To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
To describe symptom expression and functional outcome in psychotic disorders in relation with temperament traits assessed with the Temperament and Character Inventory (TCI) in a population-based sample.
As part of the 31-year follow-up survey of the Northern Finland 1966 Birth Cohort, TCI temperament items were filled in by 4349 members of the cohort. In individuals with psychotic disorders, also positive and negative symptoms and outcome variables were assessed in a 35-year follow-up. Information of TCI and outcomes were available for altogether 41 individuals with psychosis.
Reward dependence (RD) (rho = −0.45) and Persistence (P) (rho = −0.52) were significantly correlated with Positive and Negative Syndrome Scale (PANSS) negative symptoms. Higher P scores predicted higher social and occupational functioning (as measured by Social and Occupational Functioning Assessment Scale [SOFAS]), and higher Harm avoidance (HA) predicted a higher likelihood of being on a disability pension.
Results indicate that understanding of personality dimensions support better understanding of outcome and symptom expressions in psychotic disorders.
Social withdrawal is among the first signs of the prodromal state of psychosis seen in clinical samples. The aim of this prospective study was to find out whether difficulty in making contact with others and social withdrawal precede first episode psychosis in the young general population.
The members of the Northern Finland Birth Cohort 1986 (n = 6274) completed the PROD-screen questionnaire in 2001–2002. The Finnish Hospital Discharge Register was used to detect both new psychotic and non-psychotic disorders requiring hospitalisation during 2003–2008.
Twenty-three subjects developed psychosis and 89 developed a non-psychotic mental disorder requiring hospitalisation during the follow-up. Of those who developed psychosis, 35% had reported difficulty or uncertainty in making contact with others and 30% social withdrawal in adolescence. In hospitalised non-psychotic disorder, the corresponding precentages were 10 and 13% and in the control group without hospital-treated mental disorder 9 and 11%. The differences between psychotic and non-psychotic hospitalised subjects (P < 0.01) as well as controls (P < 0.001) were statistically significant regarding difficulty or uncertainty in making contact with others.
In this general population-based sample self-reported difficulty or uncertainty in making contact with others in adolescence preceded psychosis specifically compared to hospitalised non-psychotic mental disorders and controls.
To analyse associations between brain morphology and longitudinal and cross-sectional measures of outcomes in schizophrenia in a general population sample.
The sample was the Northern Finland 1966 Birth Cohort. In 1999–2001, structural brain MRI and measures of clinical and functional outcomes were analysed for 54 individuals with schizophrenia around the age of 34. Sex, total grey matter, duration of illness and the use of antipsychotic medication were used as covariates.
After controlling for multiple covariates, increased density of the left limbic area was associated with less hospitalisations and increased total white matter volume with being in remission. Higher density of left frontal grey matter was associated with not being on a disability pension and higher density of the left frontal lobe and left limbic area were related to better functioning. Higher density of the left limbic area was associated with better longitudinal course of illness.
This study, based on unselected general population data, long follow-up and an extensive database, confirms findings of previous studies, that morphological abnormalities in several brain structures are associated with outcome. The difference in brain morphology in patients with good and poor outcomes may reflect separable aetiologies and developmental trajectories in schizophrenia.
Recent studies have shown that cannabis use acts as a specific risk factor provoking the onset of psychosis in vulnerable individuals. Association of adolescent cannabis use and psychosis risk was studied after adjustment with prodromal symptoms.
To assess possible causality between cannabis use and the risk of psychosis.
To examine associations between cannabis use and the risk of psychosis in 10 years follow-up while taking into account the prodromal symptoms of psychosis in a prospective general population sample.
The sample (N=6258) composed of a prospective Northern Finland Birth Cohort 1986. Questionnaire on prodromal symptoms for psychosis (PROD-screen) and on drug use was conducted when the cohort members were 15-16 years old. The participants were asked if they had tried cannabis: never, once, 2-4 times, 5 times or more. Information on psychoses was gathered from registers until age 27 years.
In total 102 new psychoses emerged. The proportion of psychoses in the groups 'never”, 'once”, '2-4 times”, '5 times or more” were 1.5%, 2.8%, 3.6%, and 8.5%, respectively. The hazard ratio (HR) for risk of psychosis in subjects who had tried cannabis 5 times or more was 5.9 (95% CI 2.4-14.4) when compared to non-users. The association remained statistically significant when adjusted for prodromal symptoms and parental psychosis (HR 2.6, 1.0-6.6). When gender and smoking was taken into account association was no longer significant (HR 2.3, 0.9-6.0).
Adolescent cannabis use associates with increased risk of first-episode psychosis even after controlling for baseline prodromal symptoms.
There are limited amount of studies comparing time trends of incidence and risk factors of psychosis.
To compare time trends of incidence of psychosis in two population samples.
To study 1) onset age and cumulative incidence of psychoses in two Northern Finland Birth Cohorts (NFBC), 2) changes in type of diagnosis and risk factors.
The NFBC 1966 (N=12,058) and NFBC 1986 (N=9,432) are prospective cohorts of the two provinces of Finland with the live born children followed since pregnancy. The data for psychosis and risk factors were collected from variety of nationwide registers and earlier collected data of the NFBCs. The follow-up time was in both cohorts in average 26.5 years.
Proportion of all psychoses was higher in NFBC 1986 than in the NFBC 1966 (1.81% vs 1.0%). There were more affective psychoses in NFBC 1986 (0.5% vs 0.1%), but incidence of schizophrenia was the same (0.4%) in both cohorts. The age of onset was lower in NFBC 1986 than in NFBC 1966 and majority of this cases were females. Only parental psychosis was a significant risk factor predicting psychosis (Hazard Ratios >3.0) in both cohorts.
In conclusion, two birth cohorts within 20 years covering altogether about 40 years showed changes in terms of incidence, age of onset, and type of psychosis.
The effects of long-term antipsychotic medication on cognition in schizophrenia are unclear (Husa A.P. et al., Schizophr. Res. 2014).
Understanding how long-term antipsychotic treatment affects cognition is crucial for the development of safe, evidence-based treatment of schizophrenia.
To analyse the association between cumulative lifetime antipsychotic dose and cognition in schizophrenia at age 43 years in a general population sample.
Sixty (33 males) schizophrenia spectrum subjects from the Northern Finland Birth Cohort 1966 were assessed at age 43 years by California Verbal Learning Test, Visual Object Learning Test, Abstraction Inhibition and Working Memory task, Verbal fluency, Visual series, Vocabulary, Digit Span and Matrix reasoning. Cumulative lifetime antipsychotic dose-years were collected from treatment records and interviews. A factor analysis based on the cognitive tests resulted in one cognitive factor. The association between this cognitive composite score and antipsychotic dose-years was analysed by linear regression.
Higher lifetime antipsychotic dose-years were statistically significantly associated with poorer cognitive composite score at age 43 years (B=-0.32, p>0.001), also when adjusted for gender, onset age, remission and number of hospital treatment days (B=-0.42, p=0.008).
To our knowledge, this is the first report of an association between cumulative lifetime antipsychotic dose and cognition in midlife in schizophrenia. Based on this data, the use of high antipsychotic doses may relate to poorer cognitive functioning in schizophrenia after twenty years of illness. These results do not support the view that antipsychotics prevent cognitive decline or promote cognitive recovery in schizophrenia.
Though neurocognitive dysfunctions are common in schizophrenia, the course and predictors of change of cognition remain uncertain.
To understand the longitudinal changes and their predictors in cognition, which is important for the etiological investigation of schizophrenia.
Aims. To analyse if premorbid school performance, age of illness onset and the severity of illness predicts change in cognition in schizophrenia in a general population sample.
The sample included cases with schizophrenia spectrum disorder from the Northern Finland 1966 Birth Cohort. Data on school marks at age 16 yearsand severity of symptoms and occupational functioning around first episode and after years of illness were gained from national registers, hospital notes and interviews. Verbal and visual memory and executive functioning were measured twice, at ages 34 and 43 years. The number of cases varied in analyses from 29 to 41, depending on the analysed cognitive test.
Association between lower school marks at age 16-years and decrease in executive functioning (p=0.032) and visual learning and memory (p=0.039) was found, even when adjusted by age of illness onset and cognitive functioning at age 34-years. Change of cognition was not predicted by severity of symptoms nor occupational functioning. Male gender associated to decrease of executive functioning (p=0.032) and earlier age of illness onset to decrease of visual learning and memory (p=0.045).
School performance at age 16 years associates to later longitudinal change of cognition. Based on our results, later cognitive functioning may reflect the evolution of schizophrenia illness.
Our aim was to investigate how age of achieving early motor developmental milestones differ among subjects with and without a history of parental psychosis and whether parental psychosis may alter the effects of the age of achievement on the risk of schizophrenia.
The study sample comprised 10,307 individuals from the prospective Northern Finland Birth Cohort 1966. A total of 139 (1.3%) cohort members suffered from schizophrenia by the age of 46 years. Out of them 19 (13.7%) had a parent with a history of psychosis, while among the non-psychotic cohort members this figure was 524 (5.2%).
Out of eight different motor milestones investigated, parental psychosis associated (p>0.05) with later learning of holding head up, grabbing object, and walking without support. In the parental psychosis group, significant risk factors for schizophrenia included later learning of holding head up and touching thumb with index finger. In the non-parental psychosis group risk estimates were lower and statistical significant milestones were different i.e. turning over, sitting without support, standing up, standing and walking without support. Interactions between parental psychosis and touching thumb with index finger and walking without support was found.
Although parental psychosis associated with delays in motor milestones in the first year of life, it does not explain the association between late achievement of motor milestones and later risk for schizophrenia
Higher lifetime antipsychotic exposure has been associated with poorer cognition in schizophrenia. The cognitive effects of adjunctive psychiatric medications and lifetime trends of antipsychotic use remain largely unclear. We aimed to study how lifetime and current benzodiazepine and antidepressant medications, lifetime trends of antipsychotic use and antipsychotic polypharmacy are associated with cognitive performance in midlife schizophrenia.
Sixty participants with DSM-IV schizophrenia from the Northern Finland Birth Cohort 1966 were examined at 43 years of age with an extensive cognitive test battery. Cumulative lifetime and current use of psychiatric medications were collected from medical records and interviews. The associations between medication and principal component analysis-based cognitive composite score were analysed using linear regression.
Lifetime cumulative DDD years of benzodiazepine and antidepressant medications were not significantly associated with global cognition. Being without antipsychotic medication (for minimum 11 months) before the cognitive examination was associated with better cognitive performance (P = 0.007) and higher lifetime cumulative DDD years of antipsychotics with poorer cognition (P = 0.020), when adjusted for gender, onset age and lifetime hospital treatment days. Other lifetime trends of antipsychotic use, such as a long antipsychotic-free period earlier in the treatment history, and antipsychotic polypharmacy, were not significantly associated with cognition.
Based on these naturalistic data, low exposure to adjunctive benzodiazepine and antidepressant medications does not seem to affect cognition nor explain the possible negative effects of high dose long-term antipsychotic medication on cognition in schizophrenia.
Delayed motor development in infancy and family history of psychosis are both associated with increased risk of schizophrenia, but their interaction is largely unstudied.
To investigate the association of the age of achieving motor milestones and parental psychosis and their interaction in respect to risk of schizophrenia.
We used data from the general population-based prospective Northern Finland Birth Cohort 1966 (n = 10,283). Developmental information of the cohort members was gathered during regular visits to Finnish child welfare clinics. Several registers were used to determine the diagnosis of schizophrenia among the cohort members and psychosis among the parents. Altogether 152 (1.5%) individuals had schizophrenia by the age of 46 years, with 23 (15.1%) of them having a parent with psychosis. Cox regression analysis was used in analyses.
Parental psychosis was associated (P < 0.05) with later achievement of holding the head up, grabbing an object, and walking without support. In the parental psychosis group, the risk for schizophrenia was increased if holding the head up (hazard ratio [HR]: 2.46; degrees of freedom [df] = 1; 95% confidence interval [95% CI]: 1.07–5.66) and touching the thumb with the index finger (HR: 1.84; df = 1; 95% CI: 1.11–3.06) was later. In the group without parental psychosis, a delay in the following milestones increased the risk of schizophrenia: standing without support and walking without support. Parental psychosis had an interaction with delayed touching thumb with index finger (HR: 1.87; df = 1; 95% CI: 1.08–3.25) when risk of schizophrenia was investigated.
Parental psychosis was associated with achieving motor milestones later in infancy, particularly the milestones that appear early in a child's life. Parental psychosis and touching the thumb with the index finger had a significant interaction on risk of schizophrenia. Genetic risk for psychosis may interact with delayed development to raise future risk of schizophrenia, or delayed development may be a marker of other risk processes that interact with genetic liability to cause later schizophrenia.
Email your librarian or administrator to recommend adding this to your organisation's collection.