Cambridge A Level Psychology 9990: Clinical Psychology (Specialist Option 1)

Clinical Psychology is Specialist Option 1 of Cambridge International A Level Psychology 9990. It covers five groups of disorders: schizophrenia, mood disorders, impulse control disorders, anxiety and fear-related disorders, and obsessive-compulsive disorder (OCD). For each one you must know the ICD-11 diagnostic criteria and a named measure, then biological and psychological explanations, then biological and psychological treatments. The exam expects you to describe, evaluate and compare these, and to link them to issues and debates and research methods.

This guide follows the Cambridge International AS & A Level Psychology 9990 syllabus for 2024, 2025 and 2026. It covers every numbered sub-topic (1.1.1 to 1.5.3) and the five key studies. Use it with the Clinical Psychology revision notes and the Clinical Psychology practice questions. For how the four options fit together, see the Specialist Options overview.

How is Clinical Psychology examined in 9990?

If your school teaches this option, it is examined on both Paper 3 (Specialist Options: Approaches, Issues and Debates) and Paper 4 (Specialist Options: Application and Research Methods). On Paper 3, each option has three short-answer questions worth 14 marks in total, then a structured essay with a 6-mark “describe” part (a) and a 10-mark “evaluate” part (b). On Paper 4 Section A, there are two structured questions on each option. The syllabus states that the topic areas tested on Paper 3 will be different from those tested on Paper 4, so you cannot skip any of the five topics.

The syllabus also introduces two umbrella terms for this option. Biological covers explanations (genetic, biochemical), measures (such as blood pressure) and treatments (such as electro-convulsive therapy). Psychological covers explanations (behavioural, cognitive and psychodynamic) and therapies (such as systematic desensitisation). The syllabus uses ICD-11 terms but accepts other terms used appropriately.

Syllabus coverage

Number	Sub-topic	What you must know
1.1.1	Diagnostic criteria for schizophrenia	ICD-11 criteria, positive and negative symptoms, a case study; types of delusions; key study Freeman et al. (2003)
1.1.2	Explanations of schizophrenia	Genetic; biochemical (dopamine hypothesis); psychological (cognitive)
1.1.3	Treatment and management	Typical and atypical antipsychotics; ECT; CBT, e.g. Sensky et al. (2000)
1.2.1	Diagnostic criteria for mood disorders	ICD-11 depressive disorder and bipolar disorders; Beck Depression Inventory
1.2.2	Explanations of mood disorders	Biochemical; genetic, key study Oruč et al. (1997); Beck’s cognitive theory; learned helplessness and attributional style, e.g. Seligman et al. (1988)
1.2.3	Treatment and management	Tricyclics, MAOIs, SSRIs; Beck’s cognitive restructuring; Ellis’s REBT
1.3.1	Diagnostic criteria for impulse control disorders	Kleptomania, pyromania, gambling disorder; Kleptomania Symptom Assessment Scale (K-SAS)
1.3.2	Explanations	Dopamine; positive reinforcement; Miller’s feeling-state theory
1.3.3	Treatment and management	Drug treatment, key study Grant et al. (2008); covert sensitisation, e.g. Glover (1985); imaginal desensitisation, e.g. Blaszczynski and Nower (2003)
1.4.1	Diagnostic criteria for anxiety and fear-related disorders	Generalised anxiety disorder, agoraphobia, blood-injection-injury phobia; GAD-7; BIPI, e.g. Mas et al. (2010)
1.4.2	Explanations of fear-related disorders	Genetic, e.g. Öst (1992); classical conditioning, e.g. Watson and Rayner (1920); psychodynamic, e.g. Freud (1909)
1.4.3	Treatment and management	Systematic desensitisation; CBT with applied tension, key study Chapman and DeLapp (2013)
1.5.1	Diagnostic criteria for OCD	Types of obsessions and compulsions, e.g. Rapoport (1989); MOCI and Y-BOCS
1.5.2	Explanations of OCD	Biochemical; genetic; cognitive (thinking error); behavioural (operant); psychodynamic
1.5.3	Treatment and management	SSRIs; exposure and response prevention, e.g. Lehmkuhl et al. (2008); CBT, key study Lovell et al. (2006)

Studies marked “e.g.” are examples the syllabus suggests; a different suitable study can be used. The five “key studies” are named and must be known in detail: context, theory, aims, method, sample, procedure, results, conclusions and discussion points.

1.1 What do you need to know about schizophrenia?

Diagnosis (1.1.1). ICD-11 requires at least two symptoms present most of the time for at least one month, with at least one from a core group: persistent delusions, persistent hallucinations, disorganised thinking, or experiences of influence, passivity or control. Positive symptoms are additions to normal experience, such as hallucinations and delusions. Negative symptoms are losses, such as avolition (lack of motivation), alogia (poverty of speech), flat affect and social withdrawal. Delusions can be of persecution, reference, grandeur or control. A well-known case study is the Genain quadruplets, identical sisters who were all diagnosed with schizophrenia and studied by Rosenthal (1963).

Key study: Freeman et al. (2003). This pilot study asked whether virtual reality (VR) could be used to investigate persecutory ideation. Twenty-four non-clinical participants entered a neutral VR library scene containing computer-generated people, then completed measures of psychiatric symptoms and of their thoughts about the characters. Positive views of the characters were common, but some participants reported ideas of reference and persecution about them. Those who had persecutory thoughts scored significantly higher on interpersonal sensitivity and anxiety. The researchers concluded that people attribute mental states to VR characters, and that anxiety and interpersonal vulnerability may feed persecutory thinking even in a neutral setting. Evaluation points: the environment was highly standardised (a strength for reliability and for controlling situational variables), but the sample was small and non-clinical, which limits generalisation to people with schizophrenia.

Explanations (1.1.2). The genetic explanation is supported by family and twin studies: Gottesman (1991) reported a lifetime risk of around 48% for the identical twin of a person with schizophrenia, compared with about 1% in the general population. Because concordance is not 100%, environment must also matter (nature versus nurture). The dopamine hypothesis proposes that excess dopamine activity, or over-sensitive D2 receptors, in the mesolimbic pathway produces positive symptoms. Evidence includes amphetamines (which raise dopamine) worsening symptoms and antipsychotics (which block D2 receptors) reducing them. The cognitive explanation, for example Frith’s account, proposes a fault in self-monitoring: a person fails to recognise their own inner speech as self-generated, experiencing it as an external voice or inserted thought.

Treatment (1.1.3). Typical antipsychotics such as chlorpromazine block dopamine D2 receptors; they reduce positive symptoms but can cause movement side effects such as tardive dyskinesia. Atypical antipsychotics such as clozapine act on dopamine and serotonin receptors, have fewer movement side effects and may help negative symptoms, but clozapine needs regular blood monitoring. Electro-convulsive therapy (ECT) passes a brief current through the brain under anaesthetic to induce a seizure; it is used mainly when drugs fail or with catatonia. CBT helps patients test the evidence for delusional beliefs and develop coping strategies. Sensky et al. (2000) randomly allocated 90 patients with medication-resistant schizophrenia to CBT or a befriending control. Both groups improved by the end of treatment, but at follow-up nine months later only the CBT group had kept improving.

1.2 How are mood disorders diagnosed, explained and treated?

Diagnosis (1.2.1). A depressive episode in ICD-11 is a period of at least two weeks of depressed mood or loss of interest nearly every day, with other symptoms such as poor concentration, feelings of worthlessness or excessive guilt, hopelessness, thoughts of death, changes in appetite or sleep, psychomotor change and low energy. Bipolar type I requires at least one manic (or mixed) episode; a manic episode lasts at least one week and involves euphoria or irritability with increased activity or energy. Bipolar type II involves at least one hypomanic episode and at least one depressive episode. The Beck Depression Inventory (BDI) is a 21-item self-report questionnaire; each item is scored 0 to 3, so higher totals indicate more severe depression. It produces quantitative, comparable data but relies on honest self-report.

Explanations (1.2.2). The biochemical explanation links depression to low levels of monoamine neurotransmitters, especially serotonin and noradrenaline. The genetic explanation is examined through the key study. Oruč et al. (1997) compared DNA from 42 patients with bipolar I disorder and 40 healthy controls, looking at polymorphisms in the serotonin 2C receptor gene (5-HT2C) and the serotonin transporter gene (5-HTT). There was no significant association in the whole sample, but when split by gender, female patients showed trends towards association with both genes. The authors concluded that variation in these genes may cause only a minor increase in susceptibility to bipolar disorder in women. This is useful for discussing reductionism: a small genetic effect cannot be the whole explanation.

Beck’s cognitive theory proposes that depressed people hold negative schemas and show a negative triad: negative views of the self, the world and the future. These are maintained by cognitive errors such as overgeneralisation and selective abstraction. Learned helplessness comes from Seligman’s research showing that animals exposed to unavoidable shocks later stopped trying to escape. The reformulated version focuses on attributional style: depressed people explain bad events as internal, stable and global (“it’s my fault, it will last, it affects everything”). Seligman et al. (1988) found that depressed patients’ explanatory style became more optimistic during cognitive therapy, and that this change went with a reduction in depression.

Treatment (1.2.3). Tricyclics block the reuptake of serotonin and noradrenaline. MAOIs inhibit the enzyme monoamine oxidase, which breaks down monoamines; patients must avoid foods high in tyramine. SSRIs such as fluoxetine selectively block serotonin reuptake and generally have fewer side effects. Beck’s cognitive restructuring helps the client identify automatic negative thoughts and test them against evidence, for example with a thought diary. Ellis’s REBT uses the ABC model (Activating event, Belief, Consequence), then disputes irrational beliefs, especially rigid “musts”, to replace them with rational ones.

1.3 What are impulse control disorders and how are they treated?

Diagnosis (1.3.1). ICD-11 describes these as repeated failure to resist an impulse, drive or urge to perform an act that is rewarding in the short term despite longer-term harm. Kleptomania is a recurrent failure to control impulses to steal objects that are not needed for personal use or money, with tension before the act and pleasure or relief during or after it. Pyromania is repeated fire-setting without an obvious motive, with mounting tension before and fascination with fire. Gambling disorder involves impaired control over gambling, increasing priority given to it, and continuing despite negative consequences. The Kleptomania Symptom Assessment Scale (K-SAS) is a self-report scale that rates urges, thoughts and stealing behaviour over the past week; higher scores show more severe symptoms.

Explanations (1.3.2). The biological explanation focuses on dopamine in the brain’s reward pathway; the act gives a dopamine-linked “high”, which is why some patients taking dopamine-boosting medication have developed gambling problems. The behavioural explanation is positive reinforcement: the pleasure or win after the act makes it more likely to be repeated, and unpredictable wins in gambling act as a powerful variable-ratio schedule. Miller’s feeling-state theory proposes that an intense positive feeling (such as a sense of power or excitement) becomes fixed to a specific behaviour during a past experience; later, the urge to re-experience that feeling drives the behaviour. His treatment, the Feeling-State Addiction Protocol, aims to break this link.

Key study: Grant et al. (2008). The researchers pooled data from two double-blind, placebo-controlled trials of opiate antagonists (nalmefene for 16 weeks or naltrexone for 18 weeks) in 284 people with pathological gambling (137 women). Severity was measured with a version of the Yale-Brown scale adapted for gambling, and a positive response was a reduction of at least 35% sustained for at least a month. The variable most strongly associated with a good response to the drug was a family history of alcoholism. Among those on higher doses, stronger gambling urges at the start were linked to better response; among those on placebo, younger age was linked to better outcome. The use of a placebo group and double-blind design supports internal validity.

Psychological treatments (1.3.3). Covert sensitisation pairs the imagined urge or act with an imagined unpleasant consequence (such as nausea or being caught), so the behaviour becomes associated with aversion; Glover (1985) used this with a woman with kleptomania. Imaginal desensitisation teaches relaxation and then has the client imagine the trigger situation and leaving without acting on the urge; Blaszczynski and Nower (2003) describe its use with gambling.

1.4 How are anxiety and fear-related disorders explained and treated?

Diagnosis (1.4.1). Generalised anxiety disorder (GAD) involves marked anxiety for at least several months, on more days than not, shown as general apprehension or excessive worry about many everyday events, with symptoms such as muscle tension, restlessness, poor concentration and sleep disturbance. Agoraphobia is marked fear of situations where escape might be difficult or help unavailable, such as public transport or crowds. Specific phobia (blood-injection-injury) is excessive fear of seeing blood, injections or injury; unlike most phobias it often produces a sudden drop in blood pressure and fainting. The GAD-7 is a seven-item self-report questionnaire about the last two weeks, each item scored 0 to 3 (total 0 to 21). The Blood Injection Phobia Inventory (BIPI), associated with Mas et al. (2010), measures cognitive, physiological and behavioural responses across blood and injection situations.

Explanations (1.4.2). The genetic explanation is supported by Öst (1992), who found that many people with blood-injection phobia had a close relative with the same fear. The behavioural explanation is classical conditioning: Watson and Rayner (1920) paired a white rat with a loud noise until “Little Albert”, aged about 11 months, showed fear of the rat, and the fear generalised to similar furry objects. The psychodynamic explanation is illustrated by Freud (1909): “Little Hans” developed a fear of horses, which Freud interpreted as displaced fear of his father linked to the Oedipus complex.

Treatment (1.4.3). Systematic desensitisation teaches relaxation, builds an anxiety hierarchy and then works up the hierarchy, so relaxation replaces fear (reciprocal inhibition). CBT combines psychoeducation, challenging catastrophic thoughts and graded exposure. Applied tension teaches the patient to tense large muscle groups to raise blood pressure and prevent fainting during exposure.

Key study: Chapman and DeLapp (2013). This is a case study of “T”, a 42-year-old man who self-referred because he had panic-like fear of medical procedures and fainted (vasovagal syncope) during routine blood tests. He had been unable to have routine check-ups and could not watch the medical procedures his child needed. He was assessed with a diagnostic interview and questionnaires, including the Beck Anxiety Inventory (BAI), and treated over nine sessions of manualised CBT. Sessions 1 and 2 covered assessment and psychoeducation, session 3 introduced cognitive restructuring and exposure, and in session 4 T built a fear hierarchy of up to ten items rated in SUDS (0 to 100). Applied muscle tension was introduced in session 5 and used during graded exposure: wrapping a tourniquet round his arm, watching videos of blood being taken, pricking his finger with a glucometer, watching phlebotomy at a blood bank, and finally having his own blood drawn and taking his own blood pressure in session 9. His SUDS ratings fell within and across sessions, and he needed applied tension less by the end. Gains were maintained at follow-ups 4, 10 and 12 months after treatment, when his BAI score had fallen from 41 to 7. As a case study it gives rich, idiographic detail and shows how the manual works in practice, but one client cannot show that the treatment works for everyone.

1.5 What do you need to know about OCD?

Diagnosis (1.5.1). ICD-11 describes persistent obsessions (repetitive, intrusive and unwanted thoughts, images or urges that cause anxiety) and/or compulsions (repetitive behaviours or mental acts performed in response to an obsession or rigid rules, to reduce anxiety). They are time-consuming or cause significant distress or impairment. Common types include contamination and washing, checking, and symmetry and ordering. Rapoport (1989) described “Charles”, a teenage boy whose compulsive washing took hours each day. The Maudsley Obsessive-Compulsive Inventory (MOCI) is a 30-item true/false self-report questionnaire covering checking, cleaning, slowness and doubting. The Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) is a clinician-rated scale of 10 items (five on obsessions, five on compulsions), scored 0 to 4 each, for a total of 0 to 40.

Explanations (1.5.2). Biochemical: low serotonin activity is implicated, supported by the fact that SSRIs reduce symptoms. Genetic: twin studies show higher concordance for identical than non-identical twins. Cognitive (thinking error): people with OCD overestimate threat and their own responsibility, and may believe that thinking about an event makes it more likely. Behavioural (operant conditioning): a compulsion reduces anxiety, so it is negatively reinforced and repeated. Psychodynamic: Freud linked OCD to conflict between the id and ego and to fixation in the anal stage, with defences such as undoing and reaction formation.

Treatment (1.5.3). SSRIs increase available serotonin; they help many patients but symptoms can return when the drug is stopped. Exposure and response prevention (ERP) exposes the patient to the feared trigger while preventing the compulsion, so anxiety falls without it. Lehmkuhl et al. (2008) reported a case of a 12-year-old boy with autism and OCD who improved with CBT that included ERP.

Key study: Lovell et al. (2006). This randomised controlled non-inferiority trial in two UK outpatient departments allocated 72 patients with OCD to ten weekly sessions of exposure and response prevention by telephone or face to face. Outcomes were the Y-BOCS, the Beck Depression Inventory and a client satisfaction questionnaire. At six months, Y-BOCS scores in the two groups were almost identical, and satisfaction was high in both. Telephone CBT was therefore as effective as face-to-face treatment, which matters for people who cannot easily travel to therapy.

How should you evaluate clinical explanations and treatments?

Use the issues and debates the syllabus lists after each topic. The most useful are:

• Nature versus nurture: genetic evidence never shows 100% concordance, so environment matters.
• Reductionism versus holism: the dopamine hypothesis and drug treatments reduce a disorder to one chemical; CBT and REBT consider thought and behaviour.
• Determinism versus free will: biological explanations imply less personal control, which can reduce blame but also reduce a sense of agency.
• Idiographic versus nomothetic: case studies (Little Hans, Charles, Chapman and DeLapp) are idiographic; trials such as Lovell et al. and Grant et al. are nomothetic.
• Validity and reliability of measures: self-report scales such as the BDI and GAD-7 are quick and quantitative but open to social desirability bias.

When comparing treatments, judge effectiveness, side effects, how long the benefit lasts, cost and whether the patient must be motivated to take part.

Frequently asked questions

How many disorders are in Cambridge 9990 Clinical Psychology? There are five topics: schizophrenia, mood disorders (depressive and bipolar), impulse control disorders, anxiety and fear-related disorders, and OCD. Each has three sub-topics: diagnosis, explanations, and treatment and management.

Which classification system does the 9990 syllabus use? It uses ICD-11 terms for the subject content and assessment material. Cambridge states it will accept alternative terms if they are used appropriately.

Do I need to learn the “e.g.” studies? You need a study for each point marked “including a study”, and the suggested one is the safest choice. The five named key studies (Freeman et al., Oruč et al., Grant et al., Chapman and DeLapp, Lovell et al.) must be known in full.

What is the difference between a measure and a treatment in this option? A measure, such as the BDI or Y-BOCS, assesses how severe symptoms are. A treatment, such as an SSRI or ERP, aims to reduce them. Measures are often used before and after a treatment to judge whether it worked.

Official syllabus

Cambridge International AS & A Level Psychology 9990 syllabus for 2024, 2025 and 2026, section 3 Subject content, Specialist Option 1: Clinical Psychology — cambridgeinternational.org.

Related resources

• Clinical Psychology revision notes
• Clinical Psychology practice questions
• Specialist Options overview
• Paper 2 Research Methods study guide