IN REVIEW

Epidemiology of Schizophrenia


Heinz Hfner , Wolfram an der Heiden

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 years 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.

(Can J Psychiatry 1997;42:139151)

Key Words: schizophrenia, epidemiology, incidence, prevalence, ecology, symptomatology, age at onset, gender
differences

ne hundred years of research efforts have failed to produce biological indicators specific to a diagnosis of
schizophrenia. Studies on schizophrenia morbidity, therefore,
continue to rely on descriptive case definitions, and the quality of their results depends on the diagnostic definitions used.

comparable findings. The standards include a precise, operational case definition, the collection of comprehensive data
on all cases from a sufficiently large, statistically welldocumented population, symptom assessment by transculturally standardized instruments, and computerized diagnosis
independent of the interviewer. The World Health Organization (WHO) Determinants of Outcome study (2) was the
first to satisfy nearly all of these requirements at each study
site in the determination of the incidence of schizophrenia (12
centres, 10 countries). Recently, Thornicroft and Johnson (3)
have added a further methodological standard that calls for
the assessment of met and unmet needs for care in psychiatric
surveys.

In a historical analysis, Dohrenwend (1) distinguished 3

periods of epidemiological studies in psychiatry. According
to his methodological standards, only the last period, beginning around 1980, has produced valid and transnationally
1

Director, Schizophrenia Research Unit, Central Institute of Mental Health,

Mannheim, Germany.
2
Senior Scientist, Schizophrenia Research Unit, Central Institute of Mental
Health, Mannheim, Germany.
Address for correspondence: Dr H Hfner, Durchwahl 17 03-726, J 5,
Mannheim 68159 Germany

Ecological Epidemiology
With their ecological Chicago study, Faris and Dunham
(4) began an important chapter in the epidemiology of schizophrenia. The authors found the highest first-admission rates

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for schizophrenia in the inner city, characterized by social

disintegration and low-standard housing. The lowest incidence was on the outskirts of the city, in high-standard
residential areas. In the wake of their study, similar zonal
distribution patterns were reported from several American
cities, but also from Oslo, Norway (5), Nottingham, United
Kingdom (6), and Mannheim, Germany (7). In Mannheim,
the incidence of schizophrenia was reassessed 10 to 15 years
(8) and 22 to 23 years (9) later. Parallelling the citys stable
socioecological structure, the ecological distribution pattern
of first-admission rates for schizophrenia proved stable.
Besides the uneven ecological distribution of the rates,
individuals with schizophrenia at first admission are usually
found to be personally and socially disadvantaged as well.
Dohrenwend and Dohrenwend (10) found the highest rates in
the lowest social class in 5 out of 7 first-admission studies,
and Eaton (11) found the same in 15 out of 17 studies. In a
later metaanalysis of studies on the topic, Eaton and others
(12) calculated a ratio of 3 to 1 for the risk of schizophrenia
between the lowest and the highest of 3 social classes.
Social Drift versus Social Causation
Although time and cause were unclear, the social gradient
provided the impetus for a causal link between severe social
disadvantage and schizophrenia onset (10,13,14). The socialdrift hypothesissocial decline after illness onsetmerely
explained the uneven social distribution of prevalence rates.
Since first admission or first contact, at that time, was taken
as the operational definition of the onset of the disorder, any
social consequences of the emerging disorder were not
considered.
Retrospectively studying individual ecological mobility
before first admission, Dauncey and others (15) found that the
ecological disadvantage observed in schizophrenic patients
at first admission had emerged, on average, 5 years before.
The ecological selection is brought about by a tendency of
individuals later admitted with a diagnosis of schizophrenia
to remain during the premorbid period in decaying housing
areas, while their healthy and socially more successful peers
move on from these areas into better neighbourhoods. Similar
conclusions were drawn by Wiersma and others (16) using
Dutch data.
On the basis of the national Norwegian case register,
degaard (17) early pointed out that people with schizophrenia tend to cluster in rapid-turnover and low-status jobs prior
to their first admission. He implicated premorbid schizoid
personality traits in the explanation.
It seems that at least a part of the social disadvantage
involved in schizophrenia emerges before first admission.
The question of it already being present in the patients
parents was investigated by Goldberg and Morrison (18) in a
methodologically sound intergenerational study in London.
They demonstrated, for schizophrenic men, that the lack of
upward social mobility emerges after birth. In another study,
conducted by Turner and Wagenfeld (19) in New York, the
fathers of schizophrenic men showed slightly lower social
statuses compared with controls, but this result is probably

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attributable to the selection of a socially disadvantaged study

population, that is, first admissions to state mental hospitals.
Meanwhile, 3 large studies of birth cohorts from Great Britain
(20,21) and Northern Finland (22) followed into the age of
risk for schizophrenia have demonstrated that schizophrenic
patients are not socially disadvantaged at birth.
Dohrenwend and others (23) tested the alternative hypothesis of social causation versus social selection in a methodologically sophisticated study in Israel. They found
compelling evidence for the social selection hypothesis in
schizophrenia, in contrast to the risk for major depressive
disorder in women or substance abuse in men.
Hence social causation does not appear to play an essential
etiological role in schizophrenia, as is also indicated by the
fairly similar morbidity risk in all the populations investigated
(2).
Prevalence
Prevalence is a product of incidence and length of illness.
Length of illness is determined by various factors, for example, variation in the life expectancies of the populations
studied, excess mortality after disease onset, and varying
proportions of symptom-free cases due to differences in treatment, so that comparisons of prevalence rates across studies
are difficult. Prevalence rates are primarily used as an indicator of the morbidity of a given population and its need for
care.
Table 1 lists selected prevalence studies of schizophrenia
and their results according to the following criteria: 1) studies
published in 1980 or later, 2) population studies or sufficiently representative utilization studies (for example, case
registers).
For the reasons stated above, the marked variation in the
total rates cannot be interpreted as reflecting differences in
the morbidity of the populations under study. The point versus
period prevalence rates differ only minutely which, as pointed
out by Eaton and others (24), is accounted for by the primarily
chronic course of the illness involving only slight annual
excess mortality.
The dependence of the study results on the diagnostic
definition is reflected in the fact that only 30% of a representative sample of first-admission cases (N = 276) assigned
to a broad clinical diagnosis of schizophrenia according to
ICD-9 (295, 297, 298.3/4) (the ABC schizophrenia study
sample) qualified for a DSM-III diagnosis of schizophrenia
(25). The lifetime prevalence rate of 1.5% reported from the
Epidemiologic Catchment Area study (26) is probably too
high. A possible reason is that the assessments were
conducted by lay persons using instruments of low
discriminative power (27). The most precise estimates of the
lifetime risk so far, though only up to the fifth decade of life,
have been reported from the British birth cohort study (28).
The directly assessed cumulative prevalence until age 43 was
0.63. Assuming that the share of late-onset schizophrenias in
the total schizophrenic morbidity is fairly low (15%), this
figure presumably represents a fairly close estimate of the true

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Epidemiology of Schizophrenia

141

Table 1. The prevalence of schizophreniaa

Authors

Prevalence per 1000

population

Country

Period

Babigian (98)

USA

1 year

4.1

Bamrah and others (99)

UK

1 year

7.5

No

Bebbington and others (100)

UK

Point

10.9

Yes

Ben-Tovim and Cushnie (101)

Botswana

1 year

5.3

No

Canada

Lifetime

0.3

USA
USA
Puerto Rico

6 months
6 months
6 months

6.0 to 11.0
3.0 to 6.0
15.0

No
No
No

China
Germany

1 year
Point

1.9 to 4.7
3.9

Yes
No

Croatia
UK

3 months
1 year

1.5 to 5.1
6.8

No
No

Bland and others (102)

Blazer and others (103)
Burnam and others (104)
Canino and others (105)
Cheung (106)
Dilling and Weyerer (107)
Folnegovic and Folnegovic-Smalc (108)
Freeman and Alpert (109)
Halldin (110)

Age correction
Yes

No

Sweden

1 year

6.0

No

Netherlands

Point

7.3

Yes

Hwu and others (112)

Taiwan

Lifetime

3.1

No

Lee and others (25,113)

Lehtinen and others (114,115)

Korea
Finland

Lifetime
Point

Hodiamont and others (111)

Lin and others (116)

3.1 to 5.4
1.3

No
No

China

Point

4.2

Yes

Mavreas and Bebbington (117)

UK

Point

13.0

No

Murphy and Taumoepeau (118)

Myers and others (119)
Nandi and others (120)

Tonga
USA
India

1 year
6 months
Point

0.9 to 1.3
6.0 to 11.0
2.2

No
No
Yes

Shen and others (121,122)

China

Point

1.8

Sikanerty and Eaton (123)

Ghana

Point

1.1

No

Bulgaria

Point

2.8

Yes

Temkov (124)

Yes

Vasquez-Barquero (125)

Spain

Point

5.6

No

Walsh (126)

Ireland

Point

9.8

No

4.0

No

Weissman and Myers (127)

Widerlv and others (128)
Zimmerman-Tansella and others (129)
a

USA

Point

Sweden
Italy

Lifetime
1 year

0.7 to 5.0
1.3

No
No

Abridged version of a compilation by Warner and de Girolamo (36), supplemented by own review of literature.

cumulative lifetime prevalence as based on the ICD-9

diagnosis 295.
The prevalence rates for old age probably need to be
adjusted. It is still unclear how many of the delusional disorders of the old and the very old can be subsumed under the
diagnosis of schizophrenia and, thus, be considered part of
the prevalence and incidence of schizophrenia in these age
groups (29). The reason is that attempts at a precise empirical
distinction at the psychopathological level have failed.
Incidence
As stated, incidence rates are the key indicator of morbidity risk. Their distribution patterns across geographic, cultural
and social units, family membership, age, and sex also
provide some external criteria for testing the validity of a
diagnosis (30) and for formulating etiological and pathogenetic hypotheses.
Since the onset of schizophrenia is a comparatively rare
event, the accurate assessment of incidence figures is faced

with considerable practical and methodological problems.

This is especially the case when age distributions are studied
or risks for certain age groups are estimated. To ensure
accuracy, the following preconditions should be fulfilled: 1)
the population at risk must be sufficiently large, geographically stable, and statistically well documented to provide
exact data on age, sex, and social status for the denominator
in the calculation; 2) the study sample must be representative,
that is, comprise all the cases fulfilling the diagnostic criteria
during the study period; 3) the study sample must be large
enough to cover the whole age-of-risk range for schizophrenia; 4) the cases should be entered in the study as soon after
onset as possible in order to keep recall deficits, postonset
deaths, and other distorting effects to a minimum; 5) onset
must be defined and its occurrence determined precisely. The
common administrative definition of onset, first admission to
hospital or first psychiatric contact, is flawed by uncertainty
about the duration of the time period of illness preceding that
event. The more precise, but still artificial, definition of a
diagnostic onset (the time point when a set of diagnostic

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criteria is fulfilled for the first time), proposed by Pogue-Geile

(unpublished observation), is an acceptable basis for rough
estimates of the incidence. If, however, the intention is to
determine the time point or age of onset precisely, both the
prodromal phase and the development of illness before the
diagnostic criteria are met must be taken into account.
An ideal approach to studying incidence would be a prospective birth cohort design with cross-sectional assessments
at short intervals. A prospective birth cohort design is adopted
in studies of the offspring of schizophrenic mothers, but for
cost reasons, the cross-sectional assessments are carried out
at lengthy intervals. Moreover, the incidence rates calculated
for these high-risk groups do not provide any information on
incidence in the population at large. Birth cohorts of general
populations were studied retrospectively by Fremming (31)
in Denmark and for over 70 years by Helgason (32) in Iceland,
but the number of 34 or 36 cases of schizophrenia is too low
for calculating age-specific risks. The British birth cohort
study (28) provided population-based first-admission rates
for schizophrenia until age 43 years, but did not produce data
on the age distribution of onset.
Only in a minority of cases is the onset of schizophrenia
marked by conspicuous symptoms. In three-quarters of the
cases, the first psychotic episode is preceded by a prodromal
phase of several years duration, during which nonspecific
symptoms predominate. The psychotic prephase, too, frequently evolves unnoticed by others, at least for some time
(33). This means that schizophrenia is currently diagnosable
only after it has started to produce psychotic symptoms and
is perceived by the patient himself or herself or by others. Its
onset and all associated variables, such as age distribution of
the morbidity risk, must therefore be determined retrospectively by suitable methods.
The problems involved and possible solutions have been
discussed by Maurer and Hfner (34) in the context of the
standardized interview developed to address them: Instrument for the Retrospective Assessment of the Onset of
Schizophrenia (IRAOS) (35). The interview was designed to
produce data on prodromal signs, symptoms, functional impairment, social disability, and objective social development
from 3 sources and on the basis of a time matrix, which
enables accurate timing by means of anchor events.
Population studies are impractical because of the low
morbidity risk. A 2-stage design should be used, therefore,
that is, one which identifies all incidence cases of nonaffective psychosis from all the clinical records of a large, defined
population over the course of one or 2 years. For this method
to be accurate, however, the lifetime likelihood of schizophrenic patients coming into contact with the mental health
services of the catchment area must be close to 100%. This
percentage, depending on the availability and cost of mental
health services, is bound to decline with time because of the
growing proportion of patients with schizophrenia treated by
general practitioners. An additional search for incidence
cases not in contact with mental health services can improve

Vol 42, No 2

epidemiological validity, especially in developing

countries (2).
At the second stage, standardized interviews are administered to the index population obtained through the initial
screening. The operational accuracy of the diagnosis and all
the other design variables ensured, onset is then assessed
retrospectively.
Comparative Epidemiology
Table 2 is based on a review by Warner and de Girolamo
(36) but restricted to studies published after 1980. Rates
calculated with populations not corrected for age are so
indicated. The incidence rates range from a minimum of 0.07
to a maximum of 7.1. Tempting though it would be to explain
these differences as secondary to regional heterogeneity of
environmental or genetic factors, the studies should first be
compared for their methodological standards.
In the WHO Determinants of Outcome study (2), all
patients were assessed for psychopathology with a semistructured interview, the Present State Examination (PSE) (37).
The PSE is supplemented by a computer algorithm, known as
CATEGO, that can be used at several levels of classification.
The patients are allocated to 1 of 9 descriptive CATEGO
classes, depending on the prevailing symptomatology as, for
example, S+, representing central schizophrenic conditions
(thought intrusion and delusions of control), P (paranoid
symptomatology), or O (other psychoses).
The results from 7 countries are illustrated by data for 8
study sites, depicted in Figure 1 in sections II and III. For
comparison, section I gives the rates from 8 selected national
studies. The transnational variability of the incidence rates
decreases as the stringency of studies increases. The national
studies show the greatest variation in methodology, for example, diagnostic definitions and case findings. In the intermediate section, annual incidence rates for a broadly defined
diagnosis of schizophrenia (ICD 295 or CATEGO S, P, and
O), based on the same sample as in section III, show less but
still considerable variation, whereas in section III, based on a
restrictive and highly reliable diagnosis of nuclear schizophrenia (CATEGO S), no significant differences can be seen,
the annual rates varying around 10/100 000.
Incidence rates of the same size in all populations and
cultures studied render a substantial role of cultural, social,
or climatic factors in the morbidity risk for schizophrenia
inconceivable.
Zubin (38) tried to explain this unusual epidemiological
pattern by assuming that schizophrenia is the common final
pathway arising from a great number of causes. Another
common disorder with an almost identical age-corrected incidence throughout the world is dementia in old age (39,40),
which shows a clear-cut causal heterogeneity, but largely
identical symptoms.
Age at Onset
In the majority of studies (age of risk beyond 60 years
unconsidered), the mean age at first contact or first admission

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Epidemiology of Schizophrenia

143

Table 2. The incidence of schizophreniaa

Country

Diagnosis

Incidence per 1000

population per year

Age correction

Babigian (98)

USA

Clinical diagnosis

0.94

No

Bamrah and others (99)

UK

ICD

0.19

No

Bates and van Dam (130)

Canada

Clinical diagnosis

0.10

Yes

Der (76)
Dilling and others (131)

UK
Germany

Clinical diagnosis
Clinical diagnosis

0.09 to 0.16

No
Yes

Eagles and Whalley (75)

Folnegovic and others (132)

Scotland
Croatia

ICD
ICD

0.12 to 0.20
0.27

Yes
No

Netherlands

ICD

0.11

No

Authors

Giel and others (133)

0.48

Hfner (1996, unpublished observations)

Germany

ICD

0.16

No

Hagnell and others (134)

Sweden

Clinical diagnosis / PSE-CATEGO

0.24

Yes

Jablensky and others (2)

Jablensky and others (2)
Jablensky and others (2)
Jablensky and others (2)
Jablensky and others (2)
Jablensky and others (2)
Jablensky and others (2)
Krasik and Semin (135)
Krupinski (1983, unpublished observations)

Denmark
India
USA
USSR
Japan
UK
Ireland
USSR
Australia

Clinical diagnosis / PSE-CATEGO

Clinical diagnosis / PSE-CATEGO
Clinical diagnosis / PSE-CATEGO
Clinical diagnosis / PSE-CATEGO
Clinical diagnosis / PSE-CATEGO
Clinical diagnosis / PSE-CATEGO
Clinical diagnosis / PSE-CATEGO
Clinical diagnosis

0.07 to 0.18
0.09 to 0.35
0.09 to 0.16
0.12 to 0.28
0.10 to 0.21
0.14 to 0.24
0.09 to 0.22
0.08 to 0.23

No
No
No
Yes
No
No
No
Yes
Yes

Munk-Jrgensen (42)
Ninuallain (136)

Denmark
Ireland

Clinical diagnosis
Clinical diagnosis / ICD / PSE-CATEGO

0.07 to 0.11

0.18
0.37

No
No

Eaton (137)

India

0.58

No

Shen (121,122)

China

Clinical diagnosis

0.11

Yes

Tien and Eaton (138)

USA

DSM

1.0 to 7.1

No

Abridged version of a compilation by Warner and de Girolamo (36), supplemented by own review of literature.

lies between 25 and 35 years for men and women (41,42). In

the ABC schizophrenia study (43), mean age at onset
according to different definitions as assessed by the IRAOS
interview (35) was 24.0 years for the first sign of the disorder,
25.5 years for the first negative symptom, 29.0 years for the
first positive symptom, 30.1 years for a first peak of positive
symptoms (climax of the first psychotic episode), and 30.3
years for the first admission to hospital.

women. On the basis of first admissions with a clinical

diagnosis of schizophrenia to other British registers and to the
Dutch national case register, van Os and others (45) recently
found an increase from about 10/100 000 in the age group 60

Late-Onset Schizophrenia and Late Paranoid Psychoses

The question whether first episodes of schizophrenia also
occur beyond age 60 is still unclarified. A great obstacle to
epidemiological studies of nonaffective functional psychoses
in old age is not only the diagnosis but also the fact that neither
psychiatric nor general medical services nor population
studies guarantee access to all the cases with paranoid or
schizophrenic symptoms. This is why the results from recent
studies continue to vary considerably.
Harris and Jestes (44) review of European studies on
late-onset schizophrenia, as well as national Danish
case-register data (41), showed a decrease in first-admission
rates after age 60 based on a clinical diagnosis of schizophrenia. In contrast, applying the more restrictive DSM-III-R
diagnosis of schizophrenia, Castle and Murray (29), who
rated Camberwell register data for 1965 to 1984, demonstrated a considerable increase in old age, particularly in

Figure 1. Incidence rates from selected national studies and the

WHO Determinants of Outcome study per 100 000
population, aged 15 to 54 (both sexes), and for a broad
and restrictive definition of schizophrenia.

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Vol 42, No 2

Table 3. Studies on the psychopathology of late-onset schizophrenia

Author
Fish 1960 (47)

Kay and Roth 1961 (139)

Sample
All 41 paranoid states
> 60 years admitted in 1957,
including 9 late-onset and 7
early-onset schizophrenia
(cut-off 60 years)
99 admissions > 60 years
diagnosed with late
paraphrenia

Type of study/assessment
Case notes, partly personal
examination

Case records and clinical

assessment

Harris and others 1988 (140)

5 cases aged 56 to 67 years

with late-onset
schizophrenia (first and
readmissions)

Case study

Pearlson and others 1989 (51)

54 late-onset (> 45 years)

versus 54 early-onset (young)
versus 22 early-onset
(elderly); first and
readmissions

Rating of case records

Howard and others 1993 (53)

134 late-onset (> 45 years)

versus 336 early-onset cases;
first admissions

Rating of case records

Mayer and others 1993 (52)

130 first admissions 40 to 63

years versus 126 first
admissions 18 to 23 years

Evaluation of systematic clinical

assessment

Yassa and Suranyi-Cadotte

1993 (141)

20 late-onset schizophrenia
(> 45 years) versus 7
paraphrenia versus 13
late-onset paranoia (first
and readmissions)

Clinical assessment

Jeste and others 1995 (142)

25 late-onset schizophrenia
versus 39 early-onset
schizophrenia versus 35
normals

Clinical and neuropsychological

assessment

Symptomatology in
late-onset schizophrenia
No specific schizophrenia
syndrome

Risk factors for late-onset

schizophrenia
Paranoid personality traits

Auditory hallucinations and

many typically
schizophrenic symptoms;
systematic and fantastic,
usually persecutory
delusions; rare incoherence
of thought
Bizarre (persecutory)
delusion, auditory
hallucinations, visual
hallucinations, paranoid
subtype
More visual, tactile, olfactory
hallucinations, more diversity
of hallucinations, more
persecutory delusions; less
affective flattening, fewer
thought disorders
Persecutory and organized
delusions; third person
running commentary;
auditory hallucinations
More depression; more
symptoms of autonomic
nervous system, less
psychosocial impairment
Late-onset schizophrenia:
bizarre delusions, auditory
hallucinations; paraphrenia:
nonbizarre delusions;
late-onset paranoia:
nonbizarre delusions, organic
conditions
Paranoid subtype, better
work adjustment

Female gender, deafness,

personality disorder, few
relatives

Sensory impairment,
schizoid premorbid
personality, female gender,
living alone

Female gender

Female gender

Female gender (all

diagnoses); no increased
sensory deprivation

to 74 to 19/100 000 in the group 75 and over in England and

Wales and to 25/100 000 for those aged 90 and over in the
Netherlands (Figure 2).

age at the symptom level in sufficiently large study

populations did the methods adopted produce a clear-cut
empirical demarcation (44,51,52).

There are, however, ongoing controversies whether

early-onset and late-onset schizophrenia are different or
similar disorders and which delusional disorders of the elderly should be included with late-onset schizophrenia and
which of them classified separately as, for example, late
paraphrenia, paranoid psychoses, or merely persistent delusional syndromes. Behind the question of a valid diagnosis is
the issue of the underlying etiologies or, at least, of the
similarities or differences of symptoms and course (4650).

The main risk factors for paranoid disorders in old age are
cognitive and sensory impairment (44,53), whereas in
early-onset schizophrenia, signs of delayed development,
including cognitive impairment, predominate. It is therefore
reasonable to assume that in early-onset and very late-onset
schizophrenia, respectively, disordered or delayed brain development and degenerative processes of the brain, in both
instances ranging from mild to moderate in severity, are the
key risk factors. The reaction pattern of schizophrenia or
paranoid psychosis as a common final pathway shows clearcut psychopathological similarities but also some age-related
differences in both periods of life (54).

Studies focusing on the differentiation of delusional syndromes in later life are reviewed in Table 3. Final conclusions
are difficult to draw because of methodological limitations:
all of these studies employed small convenience or treatment
samples (44,47). Often first-episode cases as well as readmissions were included or no information was given on this issue.
In none of the recent studies attempting to distinguish
between primary paranoid disorder and schizophrenia in old

Sex Differences in Age at First-Ever Onset and Lifetime

Risk
As early as 1909, Kraepelin observed that women with
dementia praecox, when hospitalized for the first time, were
several years older than men. In their review of 53 studies,

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Epidemiology of Schizophrenia

145

25 years, steadily fell. Female onsets were slower to increase,

reached a lower peak somewhat later in life and, after decreasing, peaked again, but less markedly in the age group 40 to
45 years. In first-admission rates, a peak would be expected
to occur about 5 years later, which we were able to demonstrate on first-admission rates from the Danish national case
register (Hfner and others 1996, unpublished observations).
The distribution pattern published by Castle and others (57),
based on Camberwell case-register data over 20 years, also
displayed a second peak of female onsets just prior to
menopause.

Figure 2. Annual first-contact rates of nonaffective psychosis at age

60+ (based on administrative data).

Loranger (58), Seeman (59), Lewine (60), and Seeman and

Lang (61) have previously suggested that the sex difference
in age at onset might be accounted for by a protective effect
of estrogen. Animal experiments have shown that acute and
long-term estrogen applications actually reduce dopaminergic behaviour by attenuating the sensitivity of central D2
receptors (62,63). Estrogen effects on serotonin receptors at
the neurochemical and the molecular level (gene expression)
have been reported by Sumner and Fink (64) and on glutamate
receptors by Woolley and McEwen (65). In a controlled
clinical study of schizophrenic and depressive women with
normal menstrual cycles, Riecher-Rssler and others (66)
showed that, when estrogen levels were at their peak, schizophrenic and nonspecific symptom measures were significantly reduced but depressive symptoms were unaffected in
both diagnostic groups of women.
The sex difference in age of onset, however, disappears in
cases with a high genetic load, as shown by DeLisi and others
(67), Leboyer and others (68), and Albus and Maier (69),
whereas in the definitely nonfamilial cases of Albus and
Maiers sample, the onset-age difference grew to 5.7 years.
Evidently, the protective effect of estrogen is the more likely
to prevail, the lower the genetic liability. In addition, patients
of both sexes with a high genetic load seem to develop
schizophrenia at a relatively young age (69).

Figure 3. Mean age values at 5 definitions of onset until first admission. First-episode sample of schizophrenia, broad definition (N = 232).

Angermeyer and Khn (55) found that women at first admission and frequently also at onset, which has been defined and
ascertained in different ways, were older than men. Figure 3,
taken from the ABC schizophrenia study and based on a
representative sample of 232 first-episode cases, shows a
significant age difference of about 3 to 4 years for all definitions of onset. The pooled data of the WHO Determinants of
Outcome study revealed a mean age difference of 3.4 years
(56).
A comparison of the distribution patterns of onset for men
and women on the basis of ABC study data showed that onset
for males started to increase somewhat earlier and more
steeply and, after a pronounced peak in the age group 15 to

The lifetime risk for schizophrenia until age 60 appears to

be the same for men and women. In earlier studies in the
United States, higher lifetime incidence rates for men predominated, in part because of the age cut-off of 45 years in
the DSM-III diagnosis, in part because of the samples
recruited from public mental hospitals with higher
proportions of male patients. The use of criteria representing
more stringently defined schizophrenia (for example, duration criterion in DSM-III and DSM-IV) seems to yield a
significantly more disparate male-to-female ratio (70). Hambrecht and others (56) have recently discussed the methodological pitfalls that explain the predominance of men in some
studies, for example, an underrepresentation of primarily
female late-onset cases.
A cumulative depiction of the incidence rates for men and
women in 5-year age bands until age 59 from the ABC study
shows that the cumulative incidence, a good indicator of the
lifetime risk as based on an ICD-9 295 diagnosis of schizophrenia is practically the same for both sexes at 13.2/100 000
for men and 13.1/100 000 for women. Men clearly consume

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The Canadian Journal of Psychiatry

Table 4. Symptomatology at first admission: CATEGO syndrome

scores and total score by 3 age groups (N = 232)
Syndrome
DAH

12 to 20

Onset agea in years

21 to 35

36 to 59

11.2

10.3

10.1

ANOVA
P < 0.7

BSO

8.7

7.8

7.4

P < 0.4

SNR

9.6

6.7

6.6

P < 0.003

NSN

16.3

15.5

13.3

P < 0.08

Total score

45.9

40.4

37.7

P < 0.03

Onset defined by first psychotic symptom.

their lifetime risk more rapidly than women do, but from age
30 to 35 on, the rates for women approximate and finally meet
those for men.
Temporal Trends
Considering the even distribution of morbidity across
countries and cultures (see Figure 1), great variation over
historical time is unlikely. This is a difficult assumption to
verify, however, because it requires the registration and diagnosis on a fairly identical basis of all cases from a large,
statistically well-prepared population over a long period controlling for demographic changes.
The belief that schizophrenia did not exist before the 18th
century (71) is extremely unlikely to be true, and so is the
conviction that its incidence has increased with the bourgeoning population in the 19th and 20th centuries (7174). Decreases of 40% to 50% in the first-admission rates for
schizophrenia from the mid-1960s to about the mid-1980s
were recently reported by Munk-Jrgensen (42) from Denmark, Eagles and Whalley (75) from Scotland, and Der (76)
from England and Wales. Ders interpretation of the findings
as true morbidity trends triggered a critical debate in The
Lancet and the European Archives of Psychiatry and Clinical
Neuroscience. The main point raised was that the number of
available hospital beds and first admissions for a few other
diagnoses, such as affective psychoses and neurotic disorder,
also fell by approximately the same amount in these countries
over the same period (77,79). Strmgren (78) and Kendell and
others (80) also pointed out that the diagnosis of schizophrenia had become more restrictive during this period.
Warner and de Girolamo (36), referring to repeated, crosssectional investigations with the same methodology at some
study sites over the period in question, found stable,
age-corrected rates. Only 3 longitudinal studies fulfilled the
requirements mentioned for the investigation of long-term
morbidity trends in schizophrenia (17,81,82). They were
conducted on case-register data for Norway, Iceland, and the
state of Victoria, Australia. The longest period was covered
in the Australian study, in which a retrospective application
of operationalized diagnoses to random samples of case records was used. All of these studies found fairly stable rates,
indicating that temporal changes in schizophrenia morbidity
currently or in the recent past must be considered unlikely.

Vol 42, No 2

Clinical Epidemiology
Clinical epidemiology aims at generally valid conclusions
from clinical samples. The precondition is that study samples
are representative of the disorder in question or at least of a
defined subtype. The diagnostic definition should not include
any course criteria, such as the 6-month criterion in DSM-III
and DSM-IV, which is bound to lead to a biased selection in
the sample and thus to distorted results. Some epidemiological aspects of a disorder with an irregular, episodic course
also require comparisons at an identical stage of illness to
avoid confounds from different duration of illness (83). This
requirement has been fulfilled only recently in primarily
first-episode studies (43,84).
Symptomatology of the First Episode across the Life Cycle
Early-onset schizophrenia (under age 21) and very earlyonset schizophrenia (under age 14) are characterized by disorganization and a high frequency of poorly differentiated
and nonspecific symptoms, severe conduct disorders, and
functional impairment: the more prominent these symptoms,
the younger the patients are at onset (85,86). The sex distribution of early-onset schizophrenia shows a slight predominance of males in most studies, but the opposite has been
demonstrated in other studies. The studies, mostly based on
first-contact samples at child psychiatric institutions, however, usually do not include admissions after age 18. For this
reason, some young male cases of schizophrenia may be
missed because their asocial behaviour brings them into contact with social and youth guidance services as well as juvenile courts before reference to mental health services (87).
Testing the conclusion drawn from several studiesthat
early-onset schizophrenias are more severe than late-onset
schizophreniasinvestigators from the ABC schizophrenia
study, on the basis of PSE and CATEGO syndrome scores
(37), found that the PSE total scores were significantly lower
for late-onset patients, men and women taken together. As
shown in Table 4, the result was accounted for to a lesser
extent by the specific symptom scores DAH (delusional and
hallucinatory syndromes) and BSO (behaviour and speech),
and primarily by the 2 nonspecific scores SNR (specific
neurotic syndromes) and NSN (nonspecific neurotic syndromes). The implication of this finding is that the greater
severity of early-onset schizophrenia is primarily attributable
to a higher frequency of symptoms not specific to psychosis.
A comparison of the symptom scores in early- and lateonset schizophrenia (< 21 years versus 40 years) by sex
yielded different age trends for men and women. On 4 out of
8 symptom dimensions, late-onset men scored significantly
lower than early-onset men. For late-onset women, not a
single indicator was significantly more favourable and one,
the SANS global score, was more unfavourable in late-onset
women (Table 5).
This means that the milder symptomatology in late-onset
schizophrenia as a whole was accounted for by men alone,
while the total scores for late-onset women did not decrease,
and the SANS score, measuring negative symptoms, even

March 1997

Epidemiology of Schizophrenia

147

Table 5. Sex differences in symptom scores at time of first psychotic episodeearly versus late onseta
Men
Symptomatology
DAH

Women
Late (n = 9)

12.1

Wilcoxon
0.02a

5.7

8.6

0.29

7.3

SNR

10.7

0.11

NSN

18.9

0.03b

Total score

50.3

0.02b

31.8

SANS

9.3

0.29

PIRS

10.7

0.26

3.0

0.06c

1.8

BSO

DAS-M

Early (n = 28)

Early (n = 21)

Late (n = 24)

10.0

Wilcoxon
0.95

8.9

0.44

7.9

7.3

8.2

0.42

7.1

11.4

13.0

0.58

13.8

40.0

0.80

39.2

6.6

6.7

0.08c

9.5

8.4

9.8

0.73

10.5

1.9

0.61

1.8

10.5

Age at first psychotic symptom < 21 years versus 40 years.

P 0.1.
c
P 0.05.
Arrows mark the direction of the age difference.
b

increased in comparison with early-onset cases. In keeping

with the estrogen hypothesis (5860,62,88), we assume that
this finding resulted from the waning protective effect of
estrogenresponsible for the delay in onset and the milder
early symptomatology in women. In the premenopausal
period, this would explain the higher frequency and severity
of schizophrenias developed by women at this age. The
protective effect of estrogen lacking, men develop relatively
severe cases at a young age, but relatively milder cases with
growing age of onset.

By using syndrome scores derived from the systematic

Arbeitsgemeinschaft fr Methodik und Dokumentation in der
Psychiatrie (AMDP) symptom check list (93), the main items
of which are identical with the PSE, we compared a large,
consecutive, first-admission sample of schizophrenic patients
(n = 1109) from the Mannheim-based CIMH in the years 1978
to 1992 by 5-year age bands across the total age range (> 15
to 75). Neither significant sex differences nor age trends
were found in any of the schizophrenic and affective syndrome scores.

Age and Sex Differences in Illness Behaviour

At the level of single symptoms, the majority showed only

little variation with age. Only very few symptoms showed
highly significant and pronounced age differences: as illustrated in Figure 4, based on 5-year age groups from 15 to 19
years until 75 to 79 years, all the percentages of cases presenting systematic and paranoid delusions increased linearly with
age across the total age-of-onset range. Systematic delusions
showed a sixfold increase from 7% in the youngest age group
to 44% in the oldest group. Goodness of fit tests (linear logit
model) demonstrated highly significant linear increases or
decreases in frequency in logits with age.

A series of studies has consistently reported a higher

frequency of conduct disorders, especially asocial and criminal behaviours, and of substance abuse in schizophrenic men
(89). The WHO Determinants of Outcome study (2) also
found more first admissions triggered by acts of violence in
men than in women (22.2% versus 13.9%) (56).
In the ABC schizophrenia study, comparisons by sex, age
not taken into account, did not reveal any significant differences in the core symptoms. As stated by Goldberg and Gold
(90) with respect to neuropsychological test results in firstepisode patients, the disorder itself appears to be fairly similar
in men and women. The most pronounced sex difference
emerged in behavioural items, such as self-neglect, reduced
interest in a job, social withdrawal, and deficits of communication, which were all significantly more frequent in men
(Table 6). The socially negative items in men showed the
highest frequency before age 25 and the lowest frequency
after age 35.
Considering that population studies have shown conduct
disorders, antisocial and violent behaviour, and substance
abuse to be significantly overrepresented in men from puberty
to early adulthood (91), it is more plausible to classify this sex
difference in schizophrenia as illness behaviour rather than as
a direct expression of the illness. This presumes that the
socially negative behaviour of young males, also reflected in
a deficient compliance with care provision, has an unfavourable impact on outcome (92).

Unlike the delusional symptoms, the key symptoms of

incoherence of thought and disordered sense of self,
indicators of the disorganizational syndrome dimension particularly frequent in early-onset schizophrenia (85,87), decreased linearly over the entire age range. These 2 trends are
probably attributable to developmental factors and, again, are
not expressions of the basic psychophysiological process of
the disease. This means that the level of cognitive and personality development at the onset of the disorder is reflected
in symptoms (85,94,95). As the increase in paranoid and
systematic delusions indicates, the cognitive and coping abilities of personality at more mature stages of personality development become more differentiated and increasingly stable,
thus reducing the disorganizing effect of the psychosis on
overall mental functioning.
Like the socially negative illness behaviour of young
males, the age trends in the leading positive symptoms

148

The Canadian Journal of Psychiatry

Vol 42, No 2

Table 6. Gender differences in symptomatology at first admission and during early course
(ABC Schizophrenia First-Episode Sample, N = 232)
Symptom

Males (%)

Females (%)

P(2)a

Cross-sectional at first admission (PSE, PIRS, SANS, DAS)

Behaviours:
Overadaptiveness/conformity

5.8

14.9

0.029

38.1
81.9
76.4
68.3
84.7
58.1
36.5
48.0

18.0
54.1
50.7
31.3
62.7
39.5
19.5
31.3

0.001
0.001
0.001
0.002
0.002
0.005
0.005
0.012

79.6

92.7

0.003

39.8
31.5
74.1

21.0
16.9
55.6

0.002
0.009
0.003

Behaviours more frequent in men:

Self-neglect
Deficits of free-time activities
Deficits of communication
Reduced interest in a job
Social disability (overall estimate)
Loss of interests
Deficits in personal hygiene
Social inattentiveness
Cumulative prevalence during early course (IRAOS)
Behaviours more frequent in women:
Restlessness
Behaviours more frequent in men
Drug abuse
Alcohol abuse
Reduced activities in free time
a

The table gives results only for those items (out of the total of 303 items of PSE, PIRS, SANS, DAS, and IRAOS) in which (for alpha-correction) a significant gender difference
was validated with at least a statistical trend (P < 0.10) in both randomly split subsamples.

Eugen Bleuler (96) regarded them as secondary symptomsbut not in the negative symptoms, illustrate the extent
to which personality development, together with genetic and
probably also environmentally determined brain processes,
influences the clinical expression and probably also the
course of the disorder. This issue was recently raised by
Galdos and van Os (97) with reference to the fact that fully
elaborated positive symptoms, such as paranoid and
systematic delusions, require a certain degree of cognitive
maturity and education, for example, knowledge of the systems included as explanatory principles in the delusions. The
interaction of disease and development is likely to become
one of the key topics for future schizophrenia research and to
help build a bridge between genetic, epidemiological, and
personality research.

morbidity risk, and the distinction of empirical subtypes of

schizophrenia.
The knowledge available allows some fairly reliable conclusions about the epidemiology of schizophrenia, however:
the average age-corrected morbidity risk for schizophrenia of
a restrictive definition is 0.1/1000 population per year, with

Discussion
The epidemiology of schizophrenia is still faced with a
series of unsolved methodological problems, making conclusive interpretations and meaningful comparisons difficult.
Among these problems are the definition of the diagnosis by
conventional criteria, the variability of illness courses despite
the similarity of psychopathological symptoms, and the heterogeneity of the study populations. The difficulties resulting
from nonrepresentative study populations or from a failure to
check the findings against alternative interpretations are
reflected in the controversy produced by the reports of decreasing first-admission rates for schizophrenia from the mid1960s to the 1980s in some regions. Equally controversial
issues are the similarity or difference of age at onset in men
and women, the association between social class and the

Figure 4. Psychotic symptoms with significant age trends.

March 1997

Epidemiology of Schizophrenia

a range from 0.07 to 0.14/1000. It is unlikely that cultural,

social, or ecological factors play a crucial part in the etiology
of schizophrenia.

7.

Schizophrenia is primarily a disorder of adolescents and

young adults. The mean age at first contact with mental health
services is 25 to 35 years for both sexes together. In threequarters of first-episode cases, the first psychotic symptom is
preceded by a prodromal period of 6 years on average.
Negative and nonspecific symptoms emerge, on average, 5
years earlier than positive symptoms. Both symptom categories show an exponential accumulation until the climax of the
first episode and disappear altogether or at least partly after
that. Irrespective of how onset is defined, women fall ill 3 to
4 years later than men. The age distribution of onsets for
women shows a second peak in those aged 40 to 45 years.
Despite the difference in age of onset, the core symptoms and
almost all the other actual disease variables do not differ
between the sexes. A pronounced difference is the predominance of socially negative behaviour and substance abuse in
young male patients, but this finding very likely reflects ageand sex-specific illness behaviour and is not a direct expression of the disorder.

9.

Overall, the onset of schizophrenia is determined by various factorsgenetic and general biological (for example,
estrogen)and these same factors, interacting with age- and
sex-specific behaviour and level of development at onset,
influence the clinical expression and social course.

8.

10.
11.
12.

13.
14.
15.
16.
17.
18.
19.
20.

21.

22.
23.
24.

Clinical Implications
Incidence rates of schizophrenia appear stable across countries,

25.

cultures, and over time.

Given a narrow definition of schizophrenia, the annual incidence rates vary around 1 in 10 000.

On average, women fall ill 3 to 4 years later than men, probably

26.
27.

because of a protective effect of estrogen.

28.

Limitations

29.

Comparisons among studies are difficult because of differential

30.

standards in methodology.

It is still unclear whether schizophrenia-like late-onset psychoses should be classified as schizophrenia.

31.
32.
33.

References

34.
35.

1.

2.

3.
4.
5.
6.

Dohrenwend BP. The problem of validity in field studies of psychological

disorders. In: Robins LN, Barrett JE, editors. The validity of psychiatric diagnosis.
New York: Raven Press; 1989. p 3555.
Jablensky A, Sartorius N, Ernberg G, Anker M, Korten A, Cooper JE, and others.
Schizophrenia: manifestations, incidence and course in different cultures: a World
Health Organization ten-country study. Psychol Med 1992;20:127.
Thornicroft G, Johnson S. True versus treated prevalence of psychosisthe Prism
Case Identification Study. European Psychiatry 1996;11:185.
Faris REL, Dunham HW. Mental disorders in urban areas: an ecological study of
schizophrenia and other psychosis. Chicago: University of Chicago Press; 1939.
Sundby P, Nyhus P. Major and minor psychiatric disorders in males in Oslo: an
epidemiological study. Acta Psychiatr Scand 1963;39:51949.
Giggs J, Cooper JE. Ecological structure and the distribution of schizophrenia and
affective psychosis in Nottingham. Br J Psychiatry 1987;151:62733.

36.
37.
38.
39.
40.

149

Hfner H, Reimann H, Immich H, Martini H. Inzidenz seelischer erkrankungen

in Mannheim 1965. Social Psychiatry 1969;4:12535.
Weyerer S, Hfner H. The stability of ecological distribution of the incidence of
treated mental disorders in the city of Mannheim. Soc Psychiatry Psychiatr
Epidemiol 1989;24:5762.
Lffler W, Hfner H. Die kologische verteilung schizophrener ersterkrankungen
in zwei deutschen grossstdten (Mannheim und Heidelberg). Fundamenta Psychiatrica 1994;8:10315.
Dohrenwend BP, Dohrenwend BS. Social status and psychological disorder: a
causal inquiry. New York: J Wiley; 1969.
Eaton WW. Residence, social class, and schizophrenia. J Health Soc Behav
1974;15:289.
Eaton WW, Day R, Kramer MS. The use of epidemiology for risk factor research
in schizophrenia: an overview and methodological critique. In: Tsuang MT,
Simpson JL, editors. Handbook of schizophrenia, Volume 3, Nosology,
epidemiology and genetics. Amsterdam: Elsevier Science; 1988. p 169204.
Kohn M. Social class and schizophrenia: a critical review and reformulation.
Schizophr Bull 1973;7:6079.
Hollingshead A, Redlich F. Social class and mental illness. New York: J Wiley;
1958.
Dauncey K, Giggs J, Baker H, Harrison G. Schizophrenia in Nottingham: lifelong
residential mobility of a cohort. Br J Psychiatry 1993;163:6139.
Wiersma D, Giel R, de Jong A, Slooff CJ. Social class and schizophrenia in a
Dutch cohort. Psychol Med 1983;13:14150.
degaard O. Epidemiology der psychosen. Nervenarzt 1971;42:56975.
Goldberg EM, Morrison SL. Schizophrenia and social class. Br J Psychiatry
1963;109:785802.
Turner RJ, Wagenfeld MO. Occupational mobility and schizophrenia. American
Sociological Review 1967;32:10413.
Done DJ, Crow TJ, Johnstone EC, Sacker A. Childhood antecedents of schizophrenia and affective illness: social adjustment at ages 7 and 11. BMJ
1994;309:699703.
Crow TJ, Done DJ, Sacker A. Birth cohort study of the antecedents of psychosis:
ontogeny as witness to phylogenetic origins. In: Hfner H, Gattaz WF, editors.
Search for the causes of schizophrenia, vol.III. Berlin: Springer-Verlag; 1995. p
320.
Jones PB. Does schizophrenia result from pregnancy, delivery and perinatal
complications? a 28-year study in the 1966 North Finland birth cohort [abstract].
European Psychiatry 1996;11(4 Suppl):243S.
Dohrenwend BP, Levav I, Shrout PE, Schwartz SL, Naveh G, Link BG, and others.
Socioeconomic status and psychiatric disorders: the causation-selection issue.
Science 1992;255:94652.
Eaton WW, Mortensen PB, Herrman H, Freeman HE, Bilker W, Burgess P, and
others. Long-term course of hospitalization for schizophrenia, part I: risk for
rehospitalization. Schizophr Bull 1992;18:21727.
Lee CK, Kwak YS, Yamamoto J, Rhee H, Kim YS, Han JH, and others. Psychiatric
epidemiology in Korea, part II: urban and rural differences. J Nerv Ment Dis
1990;178:24752.
Eaton WW, Kessler LG. Epidemiologic field methods in psychiatry: the NIMH
Epidemiologic Catchment Area Program. New York: Academic Press; 1985.
Anthony J, Folstein MF, Romanoski A. Comparison of the lay Diagnostic
Interview Schedule and a standardized psychiatric diagnosis: experience in Eastern Baltimore. Arch Gen Psychiatry 1985;42:66775.
Jones PB, Rodgers B, Murray RM, Marmot M. Child development risk factors for
adult schizophrenia in the British 1946 birth cohort. Lancet 1994;344:1398402.
Castle D, Murray RM. The epidemiology of late-onset schizophrenia. Schizophr
Bull 1993;19:691700.
Hfner H, Maurer K. The contribution of epidemiology to the study of diagnosis.
European Psychiatry 1994;9:312.
Fremming KH. The expectations of mental infirmity in a sample of the Danish
population. London: Cassell; 1996.
Helgason T. Epidemiology of mental disorders in Iceland. Acta Psychiatr Scand
1964;40 (173 Suppl):1S258S.
Hambrecht M, Hfner H, Lffler W. Beginning schizophrenia observed by
significant others. Soc Psychiatry Psychiatr Epidemiol 1994;29:5360.
Maurer K, Hfner H. Methodological aspects of onset assessment in schizophrenia. Schizophr Res 1995;15:26576.
Hfner H, Riecher-Rssler A, Hambrecht M, Maurer K, Meissner S, Schmidtke
A, and others. IRAOS: an instrument for the assessment of onset and early course
of schizophrenia. Schizophr Res 1992;6:20923.
Warner R, de Girolamo G. Schizophrenia. Geneva: World Health Organization;
1995.
Wing JK, Cooper JE, Sartorius N. Measurement and classification of psychiatric
symptoms. London: Cambridge University Press; 1974.
Zubin J. Epidemiology and course of schizophrenia: discussion. In: Hfner H,
Gattaz WF, Janzarik W, editors. Search for the causes of schizophrenia, vol I.
Berlin: Springer-Verlag; 1987. p 1149.
Jorm AF. Cross-national comparisons of the occurrence of Alzheimers and
vascular dementias. Eur Arch Psychiatry Neurol Sci 1991;240:21822.
Haass C, Lemare C, Capell A, Citron M, Seubert T, Schenk D, and others. The
Swedish mutation causes early-onset Alzheimers disease by beta-secretare clevage within the secretory pathway. Natural Medicine 1995;1:12916.

150

41.
42.
43.

44.
45.
46.
47.
48.
49.
50.

51.
52.
53.
54.

55.
56.

57.
58.
59.
60.
61.
62.

63.

64.
65.
66.
67.
68.
69.
70.
71.
72.
73.

The Canadian Journal of Psychiatry

Hfner H, Riecher A, Maurer K, Lffler W, Munk-Jrgensen P, Strmgren E.

How does gender influence age at first hospitalization for schizophrenia? a
transnational case register study. Psychol Med 1989;19:90318.
Munk-Jrgensen P. Schizophrenia in Denmark: incidence and utilization of
psychiatric institutions. Acta Psychiatr Scand 1986;73:17280.
Hfner H, Maurer K, Lffler W, Bustamante S, an der Heiden W, Riecher-Rssler
A, and others. Onset and early course of schizophrenia. In: Hfner H, Gattaz WF,
editors. Search for the causes of schizophrenia, vol.III. Berlin: Springer-Verlag;
1995. p 4366.
Harris MJ, Jeste DV. Late-onset schizophrenia: an overview. Schizophr Bull
1988;14:3955.
van Os J, Howard R, Takei N, Murray RM. Increasing age is a risk factor for
psychosis in the elderly. Soc Psychiatry Psychiatr Epidemiol 1995;30:1614.
Roth M, Morrissey J. Problems in the diagnosis and classification of mental
disorders in old age. Journal of Mental Science 1952;98:6680.
Fish F. Senile schizophrenia. Journal of Mental Science 1960;106:93846.
Grahame PS. Schizophrenia in old age (late paraphrenia). Br J Psychiatry
1984;145:4935.
Holden NL. Late paraphrenia or the paraphrenias? a descriptive study with a
10-year follow-up. Br J Psychiatry 1987;150:6359.
Almeida OP, Howard R, Frstl H, Levy R. Late onset paranoid disorders, part I:
coming to terms with late paraphrenia. In: Chiu E, Ames D, editors. Functional
psychiatric disorders of the elderly. Cambridge: Cambridge University Press;
1994. p 30316.
Pearlson GD, Kreger L, Rabins PV, Chase GA, Cohen BM, Wirth JB, and others.
A chart review study of late-onset and early-onset schizophrenia. Am J Psychiatry
1989;146:156874.
Mayer C, Kelterborn G, Naber D. Age of onset in schizophrenia: relations to
psychopathology and gender. Br J Psychiatry 1993;162:66571.
Howard R, Castle D, Wessely S, Murray RM. A comparative study of 470 cases
of early-onset and late-onset schizophrenia. Br J Psychiatry 1993;163:3527.
Hfner H, Maurer K. Epidemiology of positive and negative symptoms in schizophrenia. In: Shriqui CL, Nasrallah HA, editors. Contemporary issues in the
treatment of schizophrenia. Washington (DC): American Psychiatric Press; 1993.
p 12554.
Angermeyer MC, Khn L. Gender differences in age at onset of schizophrenia:
an overview. Eur Arch Psychiatry Neurol Sci 1988;237:35164.
Hambrecht M, Maurer K, Hfner H, Sartorius N. Transnational stability of gender
differences in schizophrenia? an analysis based on the WHO study on determinants of outcome of severe mental disorders. Eur Arch Psychiatry Clin Neurosci
1992;242:612.
Castle D, Wessely S, Der G, Murray RM. The incidence of operationally defined
schizophrenia in Camberwell, 1965-84. Br J Psychiatry 1991;159:7904.
Loranger AW. Sex differences in age of onset of schizophrenia. Arch Gen
Psychiatry 1984;41:15761.
Seeman MV. Interaction of sex, age, and neuroleptic dose. Compr Psychiatry
1983;24:1258.
Lewine RRJ. Gender and schizophrenia. In: Tsuang MT, Simpson JC, editors.
Handbook of schizophrenia. Volume III, Nosology, epidemiology and genetics
of schizophrenia. Amsterdam: Elsevier Science; 1988. p 37997.
Seeman MV, Lang M. The role of estrogens in schizophrenia gender differences.
Schizophr Bull 1990;16:18594.
Hfner H, Behrens S, De Vry J, Gattaz WF. Oestradiol enhances the vulnerability
threshold for schizophrenia in women by an early effect on dopaminergic
transmissionevidence from an epidemiological study and from animal experiments. Eur Arch Psychiatry Clin Neurosci 1991;241:658.
Gattaz WF, Behrens S, De Vry J, Hfner H. stradiol hemmt dopamin-vermittelte
verhaltensweisen bei ratten: ein tiermodell zur untersuchung der geschlechtsspezifischen unterschiede bei der schizophrenie. Fortschr Neurol Psychiatr
1992;1:816.
Sumner BEH, Fink G. Oestradiol-17 in its positive feedback mode significantly
increases 5-HT2a receptor density in the frontal, cingulate and piriform cortex of
the female rat. J Physiol 1995;483:52.
Woolley CS, McEwen BS. Estradiol regulates hippocampal dendritic spine density via an N-methyl-D-aspartate receptor-dependent mechanism. J Neurosci
1994;14:76807.
Riecher-Rssler A, Hfner H, Dtsch-Strobel A, Oster M, Stumbaum M, van
Glick-Bailer M, and others. Further evidence for a specific role of estradiol in
schizophrenia? Biol Psychiatry 1994;36:4925.
DeLisi LE, Bass N, Boccio A, Shields G, Morganti C, Vita A. Age of onset in
familial schizophrenia. Arch Gen Psychiatry 1994;51:3345.
Leboyer M, Filteau M-J, Jay M, Campion D, Rochet T, dAmato T, and others.
No gender effect on age at onset in familial schizophrenia [letter]. Am J Psychiatry
1992;149:1409.
Albus M, Maier W. Lack of gender differences in age at onset in familial
schizophrenia. Schizophr Res 1995;18:517.
Lewine RRJ, Burbach D, Meltzer HY. Effect of diagnostic criteria on the ratio of
male to female schizophrenic patients. Am J Psychiatry 1984;141:847.
Torrey EF. Schizophrenia and civilization. New York: Jason Aronson; 1996.
Astrup C. Nervse erkrankungen und soziale verhltnisse. Berlin: Volk und
Gesundheit; 1956.
Eaton WW. A formal theory of selection for schizophrenia. American Journal of
Sociology 1980;86:14958.

74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
94.

95.
96.
97.
98.
99.
100.
101.
102.
103.
104.

105.
106.
107.

Vol 42, No 2

Hare E. Was insanity on the increase? Br J Psychiatry 1983;142:43945.

Eagles JM, Whalley LJ. Decline in the diagnosis of schizophrenia among first
admissions to Scottish mental hospitals from 1969-78. Br J Psychiatry
1985;146:1514.
Der G. Is schizophrenia disappearing? [letter]. Lancet 1990;335:5136.
Angst J. Is schizophrenia disappearing? Eur Arch Psychiatry Clin Neurosci
1991;240:373.
Strmgren E. Changes in the incidence of schizophrenia? Br J Psychiatry
1987;150:17.
Hfner H, Gattaz WF. Reply: is schizophrenia disappearing? Eur Arch Psychiatry
Clin Neurosci 1991;240:3746.
Kendell RE, Malcolm DE, Adams W. Is the incidence of schizophrenia falling?
Schizophr Res 1992;6:100.
Helgason T. Expectancy of schizophrenia in Iceland during the twentieth century.
In: Glel R, editor. Changing the course and outcome of mental disorder. World
Psychiatric Association meeting; Groningen, The Netherlands; 1993 Sept 13.
Krupinski J, Alexander L. Patterns of psychiatric morbidity in Victoria, Australia,
in relation to changes in diagnostic criteria 1848-1978. Social Psychiatry
1983;18:617.
Hfner H. The epidemiology of onset and early course of schizophrenia. In: Hfner
H, Wolpert EM, editors. New research in psychiatry. Toronto: Hogrefe & Huber;
1996. p 3361.
Loebel AD, Lieberman JA, Alvir JMJ, Mayerhoff D, Geisler SH, Szymanski SR.
Duration of psychosis and outcome in first-episode schizophrenia. Am J Psychiatry 1992;149:11838.
Remschmidt H, Schulz E, Martin M, Warnke A, Trott G-E. Childhood-onset
schizophrenia: history of the concept and recent studies. Schizophr Bull
1994;20:72745.
Asarnow RF, Asamen J, Granholm E, Sherman T, Watkins JM, Williams ME.
Cognitive/neuropsychological studies of children with a schizophrenic disorder.
Schizophr Bull 1994;20:64769.
Hfner H, Nowotny B. Epidemiology of early-onset schizophrenia. Eur Arch
Psychiatry Clin Neurosci 1995;245:8092.
Riecher-Rssler A, Hfner H, Stumbaum M, Maurer K, Schmidt R. Can estradiol
modulate schizophrenic symptomatology? Schizophr Bull 1994;20:20314.
Hfner H, Bker W. Crimes of violence by mentally abnormal offenders. London:
Cambridge University Press; 1982.
Goldberg TE, Gold JM. Neurocognitive deficits in schizophrenia. In: Hirsch SR,
Weinberger DR, editors. Schizophrenia. London: Blackwell Science; 1995.
p 14662.
Choquet M, Ledoux S. Epidmiologie et adolescence. Rhne-Poulenc rorer specia
1994;27:287309.
Hfner H, Ftkenheuer B, Nowotny B, an der Heiden W. New perspectives in the
epidemiology of schizophrenia. Psychopathology 1995;28:2640.
Gebhardt R, Pietzker A, Strauss A, Stoeckel M, Langer C, Freudenthal K.
Skalenbildung im AMDP-System. Archiv fr Psychiatrie und Nervenkrankheiten
1983;233:22345.
Asarnow RF, Caplan R, Asarnow JR. Neurobehavioral studies of schizophrenic
children: a developmental perspective on schizophrenic disorders. In: Hfner H,
Gattaz WF, editors. Search for the causes of schizophrenia, vol.III. Berlin:
Springer-Verlag; 1995. p 87113.
Blanz B, Schmidt MH, Detzner U, Lay B. Is there a sex-specific difference in
onset age of schizophrenia that started before age of 18? European Child and
Adolescent Psychiatry 1996;3:26776.
Bleuler E. Dementia praecox oder die gruppe der schizophrenien. Leipzig-Wien:
Deuticke; 1911.
Galdos PM, van Os J. Gender, psychopathology, and development: from puberty
to early adulthood. Schizophr Res 1995;14:10512.
Babigian HM. Schizophrenia: epidemiology. In: Kaplan HI, Freedman AM,
Sadock BJ, editors. Comprehensive textbook of psychiatry. Baltimore: Williams
& Wilkins; 1980. p 8606.
Bamrah JS, Freeman HL, Goldberg DP. Epidemiology in Salford, 1974-84:
changes in an urban community over ten years. Br J Psychiatry 1991;159:80210.
Bebbington P, Hurry J, Sturt E, Wing JK. Epidemiological study of mental
disorders in Camberwell. Psychol Med 1981;11:56179.
Ben-Tovim DI, Cushnie JM. The prevalence of schizophrenia in a remote area of
Botswana. Br J Psychiatry 1986;148:57680.
Bland RC, Orn H, Newman SC. Lifetime prevalence of psychiatric disorders in
Edmonton. Acta Psychiatr Scand 1988;338:2432.
Blazer D, George LK, Landerman R, Pennybacker M, Melville ML, Woodbury
M, and others. Psychiatric disorders: a rural/urban comparison. Arch Gen Psychiatry 1985;42:6516.
Burnam MA, Hough RL, Escobar JI, Karno M, Timbers DM, Teller CA, and
others. Six-month prevalence of specific psychiatric disorders among Mexican
Americans and non-Hispanic whites in Los Angeles. Arch Gen Psychiatry
1987;44:68794.
Canino GJ, Bird HR, Shrout PE, Rubio-Stipec M, Bravo M, Martinez R, and
others. The prevalence of specific psychiatric disorders in Puerto Rico. Arch Gen
Psychiatry 1987;44:72735.
Cheung P. Adult psychiatric epidemiology in China in the 80s. Culture, Medicine
and Psychiatry 1991;15:47996.
Dilling H, Weyerer S. Prevalence of mental disorders in the small-town, rural
region of Traunstein (Upper Bavaria). Acta Psychiatr Scand 1984;69:6079.

March 1997

Epidemiology of Schizophrenia

108. Folnegovic Z, Folnegovic-Smalc V. Schizophrenia in Croatia: interregional differences in prevalence and a comment on constant incidence. J Epidemiol Community Health 1992;46:24855.
109. Freeman HL, Alpert M. Prevalence of schizophrenia in an urban population. Br J
Psychiatry 1986;149:60311.
110. Halldin T. Prevalence of mental disorder in an urban population in central Sweden.
Acta Psychiatr Scand 1984;69:50318.
111. Hodiamont P, Peer N, Sybern N. Epidemiological aspects of psychiatric disorder
in a Dutch health area. Psychol Med 1987;17:495505.
112. Hwu HG, Yeh E-K, Chang L-Y. Prevalence of psychiatric disorders in Taiwan
defined by the Chinese diagnostic interview schedule. Acta Psychiatr Scand
1989;79:13647.
113. Lee CK, Kwak YS, Yamamoto J, Rhee H, Kim YS, Han JH, and others. Psychiatric
epidemiology in Korea, part I: gender and age differences in Seoul. J Nerv Ment
Dis 1990;178:2426.
114. Lehtinen V, Joukamaa M, Lahtela K, Raitasalo R, Jyrkinen E, Maatela J, and
others. Prevalence of mental disorders among adults in Finland: basis results from
the Mini Finland Health Survey. Acta Psychiatr Scand 1990;81:41825.
115. Lehtinen V. The prevalence of PSE-CATEGO disorders in a Finnish adult
population cohort. Soc Psychiatry Psychiatr Epidemiol 1990;25:18792.
116. Lin KM. Overview of mental disorders in Chinese cultures: review of
epidemiological and clinical studies. In: Kleinman A, Lin TY, editors. Normal
and abnormal behaviour in Chinese cultures. Dordrecht: Reidel; 1981. p 23772.
117. Mavreas VG, Bebbington P. Psychiatric morbidity in Londons Greek-Cypriot
immigrant community. Social Psychiatry 1987;22:1509.
118. Murphy HB, Taumoepeau BM. Traditionalism and mental health in the South
Pacific: a re-examination of an old hypothesis. Psychol Med 1980;10:47182.
119. Myers JK, Weissman MM, Tischler GL, Holzer CE, Leaf P, Orvaschel H, and
others. Six month prevalence of psychiatric disorders in three sites. Arch Gen
Psychiatry 1984;41:95967.
120. Nandi DN, Mukherjee S, Boral GC, Banerjee G, Ghosh A, Sarkas S, and others.
Socio-economic status and mental morbidity in central tribes and castes in India:
a cross-cultural study. Br J Psychiatry 1980;136:7385.
121. Shen Y. Investigations of mental disorders in Beijing suburban district. Chinese
Medical Journal 1981;94:1536.
122. Shen Y. A survey of mental disorders in a suburb of Beijing. International Journal
of Mental Health 1988;16:7580.
123. Sikanerty T, Eaton WW. Prevalence of schizophrenia in the Labadi district of
Ghana. Acta Psychiatr Scand 1984;69:15661.
124. Temkov I. Use of reported prevalence data in cross-national comparisons of
psychiatric morbidity. Social Psychiatry 1980;3:1117.
125. Vasquez-Barquero JL. A community mental health survey in Cantabria: a general
description of morbidity. Psychol Med 1987;17:22741.

151

126. Walsh D. The treated prevalence of mental illness in the Republic of Ireland: the
three county case register study. Psychol Med 1980;10:46570.
127. Weissman MM, Myers JK. Psychiatric disorders in a U.S. community: the
application of research diagnostic criteria to a resurveyed community sample. Acta
Psychiatr Scand 1980;62:99111.
128. Widerlv B, Borg P, Cullberg J, Stefansson CG, Lindqvist G. Epidemiology of
long-term functional psychosis in three different areas in Stockholm County. Acta
Psychiatr Scand 1989;80:406.
129. Zimmerman-Tansella C. Bringing into action the psychiatric reform in SouthVerona: a five year experience. Acta Psychiatr Scand 1985;71:7186.
130. Bates CE, van Dam CH. Low incidence of schizophrenia in British Columbia
coastal Indians. J Epidemiol Community Health 1984;38:12730.
131. Dilling H, Weyerer S, Fichter M. The Upper Bavarian studies. Acta Psychiatr
Scand 1989;348:11340.
132. Folnegovic Z, Folnegovic-Smalc V, Kulcar Z. The incidence of schizophrenia in
Croatia. Br J Psychiatry 1990;156:3635.
133. Giel R, Sauer HC, Slooff CJ, Wiersma D. Epidemiological observations on
schizophrenia and disability in the Netherlands. Tijdschrift voor Psychiatrie
1980;11-12:71022.
134. Hagnell O, Essen-Mller E, Lanke J. The incidence of mental illness over a quarter
of a century: the Lundby longitudinal study of mental illness in a total population
based on 42,000 observation years. Stockholm: Almquist & Wiksell International;
1990.
135. Krasik ED, Semin IR. Epidemiological aspects of first admissions of schizophrenic patients. Zhurnal Nevropatologij Psikijatrii 1980;80:13549.
136. Ninuallain M, OHare A, Walsh D. Incidence of schizophrenia in Ireland. Psychol
Med 1987;17:9438.
137. Eaton WW. Update on the epidemiology of schizophrenia. Epidemiol Rev
1991;13:3208.
138. Tien AY, Eaton WW. Psychopathologic precursors and sociodemographic risk
factors for the schizophrenia syndrome. Arch Gen Psychiatry 1992;49:3746.
139. Kay DWK, Roth M. Environmental and hereditary factors in the schizophrenia of
old age (late paraphrenia) and their bearing on the general problem of causation
in schizophrenia. Journal of Mental Science 1961;107:64986.
140. Harris MJ, Cullum CM, Jeste DV. Clinical presentation of late-onset schizophrenia. J Clin Psychiatry 1988;49:35660.
141. Yassa R, Suranyi-Cadotte B. Clinical characteristics of late-onset schizophrenia
and delusional disorder. Schizohpr Bull 1993;19:7017.
142. Jeste DV, Harris MJ, Krull A, Kuck J, McAdams LA, Heaton RK. Clinical and
neuropsychological characteristics of patients with late-onset schizophrenia. Am
J Psychiatry 1995;152:72230.

Rsum
Objectif : Caractriser lpidmiologie de la schizophrnie.
Mthode : Analyse documentaire narrative.
Rsultats : Chaque anne, un adulte sur 10 000 (g entre 12 et 60 ans) est atteint de schizophrnie. Lorsquon utilise
une dfinition restrictive et prcise du diagnostic, des mthodes dvaluation normalises et des populations larges et
reprsentatives, on constate que les taux dincidence semblent tre demeurs stables, dun pays et dune culture lautre
ainsi quau fil des ans, et ce depuis au moins 50 ans. Les malades schizophrnes ne viennent pas au monde socialement
dfavoriss, ni dfavoriss quant leur milieu. La rpartition ingale des taux de prvalence est le rsultat de la slection
sociale : lapparition prcoce de la maladie mne une stagnation sociale alors quune apparition tardive entrane une
diminution du statut social. La principale zone dge, pour ce qui est des risques de schizophrnie, se situe entre 20 et
35 ans. On ne sait pas encore si les psychoses dallure schizophrnique dbut tardif (comme les paraphrnies tardives),
qui se dclarent aprs lge de 60 ans, devraient tre classes comme des schizophrnies, que ce soit au plan
psychopathologique ou tiologique.
Dans 75 % des cas, la premire hospitalisation est prcde dune phase prodromique dune dure moyenne de 5 ans
et dune prphase psychotique dun an. Chez les femmes, la maladie se manifeste gnralement 3 ou 4 ans plus tard que
chez les hommes et une deuxime priode dapparition leve concide peu prs avec la mnopause. Les schizophrnies
dbut tardif sont donc plus frquentes et plus graves chez les femmes que chez les hommes. Les diffrences entre les
sexes quant lge dapparition de la maladie sont moindres lorsque le fardeau gntique est lev et elles sont plus
grandes lorsque le fardeau gntique est faible. Le mode dapparition et les principaux symptmes de la maladie sont
similaires chez les deux sexes. Les diffrences les plus marques entre les sexes se situent au niveau du comportement
socialement ngatif d la maladie, qui est observ chez les jeunes hommes.
Conclusions : Parmi les facteurs qui dterminent lvolution sociale et lissue figurent le niveau de dveloppement social
au moment de lapparition de la maladie, le trouble lui-mme (par exemple le fardeau gntique, la gravit des
symptmes et les dficits fonctionnels), les facteurs biologiques gnraux (par exemple, loestrogne) et les comportements pathologiques spcifiques au sexe et lge.