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24:[["$","$L33",null,{"feature":"flashcards"}],"$L34",["$","$L35",null,{"href":"/a-level/psychology/eduqas/schizophrenia-explanations/flashcards","label":"Schizophrenia: explanations","subjectCode":"a_level_psychology__eduqas","surface":"flashcards"}],["$","$L36",null,{"runner":["$","div",null,{"className":"min-h-0 flex-1 overflow-hidden bg-background","children":["$","$L37",null,{"decks":[{"id":"0467c75b-5b61-4ad0-b151-287dc79b08e0","title":"Schizophrenia: explanations Flashcards","topicId":"025f0750-ef4a-542b-8c2a-37b614a8d7aa","topicSlug":"schizophrenia-explanations","cards":[{"id":"35f86056-0f79-460e-98b7-1ca4f157831b","cardType":"basic","points":1,"front":"In schizophrenia, what type of symptom is a hallucination?","back":"A positive symptom.","mcqOptions":[{"text":"A positive symptom.","correct":true,"explanation":"Hallucinations add perceptions that are not present in reality, so they are classified as positive symptoms rather than losses of normal functioning."},{"text":"A negative symptom.","correct":false,"explanation":"Negative symptoms involve reductions in normal functioning, such as avolition or speech poverty. Hallucinations add an abnormal experience, so they are positive symptoms."},{"text":"A cognitive symptom.","correct":false,"explanation":"Cognitive symptoms concern impaired mental processes such as attention or working memory. A hallucination is an added perceptual experience, making it a positive symptom."},{"text":"An affective symptom.","correct":false,"explanation":"Affective symptoms concern mood and emotion, whereas hallucinations are perceptions without an external stimulus. They are therefore classified as positive symptoms."}]},{"id":"0cc0ad69-4e80-4296-9b7a-3ed75efcf425","cardType":"cloze","points":null,"front":"Avolition is a [ ] symptom involving reduced [ ].","back":"Avolition is a negative symptom involving reduced motivation.","mcqOptions":[{"text":"Avolition is a negative symptom involving reduced motivation.","correct":true,"explanation":"Avolition is a negative symptom because it represents a loss of normal functioning, specifically a reduced drive to begin or continue purposeful activities."},{"text":"Avolition is a positive symptom involving reduced motivation.","correct":false,"explanation":"Calling avolition positive confuses added abnormal experiences with losses of functioning. Avolition is a negative symptom characterised by reduced motivation."},{"text":"Avolition is a negative symptom involving reduced perception.","correct":false,"explanation":"Reduced perception does not define avolition and is more closely associated with sensory processing. Avolition is a negative symptom involving reduced motivation."},{"text":"Avolition is a cognitive symptom involving reduced memory.","correct":false,"explanation":"This confuses avolition with cognitive impairment. Avolition is classified as a negative symptom because it involves reduced motivation and goal-directed behaviour."}]},{"id":"c7f3d6f7-5eef-42b9-85e5-b2364c07ccff","cardType":"basic","points":3,"front":"For Eduqas, what three broad groups organise schizophrenia explanations?","back":"

Biological
Individual differences
Social psychological

","mcqOptions":[{"text":"

Biological
Individual differences
Social psychological

","correct":true,"explanation":"The Eduqas specification groups explanations into biological, individual differences, and social psychological approaches, allowing theories to be compared across these three levels."},{"text":"

Biological
Cognitive
Social psychological

","correct":false,"explanation":"Cognitive is a specific type of explanation rather than one of the three Eduqas headings. The required groups are biological, individual differences, and social psychological."},{"text":"

Behavioural
Psychodynamic
Social psychological

","correct":false,"explanation":"Behavioural and psychodynamic approaches are narrower theoretical perspectives, not the Eduqas organising headings. The groups are biological, individual differences, and social psychological."},{"text":"

Clinical symptoms
Medical treatments
Social influences

","correct":false,"explanation":"Clinical symptoms and medical treatments do not form the three explanation groups. Eduqas organises explanations as biological, individual differences, and social psychological."}]},{"id":"35e5268b-118e-4883-92de-0bcab8540c79","cardType":"cloze","points":null,"front":"The traditional dopamine hypothesis links positive symptoms to [ ], especially in [ ].","back":"The traditional dopamine hypothesis links positive symptoms to excess dopamine activity, especially in subcortical pathways.","mcqOptions":[{"text":"The traditional dopamine hypothesis links positive symptoms to excess dopamine activity, especially in subcortical pathways.","correct":true,"explanation":"The traditional hypothesis proposes that excessive dopamine signalling in subcortical areas, particularly the mesolimbic pathway, contributes to positive symptoms such as hallucinations and delusions."},{"text":"The traditional dopamine hypothesis links positive symptoms to reduced dopamine activity, especially in subcortical pathways.","correct":false,"explanation":"Underactivity reverses the traditional account of positive symptoms. That account links positive symptoms to excess dopamine activity in subcortical pathways."},{"text":"The traditional dopamine hypothesis links positive symptoms to excess dopamine activity, especially in cortical pathways.","correct":false,"explanation":"Excess cortical dopamine is not the traditional explanation for positive symptoms. The theory instead identifies excess dopamine activity in subcortical pathways."},{"text":"The traditional dopamine hypothesis links positive symptoms to excess serotonin activity, especially in subcortical pathways.","correct":false,"explanation":"This substitutes serotonin for the neurotransmitter named by the dopamine hypothesis. The traditional account proposes excess dopamine activity in subcortical pathways."}]},{"id":"099da4b5-7a4b-462d-9997-016a587b35dc","cardType":"basic","points":2,"front":"Why do antipsychotic drugs support the dopamine hypothesis?","back":"Many reduce dopamine activity at D2 receptors.","mcqOptions":[{"text":"Many reduce dopamine activity at D2 receptors.","correct":true,"explanation":"Many antipsychotics antagonise D2 receptors, reducing dopamine signalling. Their ability to lessen symptoms therefore supports a role for excessive dopamine activity in schizophrenia."},{"text":"Many increase dopamine activity at D2 receptors.","correct":false,"explanation":"Increasing D2 activity would intensify rather than counter the excessive dopamine signalling proposed by the hypothesis. Many antipsychotics instead reduce dopamine activity at D2 receptors."},{"text":"Many reduce dopamine activity at D1 receptors.","correct":false,"explanation":"D1 receptors are not the principal target used as evidence for this hypothesis. Support comes from many antipsychotics reducing dopamine activity at D2 receptors."},{"text":"Many reduce glutamate activity at NMDA receptors.","correct":false,"explanation":"NMDA receptors respond primarily to glutamate, so blocking them would not provide the standard drug evidence for the dopamine hypothesis. Many antipsychotics reduce D2 activity."}]},{"id":"97dcdc72-564a-4f04-a45b-6c11bfac0c9e","cardType":"basic","points":1,"front":"In the modern dopamine account, prefrontal dopamine underactivity is linked to which symptoms?","back":"Negative and cognitive symptoms.","mcqOptions":[{"text":"Negative and cognitive symptoms.","correct":true,"explanation":"Modern accounts associate reduced dopamine signalling in prefrontal cortical pathways with diminished motivation and impaired executive processes, producing negative and cognitive symptoms."},{"text":"Positive and disorganised symptoms.","correct":false,"explanation":"Positive symptoms are primarily associated with excessive dopamine activity in subcortical pathways. Prefrontal dopamine underactivity is linked instead to negative and cognitive symptoms."},{"text":"Hallucinations and delusions.","correct":false,"explanation":"Hallucinations and delusions are both positive symptoms associated with excessive subcortical dopamine activity, not prefrontal underactivity. The latter is linked to negative and cognitive symptoms."},{"text":"Motor and sensory symptoms.","correct":false,"explanation":"Motor and sensory symptoms are not the symptom pairing proposed by the modern dopamine account. Prefrontal dopamine underactivity is linked to negative and cognitive symptoms."}]},{"id":"9c79d01c-b1d2-4aea-b741-d7388e2c3325","cardType":"basic","points":1,"front":"What medication-response problem weakens the dopamine hypothesis?","back":"Not everyone responds to dopamine-blocking medication.","mcqOptions":[{"text":"Not everyone responds to dopamine-blocking medication.","correct":true,"explanation":"A substantial minority of patients show little improvement with D2-blocking drugs, suggesting that dopamine dysfunction alone cannot explain every case of schizophrenia."},{"text":"Everyone responds fully to dopamine-blocking medication.","correct":false,"explanation":"Universal full recovery would strongly support rather than weaken a simple dopamine explanation, but it does not occur. Some patients do not respond to dopamine-blocking medication."},{"text":"Only people with negative symptoms respond to dopamine-blocking medication.","correct":false,"explanation":"Response is not restricted to people with negative symptoms, and these symptoms may respond less well. The key problem is that not everyone responds to dopamine-blocking medication."},{"text":"Stopping dopamine-blocking medication never affects symptoms.","correct":false,"explanation":"Symptoms can return after medication is stopped, so this is not the relevant response problem. The challenge is that some patients never respond adequately to dopamine blockade."}]},{"id":"d339f29e-a685-497d-9809-2c7ebdefded9","cardType":"cloze","points":null,"front":"THC acts on the brain’s [ ] and can indirectly affect [ ].","back":"THC acts on the brain’s endocannabinoid system and can indirectly affect dopamine pathways.","mcqOptions":[{"text":"THC acts on the brain’s endocannabinoid system and can indirectly affect dopamine pathways.","correct":true,"explanation":"THC binds to cannabinoid receptors within the endocannabinoid system. Its effects on this system can alter dopamine pathways implicated in psychotic symptoms."},{"text":"THC acts on the brain’s opioid system and can indirectly affect dopamine pathways.","correct":false,"explanation":"THC primarily acts at cannabinoid receptors rather than opioid receptors. It affects the endocannabinoid system and can indirectly alter dopamine pathways."},{"text":"THC acts on the brain’s endocannabinoid system and can indirectly affect acetylcholine pathways.","correct":false,"explanation":"The first term is correct, but acetylcholine is not the pathway emphasised in explanations of cannabis-related psychosis. THC can indirectly affect dopamine pathways."},{"text":"THC acts on the brain’s serotonin system and can indirectly affect GABA pathways.","correct":false,"explanation":"This confuses THC with drugs acting primarily through serotonin or GABA. THC acts on the endocannabinoid system and can indirectly influence dopamine pathways."}]},{"id":"de62d383-b010-4f4c-9799-2760c986a45f","cardType":"basic","points":2,"front":"Which cannabis-use pattern did Di Forti et al. (2015) link to increased psychosis risk?","back":"High-potency cannabis, especially with frequent use.","mcqOptions":[{"text":"High-potency cannabis, especially with frequent use.","correct":true,"explanation":"Di Forti et al. found that using high-potency cannabis, particularly when use was frequent, was associated with a greater likelihood of experiencing psychosis."},{"text":"Low-potency cannabis, especially with infrequent use.","correct":false,"explanation":"Low-potency, infrequent use was not the pattern associated with the greatest psychosis risk. Di Forti et al. particularly linked high-potency cannabis and frequent use to increased risk."},{"text":"Low-potency cannabis, especially with occasional use.","correct":false,"explanation":"The study did not identify occasional use of low-potency cannabis as the key high-risk pattern. Increased psychosis risk was associated particularly with frequent use of high-potency cannabis."},{"text":"High-potency cannabis, especially with infrequent use.","correct":false,"explanation":"Although frequency matters, the reported high-risk combination was not infrequent use of high-potency cannabis. Di Forti et al. linked high potency especially with frequent use to psychosis risk."}]},{"id":"ae828ec0-3e9c-42fe-bbad-a46c8195da12","cardType":"basic","points":2,"front":"Why does cannabis evidence struggle to prove causation?","back":"It is often correlational, with possible pre-existing risk/confounds.","mcqOptions":[{"text":"It is often correlational, with possible pre-existing risk/confounds.","correct":true,"explanation":"Correlational evidence establishes an association but cannot show that cannabis causes psychosis. Existing vulnerability or another confounding variable could independently increase both cannabis use and psychosis risk."},{"text":"It is often experimental, with effective random allocation/controls.","correct":false,"explanation":"Cannabis research generally does not use controlled experiments with random allocation because exposing participants would be unethical. The evidence is often correlational and may reflect pre-existing risks or confounds."},{"text":"It is often longitudinal, with proven temporal precedence/causation.","correct":false,"explanation":"Longitudinal evidence can establish that cannabis use preceded psychosis, but it still cannot eliminate every confound. The main limitation is correlational evidence and possible pre-existing vulnerability."},{"text":"It is often objective, with reliable biological measures/scans.","correct":false,"explanation":"Objective measurement would improve reliability rather than prevent causal conclusions. Causation remains uncertain because much cannabis evidence is correlational and pre-existing vulnerabilities or confounding variables may explain the association."}]},{"id":"992a0572-bc07-4f35-97c2-e396c753029c","cardType":"basic","points":1,"front":"What can enlarged ventricles suggest about surrounding brain tissue?","back":"Reduced volume in surrounding brain tissue.","mcqOptions":[{"text":"Reduced volume in surrounding brain tissue.","correct":true,"explanation":"Ventricles are fluid-filled spaces, so their enlargement can indicate that nearby brain tissue occupies less space. This suggests reduced volume or loss of surrounding tissue."},{"text":"Increased volume in surrounding brain tissue.","correct":false,"explanation":"Enlarged ventricles occupy more intracranial space and therefore do not indicate greater surrounding tissue volume. They can instead suggest reduced volume in nearby brain tissue."},{"text":"Increased activity in surrounding brain tissue.","correct":false,"explanation":"Ventricle size is a structural measure and does not directly demonstrate heightened neural activity. Enlarged ventricles can suggest reduced volume in the surrounding brain tissue."},{"text":"Reduced activity in surrounding brain tissue.","correct":false,"explanation":"Reduced neural activity is a functional claim that cannot be inferred solely from enlarged ventricles. The structural implication is reduced volume in the tissue surrounding them."}]},{"id":"29446136-8480-4948-b603-8fe29c3bccf0","cardType":"cloze","points":null,"front":"Johnstone et al. (1976) found some people with [ ] had larger ventricles than [ ].","back":"Johnstone et al. (1976) found some people with chronic schizophrenia had larger ventricles than controls.","mcqOptions":[{"text":"Johnstone et al. (1976) found some people with chronic schizophrenia had larger ventricles than controls.","correct":true,"explanation":"Johnstone et al. reported that some people with chronic schizophrenia had enlarged ventricles compared with control participants, supporting an association between schizophrenia and structural brain differences."},{"text":"Johnstone et al. (1976) found some people with acute schizophrenia had larger ventricles than controls.","correct":false,"explanation":"The finding concerned people with chronic schizophrenia, not specifically those experiencing acute schizophrenia. Their ventricles were compared with those of control participants."},{"text":"Johnstone et al. (1976) found some people with chronic schizophrenia had larger ventricles than other patients.","correct":false,"explanation":"The comparison was with controls, not with other people diagnosed with chronic schizophrenia. Johnstone et al. found that some chronic patients had larger ventricles than controls."},{"text":"Johnstone et al. (1976) found some people with chronic depression had larger ventricles than relatives.","correct":false,"explanation":"Johnstone et al. studied chronic schizophrenia rather than depression and compared participants with controls rather than relatives. The reported ventricular enlargement was in some chronic schizophrenia patients."}]},{"id":"d6090391-5331-4a75-abc4-be07ac11e9a4","cardType":"basic","points":2,"front":"Why can enlarged ventricles not diagnose schizophrenia by themselves?","back":"

Not found in all patients.
Not unique to schizophrenia.

","mcqOptions":[{"text":"

Not found in all patients.
Not unique to schizophrenia.

","correct":true,"explanation":"Enlarged ventricles lack both sensitivity and specificity: some people with schizophrenia do not have them, while people with other conditions may also show them."},{"text":"

Found in all patients.
Unique to schizophrenia.

","correct":false,"explanation":"If enlarged ventricles occurred in every patient and only in schizophrenia, they would support diagnosis rather than undermine it. In reality, they are neither universal nor unique."},{"text":"

Not found in any patients.
Only found in healthy controls.

","correct":false,"explanation":"Enlarged ventricles are not consistently absent from patients or restricted to healthy people. They occur in some schizophrenia patients, but are neither present in all cases nor unique to the disorder."},{"text":"

Clearly visible in all scans.
Easy for clinicians to measure.

","correct":false,"explanation":"Being visible and easy to measure would not explain poor diagnostic value. Enlarged ventricles cannot diagnose schizophrenia because they are absent in some patients and occur outside schizophrenia."}]},{"id":"dfd04977-0035-4ba6-ac5b-870d6d479713","cardType":"basic","points":2,"front":"How does Frith’s cognitive explanation account for auditory hallucinations?","back":"The person misattributes inner speech to an external source.","mcqOptions":[{"text":"The person misattributes inner speech to an external source.","correct":true,"explanation":"Frith proposed that defective self-monitoring prevents internally generated speech from being recognised as one’s own. The person consequently experiences inner speech as an external voice."},{"text":"The person misattributes external speech to an internal source.","correct":false,"explanation":"Frith’s account does not propose that genuine external speech is mistaken for thought. It argues that internally generated speech is misattributed to an external source."},{"text":"The person misinterprets spoken language as a meaningless sound.","correct":false,"explanation":"Failure to understand other people’s speech is not Frith’s explanation of hallucinations. His account focuses on faulty self-monitoring, causing inner speech to be experienced as externally produced."},{"text":"The person converts inner speech to an external sound.","correct":false,"explanation":"Deliberately producing external speech would not create the experience of an involuntary voice. Frith argued that inner speech is mistakenly attributed to an external source."}]},{"id":"4f1ed248-49e4-461b-a1ab-a3b961b7481f","cardType":"basic","points":1,"front":"Why be cautious calling thought disorder a root cause of schizophrenia?","back":"It may be a symptom, not an original cause.","mcqOptions":[{"text":"It may be a symptom, not an original cause.","correct":true,"explanation":"Disorganised thinking may arise as part of schizophrenia rather than initiate the disorder. Treating it as causal risks confusing an observable symptom with the original underlying cause."},{"text":"It may be an original cause, not a symptom.","correct":false,"explanation":"Calling thought disorder an original cause assumes the direction of explanation that is in question. It may instead be a symptom produced by schizophrenia."},{"text":"It may be a genetic mutation, not a symptom.","correct":false,"explanation":"Thought disorder is a cognitive and behavioural feature, not a confirmed genetic mutation. Caution is needed because it may be a symptom of schizophrenia rather than its original cause."},{"text":"It may be a treatment effect, not an original cause.","correct":false,"explanation":"Thought disorder is not an antipsychotic side effect that can explain untreated schizophrenia. The key caution is that it may be a symptom rather than the disorder’s root cause."}]},{"id":"3f4fd927-2aa8-4cfd-9ebc-889a6f748f60","cardType":"basic","points":2,"front":"Why is the schizophrenogenic mother theory ethically criticised?","back":"It blames mothers and is sexist.","mcqOptions":[{"text":"It blames mothers and is sexist.","correct":true,"explanation":"The theory places responsibility for schizophrenia on mothers by portraying their parenting as cold and rejecting. This unfair gendered attribution is both blaming and sexist."},{"text":"It defends mothers and is gender-neutral.","correct":false,"explanation":"The theory does not defend mothers or distribute responsibility equally between parents. It specifically attributes schizophrenia to supposedly harmful maternal behaviour, making it mother-blaming and sexist."},{"text":"It blames fathers and is sexist.","correct":false,"explanation":"The schizophrenogenic mother theory focuses blame on mothers rather than fathers. Its gendered portrayal of maternal parenting as pathogenic is why it is criticised as sexist."},{"text":"It empowers mothers and is feminist.","correct":false,"explanation":"The theory is not ethically praised for empowering women. By assigning mothers responsibility for their child’s schizophrenia, it creates guilt and reflects a sexist assumption."}]},{"id":"d6cabe0b-853f-401c-9667-dace71e915c0","cardType":"cloze","points":null,"front":"The oestrogen hypothesis says oestrogen may protect [ ], with risk increasing after [ ].","back":"The oestrogen hypothesis says oestrogen may protect dopamine systems, with risk increasing after menopause.","mcqOptions":[{"text":"The oestrogen hypothesis says oestrogen may protect dopamine systems, with risk increasing after menopause.","correct":true,"explanation":"Oestrogen may regulate or protect dopamine systems, helping explain women’s later average onset. Falling oestrogen levels after menopause may therefore increase vulnerability to schizophrenia."},{"text":"The oestrogen hypothesis says oestrogen may protect serotonin systems, with risk increasing after puberty.","correct":false,"explanation":"The hypothesis does not propose that oestrogen protects serotonin systems or that puberty increases risk. It concerns protection of dopamine systems, which declines after menopause as oestrogen levels fall."},{"text":"The oestrogen hypothesis says oestrogen may protect GABA systems, with risk increasing after pregnancy.","correct":false,"explanation":"GABA systems are not the proposed target of oestrogen’s protective effect, and pregnancy involves high rather than declining oestrogen. The hypothesis identifies dopamine systems and increased risk after menopause."},{"text":"The oestrogen hypothesis says oestrogen may protect acetylcholine systems, with risk increasing after adolescence.","correct":false,"explanation":"The hypothesis focuses on dopamine rather than acetylcholine systems. Risk is proposed to increase after menopause, when oestrogen falls, rather than after adolescence."}]},{"id":"c0e7516d-a012-49bf-89f6-c035df84d31a","cardType":"basic","points":1,"front":"According to Häfner et al. (1993), which sex often shows earlier onset and more negative symptoms?","back":"Males.","mcqOptions":[{"text":"Males.","correct":true,"explanation":"Häfner et al. found that males commonly developed schizophrenia earlier and showed more negative symptoms, whereas females tended to have later onset and a more favourable course."},{"text":"Females.","correct":false,"explanation":"Females generally showed later onset and fewer negative symptoms in Häfner et al.’s findings. Males were the group associated with earlier onset and more negative symptoms."},{"text":"Both sexes.","correct":false,"explanation":"The study reported a sex difference rather than an identical pattern. Males, not both sexes equally, often experienced earlier onset and more negative symptoms."},{"text":"Neither sex.","correct":false,"explanation":"Häfner et al. did identify a group with this characteristic pattern. Males often showed earlier onset and more negative symptoms than females."}]},{"id":"8612acee-3d1c-4355-98e6-9b8c1fae35a6","cardType":"basic","points":2,"front":"How can cultural norms affect voice-hearing?","back":"They shape whether voices are seen as spiritual or as symptoms.","mcqOptions":[{"text":"They shape whether voices are seen as spiritual or as symptoms.","correct":true,"explanation":"Cultural beliefs provide frameworks for interpreting voice-hearing. Some cultures understand voices as spiritual experiences, while others are more likely to interpret them as symptoms of mental disorder."},{"text":"They shape whether voices are seen as loud or as quiet.","correct":false,"explanation":"Cultural norms influence the meaning assigned to voices, not whether they are objectively loud or quiet. Voices may be interpreted as spiritual experiences or as symptoms."},{"text":"They shape whether voices are seen as positive or as negative.","correct":false,"explanation":"Positive and negative are symptom classifications, not the contrasting cultural interpretations in this explanation. Cultural norms can frame voices as spiritual experiences or as symptoms."},{"text":"They shape whether voices are seen as internal or as external.","correct":false,"explanation":"Internal and external describe perceived location rather than culturally shaped meaning. Cultural norms affect whether voice-hearing is understood as spiritual or regarded as a symptom."}]},{"id":"ceb1eadb-fda4-434b-8582-4661c37298b8","cardType":"basic","points":2,"front":"In double-bind theory, what family communication pattern increases stress?","back":"Contradictory messages make communication confusing and stressful.","mcqOptions":[{"text":"Contradictory messages make communication confusing and stressful.","correct":true,"explanation":"Double-bind theory proposes that repeated contradictory messages place a person in an impossible communicative situation, creating confusion and stress because no response can resolve the contradiction."},{"text":"Consistent messages make communication confusing and stressful.","correct":false,"explanation":"Consistent messages reduce ambiguity rather than creating the no-win situation described by double-bind theory. The proposed source of stress is repeated contradictory communication."},{"text":"Supportive messages make communication confusing and stressful.","correct":false,"explanation":"Supportive messages would generally reduce family stress and are not the pattern identified by double-bind theory. The theory emphasises contradictory messages that cannot be satisfactorily answered."},{"text":"Direct messages make communication confusing and stressful.","correct":false,"explanation":"Direct messages are clear rather than inherently confusing. Double-bind theory specifically identifies contradictory messages, often delivered at different verbal and non-verbal levels, as stressful."}]},{"id":"59472f55-e2c8-4ddc-b29c-13cf4b46cf31","cardType":"cloze","points":null,"front":"High expressed emotion involves relatives’ criticism, hostility and emotional over-involvement, and is linked to higher [ ] risk.","back":"High expressed emotion involves relatives’ criticism, hostility and emotional over-involvement, and is linked to higher relapse risk.","mcqOptions":[{"text":"relapse","correct":true,"explanation":"High expressed emotion creates a stressful family environment and predicts a greater likelihood that symptoms will return after treatment, so it is associated specifically with relapse risk."},{"text":"onset","correct":false,"explanation":"High expressed emotion is primarily linked to symptoms returning in someone already diagnosed, not to the initial onset of schizophrenia. The required term is relapse."},{"text":"remission","correct":false,"explanation":"Remission means symptoms have reduced or disappeared, so a higher remission risk does not describe the harmful association. High expressed emotion raises relapse risk."},{"text":"recovery","correct":false,"explanation":"Recovery is a beneficial outcome rather than the adverse outcome predicted by criticism, hostility and over-involvement. High expressed emotion is associated with an increased risk of relapse."}]},{"id":"be31794f-118c-417c-9cfc-309d67543cc2","cardType":"basic","points":2,"front":"How does the diathesis-stress model explain schizophrenia?","back":"A vulnerability interacts with an environmental stressor.","mcqOptions":[{"text":"A vulnerability interacts with an environmental stressor.","correct":true,"explanation":"The diathesis-stress model argues that schizophrenia develops when an underlying biological or psychological vulnerability combines with sufficient environmental stress; neither factor necessarily causes the disorder alone."},{"text":"A vulnerability acts without an environmental stressor.","correct":false,"explanation":"A vulnerability is a predisposition, not a guaranteed independent cause. The model proposes that vulnerability interacts with an environmental stressor to produce schizophrenia."},{"text":"A stressor interacts with an environmental protection.","correct":false,"explanation":"Protection may reduce the likelihood of disorder rather than trigger it. The diathesis-stress model describes an underlying vulnerability interacting with an environmental stressor."},{"text":"A vulnerability interacts with an environmental cure.","correct":false,"explanation":"A cure is a response to illness, not one of the causal components in this model. Schizophrenia is explained through vulnerability interacting with an environmental stressor."}]}]}],"examCountdown":{"examDate":"2027-05-18","paperLabel":"Component 1"},"heading":"Schizophrenia: explanations","title":"Schizophrenia: explanations Flashcards","topbar":{"backHref":"/a-level/psychology/eduqas/flashcards"},"topicSidebar":"$L38"}]}],"topicId":"025f0750-ef4a-542b-8c2a-37b614a8d7aa","walled":"$L39"}],"$L3a","$L3b"]