EPIDEMIOLOGY OF SCHIZOPHRENIA

Citation
H. Hafner et W. Anderheiden, EPIDEMIOLOGY OF SCHIZOPHRENIA, Canadian journal of psychiatry, 42(2), 1997, pp. 139-151
Citations number
141
Categorie Soggetti
Psychiatry,Psychiatry
ISSN journal
07067437
Volume
42
Issue
2
Year of publication
1997
Pages
139 - 151
Database
ISI
SICI code
0706-7437(1997)42:2<139:EOS>2.0.ZU;2-J
Abstract
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 an d precise definition of the diagnosis and using standardized assessmen t methods and large, representative populations, the incidence rates a ppear stable across countries and cultures and over time, at least for the last 50 years. Schizophrenic patients are not born into ecologica l and social disadvantage. The uneven distribution of prevalence rates is a result of social selection: an early onset leads to social stagn ation, a late onset to descent from a higher social status. The main a ge range of risk for schizophrenia is 20 to 35 years. It is still uncl ear whether schizophrenia-like late-onset psychoses (for example, late paraphrenia) after age 60 should be classified as schizophrenia eithe r psychopathologically or etiologically. In 75% of cases, first admiss ion is preceded by a prodromal phase with a mean length of 5 years and a psychotic prephase of one year 's duration. On average, women fall ill 3 to 4 years later than men and show a second peak of onset around menopause. Consequently, late-onset schizophrenias are more frequent and more severe in women than in men. The sex difference in age of ons et is smaller in cases with a high genetic load and greater in cases w ith a low genetic load. Type of onset and core symptoms do nor differ between the sexes. The most pronounced sex difference is the socially negative illness behaviour of young men. Conclusions: Among the factor s determining social course and outcome are level of social developmen t at onset, the disorder itself (for example, genetic liability, sever ity of symptoms, and functional deficits), general biological factors (for example, estrogen), and sex- and age-specific illness behaviour.