Schizophrenia: Epidemiology

Current Opinion in Psychiatry

Volumn 12, Issue 1, 1999, Pages 19-28

  Jablensky, Assen ^a  

^a Children's Hospital Medical Centre   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

BIRTH; BREAST FEEDING; DATA BASE; DEMOGRAPHY; ENVIRONMENTAL FACTOR; EPILEPSY; ETHNIC GROUP; GENETIC PREDISPOSITION; HUMAN; INCIDENCE; INTELLIGENCE QUOTIENT; LANGUAGE ABILITY; LIFESPAN; MATERNAL DISEASE; MOLECULAR BIOLOGY; PERINATAL MORBIDITY; POPULATION; PREGNANCY COMPLICATION; PREVALENCE; REVIEW; RHEUMATOID ARTHRITIS; RISK FACTOR; SCHIZOPHRENIA; SEASON; SEX DIFFERENCE; URBAN AREA;

EID: 0032998471     PISSN: 09517367     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001504-199901000-00013     Document Type: Review

References (49)

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2. Jones P, Cannon M. The new epidemiology of schizophrenia. Psychiatr Clin North Am 1998; 21:1-25. This is an excellent review of the trends towards convergence of epidemiological, genetic and developmental approaches to the study of risk and causal factors in schizophrenia.
3. Jablensky A, Sartorius N, Ernberg G, Anker M, Korten A, Cooper JE, et al. Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization Ten-country study. Psychol Med 1992; (Monograph Suppl) 20:43-55.
4. Jablensky A. Schizophrenia: recent epidemiologic issues. Epidemiol Rev 1995; 17:10-20.
5. Balestrieri M, Rucci P, Nicolaou S. Gender-specific decline and seasonality of births in operationally defined schizophrenics in Italy. Schizophr Res 1997; 27:73-81.
6. Jeffreys S, Harvey CA, McNaught AS, Quayle AS, King MB, Bird AS. The Hampstead Schizophrenia Survey 1991. I: Prevalence and service use comparisons in an inner London health authority, 1986-1991. Br J Psychiatry 1997; 170:301-306. This is a report on a repeat census in 1991 of area residents with schizophrenia, using the same methods as in a previous census in 1986. The point prevalence of 'broad' schizophrenia in 1991 was 5.1 per 1000 total general population (or 8.0 per 1000 using the age range 15-54 years in the denominator) compared with 4.7 per 1000 total general population in 1986.
7. Brewin J, Cantwell R, Dalkin T, Fox R, Medley I, Glazebrook C, et al. Incidence of schizophrenia in Nottingham. A comparison of two cohorts, 1978-80 and 1992-94. Br J Psychiatry 1997; 171:140-144. This study is a repeat of a first-contact incidence investigation in the same area which was part of the WHO 10-country study. Because the 1992-1994 study used ICD-10 diagnostic criteria that were not available in 1978-1980, the earlier cases were rediagnosed according to ICD-10. The 1992-1994 age-standardized annual incidence rate for ICD-10 schizophrenia and related disorders was 1.4 per 10 000 and was identical to the 1978-1980 rate for the same group of conditions. In 1992-1994 the rate for ICD-10 schizophrenia (0.87 per 10 000) was lower than the 1978-1980 rate (1.41 per 10 000), but there were relative increases in the diagnoses of delusional disorders, acute psychoses and drug-related psychoses.
8. Torrey EF, Miller J, Rawlings R, Yolken RH. Seasonality of births in schizophrenia and bipolar disorder: a review of the literature. Schizophr Res 1997; 28:1-38. A comprehensive review is provided of some 250 studies published since Tramer (1929) first drew attention to the month of birth and a possible seasonal factor predisposing to psychoses - a most useful reference.
9. Castle D, Murray RM. The neurodevelopmental basis of sex differences in schizophrenia. Psychol Med 1991; 21:565-575.
10. Häfner H, an der Heiden W, Behrens S, Gattaz WF, Hambrecht M, Löffler W, et al. Causes and consequences of the gender difference in age at onset of schizophrenia. Schizophr Bull 1998; 24:99-113. This is an overview of the Mannheim 'ABC' (age, beginning, course) schizophrenia study, which comprises 12 substudies, all focusing on aspects of age, sex, severity of illness and disability in a sample of 232 first-episode cases (consecutive admissions) followed up for 5 years. A detailed assessment of prodromal and prepsychosis signs and impairments demonstrated the following: impairments tend to appear early in the prodromal phase, which had an average duration of 5 years in the majority of the patients; men, having on average an earlier onset of both prodromal signs and overt psychosis, were more severely handicapped at the time of first contact than women; in men, but not in women, early onset schizophrenia tended to be more severe than late onset schizophrenia; and late onset schizophrenia was both more frequent and more severe in postmenopausal women. The hypothesis of a protective effect of aestrogen provides an unifying framework for the findings.
11. Häfner H, Behrens S, Vry Jde, Gattaz WF. An animal model for the effects of oestradiol on dopamine-mediated behavior: implications for sex differences in schizophrenia. Psychiatry Res; 38:125-134.
12. Riecher-Roessler A, Häfner H, Stumbaum M, Maurer K, Schmidt R. Can estradiol modulate schizophrenic symptomatology? Schizophrenia Bull; 20:203-214.
13. Kendler KS, Walsh D. Gender and schizophrenia. Results of an epidemiologically-based family study. Br J Psychiatry 1995; 167:184-192.
14. Murthy GVS, Janakiramaiah N, Gangadhar BN, Subbakrishna DK. Sex difference in age at onset of schizophrenia: discrepant findings from India. Acta Psychaitr Scand 1998; 97:321-325. The age at onset of first psychotic symptom, age at first contact and age at first admission were compared in 100 men and 100 women consecutive admitted with DSM-IV diagnosis of schizophrenia at the National Institute of Mental Health and Neurosciences in Bangalore. No sex differences were found in any one of these three indices. Contrary to other findings in the literature, survival analysis demonstrated a significantly higher risk for females of developing schizophrenia at an earlier age.
15. Jablensky A, Cole SW. Is the earlier age at onset of schizophrenia in males a confounded finding? Results from a cross-cultural investigation. Br J Psychiatry 1997; 170:234-240. Generalized linear models were used to estimate the unconfounded contributions of sex, premorbid personality, marital status and family history to male-female differences in age at onset in 778 men and 653 women in developing countries and developed countries, who participated in the WHO study. Controlling for marital status and premorbid personality traits strongly attenuated male-female differences in age at onset.
16. Goldstein JM. Sex differences in schizophrenia: epidemiology, genetics and the brain. Int Rev Psychiatry 1997; 9:399-408. A concise and useful review of the literature on sex differences in the incidence of schizophrenia, age at onset, course and treatment response, brain abnormalities and genetic transmission is provided.
17. Torrey EF, Bowler AE, Clark K. Urban birth and residence as risk factors for psychoses: an analysis of 1880 data. Schizophr Res 1997; 25:169-176. The data of the 1880 US census of the insane (point prevalence 1.8 per 1000) were reanalysed by county of origin and degree of urbanization. Urban residence was associated with an increased prevalence of psychosis. The authors discuss the sociological 'drift', 'social residue' and 'breeder' theories, but conclude in favour of biological hypotheses focusing on a greater likelihood of infectious and toxic insults on the brain in urban settings.
18. Marcelis M, Navarro-Mateu, Murray R, Selten JP, van Os J. Urbanization and psychosis: a study of 1942-1978 birth cohorts in The Netherlands. Psychol Med 1998; 28:871-879. The authors followed up through the National Psychiatric Case Register all live births in Holland, 1942-1978, and identified all first admissions for schizophrenia, affective psychosis and other psychoses during 1970-1992 (n=42 115). An 'urban risk factor', more likely to be environmental rather than genetic, was demonstrated, but its nature and mode of operation remain obscure.
19. Takei N, Persaud R, Woodruff P, Brockington I, Murray RM. First episodes of psychosis in Afro-Caribbean and White people. An 18-year follow-up population-based study. Br J Psychiatry 1998; 172:147-153. A sample of 34 Afro-Caribbean and 54 white British-born individuals with first admission for psychosis in 1973-1974 were re-examined. No difference was found between the two groups in the consistency of diagnosis over the follow-up period but Afro-Caribbeans had experienced more readmissions, longer hospitalizations and more involuntary admissions than their White counterparts.
20. Bhugra D, Leff J, Mallett R, Der G, Corridan B, Rudge S. Incidence and outcome of schizophrenia in Whites, African-Caribbeans and Asians in London. Psychol Med 1997; 27:791-798. In this study, the instruments and case-finding methods of the WHO 10-country study were used to assess all first contact cases from two health districts over 1 year (whites) or 2 years (ethnic minorities). One-year follow-up information was collected on 97 of the 100 cases with a diagnosis of schizophrenia. Adjusted census data were used for the denominator. The crude annual incidence rate per 10 000 (age 18-64 years) was 5.9 in Afro-Caribbeans, 3.0 in whites and 3.5 in Asians, and the results were similar using age-standardized rates. Afro-Caribbean males had twice the rate of white men in the age range 18-29 years, whereas Asian women had the highest incidence in the age range 30-64 years.
21. Harrison G, Glazebrook C, Brewin J, Cantwell R, Dalkin T, Fox R, et al. Increased incidence of psychotic disorders in migrants from the Caribbean to the United Kingdom. Psychol Med 1997; 27:799-806. This is a first-contact incidence study of a similar design to that of the WHO 10- country study, covering the area of Nottingham over a 24-month period. Adjusted census data were used for the denominator. The annual rate of ICD-10 schizophrenia among first-generation and second-generation Afro-Caribbean migrants was six per 10 000 (relative risk 10.75 in men and 4.46 in women, age 16-64 years) compared with 0.6 per 10 000 for the remaining population. Most of the excess incidence in Afro-Caribbeans was concentrated in the age range 20-39 years. The authors estimate at 17% the population attributable fraction of first-onset psychosis in Nottingham to the Afro-Caribbean migrant population.
22. Selten JP, Slaets JPJ, Kahn RS. Schizophrenia in Surinamese and Dutch Antillean immigrants to The Netherlands: evidence of an increased incidence. Psychol Med 1997; 27:807-811. Data from the Dutch psychiatric register were used to calculate relative risk for hospitalizations with discharge diagnosis of schizophrenia during 1970-1992. Compared with the native Dutch population, the age-adjusted and sex-adjusted relative risk for a first admission with schizophrenia were 3.8 in Surinamese-born immigrants and 3.9 for Antillean-born immigrants. The Dutch data, therefore, support the earlier UK findings of an excess of psychosis among the Afro-Caribbean migrant minority, but suggest that the effect may not be restricted to people of African background.
23. Hutchinson G, Takei N, Bhugra D, Fahy T, Gilvarry C, Mallett R, et al. Increased rate of psychosis among African-Caribbeans in Britain is not due to an excess of pregnancy and birth complications. Br J Psychiatry 1997; 171: 145-147. Obstetric histories were obtained by interviewing the mothers of 103 white and of 61 Afro-Caribbean patients admitted with diagnoses of psychoses between 1987 and 1993. White patients with psychoses were more likely to have a history of obstetric complications (odds ratio 2.34, 95% confidence interval 0.88-6.47) than their Afro-Caribbean counterparts. No difference was found between rates of obstetric complications in first-generation and second-generation migrants. This study provides no support for the hypothesis that pregnancy and birth complications may explain the increased rate of psychosis among Afro-Caribbeans in the UK.
24. Fahy TA, Jones PB, Sham PC, Murray RM. Schizophrenia in Afro-Caribbeans in the UK following prenatal exposure to the 1957 A2 influenza epidemic. Schiozophr Res 1992; 6:98-99.
25. Selten JP, Slaets J, Kahn R. Prenatal exposure to influenza and schizophrenia in Surinamese and Dutch Antillean immigrants to The Netherlands. Schizophr Res 1998; 30:101-103. Following the report by Fahy et al. [22], which suggested that maternal influenza during the 1957 pandemic may have contributed to the high rate of schizophrenia in the offspring of Afro-Caribbean immigrants to the UK, the authors examined comparable data from Holland and concluded that individuals who were in the second trimester of gestation at the peak of the epidemic were at no greater risk of developing schizophrenia than were control individuals.
26. Hutchinson G, Takei N, Fahy TA, Bhugra D, Gilvarry C, Moran P, et al. Morbid risk of schizophrenia in first-degree relatives of White and African-Caribbean patients with psychosis. Br J Psychiatry 1996; 169:776-780.
27. Cannon TD. On the nature and mechanisms of obstertric influences in schizophrenia: a review and synthesis of epidemiological studies. Int Rev Psychiatry 1997; 9:387-397. This is an excellent analytical review, describing three models of the relationship between obstetric complications and schizophrenia: (1) obstetric complications generate phenocopies of schizophrenia in their own right; (2) obstetric complications covary with the genetic predisposition to schizophrenia (those genetically predisposed experience more obstetric complications); and (3) randomly occurring obstetric complications interact with genetic vulnerability, enhancing its expression. The author's interpretation of published findings, favouring the third model, may be overestimating their consistency.
28. Hultman CM, Ihman A, Cnattingius S, Wieselgren IM, Lindström LH. Prenatal and neonatal risk factors for schizophrenia. Br J Psychiatty 1997; 170:128-133. In this study, the obstetric records of 107 consecutive admissions (82 with DSM-III schizophrenia and 25 with other psychotic disorders) and of 214 control individuals were scored using a scale based on the optimality concept of Prechtl. Both the schizophrenic patients and the total group of psychotic patients were characterized by high nonoptimality scores ( > 7 nonoptimal points) corresponding to odds ratio 3.67 (95% confidence interval 1.30-10.36) in schizophrenia and 4.58 (95% confidence interval 1.74-12.03) in all psychoses combined. Although maternal age and early rupture of membranes each had an independent effect in a logistic regression model, the main contribution to the summary score was that of gestational factors, in particular aberrant body size (disproportionately high or low body weight for body length, and a small head circumference), which results from deviations (acceleration or retardation) in intrauterine growth. This finding was not restricted to schizophrenia, but applied to the whole sample of psychotic disorders.
29. Prechtl's 'optimality' concept: Prechtl HFF. Neurological sequelae of prenatal and perinatal complications. Br Med J 1997; 4:763-767.
30. Verdoux H, Geddes JR, Takei N, Lawrie SM, Bovet P, Eagles JM, et al. Obstetric complications and age at onset in schizophrenia: An international collaborative meta-analysis of individual patient data. Am J Psychiatry 1997; 154:1220-1227. Data on 854 individual patients (47.8% of them rated as positive for obstetric complications) were contributed to this meta-analysis by 11 research groups. Logistic regression was used to examine the relationship between obstetric complications and three explanatory variables: age at onset, family history of psychosis and sex. A significant association (crude odds ratio 1.52, 95% confidence interval 1.04-2.22) was found for age at onset, but not for either family history or sex. There was a linear ('dose-response') relationship between obstetric complications and age at onset, which was interpreted as suggestive of a causal effect. Caesarean, complicated or emergency delivery and breech or abnormal presentation were the strongest contributors to the association. The authors discuss various confounding factors and methodological shortcomings of the data that could have influenced the results of this meta-analysis, but nevertheless conclude, with some caution, that the association between obstetric complications and age at onset may be a causal one.
31. Grech A, Takei N, Murray RM. Maternal exposure to influenza and paranoid schizophrenia. Schizophr Res 1997; 26:121-125. Using data on 17 247 patients born in England and Wales between 1923 and 1965, the authors tested the hypothesis that increased risk of schizophrenia associated with in-utero exposure to influenza would be particularly demonstrable in paranoid schizophrenia. The hypothesis was not supported when the data were analysed using logistic regression and controlling for birth cohort effects.
32. Morgan V, Castle D, Page A, Fazio S, Gurrin L, Burton P, et al. Influenza epidemics and incidence of schizophrenia, affective disorders and mental retardation in Western Australia: no evidence of a major effect. Schizophr Res 1997; 26:25-39. A total of 1852 patients with ICD-9 schizophrenia, affective psychoses, or neurotic depression, and 804 patients with mental retardation sampled from morbidity registers by dates of birth falling within intervals that defined exposure and nonexposure during gestation to six influenza epidemics in Western Australia during the period 1950-1960 were analysed. The data were related to population denominators of 82 963 exposed and 32 262 nonexposed (control) births. Using relative risk ratios for each of the first three gestational trimesters and for each epidemic, as well as Poisson regression to examine for a systematic effect across all the epidemics, the study found no significant effect of maternal influenza on the incidence of schizophrenia, affective psychoses and neurotic depression, although a first and second trimester effect was detected for mental retardation. Notably, the 1957 epidemic, during which influenza notifications were mandatory in Western Australia and a weekly count of all the cases was available, had no detectable impact on the subsequent incidence rate of schizophrenia.
33. Crow TJ, Done DJ. Prenatal influenza dose not cause schizophrenia. Br J Psychiatry 1992; 161:390-393.
34. Cannon M, Cotter D, Coffey VP, Sham PC, Takei N, Larkin C, et al. Prenatal exposure to the 1957 influenza epidemic and adult schizophrenia: a follow-up study. Br J Psychiatry 1996; 168:368-371.
35. van Os J, Selten JP. Prenatal exposure to maternal stress and subsequent schizophrenia. The May 1940 invasion of The Netherlands. Br J Psychiatry 1998; 172:324-326. The cumulative incidence of schizophrenia and affective disorders (National Psychiatric Case Register data) was examined in a cohort of 133 394 births, presumed to have been exposed in utero to maternal stress during the 5-day blitzkrieg against Holland in 1940. These data were compared with the incidence of schizophrenia and affective disorders in birth cohorts preceding or following the year of the invasion. There was a statistically significant, but small, effect for adult schizophrenia associated with first gestational trimester exposure (odds ratio 1.28, 95% confidence interval 1.07-1.53), but not for affective disorders.
36. Jones PB, Rantakallio P, Hartikainen AL, Isohanni M, Sipila P. Schizophrenia as a long-term outcome of pregnancy, delivery, and perinatal complications: A 28- year follow-up of the 1966 North Finland general population birth cohort. Am J Psychiatry 1998; 155:355-364. A total of 11017 members of an initial birth cohort (12 058 live births) were followed up from late gestation to their 28th year. The 76 individuals who had developed DSM-III-R schizophrenia by age 28 years (cumulative incidence 0.69%) were compared with 10 502 cohort members without psychiatric disorders on a number of maternal characteristics, pregnancy and birth complications, and perinatal events that had been recorded prospectively. A measure of perinatal brain damage was significantly associated with schizophrenia in later life (odds ratio 7.5, 95% confidence interval 3.2-17.6) and, assuming causality, could account for 6.8% population attributable risk. Other independent predictors were low birth weight, male sex and reported maternal depression in mid-pregnancy. A shortcoming of this otherwise powerful study is the lack of data on family history that would enable an exploration of gene - environment interactions.
37. Apgar score: Stedman's medical dictionary 26th edn. Baltimore: Williams & Wilkins; 1995. p. 1585.
38. Rantakallio P, Jones P, Moring J, von Wendt L. Association between central nervous system infections during childhood and adult onset schizophrenia and other psychoses: a 28-year follow-up. Int J Epidemiol 1997; 26: 837-843. The cumulative incidence of schizophrenia up to age 28 years was compared in members of the 1966 North Finland general population birth cohort (n=11 017) in relation to prospectively diagnosed central nervous system infection in infancy or childhood. Exposed individuals had a significantly increased risk (odds ratio 4.80, 95% confidence interval 1.65-14.0) compared with unexposed individuals. Postnatal Coxsackie B5 infection had been diagnosed in two out of the four instances of documented exposure to viral infection among the 76 schizophrenia cases. Other risk factors, apart from those referred to in [32], included intelligence quotient below 85 (odds ratio 4.77) and childhood convulsions (odds ratio 1.13).
39. McCreadie RG. The Nithdale Schizophrenia Surveys. 16. Breast-feeding and schizophrenia: preliminary results and hypotheses. Br J Psychiatry 1997; 170:334-337. Human milk has a high content of long-chain polyunsaturated fatty acids which represent essential constituents of neuronal membranes. In a questionairre, mothers of 45 patients with schizophrenia, born in the 1940s and 1950s, reported significantly lower rates of breast feeding for the patients (29%) and for their siblings (38%) than the population rates of breast feeding (81 and 51%) for those decades, according to Scottish surveys.
40. Malmberg A, Lewis G, David A, Allebeck P. Premorbid adjustment and personality in people with schizophrenia. Br J Psychiatry 1998; 172: 308-313. The authors identified through the Swedish National Register of Psychiatric Care all admissions between 1973 and 1983 with ICD-8 schizophrenia (n=195) and other psychoses (n=193) among a cohort of 50 087 men who had been conscripted into the Swedish army at age 18-20 years during the period 1969-1970. Their responses to self-administered questionnaires probing behaviour, attitudes and social functioning in childhood and adolescence, which had been recorded at conscription, were compared with the responses of the rest of the cohort who had no psychiatric admissions. Four variables (having fewer than two friends, preference for socializing in small groups, feeling more sensitive than others and not having a steady girlfriend) were associated with significantly increased risk of schizophrenia in later life. Individuals scoring positively on all four items had odds ratio 30.7 (95% confidence interval 12.9-73.8) of developing schizophrenia, after adjustment for possible confounders. However, because these were relatively common characteristics, and a high proportion of the total cohort was positive on any one item, the predictive value of this set of variables was low; only 3% of those who were positive on all four items developed schizophrenia during the subsequent 13 years.
41. Jones P, Rodgers B, Murray R, Marmot M. Child developmental risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet 1994; 344: 1398-1402.
42. David AS, Malmberg A, Brandt L, Allebeck P, Lewis G. IQ and risk for schizophrenia: a population-based cohort study. Psychol Med 1997; 27:1311-1323. In a related analysis of the Swedish Army 1969-1970 conscript cohort (n=50 087) data, the authors compared the performance on intelligence-quotient-related tests and tasks at conscription in the 195 individuals who subsequently developed schizophrenia, 192 individuals who developed other psychoses and the rest of the cohort. The risk of later schizophrenia increased linearly with the decrement of intelligence quotient (after controlling for confounding effects). The risk of schizophrenia was significantly associated with poor performance on verbal tasks (odds ratio 1.12) and on tests of 'mechanical' reasoning (odds ratio 1.30). The authors leave to future research the question regarding whether the association is direct and causal (cognitive impairment resulting in poor reality testing), or indirect (low intelligence quotient being one expression of abnormal brain development).
43. Cannon M, Jones P, Murray RM, Wadsworth MEJ. Childhood laterality and later risk of schizophrenia in the 1946 British birth cohort. Schizophr Res 1997; 26:117-120.
44. Done DJ, Leinonen E, Crow TJ, Sacker A. Linguistic performance in children who develop schizophrenia in later life. Evidence for normal syntactic ability. Br J Psychiatry 1998; 172:130-135.
45. Bredkjur SR, Mortensen PB, Parnas J. Epilepsy and non-organic non-affective psychosis. National epidemiologic study. Br J Psychiatry 1998; 172:235-238. This is a record-linkage study merging data from the Danish National Patient Register and the Danish Psychiatric Register for general hospital and psychiatric hospital admissions between 1977 and 1992. Excluding patients who had a psychiatric diagnosis preceding a diagnosis of epilepsy, and individuals with substance use disorders or learning disability, conservative estimates of the standardized incidence ratio for all nonorganic nonaffective psychoses in 59 416 people with epilepsy was 2.30 (all epilepsy) and 3.57 (psychomotor epilepsy). The standardized incidence ratio for schizophrenia in males with psychomotor epilepsy was 2.56. The study supports the notion that epilepsy, and in particular temporal lobe epilepsy, is a risk factor for nonaffective psychosis including schizophrenia.
46. Lauerma H, Lehtinen V, Joukamaa M, Jorvelin MR, Helenius H, Isohanni M. Schizophrenia among patients treated for rheumatoid arthritis and appendicitis. Schizophr Res 1998; 29:255-261. Contrary to previous studies and to the assumption based on their results that the negative association between schizophrenia and rheumatoid arthritis is among the few consistently replicated findings in the epidemiology of schizophrenia, the authors found rates of schizophrenia similar to those in the general population among 5626 patients treated for rheumatoid arthritis in the course of a year. Surprisingly, the comparison group, consisting of 5330 people treated for appendicitis during the same year, had a significantly lower prevalence of schizophrenia than either the rheumatoid arthritis group or the general population. The authors suggest that the schizophrenic patients among whom a lower than expected prevalence of RA had been found in previous studies, were mostly institutionalized and, hence, protected from exposures to infectious agents involved in the pathogenesis of rheumatoid arthritis. With regard to the negative association between appendicitis and schizophrenia in this study, the authors speculate that genes predisposing to schizophrenia may confer resistance to infectious agents involved in appendicitis.
47. Meehl PE. Toward an integrated theory of schizotaxia, schizotypy, and schizophrenia. J Person Disord 1990; 4:1-99.
48. Chen WJ, Hsiao CK, Hsiao LL, Hwu HG. Performance of the Continuous Performance Test among community samples. Schizophr Bull 1998; 24:163-174. This study is among the first to investigate the population distribution of a measure of sustained attention (Continuous Performance Test) that has been implicated as a vulnerability marker of schizophrenia in a community sample of 345 adults and 115 adolescents in Taiwan. The results highlight the importance of accounting for 'normal' population variation (age-, sex-, and education-related) in the interpretation of neurocognitive deficits in patients with schizophrenia and their biological relatives.
49. Shpilberg O, Dorman JS, Ferrell RE, Trucco M, Shahar A, Kuller LH. The next stage: molecular epidemiology. J Clin Epidemiol 1997; 6:633-638.