Schizophrenia

CPD

AP Staff

1 May 2000

References

American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DSM-5-TR. 5th edn. Washington, DC: American Psychiatric Association Publishing; 2022.
World Health Organization. Schizophrenia 2025. At: www.who.int/news-room/fact-sheets/detail/schizophrenia
Morgan VA, Waterreus A, Jablensky A, et al. People living with psychotic illness in 2010: The second Australian national survey of psychosis. Aust N Z J Psychiatry. 2012;46(8):735–52.
Australian Institute of Health and Welfare. Prevalence and impact of mental illness. 2025. At: www.aihw.gov.au
Therapeutic Guidelines. Psychoses. Melbourne: Therapeutic Guidelines Limited; 2023. At: www.tg.org.au
Tahmazov E, Bosse J, Glemain B, et al. Impact of Early Intervention for Early Psychosis on Suicidal Behavior—A Meta-Analysis. Acta Psychiatr Scand. 2025;151(2):127–41.
Mortensen PB, Pedersen CB, Westergaard T, et al. Effects of Family History and Place and Season of Birth on the Risk of Schizophrenia. N Engl J Med. 1999;340(8):603–8.
Besteher B, Brambilla P, Nenadić I. Twin studies of brain structure and cognition in schizophrenia. Neurosci Biobehav Rev. 2020;109:103–13.
Hilker R, Helenius D, Fagerlund B, et al. Heritability of Schizophrenia and Schizophrenia Spectrum Based on the Nationwide Danish Twin Register. Biol Psychiatry. 2018;83(6):492–8.
Davis J, Eyre H, Jacka FN, et al. A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis. Neurosci Biobehav Rev. 2016;65:185–94.
National Health Service. Causes – Schizophrenia: Crown Copyright; 2023. At: www.nhs.uk/mental-health/conditions/schizophrenia/causes/
Benrimoh D, Dlugunovych V, Wright AC, et al. On the proportion of patients who experience a prodrome prior to psychosis onset: A systematic review and meta-analysis. Molec Psychiat. 2024;29(5):1361–81.
Häfner H, Löffler W, Maurer K, et al. Depression, negative symptoms, social stagnation and social decline in the early course of schizophrenia. Acta Psychiatr Scand. 1999;100(2):105–18.
Larson MK, Walker EF, Compton MT. Early signs, diagnosis and therapeutics of the prodromal phase of schizophrenia and related psychotic disorders. Expert Rev Neurother. 2010;10(8):1347–59.
Olsen KA, Rosenbaum B. Prospective investigations of the prodromal state of schizophrenia: review of studies. Acta Psychiatr Scand. 2006;113(4):247–72.
Australian Medicines Handbook. Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd; 2026. At: www.amh.net.au
Australian Institute of Health and Welfare. National drug strategy household survey 2022–2023: Australian Government; 2024. At: www.aihw.gov.au
National Health Service. Symptoms – Schizophrenia: Crown Copyright; 2023. At: www.nhs.uk/mental-health/conditions/schizophrenia/symptoms/
National Mental Health Commission. Equally Well Consensus Statement: Improving the physical health and wellbeing of people living with mental illness in Australia. Sydney: NMHC; 2016.
Popa A-V, Ifteni PI, Țăbian D, et al. What is behind the 17-year life expectancy gap between individuals with schizophrenia and the general population? Schizophrenia. 2025;11(1):117.
Hjorthøj C, Stürup AE, McGrath JJ, et al. Years of potential life lost and life expectancy in schizophrenia: a systematic review and meta-analysis. Lancet Psychiatry. 2017;4(4):295–301.
Harris M. The metabolic syndrome. Aust J Gen Pract. 2013;42:524–7.
Lambert TJ, Velakoulis D, Pantelis C. Medical comorbidity in schizophrenia. Med J Aust. 2003;178(S9):S67–70.
Saha S, Chant D, McGrath J. A systematic review of mortality in schizophrenia: is the differential mortality gap worsening over time? Arch Gen Psychiatry. 2007;64(10):1123–31.
Bobes J, Arango C, Garcia-Garcia M, et al. Healthy lifestyle habits and 10-year cardiovascular risk in schizophrenia spectrum disorders: an analysis of the IMPACT study. Schizophr Res. 2010;119(1-3):101–9.
De Hert M, Correll CU, Bobes J, et al. Physical illness in patients with severe mental disorders. I. Prevalence, impact of medications and disparities in health care. World Psychiatry. 2011;10(1):52–77.
Correll CU, Detraux J, De Lepeleire J, et al. Effects of antipsychotics, antidepressants and mood stabilizers on risk for physical diseases in people with schizophrenia, depression and bipolar disorder. World Psychiatry. 2015;14(2):119–36.
Vancampfort D, Stubbs B, Mitchell AJ, et al. Risk of metabolic syndrome and its components in people with schizophrenia and related psychotic disorders, with and without antipsychotic therapy: a systematic review and meta-analysis. World Psychiatry. 2015;14(3):339–47.
McGrath JJ, Saha S, Chant D, et al. Schizophrenia: a concise overview of incidence, prevalence, and mortality. Epidemiol Rev. 2008;30:67–76.
Laursen TM. Life expectancy among persons with schizophrenia or bipolar affective disorder. Schizophr Res. 2011;131(1-3):101–4.
Crump C, Winkleby MA, Sundquist K, et al. Comorbidities and mortality in persons with schizophrenia: a Swedish national cohort study. Am J Psychiatry. 2013;170(3):324–33.
Heald A, Pendlebury H, Guy M, et al. Lifestyle factors and the physical health of people with schizophrenia. J Psychiatr Ment Health Nurs. 2017;24(6):403–10.
Newcomer JW. Antipsychotic medications: metabolic and cardiovascular risk. J Clin Psychiatry. 2007;68(Suppl 4):8–13.
Mitchell AJ, Vancampfort D, Sweers K, et al. Prevalence of metabolic syndrome and metabolic abnormalities in schizophrenia and related disorders—a systematic review and meta-analysis. Schizophr Bull. 2013;39(2):306–18.
Pillinger T, McCutcheon RA, Vano L, et al. Comparative effects of 18 antipsychotics on metabolic function in patients with schizophrenia, predictors of metabolic dysregulation, and association with psychopathology: a systematic review and network meta-analysis. Lancet Psychiatry. 2020;7(1):64–77.
Leucht S, Cipriani A, Spineli L, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. Lancet. 2013;382(9896):951–62.
Tandon R, Nasrallah HA, Keshavan MS. Schizophrenia, “just the facts” 4. Clinical features and conceptualization. Schizophr Res. 2009;110(1-3):1–23.
Rummel-Kluge C, Komossa K, Schwarz S, et al. Head-to-head comparisons of metabolic side effects of second generation antipsychotics in the treatment of schizophrenia: a systematic review and meta-analysis. Schizophr Res. 2010;123(2-3):225–33.
Galletly C, Castle D, Dark F, et al. Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for the management of schizophrenia and related disorders. Aust N Z J Psychiatry. 2016;50(5):410–72.
Gardner DM, Murphy AL, O’Donnell H, et al. International consensus study of antipsychotic dosing. Am J Psychiatry. 2010;167(6):686–93.
Tiihonen J, Mittendorfer-Rutz E, Majak M, et al. Real-world effectiveness of antipsychotic treatments in a nationwide cohort of 29,823 patients with schizophrenia. JAMA Psychiatry. 2017;74(7):686–93.
Kishimoto T, Hagi K, Nitta M, et al. Effectiveness of long-acting injectable vs oral antipsychotics in patients with schizophrenia: a meta-analysis of randomized controlled trials. Schizophr Bull. 2021;47(1):131–40.
Siskind D, McCartney L, Sharma R, et al. Clozapine v. first- and second-generation antipsychotics in treatment-resistant schizophrenia: a systematic review and meta-analysis. Br J Psychiatry. 2016;209(5):385–92.
Kane JM, Correll CU, Goff DC, et al. Real-world effectiveness of antipsychotic treatment in patients with schizophrenia. J Clin Psychiatry. 2020;81(3):19m12975.
Stroup TS, McEvoy JP, Ring KD, et al. A randomized trial examining the effectiveness of switching from olanzapine, quetiapine, or risperidone to aripiprazole to reduce metabolic risk: Comparison of Antipsychotics for Metabolic Problems (CAMP). Am J Psychiatry. 2011;168(9):947–56.
Mauri MC, Paletta S, Maffini M, et al. Clinical pharmacokinetics of atypical antipsychotics: a critical review of the relationship between plasma concentrations and clinical response. Clin Pharmacokinet. 2014;53(10):893–917.
Hiemke C, Bergemann N, Clement HW, et al. Consensus guidelines for therapeutic drug monitoring in neuropsychopharmacology: Update 2017. Pharmacopsychiatry. 2018;51(1-02):9–62.
Cooper SJ, Reynolds GP, Barnes T, et al. British Association for Psychopharmacology guidelines on the management of weight gain, metabolic disturbances and cardiovascular health associated with psychosis and antipsychotic drug treatment. J Psychopharmacol. 2016;30(8):717–48.
Ward M, Druss B. The epidemiology of diabetes in populations with severe mental illness. Harv Rev Psychiatry. 2015;23(2):75–88.
Smith DJ, Langan J, McLean G, et al. Schizophrenia is associated with excessive multiple physical-health comorbidities: a cross-sectional study of 1,751,841 patients in primary care. BMJ Open. 2013;3(4):e002808.
Firth J, Siddiqi N, Koyanagi A, et al. The Lancet Psychiatry Commission: a blueprint for protecting physical health in people with mental illness. Lancet Psychiatry. 2019;6(8):675–712.
Speyer H, Christiani TV, Røder ME, et al. The effect of lifestyle interventions on physical health in patients with severe mental illness: a systematic review and meta-analysis. J Clin Psychiatry. 2019;80(1):18r12134.

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

What’s on the list?

Making palliative care support easier to find

Supporting patients and families at the end of life

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

What’s on the list?

Making palliative care support easier to find

Supporting patients and families at the end of life

Case scenario

Introduction