Clinical Psychology

0. Big Picture

Clinical psychology = diagnosing and treating psychological disorders. 5 disorders: schizophrenia · mood disorders · impulse control disorders · anxiety & fear-related disorders · OCD.

Approach	Asks…	Used for
Biological	neurotransmitter imbalance? genes? (brain scans, blood tests)	drug therapy, ECT
Cognitive	faulty / irrational information processing?	CBT, REBT, cognitive restructuring
Learning (behaviourist)	classical & operant conditioning?	desensitisation, ERP, covert sensitisation
Social / psychodynamic	environment, trauma, unconscious conflict?	talking therapies

An interactionist view (biology + environment, e.g. inherited predisposition + trauma trigger) is often the most sensible.

6.1 Schizophrenia

① Diagnostic criteria (ICD-11)

Psychotic disorders = major break from reality (person perceives the world very differently from others). Schizophrenia = a very severe psychotic disorder; disturbances in thoughts, feelings, experience & behaviour.

Positive symptom = experience 'in addition to' / 'distortion of' normal experience (delusions = distorted thinking; hallucinations = distorted perception). Negative symptom = level of functioning/experience falls below normal (avolition = motivation lower than normal; flattened affect = less emotion expressed than expected).

Types of delusion

Type	Strongly held belief that…	e.g.
Persecutory	you are in danger / conspired against / others pursue you to harm you	"they're out to get me"
Grandiose	you have special abilities or powers	"I am a superhero"
Reference	events in the environment relate to you	TV programme is talking about me

All are beliefs fully believed despite strong evidence to contradict.

② Key study: Freeman et al. (2003) — VR & persecutory ideation

Freeman, Slater, Bebbington, Garety, Kuipers, Fowler… & Vinayagamoorthy (2003). Can virtual reality be used to investigate persecutory ideation? J. Nervous & Mental Disease, 191(8), 509–514.

③ Explanations of schizophrenia

A. Biological — Genetic

Genes (or combinations of genes) are passed to offspring and may cause the disorder. 3 ways to investigate:

Method	What it does
Family study	are biological relatives of someone with the disorder more likely than non-relatives to be similarly affected? Close relatives share more genes ⇒ more risk
Twin study	compares concordance in MZ (identical, 100% DNA) vs DZ (non-identical, ~50% DNA) twins. Allows nature vs nurture to be studied
Adoption study	adopted child vs biological parent (not raised by them) ⇒ truly separates genes from environment – family & twin studies can't

• Gottesman (1991): risk of developing schizophrenia = 1% general population → 48% if you have an identical twin with it.
• Hilker et al. (2017): twin study, 30 000+ twin pairs in Denmark (Danish Twin Register + Danish Psychiatric Central Research Register), included related disorders ⇒ heritability = 79%.
• Tienari et al. (2000): adoption study – schizophrenia in 6.7% of adoptees whose biological mother had it vs just 4% of controls (adoptees of mothers without it).

B. Biological — Biochemical (the dopamine hypothesis)

Neurotransmitter = chemical messenger enabling communication between neurons; it crosses a small junction called the synapse. Neurons using dopamine may fire too often or send too much information. Excess dopamine in the Broca's region (language formation) ⇒ impaired logical speech (classic symptom).

Evidence:

• Drug trials (give different drugs to groups & compare): amphetamines & cocaine ↑ dopamine ⇒ more hallucinations/delusions; in schizophrenia they make symptoms worse. L-dopa (synthetic dopamine for Parkinson's) in too-high dose ⇒ symptoms identical to schizophrenia, e.g. hallucinations (Lindström et al., 1999).
• Post-mortem studies: deceased patients' brains have more dopamine receptors. Wise et al. (1974): brain fluid had abnormally low levels of the enzyme that breaks down dopamine ⇒ dopamine probably present in excess.
• PET scans (gamma cameras detect radioactive tracer e.g. glucose; accumulates in active areas): more receptors in striatum, limbic system, cortex in schizophrenia ⇒ linked to positive symptoms. Nestler (1997): decreased dopamine activity in prefrontal cortex ⇒ negative symptoms e.g. flattened affect.

C. Psychological — Cognitive (Frith, 2015)

Accepts biology contributes to positive symptoms, but no single genetic/structural/biochemical cause found ⇒ looks for faulty mental processes. Schizophrenia = abnormality of self-monitoring.

• Hallucinations: patients fail to recognise perceived voices are inner speech ⇒ attribute them to an external source. Test: decide if items read aloud were said by themselves, an experimenter or a computer. Patients with incoherent speech did worst ⇒ linked to memory & attention difficulties crucial for self-monitoring.
• Delusions: misinterpretation of perception – self-generated thoughts seem external and get built into beliefs (logical reasoning applied to hallucinations) ⇒ delusions of alien control, auditory hallucinations, thought insertion. Inability to monitor others' intentions ⇒ paranoia & incoherence.
• Negative symptoms (e.g. avolition): difficulty generating spontaneous actions ⇒ hard to decide what to do without a prompt (can answer a question – a stimulus – but struggles to start a conversation). Partly due to impaired theory of mind (recognising intentions of others). Flat affect, lack of speech, social withdrawal ⇒ difficulty monitoring own mental states and others'.

④ Treatment & management of schizophrenia

Hard to treat: complex, many symptoms across all areas of functioning; usually positive + negative together. Patients may need help for acute episodes (period of active psychotic symptoms e.g. hallucinations/delusions) and help with independent living.

A. Biochemical — Antipsychotics

Before the 1950s (before dopamine was identified) no treatment – patients just hospitalised hoping for improvement. 1950s: antipsychotics developed → reduce dopamine activity ⇒ reduce symptoms. Usually the first treatment after diagnosis, continued alongside psychological therapy (e.g. CBT).

	Typical (1st generation)	Atypical (2nd generation)
Developed	1950s	1990s
Example	chlorpromazine	clozapine
How it works	dopamine antagonists – block dopamine receptors (must block a considerable proportion of dopamine activity)	block dopamine but rapidly dissociate (block only briefly) ⇒ normal dopamine transmission can still happen
Symptoms treated	mainly positive (hallucinations, delusions)	positive AND negative; effective for treatment-resistant patients
Side effects	many & can be severe: extrapyramidal symptoms (EPS) and tardive dyskinesia (TD) – affect motor control, involuntary spasms & abnormal movements of face/body	lower risk, less severe: weight gain, drowsiness, difficulty concentrating

• Evidence (RCTs, often double-blind placebo controlled): ~50% show significant improvement after 4–6 weeks; 30–40% partial improvement; a substantial minority little/no improvement.
• Relapse (symptoms return) rates are high. Patients told to keep taking medication after acute episodes (even in remission – at lower doses). But side effects + fewer symptoms ⇒ non-adherence to medication (stopping against the doctor's instructions).

B. Electro-convulsive therapy (ECT)

• History: inducing seizures used for hundreds of years. 1930s – mistaken belief that schizophrenia was very rare in epileptics ⇒ first ECT trials. Cerletti & Bini saw the effect of electric shocks on cattle ⇒ used on humans, but with no anaesthetic or anti-anxiety drugs patients were traumatised, some broke bones.
• Modern ECT: pass electricity through the brain to induce a seizure – the seizure is the 'treatment', not the electricity. Course of 6–12 sessions, ~twice a week (less often later to prevent relapse). Now applied unilaterally to the non-dominant hemisphere (not bilateral) ⇒ ↓ memory loss.
• Risks: affects central nervous & cardiovascular systems (dangerous with pre-existing medical conditions); memory loss common (usually temporary); rarely lasting neurological damage or death.
• No agreed explanation of why it works – maybe affects post-synaptic responses to CNS transmitters.
• Use: rarely used – no evidence it beats antipsychotics. Can work in acute episodes (fast, short-term improvement of severe symptoms); maybe best for catatonic symptoms (NICE, 2015). Still controversial.

C. Psychological — Cognitive-behavioural therapy (CBT)

Combines cognitive + behaviourist principles; departs from strict focus on observable behaviour to recognise invisible cognitive processes. A talking therapy – recognise & challenge the thoughts underlying behaviours to change them. Almost always used alongside antipsychotics – drugs first to stabilise the patient enough to engage in therapy.

Schizophrenia — Quick questions (textbook)

• Q1: predictors of persecutory ideation in VR (Freeman) ⇒ high interpersonal sensitivity + high anxiety (not thoughts about avatars / not gender).
• Q2: twin studies: genetic influence but never 100% ⇒ environment also matters ⇒ supports an interactionist view in the nature vs nurture debate; adoption studies help separate the two.
• Q3: explanation that fits antipsychotics best ⇒ the dopamine hypothesis (drugs reduce dopamine activity).

6.2 Mood (Affective) Disorders

Depressive disorder (unipolar) and bipolar disorder

① Diagnostic criteria (ICD-11)

Mood disorders = episodes of particular types of mood over time (depressive, manic, mixed, hypomanic). Episodes are not diagnosable on their own – they are the main components of mood disorders. Episodic mood disorder = episodes where mood is either very low or very high.

Depressive disorder (unipolar)

Depressed mood (sad, irritable, empty) or loss of pleasure + symptoms affecting function (poor concentration, worthlessness/guilt, recurrent thoughts of death, changes to eating/sleeping). Diagnosis only if the person has never had a manic, mixed or hypomanic episode (that would mean bipolar).

• Single-episode: one depressive episode, no previous history.
• Recurrent: ≥ 2 depressive episodes separated by several months without significant mood disturbance.

Bipolar disorders

	Type 1	Type 2
Defined by	≥ 1 manic or mixed episode	≥ 1 hypomanic episode + ≥ 1 depressive episode
Behaviour	extreme euphoria / irritability, high activity, rapid speech, impulsivity, reckless behaviour, v. high self-esteem	lesser versions (↑ talkative, ↑ self-esteem, impulsive); different from usual but NO marked impairment
Note	manic/mixed often alternate with depressive episodes	no history of manic or mixed episodes

② Measure: Beck Depression Inventory (BDI)

21-item self-report; measures attitudes & symptoms of depressive disorder; one of the most widely used tools. Each item = ≥ 4 statements; choose the one that best fits how you felt over a recent period (past week or two weeks, depending on version).

e.g. (Beck, 1979): "I get as much satisfaction out of things as I used to" (0) · "I don't enjoy things the way I used to" (1) · "I don't get real satisfaction out of anything anymore" (2) · "I am dissatisfied and bored with everything" (3)

Other items: guilt, hopelessness, fatigue, weight loss. Updated twice – current BDI-II (1996) adds increase/loss of appetite & fatigue.

③ Explanations of mood disorders

Many factors: environmental (e.g. trauma) and biological (genes, brain chemistry).

A. Biological — Biochemical

• Dopamine – signals for motivation & pleasure. Low dopamine ⇒ low motivation/pleasure = core symptoms of depression. Evidence: low dopamine often found in depression; anti-depressants reduce symptoms by increasing dopamine.
• Serotonin – regulates sleep, appetite, mood, anxiety. Normal levels ⇒ balanced. Low ⇒ low mood, anxiety, disrupted sleep & eating. Evidence: most common anti-depressants are SSRIs, which ↑ serotonin.
• Bipolar: serotonin, dopamine and noradrenaline linked to onset. Levels too high / too low ⇒ disorder.

B. Biological — Genetic

First-degree relatives share 50% of DNA. Evidence suggests some genetic explanation for depression + bipolar. Bipolar = one of the most likely to be inherited: genetic factors up to 80% of the cause – but little understanding of which genes (complex inheritance patterns + difficulty with precise diagnoses – McGuffin et al., 1994). Strategy: look at neurotransmitters involved, work back to genes (e.g. serotonin genes).

C. Psychological — Beck's cognitive theory of depression

Negative views of someone with depression form a reality for them (even if far-fetched). Cause of low mood & physiological symptoms = incorrect information processing ("cognitive distortion" = negative bias). Develops from negative experiences in childhood ⇒ negative schemas (units of knowledge about the world that underlie reasoning, memory, perception). When faced with events, the schema is activated ⇒ expect things to turn out badly ⇒ emotional, cognitive & behavioural symptoms.

• Self: unpleasant experiences attributed internally – I'm worthless, incapable of being happy.
• World: presents insurmountable obstacles; external forces misinterpreted as being against me.
• Future: negative – anticipates failure or rejection in any future task.

D. Psychological — Learned helplessness & attributional style

Basis of attributional (explanatory) style. Attribution = how we explain causes of behaviour/events (can be faulty/biased). Difficult upbringing / parental loss ⇒ more likely to perceive lack of control ⇒ negative attributional style:

Negative style = …	meaning	e.g. team loses a match
Internal	"it's my fault"	"I played badly"
Stable	"it will last forever"	"we'll always lose"
Global	"affects every area of life"	"I'm bad at everything"

④ Treatment & management of depressive disorder

A. Biological — Anti-depressant drugs

	Tricyclics	MAOIs	SSRIs
Introduced	1950s	1950s (effective by then)	more recent
How	↑ norepinephrine & serotonin by stopping reabsorption	inhibit monoamine oxidase (breaks down norepinephrine, serotonin, dopamine) ⇒ they stay at higher levels	selective serotonin reuptake inhibitors – stop serotonin being reabsorbed & broken down after crossing the synapse ⇒ ↑ serotonin
Side effects	drowsiness, nausea & vomiting, blurred vision, weight gain	headaches, drowsiness/insomnia, nausea, diarrhoea, constipation; withdrawal problems; interact with other meds (pain meds, other anti-depressants) ⇒ high blood pressure, headaches	fewer & less severe than MAOIs/tricyclics
Use today	effective, but usually only when other treatments have failed	only when other anti-depressants / treatments unsuccessful	most commonly prescribed in most countries

• Fewer side effects = ↑ quality of life and patients less likely to stop ⇒ more likely to continue ⇒ drug more effective. Different individuals respond to different drugs.
• Evidence: many large clinical studies: all three beat placebos. Fournier et al. (2010): impact far more noticeable in moderate-to-severe depression than in mild.
• Research methods: well-controlled experiments, large samples ⇒ highly replicable.

B. Psychological — Beck's cognitive restructuring

Aims to gain "entry into the patient's cognitive organisation" (Beck, 1979). One-to-one talking therapy using questioning to identify illogical thinking and discussing ways to change it. Steps:

1. Explain the theory (the cognitive triad) so the patient understands how their thinking about self/world/future contributes.
2. Train to observe & record thoughts – catch automatic, dysfunctional thoughts (practised outside sessions, in real-life context).
3. Link thoughts ↔ affect ↔ behaviour – each influences the others.
4. 'Reality testing' – challenge: is this thought an accurate reflection of reality? Use reattributing: is the cause of problems/failures internal or external? ⇒ reframe, realise they're not responsible.
5. Aim: patient can do cognitive restructuring themselves ⇒ fewer depressive symptoms.

C. Psychological — Ellis's rational emotive behaviour therapy (REBT)

Based on stoicism (philosophy: individual not directly affected by external things but by their own perception of them). Ellis (1962): people get depressed because of internal constructions – perceptions & attitudes to what happens. People with negative, fixed, irrational beliefs are at greater risk.

• Goal: create & maintain constructive, rational patterns of thinking; change thoughts leading to guilt, self-defeat, self-pity or negative behaviour (avoidance, withdrawal, addiction).
• Method – 'disputing': therapist forcefully questions irrational beliefs using many methods ⇒ reformulate dysfunctional beliefs. Client sees consequences (C) are only partly due to the event (A); holding negative beliefs (B) is destructive but can be changed by replacing with healthier thoughts.
• Ellis: holding irrational beliefs is ingrained over time ⇒ REBT focuses on the present (little interest in past, unlike psychoanalysis).
• Lyons & Woods (1991): meta-analysis of 70 REBT outcome studies, 236 comparisons with baseline/controls/other psychotherapies ⇒ REBT sig. better than baseline & controls. Iftene et al. (2015): REBT as effective as anti-depressants.

Mood disorders — Quick questions (textbook)

• Q4 (BDI useful?) ✓ quantitative, reliable, tracks improvement ✗ self-report, can't capture what depression is really like, culture bias.
• Q5 why do two family members share a disorder? ⇒ not just genes: shared environment (trauma, bereavement, upbringing, learned helplessness / negative attributional style).
• Q6 lost football match: negative style ⇒ "it's my fault (internal), we'll always lose (stable), I'm useless at everything (global)"; positive style ⇒ "bad luck today, next time will differ".

6.3 Impulse Control Disorders

① Diagnostic criteria (ICD-11)

Characterised by the repeated inability to resist an impulse/urge to carry out a behaviour that feels rewarding in the short term but has long-term negative consequences (harm to self/others, distress about the behaviour, significant impairment in family, friendships, work). Three to know: kleptomania · pyromania · gambling disorder.

Disorder	Key criteria
Kleptomania	powerful, hard-to-resist impulse to steal ⇒ often steals. Before: intense tension / affective arousal; during/immediately after: excitement, gratification or relief. Stealing not for monetary gain, sabotage or revenge. No other obvious explanation (other behavioural/mental disorder, substance use, intellectual impairment).
Pyromania	powerful, hard-to-resist impulse to set fires ⇒ many acts/attempts of setting fire to property/objects. Increasing tension just before; pleasure, excitement or gratification during, straight after, and while witnessing/participating in the aftermath. Fascination / preoccupation with fire & related stimuli (watching/building fires, firefighting equipment). No intelligible motive (money, sabotage, revenge) & no other explanation.
Gambling disorder	pattern of persistent/recurrent gambling, online or offline: ① impaired control (time spent, money spent) ② gambling takes priority over other activities/interests ③ continues or increases despite negative consequences. Significant distress/impairment (family, friends, work). Usually present ≥ 1 year (shorter if all criteria met & symptoms severe).

② Measure: Kleptomania Symptom Assessment Scale (K-SAS)

11-item self-rated scale of impulses, thoughts, feelings & behaviours about stealing, over the past 7 days. Each item rated 0–4 or 0–5 (0 = no symptoms; 4/5 = severe, frequent/enduring). Higher score = greater severity & duration.

③ Explanations

A. Biological — Dopamine (reward deficiency syndrome)

Dopamine = the 'happy' chemical; released by rewarding stimuli. Stealing stimulates reward centres ⇒ dopamine release. When behaviours become compulsive, dopamine levels in the striatum (reward & behavioural control) are reduced ⇒ deficiency ⇒ need to keep doing the behaviour ⇒ more stealing. = 'reward deficiency syndrome' (Comings & Blum, 2000) – may explain other addictions.

• Evidence: kleptomania as a side-effect of synthetic dopamine (for Parkinson's); gambling disorder & compulsive shopping appear alongside these drugs.
• Methods: brain scans (PET / fMRI = tracks oxygenated blood flow to active areas) are scientific & objective – see what's active, no subjective interpretation/self-report ⇒ ↑ validity & reliability.

B. Psychological — Behavioural: positive reinforcement

Positive reinforcement (operant conditioning) = behaviour followed by a reward (money, attention) ⇒ more likely to be repeated. e.g. birthday scratch card wins ⇒ buy more scratch cards.

Why gamblers keep playing despite losing: schedules of reinforcement – partial reinforcement (no reward every time, e.g. fruit machine pays ~1 in 500 plays) ⇒ player never fully satisfied & mistakenly believes they'll make back losses "if I play just one more time".

C. Psychological — Cognitive: Miller's feeling-state theory (2010)

Underlying thoughts about behaviours explain obsessions. Intense positive feelings become linked to specific behaviours (gambling, fire-setting) forming a 'state-dependent memory' = feeling-state (all sensations, emotions, thoughts, physiological arousal e.g. ↑ heart rate, adrenaline).

• e.g. fire-setting feeling-state: "I am a powerful human being" + positive emotions + arousal + memory of setting the fire ⇒ compulsion to set fires. States persist over time so even early positive feeling-states can affect later behaviour.
• Normal behaviours in moderation become problematic only because of fixated, intense feeling-states. An underlying negative thought (e.g. "I'm weak/unimportant") makes the feeling-state during the act highly desirable. Then more negative beliefs when behaviour goes out of control (harmful consequences).

Belief type (Table 6.3)	Example
negative belief about self/world	'I'm a loser'
positive belief during event (e.g. gambling)	'I'm a winner'
negative belief from out-of-control behaviour	'I mess up everything'

④ Treatment & management

A. Biological — Opiate antagonists

Drugs traditionally used for substance abuse; block the reward centres activated by drug/alcohol (and by gambling) ⇒ ↓ urge, extends abstinence. e.g. nalmefene, naltrexone. Work well for alcohol dependence with strong cravings, family history of alcoholism and euphoric response (O'Brien, 2005; Monterosso et al., 2001). Alcohol dependence is genetically linked to pathological gambling (PG) and the two often co-occur.

B. Psychological (cognitive-behavioural therapies)

Change distortions in thoughts/feelings to bring about behavioural change. Two therapies:

Impulse control — Quick questions (textbook)

• Q7 gambling conflicts: social (lose friends, secrecy), family (money lost, arguments, trust), occupational (late/absent, can't concentrate, job loss).
• Q8 K-SAS: ✓ quick, quantitative, reliable, tracks change ✗ self-report/shame ⇒ under-reporting, no detail.
• Q9 dopamine = correlation, not proven cause – can't say for certain reduced dopamine causes impulse disorders (could be the result of the behaviour, or a third factor).

6.4 Anxiety & Fear-Related Disorders

① Diagnostic criteria (ICD-11)

Excessive fear and anxiety + related behavioural disturbances; severe enough for significant distress / impairment (family, social, occupational). Fear = response to perceived imminent threat in the present; anxiety = focused on anticipated threat in the future. Disorders are told apart mainly by the specific stimulus.

Disorder	Key criteria
Generalised anxiety disorder (GAD)	marked anxiety on most days for at least several months. General apprehension or worry about multiple everyday events (health, family, finances, work). Muscular tension, sleep disturbance, difficulty concentrating, irritability. Not due to another medical condition/substance.
Agoraphobia	excessive fear/anxiety in situations where escape might be difficult or help unavailable (public transport, crowds, outside home alone). Afraid of panic attacks or embarrassing symptoms in public ⇒ situations avoided or endured with extreme distress. Persists several months.
Specific phobia (blood-injection-injury, BII)	excessive fear/anxiety consistently when exposed to / anticipating the sight of blood, injection or injury. Disproportionate to actual danger; stimulus avoided or endured with intense fear. Persists several months.

② Measures

③ Explanations

A. Biological — Genetic

We're born prepared to fear certain objects – stimuli posing a survival threat; genetic set-up to avoid them, transmitted through DNA.

B. Psychological — Behavioural (classical & operant conditioning)

Classical conditioning explains how a phobia starts: a harmless stimulus paired with a frightening experience, e.g. agoraphobia after being mugged in public.

Operant conditioning explains how it persists. Negative reinforcement = ↑ likelihood of repeating a behaviour because something unpleasant is removed. Avoiding the phobic stimulus reduces fear ⇒ rewarding ⇒ avoidance repeats.

Meeting other (harmless) ducks could act as counterconditioning – but avoidance prevents this.

C. Psychological — Psychodynamic (Freud)

Anxiety/fear result from impulses of the id, esp. when denied/repressed. Phobias = one way this internal conflict shows up. Sources of conflict arise at different psychosexual stages; the phobic object symbolises the conflict typical of that stage.

④ Treatment & management

A. Behavioural therapy: systematic desensitisation

Reduces undesirable responses to particular situations (esp. phobias e.g. agoraphobia). Assumes nearly all behaviour is a conditioned response – if a phobia can be learned (Little Albert) it can be unlearned = counterconditioning.

1. Teach relaxation – progressive muscle relaxation, visualisation, or even anti-anxiety drugs.
2. Build an anxiety hierarchy together – list of anxiety-provoking situations of ↑ severity, unique to the individual (Table 6.6 below).
3. Work up the hierarchy: start in vitro (imagined) then in vivo (real-life exposure). At each stage stay calm/relaxed; don't move on until no anxiety at the current stage.

• Evidence: effective for agoraphobia (Agras, 1967) & fear of snakes (Kimura et al., 1972). Declined in popularity since 1970s–80s – more direct forms of exposure now more common.
• Application: non-drug treatment; skills reusable ⇒ long-term solution; improves quality of life.

6.5 Obsessive-Compulsive Disorder (OCD)

① Diagnostic criteria (ICD-11)

Persistent obsessions or compulsions, or most commonly both.

Obsessions (Table 6.7)	Compulsions
fear of deliberately harming oneself · fear of illness/infection · fear of harming/killing others · fear of accidentally injuring self/others · strong desire for order & symmetry	frequent & excessive handwashing · putting things in order (labels facing same way) · checking repeatedly (oven 20 times) · repeating words to oneself / counting

② Measures

	MOCI (Maudsley Obsessive-Compulsive Inventory)	Y-BOCS (Yale-Brown Obsessive Compulsive Scale)
Format	30 items, true / false; ~5 min; self-report	semi-structured interview (~30 min) + checklist of obsessions/compulsions (Table 6.8) + 10-item severity scale
Measures	checking, washing, slowness, doubting; score 0–30	time spent, how hard to resist, distress caused; score 0–40; > 16 = clinical range
Purpose	quick assessment for clinicians & researchers – not a formal diagnostic tool	widely used – measures nature + severity; plan treatment / monitor progress
Example	"I frequently have to check things (gas, water taps, doors) several times" (checking) · "I do not take a long time to dress" (slowness)	categories: aggressive, contamination, sexual, hoarding, religious, symmetry, body-focused / cleaning, washing, checking, repeating, counting, ordering, hoarding

③ Explanations

A. Biological — Biochemical

• Dopamine ↑: people with OCD tend to have abnormally high dopamine. Szechtman et al. (1998): ↑ dopamine in rats ⇒ repetitive movements mirroring compulsions.
• Serotonin ↓: lower than normal. Supported by anti-depressants that ↑ serotonin (SSRIs) being more effective than those with less effect on serotonin (Pittenger & Bloch, 2014).
• Oxytocin ('love hormone' – trust, attachment, but also ↑ distrust & fear of threats): mixed evidence. Leckman et al. (1994): some forms of OCD related to oxytocin dysfunction (cerebrospinal fluid + patient accounts). Contrasting: den Boer & Westenberg (1992) – double-blind placebo-controlled study of 12 OCD patients: half got syntocinon (synthetic oxytocin) nasal spray daily, half placebo ⇒ no reduction in obsessions/compulsions ⇒ no link.

B. Biological — Genetic

• Monzani et al. (2014): large twin study ⇒ concordance MZ 52% vs DZ 21% ⇒ heritability ≈ 48%.
• Ozaki et al. (2003): mutation of the SERT gene (⇒ lower serotonin) in 6 members of 2 unrelated families with OCD.
• Mattheisen et al. (2015): 1406 OCD patients + general population ⇒ genes PTPRD and SLITRK3 implicated (both interact to regulate synapses).
• No definitive answer on which genes – but OCD runs in families and is more concordant in MZ than DZ twins ⇒ some genetic influence.

C. Psychological — Cognitive (thinking error)

OCD = cognitive obsessions + behavioural compulsions. Obsessive thinking is based on faulty reasoning (Rachman, 1977), e.g. belief that hands covered in germs could kill. Errors worsen under stress. Compulsions = outcome of such erroneous thinking – attempts to relieve unwanted thoughts and the anxiety they cause.

D. Psychological — Behavioural (operant conditioning)

Handwashing alleviates the obsession (temporarily) ⇒ negative reinforcer (relieves something unpleasant – the worry) and positive reinforcer (the person is 'rewarded' by having clean hands) ⇒ compulsive behaviours are learned.

E. Psychological — Psychodynamic

Unconscious beliefs & desires. OCD = internal conflict between id and ego, arising in the anal stage (~toilet training). Tension between child and parents who want to control how/when the child defecates/urinates. To regain control:

• anally expulsive – child soils themselves ⇒ upset, arguments;
• anally retentive – child fears harsh parental responses, holds in faeces/urine.

Individual becomes 'fixated' at this stage ⇒ id thoughts disturb the rational ego ⇒ compulsive cleaning & tidying rituals later, to deal with earlier childhood trauma.

④ Treatment & management

A. Biological — SSRIs

Range of drug therapies (anti-depressants, anti-anxiety meds). SSRIs most used: block serotonin from being reabsorbed after a message passes between neurons ⇒ serotonin stays higher. Work with or without depression; they seem to lessen the anxiety associated with OCD. Higher dosage than for depression is more effective (Pampaloni et al., 2009).

B. Psychological — Exposure & response prevention (ERP)

A form of CBT. Person is exposed to stimuli that provoke obsessions + distress while being helped to prevent the compulsive behaviour. e.g. touch a door handle ⇒ dirt/germs obsession + urge to wash ⇒ don't wash; tolerate anxiety, accept the obsession, become habituated (get used to it). Key: prevent the compulsion as a response to the obsession ⇒ learn the uncomfortable feelings go away eventually without performing the compulsion.

C. Psychological — CBT

Same principles as before (understand then challenge irrational thoughts ⇒ positive change in emotional + behavioural responses). NICE research shows CBT very effective for OCD – but traditionally face-to-face, 45–60 min weekly for several weeks ⇒ expensive, time-consuming ⇒ long waiting lists (OCD may worsen while waiting ⇒ harder to treat). Attempts to improve access: computerised CBT, facilitated self-help, telephone CBT (↑ use – Mohr et al., 2000; Taylor et al., 2003: effective & cheaper).

7. Revision Summary

Explanations at a glance

Disorder	Biological	Psychological
Schizophrenia	genetic (Gottesman 1991, Hilker 2017 – 79%, Tienari 2000) · dopamine hypothesis (↑ DA ⇒ +ve; ↓ prefrontal DA ⇒ −ve)	cognitive – Frith: abnormal self-monitoring
Mood	dopamine & serotonin (+ noradrenaline in bipolar) · genetic (Oruč 1997 – 5-HT genes, females)	Beck's cognitive triad · learned helplessness / attributional style (Seligman 1988)
Impulse control	dopamine – reward deficiency syndrome (Comings & Blum 2000)	positive reinforcement (partial reinforcement) · Miller's feeling-state
Anxiety / fear	genetic – prepared to fear (Öst 1992)	behavioural: classical (Watson & Rayner 1920) + operant (neg. reinforcement) · psychodynamic (Freud 1909 – Little Hans)
OCD	↑ dopamine, ↓ serotonin, oxytocin (mixed) · genetic (Monzani 52% vs 21%; SERT; PTPRD/SLITRK3)	cognitive (faulty reasoning – Rachman) · behavioural (operant) · psychodynamic (anal stage)

Treatments at a glance

Disorder	Biological	Psychological	Key / example study
Schizophrenia	typical & atypical antipsychotics, ECT	CBT	Sensky 2000 (CBT vs befriending, n = 90)
Mood	tricyclics, MAOIs, SSRIs	Beck's cognitive restructuring, Ellis's REBT (ABC)	Wiles 2013 · Lyons & Woods 1991 · Iftene 2015
Impulse control	opiate antagonists (nalmefene, naltrexone)	covert sensitisation · imaginal desensitisation	Grant 2008 · Glover 1985 · Blaszczynski & Nower 2003
Anxiety / fear	(anti-anxiety drugs as relaxation aid)	systematic desensitisation, CBT + applied tension	Chapman & DeLapp 2014 · Agras 1967 · Kimura 1972
OCD	SSRIs	ERP, CBT (also by phone)	Lovell 2006 · Lehmkuhl 2008 · Soomro 2008

Measures at a glance

Disorder	Measure	Quick facts
Schizophrenia	ICD-11 criteria · BSI (Freeman)	≥ 1 month; BSI 53 items, 9 dimensions
Depression	Beck Depression Inventory (BDI)	21 items; 10 mild, 19–29 moderate, 30+ severe; BDI-II 1996
Kleptomania	K-SAS	11 items; past 7 days; 0–4/5
GAD / BII	GAD-7 · BIPI	7 items 0–3 (screening) · 18 situations 0–3
OCD	MOCI · Y-BOCS	30 true/false, 0–30 · interview + 10-item, 0–40, > 16 clinical

8. Exam-Style Questions & Pointers

Q	What it asks	Pointers (from these notes)
1	Define positive / negative symptom + one example each [2+2]	+ve = 'in addition to'/distortion of normal (delusions, hallucinations, thought disorder, control); −ve = falls below normal (avolition, flat affect)
2	a) genetic explanation [4]; b) two other explanations, compare [6]	family/twin/adoption + Gottesman/Hilker/Tienari; dopamine vs Frith – both explain positive symptoms; biological = chemical, Frith = faulty mental process
3	a) Beck's theory [2]; b) learned helplessness + attributional style with a study [4]	negative schemas, triad; internal–stable–global; Seligman 1988
4	a) tricyclics, MAOIs, SSRIs [6]; b) compare any two [4]	mechanism + side effects + use today; compare e.g. MAOI vs SSRI side effects & drug interactions
5	a) criteria for kleptomania, pyromania, gambling [3 each]; b) evaluate K-SAS [4]	tension → relief/gratification, no motive; impaired control, priority, continues despite harm; reliable & valid ✓ self-report ✗
6	Grant 2008: sample [2], placebo & why [4], results [2], evaluate [4]; b) one psychological treatment with a study [6]	284 patients, USA; placebo = inactive control, double-blind; family history of alcoholism; covert sensitisation (Glover) or imaginal desensitisation
7	determinism vs free will in anxiety explanations [6]	genetic, behaviourist, psychodynamic all deterministic; but no gene 100%, not everyone conditioned develops a phobia
8	a) explain systematic desensitisation [4]; b) Chapman & DeLapp: aim [2], method [1], strength + weakness of method [4], 2 questionnaires [2], strength + weakness of questionnaires [4]	relaxation + hierarchy + reciprocal inhibition; case study; BAI, BDI, Q-LES-Q, BISS; self-report issues
9	a) analyse two OCD measures [4]; b) evaluate psychometric tests [6]	MOCI vs Y-BOCS; objective/quantitative ✓ ↓ detail, self-report, nomothetic
10	a) outline Lovell procedure + findings [4]; b) evaluate Lovell [10]	72 pts, RCT, telephone vs face-to-face ERP, Y-BOCS 25 → equal outcomes (77% vs 67%); strengths/weaknesses/application/debates