This Thesis describes the epidemiology of schizophrenia and related disorders in the defined catchment area of Camberwell, SE London, UK, over the period 1965 to 1984. Cases were ascertained through the comprehensive Camberwell Cumulative Psychiatric Case Register. All first-contact patients with a Register diagnosis of any non-affective non-organic psychotic illness were included in the study. Diagnostic uniformity was ensured by rediagnosis of all cases (n=531) using the computerised OCCPI system, which facilitates rediagnosis according to a wide range of diagnostic criteria. Trends in the incidence of non-affective functional psychoses over the two decades during which the Camberwell Register was operational, are explored. The findings, of a rising rate of illness in Camberwell, are discussed in terms of changes in the demography of the general population over the years, and suggestions offered for discrepancies with other studies of time trends in schizophrenia, particular emphasis being placed on changes in the ethnic composition of Camberwell over this period. A case-control study design is used to explore whether the rising incidence of the illness in the area is due solely or largely to drift into the area of ill individuals, or whether some of the variance can be explained in terms of a pernicious inner-city effect operating during early development (in utero or in early childhood). The findings of an excess of schizophrenia patients actually having been born in the inner city suggests that something about poor households in the inner city might predispose to the illness in later life. This is discussed in the general framework of the neurodevelopmental hypothesis of schizophrenia, which proposes that at least some individuals have a form of illness consequent upon subtle damage to the developing brain. A major focus of the analyses is gender differences in schizophrenia, and late onset schizophrenia. Early-onset males were particularly likely to fulfil stringent diagnostic criteria for the illness, and to show premorbid dysfunction. The results are interpreted in the neurodevelopmental framework, and reference made to differences in male and female brains in their vulnerability to neurodevelopmental illnesses in general. Taking this theme forward, a form of factor analysis called latent class analysis is used to further explore the notion of different subtypes of schizophrenia, one of which is an early-onset severe male-predominant form (theoretically consequent upon neurodevelopmental deviance). The analyses resulted in a "best fit" model of three subtypes, one an early-onset male-predominant type associated with premorbid dysfunction ("neurodevelopmental" type); a later-onset "paranoid" type; and an affect-laden type exclusive to females ("schizoaffective" type). There were associations with a number of variables of potential importance in terms of aetiology, namely an association of the "neurodevelopmental" type with a family history of schizophrenia and obstetric complications; an association of the "paranoid" type with winter birth; and of the "affective" type with a family history of psychiatric disorder other than schizophrenia (predominantly affective disorder). This typology does not adequately account for those patients with a late (over 45 years), or very-late onset of illness (over 60). Phenomenological, premorbid, and other differences between early- and late-onset patients are analysed, and the results discussed in the broader framework of the literature on late-onset non-affective psychoses.

No description available.

Over the past few decades, epidemiological evidence has accrued to establish variance in psychosis risk across both geographical locations and demographic characteristics such as the excess risk in migrants and their descendants. Yet, the causes of this variation in rates between places and ethnic groups are still unclear, and I aimed to address this in this thesis. I conducted a systematic review and meta-analyses to synthesise existing literature on psychosis incidence in the six countries included in the EUropean network of national schizophrenia networks studying Gene-Environment Interactions (EU-GEI) study: England, The Netherlands, Spain, France, Italy and Brazil. I subsequently analysed data from two parts of the EU-GEI study: a 17-centre service-based incidence study of psychosis, and a case-control arm utilising community volunteers. In the latter, I aimed to explain excess risk in ethnic and religious minorities using a theoretical sociocultural distance model I developed using literature from the social sciences. Here, I proposed that culturally distant minorities were particularly at risk of social exclusion, and this outsider experience led to increased psychosocial disempowerment (a lack of control over one’s life), which increased psychosis risk. I also explored if this model could explain any excess risk in those with increased genetic African ancestry in England. Incidence varied substantially between the studies included in the systematic review, although methodological differences could not be excluded as an explanation. The EU-GEI incidence study confirmed substantial variation by place, and demonstrated a higher incidence in ethnic minorities and for young men, as well as in areas characterised by a low percentage of owner-occupied housing. The sociocultural distance model could explain most of the excess psychosis risk in ethnic minorities, although some excess risk remained, particularly in the Black ethnic group. Social and cultural distance appeared to be more important predictors than psychosocial disempowerment, suggesting that chronic social injustices rather than acute stress play an important role. This model did not explain excess risk in religious minorities: those following any religion retained an excess risk. It could explain the excess risk in those with increased genetic African ancestry, although this was a small, exploratory sample and this will need replicating in larger studies. This thesis demonstrated, for the first time, that excess risk in ethnic minorities could be explained by the sociocultural distance model. Overall, the findings from this thesis confirm substantial variation in psychosis risk by person and place, and suggest that the social reality of the environment plays a crucial role in explaining this.

Epidemiological data on a wide range of mental disorders from community studies conducted in European countries are presented to determine the availability and consistency of prevalence, disability and treatment findings for the EU. Using a stepwise multimethod approach, 27 eligible studies with quite variable designs and methods including over 150,000 subjects from 16 European countries were identified. Prevalence: On the basis of meta-analytic techniques as well as on reanalyses of selected data sets, it is estimated that about 27% (equals 82.7 million; 95% CI: 78.5–87.1) of the adult EU population, 18–65 of age, is or has been affected by at least one mental disorder in the past 12 months. Taking into account the considerable degree of comorbidity (about one third had more than one disorder), the most frequent disorders are anxiety disorders, depressive, somatoform and substance dependence disorders. When taking into account design, sampling and other methodological differences between studies, little evidence seems to exist for considerable cultural or country variation. Disability and treatment: despite very divergent and fairly crude assessment strategies, the available data consistently demonstrate (a) an association of all mental disorders with a considerable disability burden in terms of number of work days lost (WLD) and (b) generally low utilization and treatment rates. Only 26% of all cases had any consultation with professional health care services, a finding suggesting a considerable degree of unmet need. The paper highlights considerable future research needs for coordinated EU studies across all disorders and age groups. As prevalence estimates could not simply be equated with defined treatment needs, such studies should determine the degree of met and unmet needs for services by taking into account severity, disability and comorbidity. These needs are most pronounced for the new EU member states as well as more generally for adolescent and older populations.

(Truncated abstract) The aims of this thesis are: (i) To estimate the prevalence of psychiatric illness among persons with intellectual disability and, conversely, the prevalence of intellectual disability among persons with a psychiatric illness; (ii) To describe the disability and service utilisation profile of persons with conjoint disorder; (iii) To examine, in particular, intellectual disability co-occurring with schizophrenia; and (iv) To explore the role of hereditary and environmental (specifically obstetric) risk factors in the aetiology of (i) intellectual disability and (ii) intellectual disability co-occurring with psychiatric illness. This thesis has a special interest in the relationship between intellectual disability and schizophrenia. Where data and sample sizes permit, it explores that relationship at some depth and has included sections on the putative nature of the link between intellectual disability and schizophrenia in the introductory and discussion chapters. To realise its objectives, the thesis comprises a core study focusing on aims (i) – (iii) and a supplementary study whose focus is aim (iv). It also draws on work from an ancillary study completed prior to the period of candidacy...This thesis found that, overall, 31.7% of persons with an intellectual disability had a psychiatric illness; 1.8% of persons with a psychiatric illness had an intellectual disability. The rate of schizophrenia, but not bipolar disorder or unipolar major depression, was greatly increased among cases of conjoint disorder: depending on birth cohort, 3.7-5.2% of individuals with intellectual disability had co-occurring schizophrenia. Down syndrome was much less prevalent among conjoint disorder cases despite being the most predominant cause of intellectual disability while pervasive developmental disorder was over-represented. Persons with conjoint disorder had a more severe clinical profile including higher mortality rates than those with a single disability. The supplementary study confirmed the findings in the core body of work with respect to the extent of conjoint disorder, its severity, and its relationship with pervasive development disorder and Down syndrome. Moreover, the supplementary study and the ancillary influenza study indicated a role for neurodevelopmental insults including obstetric complications in the adverse neuropsychiatric outcomes, with timing of the insult a potentially critical element in defining the specific outcome. The supplementary study also added new information on familiality in intellectual disability. It found that, in addition to parental intellectual disability status and exposure to labour and delivery complications at birth, parental psychiatric status was an independent predictor of intellectual disability in offspring as well as a predictor of conjoint disorder. In conclusion, the facility to collect and integrate records held by separate State administrative health jurisdictions, and to analyse them within the one database has had a marked impact on the capacity for this thesis to estimate the prevalence of conjoint disorder among intellectually disabled and psychiatric populations, and to understand more about its clinical manifestations and aetiological underpinnings.