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Journal articles on the topic 'Schizophrenia – Epidemiology'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Häfner, Heinz, and Wolfram an der Heiden. "Epidemiology of Schizophrenia." Canadian Journal of Psychiatry 42, no. 2 (March 1997): 139–51. http://dx.doi.org/10.1177/070674379704200204.

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Objective: To characterize the epidemiology of schizophrenia. Method: Narrative literature review. Results: Each year 1 in 10 000 adults (12 to 60 years of age) develops schizophrenia. Based on a restrictive and precise definition of the diagnosis and using standardized assessment methods and large, representative populations, the incidence rates appear stable across countries and cultures and over time, at least for the last 50 years. Schizophrenic patients are not born into ecological and social disadvantage. The uneven distribution of prevalence rates is a result of social selection: an early onset leads to social stagnation, a late onset to descent from a higher social status. The main age range of risk for schizophrenia is 20 to 35 years. It is still unclear whether schizophrenia-like late-onset psychoses (for example, late paraphrenia) after age 60 should be classified as schizophrenia either psychopathologically or etiologically. In 75% of cases, first admission is preceded by a prodromal phase with a mean length of 5 years and a psychotic prephase of one year's duration. On average, women fall ill 3 to 4 years later than men and show a second peak of onset around menopause. Consequently, late-onset schizophrenias are more frequent and more severe in women than in men. The sex difference in age of onset is smaller in cases with a high genetic load and greater in cases with a low genetic load. Type of onset and core symptoms do not differ between the sexes. The most pronounced sex difference is the socially negative illness behaviour of young men. Conclusions: Among the factors determining social course and outcome are level of social development at onset, the disorder itself (for example, genetic liability, severity of symptoms, and functional deficits), general biological factors (for example, estrogen), and sex- and age-specific illness behaviour.

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2

Hare, E. "Aspects of the Epidemiology of Schizophrenia." British Journal of Psychiatry 149, no. 5 (November 1986): 554–61. http://dx.doi.org/10.1192/bjp.149.5.554.

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Reasons are given why the hospital diagnosis of schizophrenia may be accurate enough for the proper study of certain aspects of its epidemiology. Studies in the seasonality of admissions and of births in schizophrenic patients have produced consistent results in different countries and at different times. The results are summarized, and causal hypotheses based on them are discussed. The idea that schizophrenia is a relatively recent disease is compatible with these hypotheses.

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3

Jablensky, Assen. "Schizophrenia: epidemiology." Current Opinion in Psychiatry 12, no. 1 (January 1999): 19–28. http://dx.doi.org/10.1097/00001504-199901000-00013.

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4

Singh, Pragya, Srinath Pandey, Ved Kumar Mishra, Swati Dwivedi, Shubhangi Dixit, and Prashant Ankur Jain. "SCHIZOPHRENIA: UNRAVELING THE LABYRINTH OF ETIOLOGY AND EPIDEMIOLOGY." International Journal of Pharmacy and Biological Sciences 7, no. 1 (January 1, 2017): 40–51. http://dx.doi.org/10.21276/ijpbs.2017.7.1.6.

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5

Häfner, H., K. Maurer, W. Löffler, B. Fätkenheuer, W. An Der Heiden, A. Riecher-Rössler, S. Behrens, and W. F. Gattaz. "The Epidemiology of Early Schizophrenia." British Journal of Psychiatry 164, S23 (April 1994): 29–38. http://dx.doi.org/10.1192/s0007125000292714.

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For the investigation of the early course of schizophrenia starting from onset, the standardised Interview for the Retrospective Assessment of the Onset of Schizophrenia was developed and validated. In a representative sample of 267 first-admitted German schizophrenics of a broad diagnosis from a population of 1.5 million, the age at which different diagnostic and onset definitions were satisfied, the symptoms at the time of the interview, and the accumulation of positive and negative symptoms until first admission were assessed. Comparison between the two sexes and three age groups yielded hardly any differences in the accumulation of symptoms and their course until first admission, except for a slightly shorter period of negative symptoms in young males and a slightly longer one in older women – which contradicts prevailing opinion. At the time of the interview, no significant sex differences were found with respect to the core symptoms of schizophrenia (negative and first-rank symptoms), but clear and substantial differences emerged in disease behaviour. The significantly higher age at first onset in women is explained, on the basis of animal experiments and a clinical study, by the neuromodulatory effect of oestrogen on D2 receptors and by a higher vulnerability threshold in women.

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6

Mortensen, P. B. "Epidemiology of schizophrenia." European Psychiatry 17 (May 2002): 32. http://dx.doi.org/10.1016/s0924-9338(02)80141-9.

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7

Ineichen, B. "Epidemiology of schizophrenia." Journal of Neurology, Neurosurgery & Psychiatry 61, no. 6 (December 1, 1996): 656. http://dx.doi.org/10.1136/jnnp.61.6.656.

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8

Wing, J. K. "Epidemiology of Schizophrenia." Journal of the Royal Society of Medicine 80, no. 3 (March 1987): 134–35. http://dx.doi.org/10.1177/014107688708000302.

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9

Mura, Gioia, Donatella Rita Petretto, Krishna M. Bhat, and Mauro Giovanni Carta. "Schizophrenia: from Epidemiology to Rehabilitation." Clinical Practice & Epidemiology in Mental Health 8, no. 1 (July 10, 2012): 52–66. http://dx.doi.org/10.2174/1745017901208010052.

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Purpose/Objective:We discuss recent evidences about schizophrenia (frequency, onset, course, risk factors and genetics) and their influences to some epidemiological myths about schizophrenia diffuse between psychiatric and psychopathology clinicians. The scope is to evaluate if the new acquisitions may change the rehabilitation approaches to schizophrenia modifying the balance about the neurodevelopmental hypothesis of schizophrenia accepting that the cognitive deficits are produced by errors during the normal development of the brain (neurodevelopmental hypothesis) that remains stable in the course of illness and the neurodegenerative hypothesis according of which they derived from a degenerative process that goes on inexorably.Research Method/Design:A review of the literature about epidemiology of schizophrenia has been performed and the contributions of some of these evidence to neurodevelopmental hypothesis and to rehabilitation has been described.Results:It cannot be definitively concluded for or against the neurodevelopmental or degenerative hypothesis, but efforts in understanding basis of schizophrenia must go on. Until now, rehabilitation programs are based on the vulnerability-stress model: supposing an early deficit that go on stable during the life under favorable circumstances. So, rehabilitation approaches (as neuro-cognitive approaches, social skill training, cognitive-emotional training) are focused on the individual and micro-group coping skills, aiming to help people with schizophrenia to cope with environmental stress factors.Conclusions/Implications:Coping of cognitive deficits in schizophrenia may represents the starting-point for further research on schizophrenia, cohort studies and randomized trials are necessary to defined the range of effectiveness and the outcome of the treatments.

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10

Maier, W. "Genetic Epidemiology of Schizophrenia." European Psychiatry 12, S2 (1997): 120s. http://dx.doi.org/10.1016/s0924-9338(97)80296-9.

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11

Goncharov, M. "Genetic Epidemiology of Schizophrenia." European Psychiatry 12, S2 (1997): 209s. http://dx.doi.org/10.1016/s0924-9338(97)80646-3.

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12

SARTORIUS, NORMAN. "The Epidemiology of Schizophrenia." American Journal of Psychiatry 161, no. 3 (March 2004): 590—a—591. http://dx.doi.org/10.1176/appi.ajp.161.3.590-a.

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13

Jablensky, Assen. "The Epidemiology of Schizophrenia." Australian & New Zealand Journal of Psychiatry 40, no. 5 (May 2006): 503. http://dx.doi.org/10.1080/j.1440-1614.2006.01832.x.

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14

Leach, Anne, and Susan Scherer. "The epidemiology of schizophrenia." Current Opinion in Psychiatry 5, no. 1 (February 1992): 20–24. http://dx.doi.org/10.1097/00001504-199202000-00005.

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15

Jablensky, Assen. "The epidemiology of schizophrenia." Current Opinion in Psychiatry 6, no. 1 (February 1993): 43–52. http://dx.doi.org/10.1097/00001504-199302000-00009.

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16

Bradford, Daniel W. "The Epidemiology of Schizophrenia." Psychiatric Services 55, no. 3 (March 2004): 324. http://dx.doi.org/10.1176/appi.ps.55.3.324.

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17

Tsuang, Ming T. "Genetic epidemiology of schizophrenia." Journal of the Neurological Sciences 120, no. 1 (December 1993): 3–4. http://dx.doi.org/10.1016/0022-510x(93)90007-l.

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18

Shepherd, Michael. "Historical epidemiology and the functional psychoses." Psychological Medicine 23, no. 2 (May 1993): 301–4. http://dx.doi.org/10.1017/s0033291700028373.

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Sixty years ago the distinguished epidemiologist Joseph Goldberger, following his outstanding achievements in clarifying the causes of pellagra, was offered a large research grant to investigate schizophrenia. He responded to the proposal by studying the available evidence concerning the schizophrenic syndrome and then politely declined to take up the challenge. ‘In five or more years’, he wrote, ‘I could probably find out nothing. Much work will be needed on the physiology of the central nervous system and on many collateral problems before dementia praecox can be understood’ (Parsons, 1943).

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19

Jones, Peter, and Mary Cannon. "THE NEW EPIDEMIOLOGY OF SCHIZOPHRENIA." Psychiatric Clinics of North America 21, no. 1 (March 1998): 1–25. http://dx.doi.org/10.1016/s0193-953x(05)70358-0.

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20

Oliver, Emily A., and Paul Fearon. "Schizophrenia: epidemiology and risk factors." Psychiatry 7, no. 10 (October 2008): 410–14. http://dx.doi.org/10.1016/j.mppsy.2008.07.011.

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21

Häfner, H., and B. Nowotny. "Epidemiology of early-onset schizophrenia." European Archives of Psychiatry and Clinical Neuroscience 245, no. 2 (April 1995): 80–92. http://dx.doi.org/10.1007/bf02190734.

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22

Gallagher, B. J., B. J. Jones, J. A. McFalls, and A. M. Pisa. "Social class and type of schizophrenia." European Psychiatry 21, no. 4 (June 2006): 233–37. http://dx.doi.org/10.1016/j.eurpsy.2006.04.001.

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AbstractObjectiveCurrent and past research strongly indicates a high prevalence of schizophrenia in the lower class in the USA and other stratified societies. To date, no study has tested for a connection between type of schizophrenia and socioeconomic status (SES). We tested for an interrelationship between schizophrenic subtype, SES and race.MethodsPositive and negative symptom scales were used to evaluate 436 schizophrenic patients at a state hospital in the USA. All patients were also diagnosed by DSM standards. Social class of origin was assessed by the Occupational Classification Distributions of the U.S. Bureau of the Census. Multivariate analysis was conducted with the likelihood ratio chi-square.ResultsWe uncovered a distinct propensity for deficit schizophrenia to be elevated among the poor. The finding presents as a pure SES effect since the likelihood of deficit schizophrenia does not vary by race when social class is held constant.ConclusionThe finding is potentially an important new insight into the epidemiology of schizophrenia. It offers a better understanding for poor outcome among lower class patients in stratified societies such as the United States. It is also consistent with longitudinal research by European investigators.

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23

Sham, Pak C., Eadbhard O'Callaghan, Noriyoshi Takei, Graham K. Murray, Edward H. Hare, and Robin M. Murray. "Schizophrenia Following Pre-natal Exposure to Influenza Epidemics Between 1939 and 1960." British Journal of Psychiatry 160, no. 4 (April 1992): 461–66. http://dx.doi.org/10.1192/bjp.160.4.461.

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We examined the relationship between the dates of births of schizophrenic patients admitted to hospitals for the first time in England and Wales between 1970 and 1979, and the occurrence of influenza epidemics between 1939 and 1960. Our results indicate that exposure to influenza epidemics between the third and seventh month of gestation is associated with schizophrenia in adult life. The hypothesis that maternal viral infection is an important cause of schizophrenia can explain many aspects of the enigmatic epidemiology of the condition.

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24

Lichtermann, Dirk, Edith Karbe, and Wolfgang Maier. "The genetic epidemiology of schizophrenia and of schizophrenia spectrum disorders." European Archives of Psychiatry and Clinical Neuroscience 250, no. 6 (December 6, 2000): 304–10. http://dx.doi.org/10.1007/s004060070005.

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25

Bromet, Evelyn J., and Shmuel Fennig. "Epidemiology and natural history of schizophrenia." Biological Psychiatry 46, no. 7 (October 1999): 871–81. http://dx.doi.org/10.1016/s0006-3223(99)00153-5.

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26

Jablensky, Assen. "The 100-year epidemiology of schizophrenia." Schizophrenia Research 28, no. 2-3 (December 1997): 111–25. http://dx.doi.org/10.1016/s0920-9964(97)85354-6.

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27

Messias, Erick, Jose Jackson Sampaio, Nidia Cordeiro Messias, and Brian Kirkpatrick. "Epidemiology of Schizophrenia in Northeast Brazil." Journal of Nervous & Mental Disease 188, no. 2 (February 2000): 118–20. http://dx.doi.org/10.1097/00005053-200002000-00009.

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28

Seidman, Larry J. "Clinical Neuroscience and Epidemiology in Schizophrenia." Harvard Review of Psychiatry 4, no. 6 (January 1997): 338–42. http://dx.doi.org/10.3109/10673229709030562.

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29

Eaton, William W. "Update on the Epidemiology of Schizophrenia." Epidemiologic Reviews 13, no. 1 (1991): 320–28. http://dx.doi.org/10.1093/oxfordjournals.epirev.a036075.

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30

Jablensky, A. "Epidemiology of Schizophrenia: A European Perspective." Schizophrenia Bulletin 12, no. 1 (January 1, 1986): 52–73. http://dx.doi.org/10.1093/schbul/12.1.52.

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31

Castle, D. J., and R. M. Murray. "The Epidemiology of Late-onset Schizophrenia." Schizophrenia Bulletin 19, no. 4 (January 1, 1993): 691–700. http://dx.doi.org/10.1093/schbul/19.4.691.

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32

Hare, Edward H. "Epidemiology of schizophrenia and affective psychoses." British Medical Bulletin 43, no. 3 (1987): 514–30. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072199.

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33

Hallmayer, Joachim. "The Epidemiology of the Genetic Liability for Schizophrenia." Australian & New Zealand Journal of Psychiatry 34, no. 1_suppl (February 2000): A47—A55. http://dx.doi.org/10.1177/000486740003401s08.

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Objective The low incidence of schizophrenia prohibits large scale prevention trials, and the question arises whether such studies become more feasible by taking into account genetic factors. The aim of the paper was to inform preventive endeavours with an account of the genetic background to schizophrenia. Method The family, twin and adoptive studies of schizophrenia are reviewed and recent molecular genetic data presented. Results Children of a parent diagnosed with schizophrenia have a ten-fold increased risk of developing the disorder. Twin and adoption studies strongly suggest the risk increase is mainly due to genetic factors. On an individual level, a positive family history is the strongest known risk factor for schizophrenia. For a prevention study, very large numbers of families have to be screened in order to reach a sufficient sample size. Conclusions One obvious way to increase the accuracy of predicting who is at high risk of developing schizophrenia would be to find specific mutations in the human genome. Attempts to isolate specific genes by means of linkage and association studies have been unsuccessful so far and, given the number of genes involved, it is extremely unlikely that the predictive value of individual genes will be high enough to warrant intervention. Genetic studies also suggest the genetic liability extends beyond the traditional clinical phenotypes. Prevention trials might become possible by adopting a broader approach.

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34

Danese, Andrea. "A public health genetic approach for schizophrenia." Epidemiologia e Psichiatria Sociale 15, no. 3 (September 2006): 185–93. http://dx.doi.org/10.1017/s1121189x00004437.

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SUMMARYBackground – Schizophrenia is a complex disease resulting from the interplay of genetic and environmental factors. However, psychiatric genetics and epidemiology have often worked as independent research fields. Aims – To review the evidence about the gene-environment interplay involved in the development of schizophrenia. Methods – Systematic review of medical and psychological databases. Results – On one hand, quantitative and molecular genetics showed high heritability for schizophrenia and identified genes likely to be involved in its pathophysiology. The strength of the association between candidate genes and schizophrenia is however modest, and the need for a more appropriate conceptualization of the genetic risk has been claimed. On the other hand, psychiatric epidemiology described several environmental factors liked with the onset or the course of schizophrenia. The observational nature of epidemiology, however, may hamper inference on causation. Gene-environment correlations and interactions influence the exposure and the vulnerability to the environment, respectively. Current findings suggest that gene-environment correlations and interactions may be common phenomena in the pathophysiology of schizophrenia. The consideration of gene-environment interplay may help to overcome many limitations of genetic and epidemiological studies in psychiatry and suggest innovative preventive and therapeutic strategies. Conclusions – Taking into account the complexity of schizophrenia pathophysiology, mental health genetics may provide a comprehensive and heuristic model of disease.Declaration of Interest: none.

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35

Craig, Thomas, and Michael Y. Hwang. "Comorbidity in Schizophrenia: Epidemiology and Clinical Implications." Psychiatric Annals 30, no. 1 (January 1, 2000): 76–78. http://dx.doi.org/10.3928/0048-5713-20000101-09.

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36

Mathew, Vinod K., Kishore Gnana Sam, Beulah Samuel, and Amit Kumar Das. "Epidemiology of Schizophrenia in an Indian Hospital." Research Journal of Pharmacy and Technology 13, no. 1 (2020): 219. http://dx.doi.org/10.5958/0974-360x.2020.00044.x.

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37

Jablensky, Assen. "Epidemiology and Cross-Cultural Aspects of Schizophrenia." Psychiatric Annals 19, no. 10 (October 1, 1989): 516–24. http://dx.doi.org/10.3928/0048-5713-19891001-05.

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38

Saha, Sukanta, Jan J. Barendregt, Theo Vos, Harvey Whiteford, and John McGrath. "Modelling disease frequency measures in schizophrenia epidemiology." Schizophrenia Research 104, no. 1-3 (September 2008): 246–54. http://dx.doi.org/10.1016/j.schres.2008.05.022.

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39

Meyer, Urs, and Joram Feldon. "Epidemiology-driven neurodevelopmental animal models of schizophrenia." Progress in Neurobiology 90, no. 3 (March 2010): 285–326. http://dx.doi.org/10.1016/j.pneurobio.2009.10.018.

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40

Häfner, H., B. Fätkenheuer, B. Nowotny, and W. an der Heiden. "New Perspectives in the Epidemiology of Schizophrenia." Psychopathology 28, no. 1 (1995): 26–40. http://dx.doi.org/10.1159/000284956.

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41

Ryan, Patricia M. "Epidemiology, etiology, diagnosis, and treatment of schizophrenia." American Journal of Health-System Pharmacy 48, no. 6 (June 1, 1991): 1271–80. http://dx.doi.org/10.1093/ajhp/48.6.1271.

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42

Wessely, Simon. "The epidemiology of crime, violence and schizophrenia." British Journal of Psychiatry 170, S32 (April 1997): 8–11. http://dx.doi.org/10.1192/s0007125000298656.

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The infamous Hungerford Massacre, the multiple murders committed by Michael Ryan in the Berkshire town of Hungerford on 19 August 1987, remain firmly in the public's imagination. It would have been difficult for anyone reviewing the newspapers of that and subsequent days not to conclude that Michael Ryan was mentally ill – headlines ranged from “Day of the Maniac” to “Matricide Points to Schizophrenia”. Because Ryan killed himself and thus there was no possibility of a court case, psychiatrists were free to comment about his mental state and psychiatric diagnosis.

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43

Beiser, Morton, and William G. Iacono. "An Update on the Epidemiology of Schizophrenia*." Canadian Journal of Psychiatry 35, no. 8 (November 1990): 657–68. http://dx.doi.org/10.1177/070674379003500803.

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44

Eagles, John M. "Incidence and epidemiology of schizophrenia in Denmark." British Journal of Psychiatry 162, no. 2 (February 1993): 268–69. http://dx.doi.org/10.1192/bjp.162.2.268.

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45

McGrath, John J. "The Surprisingly Rich Contours of Schizophrenia Epidemiology." Archives of General Psychiatry 64, no. 1 (January 1, 2007): 14. http://dx.doi.org/10.1001/archpsyc.64.1.14.

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46

McGrath, John, Sukanta Saha, Joy Welham, and David Charles Chant. "Authors' Reply: Measurement Errors in Schizophrenia Epidemiology." PLoS Medicine 2, no. 9 (September 27, 2005): e300. http://dx.doi.org/10.1371/journal.pmed.0020300.

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47

Timotijević, I., and O. Marinković. "Genetic-epidemiology of schizophrenia: A pilot study." European Neuropsychopharmacology 6 (June 1996): 173. http://dx.doi.org/10.1016/0924-977x(96)88104-1.

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48

Kendell, R. E., J. C. Chalmers, and C. Platz. "Epidemiology of Puerperal Psychoses." British Journal of Psychiatry 150, no. 5 (May 1987): 662–73. http://dx.doi.org/10.1192/bjp.150.5.662.

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Computer linkage of an obstetric register and a psychiatric case register made it possible to investigate the temporal relationship between childbirth and psychiatric contact in a population of 470 000 people over a 12-year period resulted in 54 087 births: 120 psychiatric admissions within 90 days of parturition. The ‘relative risk’ of admission to a psychiatric hospital with a psychotic illness was extremely high in the first 30 days after childbirth, particularly in primiparae, suggesting that metabolic factors are involved in the genesis of puerperal psychoses. However, being unmarried, having a first baby, Caesarian section and perinatal death were all associated with an increased risk of psychiatric admission or contact, or both, suggesting that psychological stresses also contribute to this high psychiatric morbidity. Women with a history of manic depressive illness, manic or depressive, had a much higher risk of psychiatric admission in the puerperium than those with a history of schizophrenia or depressive neuroses, and the majority of puerperal admissions met Research Diagnostic Criteria for manic or depressive disorder. Probably, therefore, puerperal psychoses are manic depressive illnesses and unrelated to schizophrenia.

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49

Bamrah, J. S., H. L. Freeman, and D. P. Goldberg. "Epidemiology of Schizophrenia in Salford, 1974–84 Changes in an Urban Community over Ten Years." British Journal of Psychiatry 159, no. 6 (December 1991): 802–10. http://dx.doi.org/10.1192/bjp.159.6.802.

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The prevalence and inception rates of treated schizophrenia in the population of inner-city Salford were compared with those from a similar survey, ten years earlier. Data were obtained from a computerised case register and a postal questionnaire sent to GPs, and case notes rated on the SCL and screened using ICD–9. The point-prevalence rate of 6.26 per 1000 adult population was higher than that previously reported (4.56), despite decreases in total inception rate and in the general population. Changes in rates are presumed to be related primarily to population movements and ageing of the schizophrenic sample. Compared with 1974, the numbers of in-patient days and long-stay in-patients had fallen substantially by 1984, although annual admissions increased over the decade; day-patient and out-patient attendances, and extramural contacts with psychiatrists, community psychiatric nurses, and social workers had also increased. Almost 62% of cases were maintained on depot injections as out-patients in 1984. Over 75% of identified schizophrenic patients were in contact with psychiatrists, but only 7 out of 557 were solely in contact with their GP. In spite of the emphasis on community care, responsibility for schizophrenic patients was still carried overwhelmingly by hospital psychiatric services.

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50

Wasow, Mona. "Chronic schizophrenia and Alzheimer's disease." Journal of Chronic Diseases 38, no. 8 (January 1985): 711–16. http://dx.doi.org/10.1016/0021-9681(85)90025-6.

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