1.2 Mood (affective) disorders: depressive disorder (unipolar) and bipolar
- Syllabus
- 9990–2028–2029
- Topic
- 1.2
- Level
- A2
Learning objectives
1.2.1Mood disorder criteria• 1.2.1 Diagnostic criteria for mood (affective) disorders- diagnostic criteria (ICD-11) of mood disorders: depressive disorder (unipolar) and bipolar disorders including manic and depressive episodes.- measure of depression: Beck depression inventory.- Relevant issues and debates and methodology for this topic include: individual and situational explanations, cultural differences, quantitative and qualitative data, psychometrics, validity.1.2.2Mood disorder explanations• 1.2.2 Explanations of mood (affective) disorders: depressive disorder (unipolar)- biological explanations:- - biochemical- - genetic (exemplified by the following key study).- Key study on association analysis of genetics of depressive disorder: Oruč et al. (1997).- psychological explanations:- - Beck's cognitive theory of depression and attributional style, including a study, e.g. Seligman et al. (1988)- - learned helplessness.- Relevant issues and debates and methodology for this topic include: nature versus nurture, reductionism versus holism, determinism versus free-will, experiments, reliability.1.2.3Mood disorder treatments• 1.2.3 Treatment and management of mood (affective) disorders- biological treatments including the use of anti-depressants (tricyclics, MAOIs and SSRIs).- psychological therapies:- - Beck's cognitive restructuring- - Ellis's rational emotive behaviour therapy (REBT).- Relevant issues and debates and methodology for this topic include: application to everyday life, individual and situational explanations, reductionism versus holism, determinism versus free-will, generalisations.
Episode history distinguishes depressive from bipolar disorders; BDI measures reported severity
| Pattern | Core episode features | Diagnostic distinction |
|---|---|---|
| Depressive episode | Persistent low/irritable mood or reduced interest/pleasure with cognitive, energy, sleep/appetite, guilt/hopelessness and possible death thoughts causing impairment | Recurrent/single depressive disorder has no history of manic or hypomanic episode |
| Manic episode | Markedly elevated/expansive or irritable mood plus increased activity/energy, reduced sleep need, pressured speech, racing thoughts, inflated self-esteem/risk behaviour and marked impairment | Presence establishes bipolar spectrum episode history rather than unipolar depression |
| Bipolar course | Manic/hypomanic and depressive episodes or mixed features across time | More than ordinary mood variation; episode pattern/severity/duration and exclusions matter |
| BDI feature | Use | Boundary |
|---|---|---|
| 21 self-report items | Samples cognitive, affective and physical depressive symptoms | Depends on insight, literacy, culture, recall and response style |
| Four response levels scored 0-3 | Sum 0-63; higher total indicates greater reported severity | Quantifies subjective experience; score is not an objective diagnosis |
| Syllabus bands | 1-10 normal ups/downs, 11-16 mild, 17-20 borderline, 21-30 moderate, 31-40 severe, >40 extreme | Interpret as taught bands alongside clinical assessment, risk and alternative causes |
| Repeat use | Track reported change over time | Practice, situation and treatment expectancy can affect scores |
Validity strengths: multiple symptom domains, graded rather than yes/no responses, overlap with recognised depressive features and concurrent relation to other depression scales. Limits: nomothetic fixed items omit unique experience, social desirability/self-report bias, somatic symptoms can have other causes, and BDI does not detect mania adequately.
Use BDI as one measure: obtain consent/privacy, explain time frame, complete all items, sum accurately, note item-level risk, combine with qualified interview/history/functional evidence and repeat consistently if monitoring. Never infer bipolar versus unipolar from total score alone.
Bipolar is defined by manic/hypomanic episode history, not simply severe depression or moment-to-moment mood change. BDI is a psychometric self-report of severity and may support assessment; it cannot independently diagnose or replace safety evaluation.
Mood-disorder explanations connect biological vulnerability, cognition, attribution and perceived control
| Explanation | Mechanism | Evidence/boundary |
|---|---|---|
| Biochemical | Dysregulated monoamine systems such as serotonin/noradrenaline affect mood, motivation and cognition | Antidepressant action supports involvement but delayed/incomplete response and correlational direction prevent a simple low-serotonin cause |
| Genetic | Polygenic vulnerability raises probability of depressive/bipolar episodes | Family/twin/association evidence is probabilistic and environment affects expression |
| Beck cognitive | Negative schemas/cognitive triad about self, world and future produce automatic biased thoughts | Explains depressive appraisals and supports restructuring; thoughts may be cause, consequence or reciprocal |
| Attributional style | Negative events attributed internally, globally and stably increase hopelessness | Seligman-style evidence links pessimistic style to later depression risk; culture/context and self-report matter |
| Learned helplessness | Repeated uncontrollable outcomes create expectation that actions cannot change events, reducing effort and mood | Explains passivity/individual differences; animal/task transfer and actual adversity limit generalisation |
| Oruč et al. (1997) | Exact evidence |
|---|---|
| Aim | Test association of serotonin 5-HT2C receptor and 5-HT transporter polymorphisms with bipolar disorder |
| Sample/design | 42 Croatian bipolar I patients (25 women, 17 men, 31-70) and 40 age/sex-matched healthy controls |
| Procedure | DNA polymorphism analysis; family history checked |
| Results | No significant total-sample 5-HT2C association; 16 patients had first-degree family history; female subgroup showed trends for both polymorphisms |
| Conclusion | Variants might make a minor sex-linked contribution to susceptibility, not a single causal bipolar gene |
| Lens | Evaluation |
|---|---|
| Reliability | Standard DNA procedures/objective genotyping replicate; historical family diagnoses/records may vary |
| Nature–nurture | Gene/biochemistry support nature; null/partial associations and stress/cognition support interaction |
| Reductionism–holism | Molecular and single-style models are testable but partial; integrated vulnerability–stress account is broader |
| Determinism | Vulnerability/processes constrain probability, not inevitable episodes; coping/treatment and environment matter |
| Individual–situational | Attribution/control expectations are individual interpretations of real situations; neither level alone suffices |
Oruč studied bipolar I and found no significant main total-sample association; subgroup trends are not proof of a female bipolar gene. Learned helplessness is an acquired expectation of no control, not a moral failure or voluntary refusal. Biochemical association/treatment effects do not settle causal direction.
Mood treatment targets monoamine availability or maladaptive appraisals and beliefs
| Class | Main mechanism | Main strengths/risks |
|---|---|---|
| Tricyclics | Block reuptake of serotonin and noradrenaline, increasing synaptic availability | Effective for some severe depression; anticholinergic, sedation, cardiovascular and overdose toxicity concerns |
| MAOIs | Inhibit monoamine oxidase so serotonin/noradrenaline/dopamine breakdown falls | Option after other failures; food/drug interactions and blood-pressure risk require strict management |
| SSRIs | Selectively inhibit serotonin reuptake | Often first-line due to tolerability/ease; delayed response, gastrointestinal/sexual/sleep effects and individual non-response |
| Therapy | Change process | Application |
|---|---|---|
| Beck cognitive restructuring | Identify negative triad/automatic thought → record mood/thought/behaviour → test evidence/reality → generate balanced alternative → homework/practice | Challenge depressive underestimation and, for bipolar management, overly positive/risky manic appraisals as well as negative depressive ones |
| Ellis REBT | A activating event → B belief → C emotional/behavioural consequence → D actively dispute irrational/demanding belief → E effective new philosophy/consequence | Show event does not directly cause mood; challenge absolutist 'must/awful/worthless' belief and rehearse rational alternative |
Treatment answer: identify specific symptom/episode and goal; explain exact mechanism; give a personalised step/example; predict measurable short/long outcome; evaluate engagement, side effects, relapse, access/culture, consent and combination with clinical monitoring. Medication and therapy are not one-size-fits-all.
| Lens | Comparison |
|---|---|
| Application | Drugs are accessible/standardised and may reduce severe symptoms; cognitive skills can transfer after therapy |
| Reductionism–holism | Drugs target biology; restructuring/REBT include meaning but may still underweight social adversity |
| Individual–situational | Drug response/side effects and beliefs are individual; stress, poverty, loss and support remain situational |
| Determinism–free will | Mechanisms constrain mood; choosing/engaging in medication/homework expresses agency within illness |
| Generalisation | Group efficacy does not predict each person, bipolar phase, culture or comorbidity |
REBT treatment requires disputation and effective new belief—ABC alone only explains the problem. Cognitive restructuring is not forced positive thinking: it tests evidence and builds balanced alternatives. Antidepressants alter transmission gradually and do not instantly create happiness or prove monoamine deficiency caused the disorder.