Clinical Psychology: Mood (Affective) Disorders Study Notes
Hello future clinical psychologists! This chapter dives into one of the most common and challenging areas in mental health: Mood Disorders. Understanding how these conditions—specifically Depressive Disorder and Bipolar Disorder—are diagnosed, explained, and treated is crucial. It’s a central part of the Clinical Psychology option, so let’s make sure these complex concepts feel approachable!
Don't worry if the terminology seems heavy; we will break down every part using simple language and memorable examples.
1.2.1 Diagnostic Criteria for Mood (Affective) Disorders
Mood disorders, also called affective disorders, are mental health conditions where a person experiences a persistent disturbance in their mood state. The two main types we study are Depressive Disorder (Unipolar) and Bipolar Disorder.
A. Depressive Disorder (Unipolar Depression)
The term 'Unipolar' means the mood disturbance goes in only one direction: down. It involves periods of severe sadness and lack of motivation that interfere with daily life.
ICD-11 Diagnostic Criteria (World Health Organization)
Diagnosis requires the presence of core symptoms for a specific duration (usually at least two weeks) and must result in significant distress or impairment.
- Core Symptoms:
- Persistent low mood (sadness, hopelessness).
- Anhedonia (loss of pleasure or interest in activities once enjoyed).
- Reduced energy or increased fatigue.
- Other Common Symptoms:
- Changes in appetite and weight (increase or decrease).
- Sleep disturbances (insomnia or hypersomnia).
- Feelings of worthlessness or excessive guilt.
- Reduced concentration and difficulty making decisions.
- Thoughts of self-harm or suicide.
Quick Tip: Depression is more than just feeling sad after a bad day; it’s a sustained illness causing severe impairment across multiple life areas.
B. Bipolar Disorder
Bipolar disorder is characterised by extreme mood swings, oscillating between two "poles": periods of intense high mood (manic episodes) and periods of deep low mood (depressive episodes).
Key Difference: Manic Episodes
During a manic episode, a person experiences abnormally and persistently elevated, expansive, or irritable mood, accompanied by increased activity or energy.
- Manic Symptoms include:
- Grandiosity: Inflated self-esteem or belief in superior abilities.
- Decreased need for sleep (e.g., feels rested after only 3 hours).
- More talkative than usual; pressure to keep talking (rapid speech).
- Flight of Ideas: Thoughts racing from one topic to the next very quickly.
- Distractibility.
- Excessive involvement in activities with high potential for painful consequences (e.g., reckless spending or risky sexual behaviour).
Did you know? Bipolar disorder used to be known as 'Manic Depression'. The shift to 'Bipolar' reflects the equal importance of both the manic and depressive states in the diagnosis.
C. Measuring Depression: Beck Depression Inventory (BDI)
To accurately measure the severity of depression, psychologists often use standardized psychometric tests, such as the Beck Depression Inventory (BDI).
- What is it? The BDI is a 21-item self-report questionnaire.
- How does it work? The patient rates the intensity of their depressive symptoms (e.g., hopelessness, irritability, fatigue, weight loss) over the past two weeks on a scale of 0 to 3.
- Why use it? The scores provide a quantitative measure of depression severity, helping clinicians track improvement or deterioration during treatment.
Key Takeaway for Diagnosis: Unipolar involves persistent low mood and anhedonia (the loss of pleasure). Bipolar involves cycles of manic highs and depressive lows. The BDI is a standard tool for quantifying the severity of depressive symptoms.
1.2.2 Explanations of Mood Disorders: Depressive Disorder (Unipolar)
Why do people develop depression? Psychological approaches offer competing explanations, often divided into biological (nature) and psychological (nurture/cognitive) factors.
A. Biological Explanations
1. Biochemical Explanation
This explanation focuses on imbalances in brain chemistry, specifically neurotransmitters.
- The Monoamine Hypothesis: Suggests that depression is caused by insufficient levels of certain neurotransmitters—particularly Serotonin and Norepinephrine (or Noradrenaline)—in the synaptic gap.
- Analogy: Imagine Serotonin is like a messenger that carries good-mood instructions across the brain. If you have depression, the brain isn't producing enough messengers, or they are being cleared away too quickly.
2. Genetic Explanation
Depression runs in families, suggesting a genetic predisposition (diathesis). This doesn't mean someone *will* get depression, but they are more *vulnerable* to it, often triggered by environmental stress.
- Key Study: Oruč et al. (1997)
This study used an association analysis of genetics to investigate the possible involvement of two specific receptor genes (5-HT2C and 5-HT transporter) in Bipolar Disorder. While the syllabus focuses on the general genetic explanation for depressive disorder, this study highlights the search for specific gene markers that may predispose individuals to mood disorders.
Although Oruč focused on Bipolar Disorder, the methodology illustrates the genetic approach applied to mood disorders—the search for specific gene linkages.
B. Psychological Explanations
1. Beck's Cognitive Theory of Depression
Aaron Beck (1967) argued that depression stems from flawed, negative thinking patterns, not just chemical imbalances.
- Negative Schemas: Depressed individuals develop rigid, negative ways of viewing the world, often established in childhood (e.g., through trauma or criticism).
- The Cognitive Triad: These negative schemas result in negative automatic thoughts about three key areas:
- The Self: "I am worthless/inadequate."
- The World: "Everything is stacked against me."
- The Future: "Things will never get better."
- Faulty Thinking (Cognitive Errors): These are systematic errors in logic that reinforce the negative triad, such as overgeneralisation ("I failed one test, so I will fail everything.") or catastrophising (blowing a small negative event out of proportion).
2. Learned Helplessness and Attributional Style
Developed primarily by Martin Seligman, this theory suggests that depression results from learning that one has no control over negative life events.
- Learned Helplessness: Originally observed in animals who were exposed to uncontrollable negative stimuli (electric shocks) and eventually stopped trying to escape, even when escape became possible.
- Attributional Style (Seligman et al., 1988): When negative events happen, how a person *explains* them (their attributional style) determines if they become depressed. A pessimistic attributional style involves explaining negative events using attributions that are:
- Internal: "It's all my fault." (e.g., I failed because I am stupid).
- Stable: "It will last forever." (e.g., I will always be stupid).
- Global: "It affects everything I do." (e.g., Because I am stupid, I will fail in relationships and work).
Mnemonic for Pessimistic Attribution: I.S.G. (Internal, Stable, Global). If you attribute failure to ISG, you are prone to learned helplessness.
Key Takeaway for Explanations: Biological theories point to low neurotransmitter levels (Serotonin) and genetics. Psychological theories focus on negative thinking patterns (Beck's triad) and believing you have no control (Learned Helplessness/ISG attribution).
1.2.3 Treatment and Management of Mood (Affective) Disorders
Treatment approaches range from biological interventions aimed at correcting chemical imbalances to psychological therapies that restructure negative thought patterns.
A. Biological Treatments: Antidepressants
Antidepressants work by adjusting the levels of key neurotransmitters (monoamines) in the brain.
- Tricyclics (TCAs) and MAOIs (Monoamine Oxidase Inhibitors): These are older classes of drugs. They block the reabsorption of norepinephrine and serotonin, or prevent their breakdown. They are effective but have significant side effects.
- SSRIs (Selective Serotonin Reuptake Inhibitors): These are the most commonly prescribed antidepressants today (e.g., Prozac).
- Function: SSRIs specifically block the reabsorption (reuptake) of serotonin back into the presynaptic neuron.
- Result: This leaves more serotonin available in the synapse (the gap between neurons), enhancing its effect on the postsynaptic neuron, thereby improving mood.
B. Psychological Therapies
1. Beck's Cognitive Restructuring (CBT Component)
This therapy aims to directly challenge the negative cognitive triad and the faulty thinking that maintains depression.
- Process:
- Identify: Help the client recognise their negative automatic thoughts (NATs).
- Challenge: Use Socratic Questioning ("What evidence do you have for this belief?") to test the validity of the NATs.
- Change/Replace: Encourage the client to replace irrational, negative thoughts with more balanced, rational alternatives.
- Example: If a client thinks, "I'm a failure," the therapist might challenge this by asking for concrete evidence of successes they achieved that week.
2. Ellis's Rational Emotive Behaviour Therapy (REBT)
Developed by Albert Ellis, REBT focuses on resolving emotional and behavioural problems by disputing irrational beliefs, which Ellis refers to as 'musts' or 'shoulds'.
- The ABC-D Model:
- A (Activating Event): A situation or event occurs (e.g., failing a test).
- B (Belief): The person holds an irrational belief about A (e.g., "I absolutely must pass every test, and since I failed, I am worthless.").
- C (Consequence): The resulting emotional consequence (Depression, anxiety).
- D (Disputing): The therapist actively challenges and disputes the irrational belief (B) to reduce the emotional consequence (C).
- Goal: To help the client achieve a more rational and effective outlook on life, leading to emotional and behavioural improvement.
Key Takeaway for Treatment: Biological treatments (SSRIs) boost neurotransmitters like serotonin. Psychological treatments (CBT/REBT) teach clients to identify and challenge their negative or irrational thought patterns, providing them with cognitive tools to manage their mood.
Quick Review Box
Unipolar: Downward spiral (depression only).
Bipolar: Cycles between mania and depression.
BDI: Measures depression severity (self-report).
Biological cause: Low serotonin/norepinephrine.
Psychological cause: Negative triad (Beck) or ISG attributions (Seligman).
Treatment goal: Use SSRIs to boost serotonin, or CBT/REBT to restructure thoughts.