: In/hyp ersomn ia Lo w ene rgy or fa ti gue Poo r se lf-estee m Troub le con centratin g/makin g deci sion s Feel ing s o f ho pel essne ss  Percentage of probable lifetime diagnoses Lifetime prevalence Males: 5-12% Females: 10-25% Some cultural variation (WHO) https://www.theguardian.com/news/ 2018/jun/04/what-is-depression-and- why-is-it-rising Smith DJ, Nicholl BI, Cullen B, Martin D, Ul-Haq Z, et al. (2013) Prevalence and Characteristics of Probable Major Depression and Bipolar Disorder within UK Biobank: Cross- Sectional Study of 172,751 Participants. PLOS ONE 8(11) https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0075362  Relapse Remission Recurrence Increasing symptoms 6-9 months  Course of MDD Tri g g e r li f e e ve n t s ~ 6 0 - 9 0 % vs. ~ 40 % (c a s e- c o nt r ol ) Hi g h re la p s e / re cu rre n c e ra t es : 5 0 - 8 5 % (J us e t a l. , 1 9 9 7 ) Af t e r t h e s ec o n d an d t h i rd ep i s od e , t h e ri sk o f re la p s e ris e s t o 7 0 a n d 90 % , re s p ec t i ve l y Re c o ve ry : 6 0 % a t 2 y e a rs , 40 % a t 4 y ea rs , a n d 30 % a t 6 y ea rs W h a t d o e s th i s tre n d s u g g e s t? Re c u rre n ce : 5 0 % 1 s t , 7 0 % 2 nd ; 9 0 % 3 rd (Ku p f e r, 1 99 1 ) 2 7 % ch ro n i c ( M a h li e t a l. 2 0 1 8 L an c e t ) Pro g n o si s wo rs e in e a rl y o n s et a n d o ld a g e o ns e t Up t o 1 0 % o f pe o p l e w it h M DD wi ll e x pe ri e n ce h y p om a n i a/ m a n i a a n d b e di a g n os e d wi t h b i po l a r  Biological Theories Genetic Factors Neurochemical Factors Brain Abnormalities AETIOLOGY Psychological Theories Behavioural & Interpersonal Theories Cognitive Theories BIOLOGICAL THEORIES Genetic factors He ritabi lity ~40% ; (Sul liva n et a l 200 0); Tw in studi es con corda nce 31-42 % (MZ) a nd ~20 % (DZ) (McGuffin e t al., 199 6, Ke ndl er et a l. 2 000 ) 2-3% i ncrea sed risk in first -de gree re lative s (Su lli van et al 20 00) He ritabi lity of ma jor de pressi on is hi ghe r i n wome n th an in me n (Kend ler et al 20 06) GxE (di athesi s-stress mode l) Gene ti c factors in fl uen ce respo nses to an en viron mental e vent (Casp i et a l 20 03) – chi ldh ood ma ltreatmen t an d interp erson al stressors BIOLOGICAL THEORIES Neurochemical f act ors Monoamine hypot hesis : low level of serot onin, dopamine & nor epinephrine in the limbic s yst em Antidepres sant s - tr icy clics and monoamine oxidas e inhibitors cause short term incr eas e of s erotonin and nor ephinephrine Alt ernativ e theor ies and t reat ments (MD MA , Ketamin, ot her psyc hadelic s, etc) Ko, K., Kopra, E. I., Cleare, A. J., & Rucker, J. J. (2023). Psychedelic therapy for depressive symptoms: A systematic review and meta-analysis. Journal of Affective Disorders, 322, 194-204. BIOLOGICAL THEORIES B ra in (a cti vat io n) abno rm al it i es PF C/ AC C have bee n sho wn to be hypoact ive → ant ic i pat e r ew ar ds , m anage em ot ions H ippo cam pus ( Red uced volum e) → cont ext uali s at ion of aff ec ti v e r esponse s – D epr essed indi vid uals wh o r em it ted w it h t re atm ent → l arg er pr e- t rea tm ent hi ppocam pal vo lum es (M acQ ueen et al 200 8) – Sm al ler hipp ocam pal vol ume s w ere r epor te d t o b e m or e p ron e t o r ela pse ( Kr onm ul ler et al 2 008) A my gdal a has been show n to be hyper acti ve → at ten ti on t o thr eat The causa l rol e such a lt era ti ons p lay in M DD i s uncl ear. We al so don ’t know i f th ese a re tr ai ts or st ate fe atur es of depr essi on. Davidson et al., 2002 BEHAVIOURAL THEORIES Decr eas ed environmental r ew ar d and insufficient positiv e reinforcement (pr edating the disorder) → the r ole of los ses and failur es How i s depression maint ai ni ng depression? Depress ion leads to f ur ther r eductions in positiv e reinforcement E. g. , people interact les s positiv ely wit h depress ed individuals (Golib & Robinson, 1982) Negat ive r einforc ement ( e. g. , depr essiv e or pas sive behaviours are r einforc ed) E. g. , Avoidance coping ( longitudinal s tudies show key role in development and maint enanc e of sy mptoms) Punishment of healthy behaviours Carvalho, J. P., & Hopko, D. R. (2011). Behavioral theory of depression: Reinforcement as a mediating variable between avoidance and depression. Journal of behavior therapy and experimental psychiatry, 42(2), 154-162. COGNITIVE THEORIES O ur b eliefs (an d so met ime s met a- b eliefs ) lead to d epress ion Exam ple o f t he vicio us cycle o f d epress ion BECK’S COGNITIVE THEORY OF DEPRESSION NE GAT I VE SC HEM AS Dy s f u nc t i o na l s e t o f b e li e f s l e ad i n g t o negative v ie w s o f o n e ’s s e lf a n d t h e world Relatively s t a bl e – early learned assumptions/views T h e y b i as s e le c t io n , e n co d i n g, c a t eg o ri s at i o n and e v al u a t io n o f s t im u l i i n n e g at i v e ways T h e y a re l i nk e d t o ad v e rs e c h i ld h o o d e v e n t s – M DD : 25 - 6 0 % se x u a l a b u se , e m o t io n a l a b u s e/ n e g l ec t (N eg e l e et a l 2 0 15 ), B D: 5 0 % ( G a rn o e t a l. 2 0 0 5 ) Early negative Formation of Cognitive experience schemas biases INFORMATION PROCESSING ERRORS Arbitrary Inference Jumping to conclusion when evidence is lacking or contrary Selective abstraction Abstracting a detail out of context and not ‘looking at the bigger picture’ Overgeneralisation Unjustified generalisation on the basis of a single incident Magnification & minimisation Perceiving events as either totally bad or neutral Personalisation Events’ interpretation on the basis of personal meaning All-or-none thinking Events labelled as black or white Discounting the positive Dismissing the positive in favour of the negative BECK’s COGNITIVE THEORY Negative Negative Activation of automatic life events schemas thoughts* Behavioural Somatic Cognitive Symptoms Affective Motivational * Characterised by COGNITIVE BIASES and Can you give THINKING ERRORS me an example?  Loss of relationship Absence of People are I will always be reliable parents untrustworthy, alone; Everyone hurtful, etc. will let me down* Behavioural Cognitive Somatic Depression Motivational Affective *Characterised by COGNITIVE BIASES and THINKING ERRORS  BECK’S COGNTIIVE THEORY NEG AT IVE AUTO MATIC T HO UG HT S: auto matic, neg ative, leading to thin king tr aps NEG AT IVE T RIA D: neg ative be liefs about th e se lf, the wo rld/other s and the fu ture SELF FU LF ILL ING PR OPH EC Y: pr edictions and beliefs ar e confirme d by con seq uences of expectations and beh aviour s COGNITIVE THEORIES LEARNED HELPLESSNESS Unavoidable negative life events (Seligman, 1975) Individuals learn to be‘helpless, lethargic and depressed’ Cognitions: No control, cannot change → lack of initiative Why only in some people? Why in events with influence? Why self-blame typically found in depression? CAUSAL ATTRIBUTION THEORY People with depression attri bute negative events to: Internal factors (likely to reduce self-esteem) Stable factors (unlikely to change) Global factors (likely to fail in several ot her aspects of life) Causal attribution has been shown to predict suicide and experimental manipulations cause depression However, some evidence that style remits in between relapses EXAMPLE: I failed my GCSE maths exam RUMINATION Repetitive thinking style, focusing on one’s depression and symptoms, and on the causes, meanings and consequences of events Why did this happen to me? Why do I feel like this? Why do I always react this way? Often dri ven by meta-cogni ti ve beliefs about i ts useful ness but often automatic and outside one’s awareness  Why did this Why can’t I happen to handle me? What does things this mean better? about me? What will others think of me? What am I doing to deserve this? Why do I feel so bad? Exacerbates negative mood and cognition in experiments Linked to less effective therapy Predicts anxiety, onset, duration, symptoms’ severity in prospective studies BIPOLAR DISORDERS Ch aracteri sed by pa th olo gica l mood sw ing s, from mani a to de pressi on. There a re severa l typ es of b ipo lar di sorde r, dep end ing o n th e patter n of th e mood sw ing s a nd thei r i ntensi ty Some ti mes, a mo od ep isod e incl ude s symp to ms o f bo th ma nia an d dep ressio n. This is cal led a mixe d sta te. MANIC EPISODE - DSM-5 D istin ctly ele vat ed o r ir rita ble mo od + at lea st 3 sym pt om s: In crea se in g oal -di rect ed a ctiv ity or p syc hom oto r ag itati on U nus ual talk ativ ene ss a nd rapi d sp eec h Fl ight of i dea s/ra cing tho ugh ts D ecre ase d n eed for slee p In crea sed se lf -es tee m D istra ctib ility R eck less nes s/R isk tak ing S ym ptom s are pre sen t m ost of t he d ay, n ear ly e ver y da y S ym ptom s last for 1 w eek , re qui re h osp ital isat ion or i nclu de psy cho sis S ym ptom s cau se s ign ifica nt f unc tion al d istr ess HYPOMANIC EPISODE – DSM-5 The same criteria apply with the following differences: Indi vidu als wi th h ypoma nia d o not expe rien ce th e marked i mpai rment in soci al or occu patio nal fun cti oni ng that chara cte rises man ia They do n ot re qui re hosp itali zation o r d ispl ay psycho ti c symp to ms, wh ich may be pre sent in a man ic epi sode Symptoms can b e prese nt for 4 da ys PERSONAL ACCOUNTS Hypomani a “At fir st when I ’m high, it’s tr emendous…ideas ar e fast...all s hy ness disappears, the right words and gest ur es are s uddenly there... uninteresting people, things bec ome intens ely interest ing. Sensuality is perv as ive; t he desire t o seduce and be s educed is irresist ible. Your marr ow is induced wit h feelings of ease, power, well -being, omnipotenc e, euphor ia...y ou c an do any thing…but somew here t his changes ” Mani a “The fast ideas become too fast and t here are far t oo many...overwhelming conf us ion replaces c lar ity... you stop keeping up with it – memory goes. I nf ec tious humour ceases t o amuse. Your friends bec ome f right ened...everything is now against the grain…y ou are ir rit able, angr y, fr ight ened, unc ontrollable and trapped. ”  MIXED STATE To q ualif y as h avin g a m anic or hy po man ic ep isod e w ith mixed fe atu res, on e m ust also have at lea st 3 o f t he fo llow ing sym pt om s du ring th e majo rity o f t he d ays o f t he c urrent or m ost recen t ep iso de o f m ania /hyp om ania : Pr om in ent dyspho ri a o r depr essed m ood D im ini shed in ter est or p leasu re in al l or al mo st all act ivi ti es Psych omo tor r et ar dati on near ly ever y d ay Fat ig ue o r loss of ene rgy Fee li ng o f wor th lessne ss or e xcessive or i nappr opr i ate gui lt ( not m er ely gui lt ab out bei ng sick) R ecur ren t thou ghts of dea th, r ecur r ent sui cidal i deat io n w it hout a speci fi c pl an, or a sui cid e at tem pt or a spe cif ic plan f or com mi tt in g sui cid e TYPES OF BIPOLAR DISORDERS BIPOLAR I AND II Bipolar I Disorder is mainly defined by manic or mixed episodes that last at least seven days, or by manic symptoms that are so severe that the person needs immediate hospital care. Usually, the person also has depressive episodes, typically lasting at least two weeks (diagnosis made regardless of these). Bipolar II Disorder is defined by a pattern of depressive episodes shifting back and forth with hypomanic episodes, but no full-blown manic episode – mixed state is possible. BP-NOS AND CYCLOTHYMIA Bipolar Disorder Unspecified (ex BP-NOS) is diagnosed when a person has symptoms of the illness that do not meet diagnostic criteria for either bipolar I or II. They symptoms may not last long enough or the person may have too few symptoms to be diagnosed with bipolar I or II Cyclothymia is a mild form of bipolar disorder. People who have cyclothymia have episodes of hypomania that shift back and forth with mild depression (no MDD) for at least two years  KEY FACTS OF BIPOLAR DISORDER Ons et: ear ly 2 0s or be for e O n se t o f f i rst m a n i c e p i so d e a f t er ag e 4 0 is a re d f la g f o r s u bs t a n ce u s e or ge n e ra l me d i ca l c o nd i t i on O n se t i n ch i ld h o o d as s o ci a t e d w it h w or st p ro g n o si s Li fe ti me preva len ce bip ola r I 1% an d bip ola r II 0.4 % Gend er distrib ution 1 :1 (g end er diffe rence s o f UD n ot fou nd) UK in cide nce hi ghe r i n bla ck/mi nori ty ethn ic grou ps 40-yea r fol low-up Zuri ch Coh ort fou nd 16 % recove ry (n o epi sode for 5 years), >50% recu rrent epi sode s COURSE OF ILLNESS EPISODIC UNSTABLE Purely episodic Radical mood course: instability: Inter-episode Inter-episode stability instability No mixed states Mixed states Infrequent Frequent episodes episodes Incomplete recovery Good recovery High incidence of Low incidence of complications complications Early onset SUICIDE IN BD Up t o 1 5 % o f pe o p l e w it h b i p ol a r c o mm i t s ui c id e ( Rh i m e r, 2 0 0 9) ~ 50 % a t t e m p t su i ci d e a t le a s t on c e ( Rh i m e r, 2 0 0 9) Su i ci d e ra t e s d ro p s ub s t a n t ia l ly wh e n a d eq u a t e ly t re a t e d Su i ci d e id e a t i on a n d b eh a v io u rs o cc u r m o st l y d ur in g e p is o d es o f m a jo r d e p re ss i o n, b u t a re l es s li k e ly i n p e o p le a f f ec t e d b y u n i po l a r d e pr es s io n – W h y c o u l d th a t b e ? T h e se ri o u sn e s s o f t h e s ui c id e a t t e m pt i s a ls o h ig h e r i n b i p o la r c o m pa re d t o u n ip o l ar s t a t es Su i ci d e ra t e s a re 4 t i me s g re a t er in m a le s t h a n f e m a l es (APA, 2 0 0 3) , wh il e a t t e mp t s a re m o re co m m o n am o n g f e ma l e s i n t h e ge n e ra l po p u l at i o n (Ku o , Ga l l o, & Ti e n , 20 0 1 ) – u n cl e a r i f t hi s ra t io re m a i ns i n BD AETIOLOGY OF BD Genetics He ritabi lity estimate up to ~85 % (McGu ffin et al 20 03) 1st deg ree rel atives: 5-10 % chan ce of BD Tw in studi es: co ncord ance 4 0-70 % in MZ (C radd ock and Jo nes 19 99) Gene ti c structure o verla ppi ng wi th sch izop hren ia spe ctru m a nd un ipo lar de pressi on Gene ti c me chan ism of cycl ing stil l not und erstood Sui cide se ems to ru n in some fami lie s w ith BD Li th ium resp onse : 1/3 resp ond s w ell , 1/3 some wha t we ll NEUROBIOLOGY D OPA MIN E ( DA ) D A in crea sed in man ic p has es and ind ucin g m ani a in peo ple wit h B D D A m ay p lay a ro le i n th e cy clic al m oo d sh ifts ➔ hi gh l eve ls o f do pam ine dur ing man ia a nd low le vels du ring dep res sive sta te fM RI Fr onta l co rtex : un der acti ve d urin g c ogn itive an d em oti ona l pro ces sin g (m ay acc oun t for imp uls ivity, di stra ctib ility, a nd emo tion dy sreg ula tion ) Li mbi c ar eas (pa rah ippo cam pa l gy rus , hip poc am pus , am ygd ala and ba sal gan glia ): ov era ctiv e du ring em oti ona l pro ces sin g (m ay be l inke d to em otio nal rea ctiv ity) Th e fr onta l co rtex wa s u nde ract ive in m ani c bu t no t de pre sse d st ates , w here as limb ic s truc ture s w ere not ove ract ive in a sso ciat ion with mo od stat es Chen et al., 2011 BD and IMMUNE DYSFUNCTION Pe o p le w it h BD ha v e h ig h ra t e s o f i n f la m m a t o ry m e d i ca l co n d i t io n s , in c lu d i n g a u t o i mm u n e d i so rd e rs , ch ro n i c i n f e ct i o n s, c a rd i ov a s cu l a r d is e a se a n d me t a b o li c d is o rd e rs ( Da n t z e r, e t a l. , 20 0 8 ). Cy t o k in e s ar e m o l e cu l e s o f t h e im m u n e sy s t em w hi c h ma y i nc re a s e o r d e c re a se i n f la m m a t or y re s p o ns e s. Me a s u rin g c yt o k i ne l e ve l s pr ov i d es i n si g h t in t o i mm u n e sy s t e m a c t iv i t y. Cy t o k in e s t ud i e s h a v e co n s is t e n t ly s ho w n e l e va t e d l ev e l s o f p ro- i n f la m m a t or y c y t ok i n es i n BD , su g g e st i v e o f c h ro n ic l ow g ra de i n f la m m a t io n. An o t h e r ke y o b se rv a t io n h a s b e e n va ri a b il i t y i n c yt o k in e p ro f i le s d ep e n d in g o n m oo d s t a t e (i. e. , d if f e rin g c yt o k i ne p ro f i le s d u rin g p e ri od s o f d ep re s s io n a n d m a n i a).  MICROBIOTA-GUT-BRAIN AXIS O ne p ote nti al pat hw ay: G ut mi cr obio ta ma y have a lar ge im pact o n t he cytoki nes that a re bei ng pro duced by t he gast r oint est inal ( G I) syst em. The G I system m ay ind uce t he pr oduct ion of pr o - i nfl am mat or y cyt okin es on an acut e o r chr onic basi s The se cyt okin es m ay have dir ect eff ects on br ain fu ncti on The re is som e e viden ce t hat t hose wi th BD have a “w or se” gut m i crob iot a H oweve r, st udie s conf ound ed b y ot her f acto rs (e.g. , peopl e wi th BD al so t ake me dicat io ns, etc. ) O the r pat hw ays: – Pa thw ays: gene ti c, substa nce u se, str ess, m ood swi ngs as t he ori gi n f or chr oni c i nfl am mat io n Rosenblat, J. D., & McIntyre, R. S. (2017). Bipolar disorder and immune dysfunction: epidemiological findings, proposed pathophysiology and clinical implications. Brain sciences, 7(11), 144. PSYCHOLOGICAL THEORIES Be ha vioura l Ac tiv ation Syste m (BAS) dysr egulation model I n d iv i d ua l s wi t h B D h a ve h i gh e r s e n si t i vi t y t o c u e s o f re w ar d ( e. g. , m a n ia c a n be t ri g g e re d b y po s i t iv e e ve n t s an d g o a l - d i re ct e d b e ha v i ou r) Cognitive theories Ne g a t i ve a t t ri b ut i o n a l s t y le a s so c ia t e d wi t h d ep re s s iv e a nd m a n ic s t a t es , BU T p o si t i ve a t t ri b ut i o n a l s t y le wa s n o t el e v at e d i n ma n i a (Re i ll y - Ha rr in g t o n et a l. , 2 0 10 ) → s o me ‘d e p re ss o g en i c c o gn i t i ve s t yl e ’ is m a in t a i n ed d u ri n g m a n i a TREATMENTS PSYCHOPHARMACOTHERAPY DEPRESSION BIPOLAR DDISORDER Enhance serotonin Lithium carbonate neuro-transmission PROBLEMS WITH CURRENT MEDS 1/3 does not remit High relapse and recurrence High Intolerance High drop out rate (i.e., 40%) 2-8 weeks for meds to be effective (increased depression in some at the beginning) Side effects (e.g., heart, liver, epileptic fits, nausea, weight gain, etc.) CLUB DRUGS as treatment? There i s need for anti depressant s with rapid effects! Ketami ne: N MD A r ecep tor a ntag onist Fou nd t o be e ffect ive ver y qu ickl y ( 4 h our s) Aca dem ics’ dr ugs ( psychot ics if not m oni to red , expensi ve b ecause mo nit or ing r equi red , indu ce peo ple to t ake i ll ici t dr ugs?) LSD: So me bene fi ts rep ort ed, on e m et a an alysi s ( K o , K. , K o pr a , E. I. , C le a r e , A. J., & R u c k e r, J. J. ( 2 0 2 3 ). P s y c h ed e l ic th e r a p y f o r d e p r e s s i v e s y m p t om s : A s y s t em a ti c r e v i e w an d m e ta - a n a ly s i s. J o u r n a l o f A ff ec t iv e D is o r d e r s , 3 2 2, 1 9 4 - 2 0 4.) ELECTROCONVULSIVE THERAPY Induces small seizures to correct brain activity (2x week, 6-8 sessions) Used for severe treatment-resistant depression, mania or catatonia 70-80% efficacy UK: 12,000 per annum, 71% women, 46% >age 65, 16% without consent Controversial: Amnesia and confusion Long-term cognitive deficits? Destroys brain cells? BRAIN STIMULATION Transcranial Magnetic Stimulation Deep brain stimulation  BEHAVIOURAL ACTIVATION In crea se acc ess to p lea san t ev ents /rew ard s D ecre ase ex peri enc e of ave rsiv e e ven ts Fe atu res D aily mo nito ring of p lea san t/un plea san t ev ent s A sse ssin g fu ncti on of de pre sse d be hav iou r (e sca ping from re spo nsib iliti es, el iciti ng sy mp athy fro m, et c.) Id enti fica tion of be hav iou ral go als w ithin m ajor lif e ar eas (activity hierarchy) S ocia l sk ills , t ime ma nag eme nt t rain ing, goa ls & sc hed ule Fo ste rs c ogn itive ch ang e C hea p & as effect ive as C BT (Ho pko et a l., 2 003 , R icha rds et a l. 2 016 , La nce t) CBT Behavioural activation Monitoring of NATs Identify negative beliefs and thoughts Challenge these thoughts as dysfunctional and irrational Reattribution training/cognitive restructuring Adopt more rational and adaptive beliefs COGNITVE RESTRUCTURING Situation Mood Automatic thoughts Evidence for ATs Evidence Alternative Rate against ATs thoughts moo d Who? What do What was going through Write an Re- What? you feel? your mind just before alternative rate When? Rate thought mood Where? mood these thoughts? At home Depres I am not making any I’ve tried many Some days I alone – sed 100% progress types of therapy do feel better Saturday which 9.30 haven’t helped EFFECTIVENESS OF CBT As effective as drug therapy, but higher efficacy in the long- run. More effective than drug therapy in reducing relapse However, still high levels of relapse (up to 40%; Bockting et al., 2005) Combination of drug therapy and cognitive therapy superior to either treatment alone GUIDED SELF-HELP FOR BD Manic/hypomanic states Depressive states: Recognize warnings signs Differentiate depression caused by Interventions and rules external factors vs. bipolar downs Medical solutions first Maintain a routine Two-person feedback rule Avoid disrupting biological rhythms Limit cash payments Keep thought logs and mood To counteract impulsivity: diaries which identify triggers Give car keys or credit cards Increase pleasurable activities Rules about staying out late or Work on negative thoughts giving out phone number Avoid alcohol and substance use 48-hours before acting rule QUESTIONS?