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Flashcards","topicId":"1148a7ca-5dd8-5323-9791-ff4bbed06412","topicSlug":"contemporary-study-schizophrenia-carlsson-et-al","cards":[{"id":"d452b91a-7237-40d8-bbad-5d43436ae639","cardType":"basic","points":1,"front":"What type of study was Carlsson et al. (2000)?","back":"A review paper of existing biological evidence.","mcqOptions":[{"text":"A review paper of existing biological evidence.","correct":true,"explanation":"Carlsson et al. brought together and evaluated existing biological research on schizophrenia. They did not collect new data from participants or manipulate variables experimentally."},{"text":"A laboratory experiment using manipulated neurotransmitter levels.","correct":false,"explanation":"No variables were directly manipulated, so this was not a laboratory experiment. Carlsson et al. produced a review paper by examining existing biological evidence."},{"text":"A case study of one patient with schizophrenia.","correct":false,"explanation":"A case study investigates an individual or small group in depth. Carlsson et al. instead wrote a review paper that synthesised existing biological evidence."},{"text":"A longitudinal study tracking patients receiving treatment.","correct":false,"explanation":"A longitudinal study follows participants over an extended period, which Carlsson et al. did not do. Their work was a review paper based on existing biological evidence."}]},{"id":"3d1a3f7d-c8d6-4b62-877a-51920da4e3b4","cardType":"cloze","points":null,"front":"Carlsson et al. used [ ] rather than collecting [ ].","back":"Carlsson et al. used secondary data rather than collecting new primary data.","mcqOptions":[{"text":"Carlsson et al. used secondary data rather than collecting new primary data.","correct":true,"explanation":"The researchers reviewed evidence already produced by other studies, making it secondary data. They did not obtain new primary data directly from participants."},{"text":"Carlsson et al. used primary data rather than collecting new secondary data.","correct":false,"explanation":"This reverses the primary-secondary distinction. Carlsson et al. analysed existing secondary data rather than collecting new primary data directly through their own research."},{"text":"Carlsson et al. used quantitative data rather than collecting new qualitative data.","correct":false,"explanation":"Quantitative and qualitative describe the form of data, not whether researchers collected it themselves. Carlsson et al. used secondary data rather than gathering new primary data."},{"text":"Carlsson et al. used laboratory data rather than collecting new field data.","correct":false,"explanation":"Laboratory and field data concern research settings, not the key methodological distinction. Carlsson et al. reviewed secondary data instead of collecting new primary data."}]},{"id":"945795cc-2828-41d8-9f5c-ccc0f4229ae7","cardType":"basic","points":2,"front":"What did Carlsson et al. aim to review?","back":"How neurotransmitter systems interact in schizophrenia and treatment.","mcqOptions":[{"text":"How neurotransmitter systems interact in schizophrenia and treatment.","correct":true,"explanation":"Carlsson et al. examined schizophrenia as the result of interactions among neurotransmitter systems, particularly dopamine, glutamate and GABA, including their relevance to treatment."},{"text":"How genetic inheritance alone operates in schizophrenia and treatment.","correct":false,"explanation":"The review did not propose that genetic inheritance alone explains schizophrenia. Its central aim was to examine how interacting neurotransmitter systems contribute to schizophrenia and treatment."},{"text":"How environmental stress independently operates in schizophrenia and treatment.","correct":false,"explanation":"Environmental stress was not the review’s central focus, and an independent environmental account misses its biological emphasis. Carlsson et al. reviewed interactions among neurotransmitter systems."},{"text":"How individual brain regions deteriorate in schizophrenia and treatment.","correct":false,"explanation":"The review was not primarily about progressive deterioration in isolated brain regions. It examined how neurotransmitter systems interact in schizophrenia and its treatment."}]},{"id":"a750aeff-7616-489a-b539-7c56d1a0128b","cardType":"basic","points":3,"front":"Which three neurotransmitter systems are central in Carlsson et al.?","back":"

Dopamine
Glutamate
GABA

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

Dopamine
Glutamate
GABA

","correct":true,"explanation":"Carlsson et al. focused on interactions among dopamine, glutamate and GABA. Their model extended beyond a dopamine-only explanation by considering a connected neurotransmitter network."},{"text":"

Dopamine
Glutamate
Serotonin

","correct":false,"explanation":"Serotonin is associated with schizophrenia research but is not one of the three systems central to this review. The correct trio is dopamine, glutamate and GABA."},{"text":"

Dopamine
GABA
Acetylcholine

","correct":false,"explanation":"Acetylcholine is not part of the review’s central three-system account, and this list omits glutamate. Carlsson et al. emphasised dopamine, glutamate and GABA."},{"text":"

Serotonin
Noradrenaline
GABA

","correct":false,"explanation":"This list substitutes serotonin and noradrenaline for two of the review’s central systems. Carlsson et al. focused specifically on dopamine, glutamate and GABA."}]},{"id":"a73ed2e4-f862-4110-8c5c-8bacf0024783","cardType":"basic","points":2,"front":"According to Carlsson et al., what happens instead of one isolated chemical imbalance?","back":"Neurotransmitter networks interact abnormally.","mcqOptions":[{"text":"Neurotransmitter networks interact abnormally.","correct":true,"explanation":"Carlsson et al. argued that schizophrenia reflects abnormal interactions across connected neurotransmitter systems, rather than a single chemical acting independently of the others."},{"text":"A single neurotransmitter causes all symptoms.","correct":false,"explanation":"This repeats the oversimplified single-imbalance approach that the review sought to move beyond. Carlsson et al. argued that neurotransmitter networks interact abnormally."},{"text":"Neurotransmitter systems operate independently.","correct":false,"explanation":"Treating each system as independent ignores the review’s network account. Carlsson et al. proposed that neurotransmitter systems influence one another and interact abnormally in schizophrenia."},{"text":"Brain structure alone determines all symptoms.","correct":false,"explanation":"This wrongly replaces a neurochemical network explanation with a purely structural one. Carlsson et al. argued that abnormal interactions within neurotransmitter networks contribute to schizophrenia."}]},{"id":"09956ac4-3a85-46a9-bbdd-72a2317bd1c1","cardType":"cloze","points":null,"front":"The simple dopamine hypothesis linked positive symptoms to [ ].","back":"The simple dopamine hypothesis linked positive symptoms to excessive dopamine activity.","mcqOptions":[{"text":"excessive dopamine activity","correct":true,"explanation":"The simple dopamine hypothesis proposed that excessive dopamine activity produces positive symptoms such as hallucinations and delusions, particularly through overactivity in mesolimbic pathways."},{"text":"reduced dopamine activity","correct":false,"explanation":"Reduced dopamine activity is associated with negative and cognitive symptoms in mesocortical pathways, not positive symptoms. The simple hypothesis linked positive symptoms to excessive dopamine activity."},{"text":"excessive glutamate activity","correct":false,"explanation":"This confuses the dopamine hypothesis with later accounts involving glutamate. The simple dopamine hypothesis specifically explained positive symptoms through excessive dopamine activity."},{"text":"reduced serotonin activity","correct":false,"explanation":"Serotonin is not the transmitter identified by the simple dopamine hypothesis. That account linked positive symptoms specifically to excessive dopamine activity."}]},{"id":"9a9b30df-4c84-452a-8f24-7c89e935c061","cardType":"basic","points":2,"front":"What symptom problem made a dopamine-only account incomplete?","back":"Negative and cognitive symptoms often remain unexplained.","mcqOptions":[{"text":"Negative and cognitive symptoms often remain unexplained.","correct":true,"explanation":"A dopamine-only account could explain positive symptoms more readily, but it did not adequately account for persistent negative symptoms or cognitive difficulties in schizophrenia."},{"text":"Hallucinations and delusions often remain unexplained.","correct":false,"explanation":"Hallucinations and delusions are positive symptoms, which excessive dopamine activity was designed to explain. Negative and cognitive symptoms exposed the limitations of a dopamine-only account."},{"text":"Positive and motor symptoms often remain unexplained.","correct":false,"explanation":"Positive symptoms are the main feature addressed by the simple dopamine hypothesis, while motor symptoms are not the key gap identified. Negative and cognitive symptoms often remained unexplained."},{"text":"Visual and sensory symptoms often remain unexplained.","correct":false,"explanation":"Visual and sensory symptoms are not the principal symptom categories that challenged the dopamine-only explanation. Its major weakness was failing to explain negative and cognitive symptoms."}]},{"id":"3c1536b3-a07a-499b-8c75-4f0dd93896b5","cardType":"cloze","points":null,"front":"Mesolimbic dopamine overactivity is linked to [ ], while mesocortical dopamine underactivity is linked to [ ].","back":"Mesolimbic dopamine overactivity is linked to positive symptoms, while mesocortical dopamine underactivity is linked to negative and cognitive symptoms.","mcqOptions":[{"text":"Mesolimbic dopamine overactivity is linked to positive symptoms, while mesocortical dopamine underactivity is linked to negative and cognitive symptoms.","correct":true,"explanation":"Excess dopamine activity in the mesolimbic pathway is associated with positive symptoms, whereas reduced dopamine activity in the mesocortical pathway is associated with negative and cognitive symptoms."},{"text":"Mesolimbic dopamine overactivity is linked to positive symptoms, while mesocortical dopamine underactivity is linked to positive symptoms.","correct":false,"explanation":"The first link is accurate, but mesocortical underactivity does not explain positive symptoms. It is associated with negative and cognitive symptoms such as avolition and impaired thinking."},{"text":"Mesolimbic dopamine overactivity is linked to negative and cognitive symptoms, while mesocortical dopamine underactivity is linked to negative and cognitive symptoms.","correct":false,"explanation":"The mesocortical link is accurate, but mesolimbic overactivity is associated with positive symptoms such as hallucinations and delusions, not negative and cognitive symptoms."},{"text":"Mesolimbic dopamine overactivity is linked to negative and cognitive symptoms, while mesocortical dopamine underactivity is linked to positive symptoms.","correct":false,"explanation":"This reverses the two pathway relationships. Mesolimbic overactivity is linked to positive symptoms, while mesocortical underactivity is linked to negative and cognitive symptoms."}]},{"id":"e7f79c4a-91f4-48f6-a74b-05d3ad8608fa","cardType":"basic","points":1,"front":"Which glutamate mechanism did Carlsson et al. emphasise?","back":"NMDA receptor hypofunction.","mcqOptions":[{"text":"NMDA receptor hypofunction.","correct":true,"explanation":"Carlsson et al. emphasised reduced functioning of NMDA-type glutamate receptors as an important mechanism contributing to the neural network disruption associated with schizophrenia."},{"text":"AMPA receptor hyperfunction.","correct":false,"explanation":"AMPA receptors also respond to glutamate, but AMPA hyperfunction was not the mechanism emphasised. Carlsson et al. focused on NMDA receptor hypofunction."},{"text":"GABA-A receptor hyperfunction.","correct":false,"explanation":"GABA-A receptors are part of the inhibitory GABA system rather than the glutamate mechanism highlighted here. The proposed mechanism was NMDA receptor hypofunction."},{"text":"D2 receptor blockade.","correct":false,"explanation":"D2 receptor blockade describes the action of many antipsychotic drugs, not the glutamate mechanism Carlsson et al. emphasised. Their focus was NMDA receptor hypofunction."}]},{"id":"51d3f93f-cb31-43e5-97b1-709bff53ee2b","cardType":"cloze","points":null,"front":"NMDA receptor hypofunction means glutamate signalling through NMDA receptors is [ ].","back":"NMDA receptor hypofunction means glutamate signalling through NMDA receptors is lower than normal.","mcqOptions":[{"text":"lower than normal","correct":true,"explanation":"Hypofunction means below-normal functioning, so glutamate transmission through NMDA receptors is reduced rather than completely absent or increased."},{"text":"higher than normal","correct":false,"explanation":"This reverses the direction of the proposed abnormality: higher signalling would be hyperfunction. NMDA receptor hypofunction means signalling is lower than normal."},{"text":"unchanged from normal","correct":false,"explanation":"Unchanged signalling would indicate normal NMDA receptor function and could not constitute hypofunction. The term means that signalling is lower than normal."},{"text":"completely absent","correct":false,"explanation":"Hypofunction indicates reduced activity, not necessarily a total absence of signalling. The model proposes NMDA receptor signalling that is lower than normal."}]},{"id":"70903d2e-85f4-4514-944a-8e15bc20a2e9","cardType":"basic","points":2,"front":"How do PCP and ketamine support NMDA hypofunction?","back":"They block NMDA receptors and can produce or worsen schizophrenia-like symptoms.","mcqOptions":[{"text":"They block NMDA receptors and can produce or worsen schizophrenia-like symptoms.","correct":true,"explanation":"PCP and ketamine are NMDA receptor antagonists. Their ability to induce or intensify positive, negative and cognitive schizophrenia-like effects supports a role for reduced NMDA activity."},{"text":"They activate NMDA receptors and can produce or worsen schizophrenia-like symptoms.","correct":false,"explanation":"PCP and ketamine antagonise rather than activate NMDA receptors. Their blockade can produce or worsen schizophrenia-like symptoms, supporting the NMDA hypofunction account."},{"text":"They block dopamine D2 receptors and can produce or worsen schizophrenia-like symptoms.","correct":false,"explanation":"D2 blockade is associated with typical antipsychotic action, not the key action of PCP and ketamine. These drugs block NMDA receptors and can generate schizophrenia-like symptoms."},{"text":"They stimulate GABA-A receptors and can produce or worsen schizophrenia-like symptoms.","correct":false,"explanation":"The relevant pharmacological action is not stimulation of GABA-A receptors. PCP and ketamine block NMDA receptors, reproducing symptoms in a way consistent with NMDA hypofunction."}]},{"id":"55f409d2-5b94-4ef7-b201-50ffaade9c4e","cardType":"basic","points":3,"front":"Why did glutamate evidence broaden the dopamine explanation?","back":"It can affect positive, negative and cognitive symptoms.","mcqOptions":[{"text":"It can affect positive, negative and cognitive symptoms.","correct":true,"explanation":"Glutamate dysfunction may contribute across all three symptom domains, giving the model broader explanatory scope than accounts centred mainly on dopamine and positive symptoms."},{"text":"It can affect positive symptoms only.","correct":false,"explanation":"Restricting the effect to positive symptoms repeats a limitation of a simple dopamine account. Glutamate dysfunction may affect positive, negative and cognitive symptoms."},{"text":"It can affect positive and negative symptoms only.","correct":false,"explanation":"This omits cognitive impairment, which is part of the broader explanatory value of glutamate evidence. It may affect positive, negative and cognitive symptoms."},{"text":"It can affect mood, anxiety and sleep symptoms.","correct":false,"explanation":"Mood and anxiety symptoms are not the three schizophrenia domains highlighted by this model. The evidence concerns positive, negative and cognitive symptoms."}]},{"id":"219e5652-e37b-4ef4-8f93-1ebc204adcdd","cardType":"basic","points":1,"front":"What is GABA’s normal effect on neural activity?","back":"GABA inhibits neural activity.","mcqOptions":[{"text":"GABA inhibits neural activity.","correct":true,"explanation":"GABA is the brain’s principal inhibitory neurotransmitter. It generally reduces the likelihood that receiving neurons will fire, helping control excessive neural activity."},{"text":"GABA excites neural activity.","correct":false,"explanation":"Excitation is principally associated with glutamate, whereas GABA normally decreases neuronal firing. GABA therefore inhibits neural activity."},{"text":"GABA does not affect neural activity.","correct":false,"explanation":"GABA directly influences neuronal excitability rather than leaving it unaffected. Its normal role is to inhibit neural activity and restrain firing."},{"text":"GABA increases neural activity.","correct":false,"explanation":"GABA can help regulate dopamine pathways, but universally increasing dopamine release is not its normal effect. Its fundamental action is to inhibit neural activity."}]},{"id":"7099ee88-042c-4715-b978-2fda77955540","cardType":"basic","points":2,"front":"If glutamate and GABA fail to regulate dopamine, what may dopamine abnormalities be?","back":"A downstream effect of wider network disruption.","mcqOptions":[{"text":"A downstream effect of wider network disruption.","correct":true,"explanation":"If upstream glutamate and GABA regulation is disrupted, abnormal dopamine activity may arise as a consequence of that broader network dysfunction rather than initiating it."},{"text":"A primary cause of wider network disruption.","correct":false,"explanation":"Calling dopamine abnormalities the primary cause ignores the model’s proposed upstream glutamate and GABA dysregulation. They may instead be a downstream effect of wider network disruption."},{"text":"An unrelated feature of wider network disruption.","correct":false,"explanation":"The model links dopamine abnormalities causally to failed glutamate and GABA regulation, so they are not unrelated. They may be a downstream effect of wider network disruption."},{"text":"A protective response to wider network disruption.","correct":false,"explanation":"Abnormal dopamine signalling contributes to symptoms rather than protecting the brain from them. In this model, it may be a downstream effect of wider network disruption."}]},{"id":"7f0c83dd-0343-479e-b7ce-23692af6f443","cardType":"cloze","points":null,"front":"Carlsson et al. imply treatments should target [ ], not only [ ].","back":"Carlsson et al. imply treatments should target multiple neurotransmitter systems, not only dopamine.","mcqOptions":[{"text":"Carlsson et al. imply treatments should target multiple neurotransmitter systems, not only dopamine.","correct":true,"explanation":"The model treats schizophrenia as involving interactions among dopamine, glutamate and GABA. Treatment should therefore address multiple neurotransmitter systems rather than concentrating solely on dopamine."},{"text":"Carlsson et al. imply treatments should target a single neurotransmitter system, not only dopamine.","correct":false,"explanation":"Focusing on one neurotransmitter system preserves the narrow approach that Carlsson et al. sought to broaden. They imply targeting multiple neurotransmitter systems, not only dopamine."},{"text":"Carlsson et al. imply treatments should target multiple neurotransmitter systems, not only glutamate.","correct":false,"explanation":"The model does not argue that dopamine should be excluded in favour of glutamate alone. It implies targeting multiple neurotransmitter systems, not only dopamine."},{"text":"Carlsson et al. imply treatments should target dopamine receptors, not only glutamate.","correct":false,"explanation":"Targeting dopamine receptors while contrasting them with glutamate reverses the model’s broader implication. Treatment should address multiple neurotransmitter systems, not only dopamine."}]},{"id":"633139dc-aa71-4def-b7e5-77dda160cd6b","cardType":"basic","points":2,"front":"What is the main limitation of typical antipsychotics in this model?","back":"They help positive symptoms more than negative or cognitive symptoms.","mcqOptions":[{"text":"They help positive symptoms more than negative or cognitive symptoms.","correct":true,"explanation":"Typical antipsychotics mainly reduce dopamine D2 activity, making them more effective against positive symptoms while providing less benefit for negative and cognitive symptoms."},{"text":"They help negative symptoms more than positive or cognitive symptoms.","correct":false,"explanation":"This reverses the usual effectiveness pattern. Typical antipsychotics generally help positive symptoms more than negative or cognitive symptoms because they chiefly reduce dopamine activity."},{"text":"They help cognitive symptoms more than positive or negative symptoms.","correct":false,"explanation":"Cognitive symptoms are not the domain most effectively treated by typical antipsychotics. These drugs generally help positive symptoms more than negative or cognitive symptoms."},{"text":"They help all symptom types more or less equally.","correct":false,"explanation":"Typical antipsychotics do not improve all three symptom domains equally. Their main benefit is for positive symptoms, with weaker effects on negative and cognitive symptoms."}]},{"id":"dfed326f-0807-43f9-bef3-cef58debdc01","cardType":"basic","points":2,"front":"Why do atypical antipsychotics fit Carlsson et al.’s network view?","back":"They affect dopamine plus other receptor systems.","mcqOptions":[{"text":"They affect dopamine plus other receptor systems.","correct":true,"explanation":"Atypical antipsychotics act on several receptor systems rather than dopamine alone, supporting Carlsson et al.’s view that schizophrenia involves interacting neurotransmitter networks."},{"text":"They affect dopamine receptors in isolation.","correct":false,"explanation":"Treating dopamine receptors in isolation reflects the older dopamine-only explanation. Atypical antipsychotics affect dopamine plus other receptor systems, fitting the broader network view."},{"text":"They affect serotonin but not dopamine receptors.","correct":false,"explanation":"This mistakenly excludes dopamine from atypical antipsychotic action. These drugs affect dopamine alongside other receptor systems, which supports an interacting network explanation."},{"text":"They affect only glutamate receptor systems.","correct":false,"explanation":"Carlsson et al. emphasised glutamate interactions, but atypical antipsychotics do not act only on glutamate. Their effects involve dopamine plus other receptor systems."}]},{"id":"7a950bda-73f1-486b-bde0-d082b4cdeee9","cardType":"basic","points":3,"front":"Which evidence sources gave Carlsson et al. converging support?","back":"

Drug effects
Clinical treatment evidence
Animal studies

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

Drug effects
Clinical treatment evidence
Animal studies

","correct":true,"explanation":"Findings from drug effects, clinical treatments and animal studies pointed towards interacting neurotransmitter systems. Agreement across these different sources provided converging support for the network account."},{"text":"

Genetic studies
Patient interviews
Longitudinal surveys

","correct":false,"explanation":"This substitutes methods that were not the stated converging evidence base. Carlsson et al. drew support from drug effects, clinical treatment evidence and animal studies."},{"text":"

Memory experiments
Family case studies
Questionnaire data

","correct":false,"explanation":"These psychological and self-report methods were not the three evidence sources identified. The review’s converging support came from drug effects, clinical treatment evidence and animal studies."},{"text":"

Twin studies
Adoption evidence
Educational records

","correct":false,"explanation":"This confuses evidence for genetic and environmental influences with Carlsson et al.’s evidence. Their network account was supported by drug effects, clinical treatments and animal studies."}]},{"id":"102a25de-edf1-4182-a5a1-42c02c964aff","cardType":"basic","points":2,"front":"Why does the review method limit causal claims?","back":"

No control/random allocation.
No new primary data.

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

No control/random allocation.
No new primary data.

","correct":true,"explanation":"As a review, Carlsson et al. did not manipulate variables using controls and random allocation or collect new primary data, so it could synthesise evidence but not demonstrate causation directly."},{"text":"

No participant consent.
No standardised diagnosis.

","correct":false,"explanation":"The review recruited no participants, so its causal limitation is not a lack of consent or diagnosis. It lacked control/random allocation and collected no new primary data."},{"text":"

No placebo medication.
No double-blind procedure.

","correct":false,"explanation":"Placebos and double-blind procedures concern particular experiments or clinical trials, not the review itself. Causal claims are limited because there was no control/random allocation or new primary data."},{"text":"

No participant matching.
No follow-up testing.

","correct":false,"explanation":"Matching and follow-up testing are design features for primary research rather than requirements of a review. Carlsson et al. lacked control/random allocation and new primary data."}]},{"id":"0fe4b400-dfd0-472c-985b-afc8e8b3fcea","cardType":"basic","points":1,"front":"What selection-bias risk exists in Carlsson et al. as a review?","back":"Chosen evidence may favour the authors’ interpretation.","mcqOptions":[{"text":"Chosen evidence may favour the authors’ interpretation.","correct":true,"explanation":"Review authors decide which studies and findings to include. Selecting evidence that supports their preferred network account could produce a biased rather than balanced conclusion."},{"text":"Reviewed participants may respond to demand characteristics.","correct":false,"explanation":"Demand characteristics affect people directly participating in research, whereas Carlsson et al. conducted a review. The relevant risk is that chosen evidence may favour the authors’ interpretation."},{"text":"Original researchers may use inconsistent diagnostic criteria.","correct":false,"explanation":"Inconsistent diagnosis can reduce comparability between studies, but it is not the review’s selection-bias risk. Selection bias occurs when chosen evidence favours the authors’ interpretation."},{"text":"Clinical patients may drop out before treatment ends.","correct":false,"explanation":"Participant attrition may bias an original clinical trial, but Carlsson et al. reviewed existing work. Their selection risk is choosing evidence that favours their interpretation."}]},{"id":"d6e269b4-908c-403a-ba49-c9a9165ff0dd","cardType":"basic","points":2,"front":"Why is PCP/ketamine evidence indirect?","back":"A drug-induced state is not identical to schizophrenia.","mcqOptions":[{"text":"A drug-induced state is not identical to schizophrenia.","correct":true,"explanation":"PCP and ketamine can produce schizophrenia-like experiences, but a temporary state caused by a drug may not reproduce the causes, development and full features of schizophrenia."},{"text":"A drug-induced state proves PCP causes schizophrenia.","correct":false,"explanation":"Producing similar symptoms does not show that PCP causes the naturally occurring disorder. The evidence is indirect because a drug-induced state is not identical to schizophrenia."},{"text":"PCP and ketamine are standard schizophrenia treatments.","correct":false,"explanation":"PCP and ketamine are used as models because they can produce schizophrenia-like effects, not as standard treatments. Such drug-induced states are not identical to schizophrenia."},{"text":"Schizophrenia is only produced by hallucinogenic drugs.","correct":false,"explanation":"Schizophrenia is not caused exclusively by hallucinogenic drugs. PCP and ketamine provide indirect evidence because the temporary states they induce are not identical to the disorder."}]},{"id":"8cb85c91-1e08-422c-b7e6-69d3b1cc4493","cardType":"cloze","points":null,"front":"Carlsson et al. is less reductionist than dopamine-only because it considers [ ], but it remains mainly [ ].","back":"Carlsson et al. is less reductionist than dopamine-only because it considers networks, but it remains mainly biological.","mcqOptions":[{"text":"Carlsson et al. is less reductionist than dopamine-only because it considers networks, but it remains mainly biological.","correct":true,"explanation":"The account considers interactions across neurotransmitter networks rather than reducing schizophrenia to dopamine alone. However, its explanation still concentrates mainly on biological processes."},{"text":"Carlsson et al. is less reductionist than dopamine-only because it considers individual neurons, but it remains mainly biological.","correct":false,"explanation":"Focusing on individual neurons would remain narrowly reductionist rather than broadening the explanation. Carlsson et al. is less reductionist because it considers networks, while remaining mainly biological."},{"text":"Carlsson et al. is less reductionist than dopamine-only because it considers networks, but it remains mainly cognitive.","correct":false,"explanation":"Networks correctly broaden the dopamine-only account, but Carlsson et al. focuses on neurotransmitters and receptors rather than thought processes. The explanation therefore remains mainly biological, not cognitive."},{"text":"Carlsson et al. is less reductionist than dopamine-only because it considers genes, but it remains mainly social.","correct":false,"explanation":"The review’s broader focus is on interacting neurotransmitter networks, not primarily genes, and it does not mainly explain schizophrenia through social influences. It remains biological."}]},{"id":"e6255703-f6da-4145-ac8f-d85eb6b04cb7","cardType":"basic","points":2,"front":"Why do consent, debrief and protection-from-harm issues mainly apply indirectly to Carlsson et al.?","back":"It did not recruit participants; ethics apply mainly to original studies.","mcqOptions":[{"text":"It did not recruit participants; ethics apply mainly to original studies.","correct":true,"explanation":"Carlsson et al. reviewed existing research rather than directly studying participants. Consent, debriefing and protection from harm therefore concern the researchers who conducted the original studies."},{"text":"It used only anonymous questionnaire data; ethics therefore did not apply.","correct":false,"explanation":"The study was a review, not an anonymous questionnaire investigation, and anonymity does not remove all ethical duties. It recruited no participants, so these issues apply mainly to original studies."},{"text":"It recruited only adult volunteers; consent was therefore unnecessary.","correct":false,"explanation":"Adults still require informed consent, and Carlsson et al. did not recruit volunteers. Ethical issues such as consent and protection mainly concern the original studies reviewed."},{"text":"It used no biological evidence; ethics apply only to drug research.","correct":false,"explanation":"The review relied heavily on biological evidence, and ethical principles apply beyond drug research. The issues are indirect because Carlsson et al. recruited no participants."}]}]}],"examCountdown":{"examDate":"2027-05-18","paperLabel":"Paper 1"},"heading":"Contemporary study (schizophrenia): Carlsson et al.","title":"Contemporary study (schizophrenia): Carlsson et al. Flashcards","topbar":{"backHref":"/a-level/psychology/edexcel/flashcards"},"topicSidebar":"$L38"}]}],"topicId":"1148a7ca-5dd8-5323-9791-ff4bbed06412","walled":"$L39"}],"$L3a","$L3b"]