Schizophrenia-Oxford shoter

Schizophrenia is the easiest psychiatric syndrome to define and describe.

The concept of schizophrenia has remained consistent across different countries and cultures throughout history.

Schizophrenia is typically characterized by a single, distinct set of symptoms.

Delusions and hallucinations are considered negative symptoms of schizophrenia.

Negative symptoms of schizophrenia involve a gain of normal functioning.

First-rank symptoms are a type of negative symptom of schizophrenia.

Schizophrenia can be easily distinguished from other psychotic disorders based on a single symptom or trait.

The classification of schizophrenia remains a settled issue in the field of psychiatry.

Psychiatry has reached a consensus on the definition and diagnosis of schizophrenia.

Schizophrenia is a well-defined and clearly understood psychiatric disorder.

The 'four As' of schizophrenia are alogia, avolition, affective flattening, and aphasia

Some patients with schizophrenia may experience tactile hallucinations

Cognitive symptoms are a subtype of positive symptoms in schizophrenia

Behavioural disorganization is a negative symptom in schizophrenia

Delusions are never present in patients with acute schizophrenia

Primary delusions are very common in patients with schizophrenia

Most patients with acute schizophrenia completely recover from the illness

Persecutory delusions are unique to schizophrenia

The chronic syndrome of schizophrenia is characterized by positive symptoms

All patients with schizophrenia have blunted affect

Formal thought disorder is a negative symptom in schizophrenia

Vorbeireden is a type of auditory hallucination

Incongruity of affect is a rare feature of schizophrenia

First-rank symptoms include delusions of reference

The 'four As' described by Bleuler are the same as the 'four As' described in the text

Neologisms are words or phrases used in an unusual way

Patients with schizophrenia always have impaired insight

Visual hallucinations are the most common type of hallucination in schizophrenia

Poverty of thought is a type of cognitive symptom in schizophrenia

The clinical picture of schizophrenia is always the same in all patients

Patients with chronic schizophrenia often exhibit increased drive and initiative.

Affect in chronic schizophrenia is often intense and congruous.

Hallucinations are a universal symptom in chronic schizophrenia.

Social behavior in chronic schizophrenia often improves over time.

Thought disorder is a rare feature of chronic schizophrenia.

Delusions in chronic schizophrenia are often accompanied by strong emotional responses.

Chronic schizophrenia is characterized by a complete lack of social withdrawal.

Patients with chronic schizophrenia often have good self-care and personal hygiene.

Speech in chronic schizophrenia is often normal and coherent.

Chronic schizophrenia is characterized by an increase in cognitive functioning.

Cognitive impairment is rare in chronic schizophrenia.

Dyskinesias are entirely due to antipsychotic medication.

Hebephrenic schizophrenia is characterized by preserved personality.

Catatonic schizophrenia is now commonly seen in industrialized countries.

Simple schizophrenia is characterized by prominent positive symptoms.

The subtypes of schizophrenia are reliable, stable over time, and associated with clear differences in pathophysiology and prognosis.

Undifferentiated schizophrenia is a subtype of schizophrenia characterized by prominent negative symptoms.

Residual schizophrenia is a subtype of schizophrenia characterized by prominent positive symptoms.

The subtypes of schizophrenia have been retained in DSM-5.

Liddle's three subsyndromes are based on the clinical features of schizophrenia during the acute phase.

Cognitive impairment in schizophrenia is typically seen in only one domain of learning and memory.

Executive function and attention are not core deficits in schizophrenia.

Social cognitive deficits in schizophrenia are limited to theory of mind.

The risk of overt dementia is not increased in later stages of schizophrenia.

Cognitive features of schizophrenia are not observed in attenuated form in unaffected first-degree relatives.

Depressive symptoms are rare in schizophrenia and only occur in the prodromal phase.

Comorbid depression in schizophrenia does not worsen the functional outcome.

The MATRICS Battery is a widely used method for cognitive assessments in schizophrenia.

Cognitive deficits are not a major determinant of poor functional outcome in schizophrenia.

Cognitive features are not being emphasized as potential targets for both drugs and psychological therapies in schizophrenia.

Liddle's three clinical subsyndromes are comparable to the groupings of positive symptoms, disorganization, and negative symptoms.

Type I schizophrenia has an insidious onset, mainly negative symptoms, and poor outcome and response to antipsychotic drugs.

The link between psychomotor poverty, impaired performance on frontal lobe tasks, and decreased frontal blood flow is a highly debated finding.

Crow's Type I and Type II schizophrenia are widely accepted and supported by subsequent research.

Regional cerebral blood flow is linked to distinct patterns of neuropsychological deficit in schizophrenia.

The clinical subsyndromes described by Liddle are only applicable to patients with acute schizophrenia.

The positive symptoms of schizophrenia are always accompanied by impaired social functioning during remissions.

Dopamine overactivity is a characteristic of Type II schizophrenia.

The ventricular enlargement in Type II schizophrenia is a reversible process.

The three clinical subsyndromes described by Liddle are mutually exclusive.

Neurological signs of schizophrenia are seen only in chronic patients.

The Calgary Depression Scale for Schizophrenia is used to assess neurological signs.

Depressive symptoms in schizophrenia can occur due to antipsychotic medication only.

Neurological signs in schizophrenia are correlated with cognitive improvement.

A neurological examination is not necessary for patients with schizophrenia.

Depressive symptoms in schizophrenia are always accompanied by negative symptoms.

Neurological signs in schizophrenia are rare in first-episode patients.

The presence of neurological signs in schizophrenia indicates a good prognosis.

The Calgary Depression Scale for Schizophrenia is used to assess neurological signs and depressive symptoms.

Neurological signs in schizophrenia are a result of antipsychotic medication only.

Patients with schizophrenia have no deficits in olfactory function.

The diminished sensitivity to pain in patients with schizophrenia is caused by medication.

The social and cultural background of the patient does not affect the content of symptoms.

Age does not affect the clinical features of schizophrenia.

Patients with intellectual disability always present with a complex clinical picture.

Pain insensitivity is not a common feature of schizophrenia.

The cognitive symptoms of schizophrenia are not affected by age.

Identifiable symptoms of schizophrenia are present before the patient typically presents for help during the prodrome.

Olfactory dysfunction is not a symptom of schizophrenia.

The longer the duration of untreated psychosis, the better the outcome.

Thalamic lesions are a proven cause of pain insensitivity in schizophrenia.

The clinical features of schizophrenia are the same in all patients regardless of age or intellectual ability.

More than 50% of people who are considered to be prodromal will progress to overt psychosis during a 2- to 3-year follow-up.

The Comprehensive Assessment of At Risk Mental State (CAARMS) is a criteria used to define and rate the severity of schizophrenia.

Psychosocial approaches to treatment aim to increase social stimulation to prevent negative symptoms.

The prodrome of schizophrenia is characterized by a sudden and distinct onset of symptoms.

Early intervention services aim to detect and treat emerging cases of schizophrenia, but this is unlikely to improve long-term outcome.

Cognitive and social functioning improve during the prodrome of schizophrenia.

The focus on the prodrome of schizophrenia is a recent development in the field of psychiatry.

Untreated psychosis is not 'neurotoxic' and does not affect the responsiveness of the illness to treatment.

The development of ideas about schizophrenia mirrors the development of ideas about psychiatric illness in general.

In the USA, psychiatrists employed Schneider’s first-rank symptoms to identify a narrowly delineated group of cases.

The first-admission rates for schizophrenia were lower in the USA than in the UK.

The concept of schizophrenia has remained consistent across different countries and cultures throughout history.

The historical development of ideas about schizophrenia is not relevant to understanding the current approach to diagnosis and classification.

The classification of schizophrenia is specified in both DSM-5 and ICD-10.

The diagnosis of schizophrenia is based solely on mental mechanisms.

The UK and continental Europe have a narrower definition of schizophrenia than the USA.

The historical development of ideas about schizophrenia is not relevant to understanding the current problems in diagnosis and classification.

The current approach to diagnosis and classification of schizophrenia is universally accepted.

The International Pilot Study of Schizophrenia was conducted by the US.

The classification of schizophrenia in DSM-5 and ICD-10 is identical.

Schizophrenia-like symptoms of less than 1-month duration are classified as schizophreniform disorder in DSM-5.

ICD-10 does not subclassify schizophrenia into the classical subtypes such as paranoid, hebephrenic, or catatonic.

DSM-5 allows the classification of schizophrenia by the number of acute episodes that have occurred after at least 6 months.

Catatonia is a subtype of schizophrenia in DSM-5.

ICD-10 requires a longer duration than DSM-5 for the diagnosis of schizophrenia.

Schizotypal disorder is classified as a personality disorder in ICD-10.

The current severity of schizophrenia can be rated on a 5-point scale in ICD-10.

The diagnostic criteria for schizophrenia in DSM-5 and ICD-10 are evidence-based.

DSM-5 and ICD-10 have the same definition for schizophrenia

Schizophrenia-like disorders can be considered within four groupings in DSM-5

Schizotypal disorder is categorized as a personality disorder in ICD-10

Brief psychotic disorder lasts for more than 1 month according to DSM-5

ICD-10 recognizes traditional subtypes of schizophrenia

DSM-5 requires a duration of illness of 1 month for schizophrenia

Delusional disorders are discussed in Chapter 11

ICD-10 does not subclassify schizophrenia into classical subtypes

Brief psychotic disorder is characterized by at least one of the acute-phase positive symptoms shown in Box 11.6 according to ICD-10

DSM-5 and ICD-10 have identical diagnostic criteria for schizophrenia

In DSM-5, schizophreniform disorder is a syndrome that lasts for less than 1 month.

Acute schizophrenia-like psychotic episode is a subtype of acute and transient psychotic disorder in ICD-10.

Schizoaffective disorder is characterized by a sudden onset of severe mental disorders in a setting of marked emotional turmoil.

The diagnosis of schizoaffective disorder requires the presence of prominent mood symptoms throughout the entire episode of illness.

ICD-10 subclassifies schizoaffective disorder according to whether the mood disturbance is depressive, manic, or mixed.

DSM-5 specifies that the diagnosis of schizoaffective disorder should only be made when both definite schizophrenic and definite affective symptoms are equally prominent and present simultaneously.

The reliability and nosological status of schizoaffective disorder is well established.

The outcome of schizoaffective disorder is generally thought to be worse than that for schizophrenia.

Complete recovery within 2-3 months is the rule for acute and transient psychotic disorder.

The category of acute and transient psychotic disorder is subdivided into several non-overlapping subtypes in ICD-10.

Patients with longstanding schizophrenia-like symptoms but which do not fully meet the diagnostic criteria are classified as residual schizophrenia in ICD-10.

Schizotypal personality disorder is classified as a personality disorder in ICD-10.

People with social withdrawal, lack of initiative, odd behavior, and blunting of emotion are diagnosed with simple schizophrenia.

Postschizophrenic depression is a type of depression that occurs only in patients with acute psychosis.

Patients with depression and schizophrenia-like symptoms are classified as having latent schizophrenia.

ICD-10 recognizes a specific type of depression that occurs in patients with schizophrenia.

People who have behaved oddly or eccentrically from an early age are classified as having residual schizophrenia.

Patients with schizophrenia who have prominent depressive symptoms are classified as having schizotypal disorder.

The diagnosis of residual schizophrenia is made in patients who have a history of schizophrenia but no longer meet the diagnostic criteria.

The term 'latent schizophrenia' is a well-established diagnostic label in ICD-10.

The lifetime prevalence of any substance abuse in patients with schizophrenia is 60%.

Post-traumatic stress disorder (PTSD) is rarely comorbid with schizophrenia, occurring in less than 10% of cases.

Delusional disorders are not considered to be part of the differential diagnosis of schizophrenia.

Schizophrenia-like disorders are clearly distinct from schizophrenia.

The classification of schizophrenia is based on aetiology or other empirically validated markers.

Obsessive-compulsive disorder is never comorbid with schizophrenia.

Panic disorder is not a common comorbidity of schizophrenia.

The prevalence of comorbid depression in patients with schizophrenia is less than 20%.

Alcohol abuse is rare among patients with schizophrenia, occurring in less than 10% of cases.

The distinction between schizophrenia and its variants is clear and universally accepted.

Schizophrenia-like disorders can occur, in clear consciousness, in a range of neurological and medical disorders.

Visual, olfactory, and gustatory hallucinations are suggestive of a psychotic disorder due to another medical condition.

A careful medical history and physical examination are not necessary for patients with schizophrenia-like psychoses.

Drug-induced states, particularly with psychostimulants or phencyclidine, can cause florid psychotic states.

A clear distinction between a drug-induced psychosis and schizophrenia is always possible.

The distinction of schizophrenia from affective psychosis depends on the degree and persistence of the mood disorder.

Delusional disorders are characterized by chronic, systematized paranoid delusions, and many areas of the mental state are remarkable.

Patients with borderline personality disorder rarely exhibit transient psychotic symptoms.

The classification of schizophrenia in DSM-5 and ICD-10 is identical.

ICD-10 subclassifies schizophrenia into classical subtypes.

The lifetime prevalence of schizophrenia is about 7 per 1000.

Schizophrenia typically begins between 20 and 30 years of age.

The gender difference in age of onset is large and robust.

Schizophrenia is more common in women than in men.

The neuroprotective effects of oestrogen are a well-established explanation for the gender difference in schizophrenia.

Patients with schizophrenia have a normal fertility rate.

The course and outcome of schizophrenia are not discussed in the chapter.

The incidence of diagnosed early-onset schizophrenia has decreased over the past four decades.

The lifetime morbid risk of schizophrenia is less than 5 per 1000.

Age at onset is the only environmental factor that affects the incidence of schizophrenia.

The incidence of schizophrenia is similar across all populations.

The annual incidence of schizophrenia is approximately 1.00 per 1000 population using a broad definition.

A meta-analysis reported a mean incidence of 0.15 per 1000 population for schizophrenia.

Schizophrenia has a high incidence and low prevalence.

The incidence of schizophrenia in England is 15.2 per 100,000 persons.

The DSM-IV criteria for schizophrenia result in a higher incidence than broader definitions.

Recent analyses have confirmed that the incidence of schizophrenia is similar across all populations.

A meta-analysis found no significant variation in the incidence of schizophrenia across different populations.

The WHO Ten-Country Study found significant variation in the incidence of schizophrenia across different populations.

The incidence of schizophrenia is higher in developing countries than in developed countries.

The current consensus is that the majority of the risk of schizophrenia is due to environmental factors.

The mode of inheritance of schizophrenia is simple and straightforward.

The genetic predisposition to schizophrenia determines the illness with certainty.

Environmental factors do not play a significant role in the development of schizophrenia.

The neurodevelopmental disturbance that leads to schizophrenia manifests itself only in adulthood.

The aetiology of schizophrenia involves only biological and psychological factors.

There is no evidence to support the role of genetic factors in the aetiology of schizophrenia.

The current understanding of the aetiology of schizophrenia is based solely on outdated views.

The classification of schizophrenia is solely based on aetiological factors.

The current understanding of the aetiology of schizophrenia is not influenced by environmental factors.

Abnormalities of the glutamate system may be secondary to excessive dopamine neurotransmission in the basal ganglia.

The interpretation of robust facts about the aetiology of schizophrenia is often clear.

The risk of schizophrenia in siblings of probands is lower than in the general population.

The liability to schizophrenia and bipolar disorder is transmitted independently.

The familial predisposition is to schizophrenia only, not a range of disorders.

The concordance rates in monozygotic twins are lower than in dizygotic twins.

There is no role for shared environmental factors in the familial aetiology of schizophrenia.

The lifetime risk of schizophrenia in various classes of relatives is not clear.

Recent findings from genome-wide studies do not support the concept of a schizophrenia spectrum.

The genetic contribution to schizophrenia is minor.

The first substantial twin study was conducted in Berlin by Luxenberger in the 1920s.

Concordance is several-fold higher in dizygotic (DZ) twins than in monozygotic (MZ) twins.

A meta-analysis of twin studies confirmed the substantial heritability of schizophrenia (50%);

The estimates of heritability make no assumptions about the genetic architecture.

Gene-environment interactions are not included in the estimates of heritability.

Twin studies can separate environmental factors into those that are shared and those that are unique to the individual.

The substantial heritability of schizophrenia suggests that inheritance contributes a small percentage of the risk for schizophrenia.

The estimates of heritability are not affected by the assumptions about the genetic architecture.

Heritability figures provide a complete understanding of the causes of schizophrenia.

Twin studies are not important in research on schizophrenia.

Among discordant MZ twins, the risk of schizophrenia is increased equally in children of both the unaffected and affected co-twin.

Estimates for schizophrenia heritability from population studies are higher than those of twin studies.

Unaffected identical co-twins do not exhibit any mild features of schizophrenia.

Adoption studies have shown that environmental factors are the primary cause of schizophrenia.

The rate of schizophrenia among the adopted-away children is lower than among children with a schizophrenic parent who remained with their biological family.

Prenatal environment is not a significant factor in the development of schizophrenia.

Adoption studies can rule out an interaction between environmental causes in the adoptive family and genetic predisposition.

Finnish data show that adoptees at low genetic risk of schizophrenia are more sensitive to adverse upbringing.

The meta-analysis showed that most of the environmental contribution to schizophrenia comes from individual-specific influences.

The rate of schizophrenia among the biological relatives of the adoptees with schizophrenia is lower than among the relatives of the controls.

Schizophrenia is a disorder caused by a single major gene.

The liability to schizophrenia is expressed when a single gene is expressed.

Some genes are necessary or sufficient for schizophrenia.

Families with a single-gene dominant or recessive disorder for schizophrenia have been identified.

The genetic mechanisms of schizophrenia are fully understood.

Identifying schizophrenia genes has been a straightforward process.

Genomics knowledge has not contributed to the progress in identifying schizophrenia genes.

Schizophrenia is a disorder with a simple genetic architecture.

The heritability of schizophrenia is low.

Schizophrenia is a disorder with a clear genetic pattern of inheritance.

The majority of genetic risk for schizophrenia comes from copy number variants (CNVs).

The largest study to date identified 108 genomic loci associated with schizophrenia risk, containing over 100 known protein-coding genes.

Each single nucleotide polymorphism (SNP) confers a significant effect on schizophrenia risk.

About 5% of patients and 2% of controls carry a copy number variant (CNV) strongly supported as a schizophrenia risk factor.

All copy number variants (CNVs) associated with schizophrenia are inherited.

The variants of the gene SETD1A are predicted to cause a gain of function of the gene concerned.

The overall importance of rare variants in schizophrenia is already well established.

Copy number variants (CNVs) can only be deletions of a length of DNA.

The odds ratio of deletion of 1.35 million nucleotides from chromosome 15q11.2 is approximately 2.

The schizophrenia-associated CNVs are not associated with a risk of one or more other neuropsychiatric phenotypes.

Crow's lateralization hypothesis proposes that schizophrenia is due to multiple genes.

The discovery of multiple loci and genes associated with schizophrenia has led to a complete understanding of the biological implications and molecular mechanisms.

Copy number variations (CNVs) likely exert their effects through gene dosage and by revealing the effects of a harmful recessive allele on the undeleted chromosome.

Genetic discoveries have led to direct clinical roles of genetic testing for schizophrenia in clinical practice.

The distinction between genetic and environmental factors is a clear-cut dichotomy.

Prenatal and perinatal factors are not identified as environmental risk factors for schizophrenia.

The classification of schizophrenia is based on aetiology or other empirically validated markers.

The genes associated with schizophrenia converge on several functional networks and biochemical pathways, including N-methyl-D-aspartate (NMDA) receptor-mediated signalling and synaptic plasticity.

The mechanism by which single nucleotide polymorphisms (SNPs) alter gene function to affect the risk of schizophrenia is straightforward to determine.

The gene DISC1 is the only genetic variant that contributes to the development of schizophrenia.

The entire genetic risk of schizophrenia can be explained by the genetic variants identified to date.

Epigenetic factors do not play a role in the development of schizophrenia.

Gene-environment interactions do not contribute to the development of schizophrenia.

The DISC1 gene is the primary cause of schizophrenia in all cases.

The majority of the genetic risk of schizophrenia can be explained by rare variants.

The genetics of schizophrenia are fully understood and well-established.

CNVs are the primary genetic variant associated with schizophrenia.

The genetics of schizophrenia are not influenced by environmental factors.

The genetic risk of schizophrenia can be fully explained by SNPs.

Obstetric complications are directly causal of schizophrenia via fetal hypoxia.

The odds ratio of schizophrenia associated with obstetric complications is around 1.

Rhesus incompatibility is not associated with an increased risk of schizophrenia.

Infective and inflammatory factors have no relation to the development of schizophrenia.

Prenatal influenza exposure has no effect on fetal brain development.

The association between obstetric complications and schizophrenia is only relevant in individuals without a genetic predisposition to the condition.

The 1957 influenza A2 pandemic is not associated with an increased risk of schizophrenia.

Serological evidence of influenza infection during early pregnancy is not associated with an increased risk of schizophrenia in the offspring.

The mechanisms underlying the association between obstetric complications and schizophrenia are well understood.

The risk of schizophrenia is not increased in individuals who experienced obstetric complications compared to their unaffected siblings or normal controls.

The relationship between maternal infection and schizophrenia risk is only observed in women with a history of psychiatric disorder.

There is no association between maternal malnutrition and increased risk of schizophrenia.

The season of birth effect on schizophrenia is observed in both the northern and southern hemispheres, but not at higher latitudes.

The mechanism of maternal malnutrition on schizophrenia is proposed to be related to general malnutrition rather than lack of specific micronutrients.

The association between paternal age and schizophrenia is only observed in those with a family history of psychosis.

The paternal age effect on schizophrenia is observed for all subsequent children, not just the first-born child.

The influence of maternal infection on schizophrenia risk is only observed during the perinatal period.

The relationship between maternal inflammation and schizophrenia risk is considered as a direct cause of schizophrenia.

The odds ratio of schizophrenia associated with maternal famine is approximately 1.

The association between schizophrenia and paternal age is not observed in the offspring of fathers below 50 years old.

The study by Parnas et al. (1982) reported that 207 children of mothers with schizophrenia developed schizophrenia as adults.

Children who developed schizophrenia could be distinguished by their better social skills at the age of 11 years.

The study by Jones et al. (1994) found that children who developed schizophrenia showed advanced milestones and better social skills.

A graded relationship between delayed milestones and schizophrenia has been disputed in several subsequent cohorts.

Parnas et al.'s (1982) study found that being socially isolated from peers was a protective factor for schizophrenia.

The study by Done et al. (1994) found that children who developed schizophrenia had better reading skills than those who remained well.

The study by Jones et al. (1994) found that children who developed schizophrenia had better education test scores than those who remained well.

Parnas et al.'s (1982) study found that poor rapport at interview was a protective factor for schizophrenia.

The study by Done et al. (1994) found that children who developed schizophrenia had better social skills than those who developed neurotic illness.

The study by Jones et al. (1994) found that children who developed schizophrenia had more social play than those who remained well.

The behaviour of children is not associated with later schizophrenia.

Cannabis use has no association with the risk of developing schizophrenia.

Tobacco smoking is not a risk factor for the development of psychosis.

Schizophrenia is not overrepresented among people of lower social class.

The findings of childhood dysfunction in individuals who later develop schizophrenia are specific to schizophrenia.

Substance misuse is not a causative factor in schizophrenia.

The association between cannabis use and psychosis is not influenced by genetic and other factors.

The relationship between tobacco smoking and psychosis is causal.

Social and psychosocial factors are not important in schizophrenia.

The findings of childhood dysfunction in individuals who later develop schizophrenia are not related to the subsequent development of the illness.

Studies have found that individuals with schizophrenia are overrepresented in disadvantaged outer-city areas.

The social drift theory suggests that people who are about to develop schizophrenia search for social isolation.

Urban birth is associated with a decreased risk of schizophrenia.

The cause of the association between urban birth and schizophrenia is fully understood and attributed to social deprivation.

Recent data suggest that genetic liability to schizophrenia plays no part in the social drift.

The distribution of schizophrenia cases in disadvantaged inner-city areas is unique to Chicago.

Unsatisfactory living conditions can prevent schizophrenia.

The association between urban birth and schizophrenia is limited to small towns and suburban areas.

The study by Pedersen and Mortensen (2001) found no association between urban birth and schizophrenia.

The social drift theory is no longer supported by recent data.

The incidence of schizophrenia is lower in Afro-Caribbean immigrants in the UK than in the white population.

Misdiagnosis due to poor diagnostic practice is a likely explanation for the high rates of schizophrenia in Afro-Caribbean immigrants in the UK.

Life events and difficulties have no proven link to the development of schizophrenia.

The increased rate of schizophrenia among migrants is solely due to social selection.

The diagnosis of schizophrenia is based solely on aetiological factors.

Environmental factors in the host country do not contribute to the increased rate of schizophrenia among migrants.

The relative risk of schizophrenia is higher in migrants from high-income countries than in those from lower- and middle-income countries.

The high incidence of schizophrenia among Afro-Caribbean immigrants in the UK is due to institutional racism.

The rate of schizophrenia among migrants is similar to that of the general population.

The relationship between ethnic density and schizophrenia is clear and well-understood.

The aberrant salience model of schizophrenia shares some features with the neuropsychological model of Gray et al.

The lifetime risk of schizophrenia in various classes of relatives is clearly established

Current psychological models of schizophrenia are more grounded in sociological aspects

The theory of Frith argues that in schizophrenia there is a breakdown in the internal representation of mental events

Palmer et al. (2009) proposed a neuropsychological model of schizophrenia that links neuropsychology to the dopamine hypothesis

The Comprehensive Assessment of At Risk Mental State (CAARMS) is a criteria used to define and rate the severity of schizophrenia

Early theories of schizophrenia are still widely used today

Menon (2011) proposed a model of aberrant connectivity and brain networks in schizophrenia

Gray et al. (1991) proposed a neuropsychological model of schizophrenia that argues that positive symptoms arise from a failure to monitor and identify one’s own willed intentions

Kretschmer suggested that both personality and schizophrenia were related to the asthenic type of body build.

Many people with schizophrenia have a clear premorbid personality disorder.

The concept of the schizophrenia spectrum is based on the idea that schizophrenia is a discrete category.

Abnormal personality features are uncommon among people who later develop schizophrenia.

The idea of a continuum between normal personality and schizophrenia is a relatively new concept in the field of psychology.

Only a small proportion of people with schizoid personalities develop schizophrenia.

There is a clear distinction between premorbid personality and the prodromal phase of emerging illness in schizophrenia.

The study of personality and psychosis has been a major area of research in the field of psychology.

The null hypothesis that there are no structural differences in the brain in schizophrenia has been disproven over the past 40 years.

The failure of Alzheimer and others to identify a neuropathology led to the view of schizophrenia as an organic disorder rather than a functional one.

Structural brain changes in schizophrenia are clinically useful in the diagnosis of individual patients.

The neurobiology of onset and first-episode psychosis is reviewed in Remington et al. (2014).

The study by Johnstone et al. is a landmark study in structural brain imaging in schizophrenia.

The search for a neuropathology associated with schizophrenia began over two centuries ago.

Alzheimer reported the case of presenile dementia with which his name is associated after studying the brains of patients with dementia praecox for a decade.

There is no evidence to suggest that there are structural brain changes in schizophrenia.

The neurobiology of relapse is reviewed in Kahn et al. (2015).

The details and interpretation of structural brain changes in schizophrenia are well understood.

Lateral ventricular enlargement in schizophrenia was first reported using computerized tomography.

The study by Johnstone and colleagues found no significant differences in ventricular volumes between patients with schizophrenia and healthy controls.

A meta-analysis of brain volumes in over 18,000 subjects found that ventricular volumes are decreased by about 30% in schizophrenia.

The results of longitudinal studies suggest that structural brain changes in schizophrenia occur primarily in adulthood.

The hippocampus and thalamus are affected equally in schizophrenia, with no significant differences in grey and white matter.

There is a clear distinction between 'organic' and 'non-organic' subtypes of schizophrenia based on structural brain imaging.

The changes in brain structure in schizophrenia are diagnostically specific and can be used to distinguish it from bipolar disorder.

Post-mortem neuropathological studies have found evidence of neurodegenerative processes in schizophrenia.

The main positive findings in neuropathological studies of schizophrenia are increases in some markers of synapses and dendrites.

The neurodevelopmental hypothesis of schizophrenia suggests that the disorder originates in late adulthood.

The meta-analysis by Hill et al. (2004) found no significant difference in perfusion of the frontal cortex compared to posterior regions in chronic, medicated patients with schizophrenia.

Functional magnetic resonance imaging (fMRI) studies of schizophrenia have shown no alterations in frontal activity during working memory tasks.

Positron emission tomography (PET) is the only imaging technique used to assess patterns of brain activity in schizophrenia.

The study by Ingvar and Franzen (1974) found increased perfusion of the frontal cortex compared to posterior regions in chronic, medicated patients with schizophrenia.

The Wisconsin Card Sorting Test is not a commonly used task in fMRI studies of working memory in schizophrenia.

Single-photon emission tomography (SPET) has not been used to assess patterns of brain activity in schizophrenia.

The association between hypofrontality and schizophrenia is not influenced by the phase of illness and symptom profile.

Functional magnetic resonance imaging (fMRI) has not been used to study altered frontal activity in schizophrenia.

The study by Minzenberg et al. (2009) found no complex changes in frontal activity in fMRI studies of schizophrenia.

Positron emission tomography (PET) is the most commonly used imaging technique in the study of schizophrenia.

Brain oscillations and network activity are not related to cognition in schizophrenia.

The electroencephalogram (EEG) in schizophrenia generally shows decreased amounts of theta activity, fast activity, and paroxysmal activity.

P300 and P50 deficits are not linked to the gene coding for a subunit of the nicotinic cholinergic receptor.

Patients with schizophrenia do not require more frontal cortex activation to achieve the same level of performance as controls.

The cortical regions activated during auditory hallucinations have not been studied using fMRI.

The activity of different brain circuits or networks is normal in schizophrenia.

The amplitude of the P300 wave is increased in patients with schizophrenia and their relatives.

Electroencephalography has not shown a decreased synchronization or coherence of electrical activity in the prefrontal cortex in schizophrenia.

The study of brain oscillations and network activity has not been a major area of research in the field of schizophrenia.

Altered 'resting state' brain activity is not a topic of emerging interest in schizophrenia research.

Dopamine-receptor agonists are used as antipsychotic drugs.

The use of PET and SPET techniques has not provided evidence to support the dopamine hypothesis of schizophrenia.

Acute amphetamine administration improves psychotic symptoms in people with schizophrenia.