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Self-reported psychotic experiences (SRPE) by individuals from the general population are often unconfirmed by clinical interview and referred to as ‘false-positive’ (FP) SRPE. FP SRPE have been suggested to represent the mildest form of risk along the extended psychosis continuum. However, little is known about their (clinical) outcome and evolution over time. Aims of this study were to prospectively examine, in individuals with FP SRPE, (1) the prevalence of remission, persistence and transition to validated PE at 3-year follow-up; (2) potential baseline psychopathological and psychosocial predictors of persistence of FP SRPE and transition to validated PE; and (3) whether those with persistent FP SRPE and validated PE already differed on psychopathology and psychosocial factors at baseline. We tested the hypotheses that (i) individuals with FP SRPE would be more likely to have SRPE and validated PE at follow-up; and (ii) that FP SRPE would be predictive of lower functioning and more psychopathology and help-seeking behaviour at follow-up.
Baseline (n = 6646) and 3-year follow-up (n = 5303) data of the second the Netherlands Mental Health Survey and Incidence Study (NEMESIS-2), a general population research project on prevalence, incidence, course and consequences of psychiatric disorders was used. Self-report of PE was followed by clinical interview to determine clinical validity. The presence of mood, anxiety and substance use disorders, childhood adversity, help-seeking and functioning as well as PE characteristics (number, frequency, distress and impact) were used in the analyses which included only individuals with complete data for both assessments waves (n = 4683).
At baseline, 454 participants had any FP SRPE; of these 372 participants had complete follow-up data available. Those with baseline FP SRPE were significantly more likely to report SRPE (OR = 3.58; 95% CI 2.38–5.40, p < 0.001) and validated PE (OR = 6.26; 95% CI 3.91–10.02, p < 0.001) at follow-up. Baseline FP SRPE also predicted the presence of mood and anxiety disorders, reduced functioning and help-seeking at follow-up. Several baseline psychopathological, psychosocial and PE characteristics were predictive for the persistence of SRPE. These factors also differentiated groups with FP SRPE or validated PE from those with remitted FP SRPE at follow-up.
‘FP SRPE’ are not truly ‘false’ as they index risk for the development of clinically relevant psychotic symptoms, development of mood and anxiety disorders and reduced functioning. Self-reported PE, even unconfirmed, warrant ‘watchful waiting’ and follow-up over time, especially when they are reported by individuals with reduced psychosocial functioning and general psychiatric problems.
Childhood maltreatment (CM) may modify the relationship between major depressive disorder (MDD) and hippocampal volume reduction. To disentangle the impact of MDD and CM on hippocampal volume we investigated the association between MDD and hippocampal volume in persons with and without a history of CM in two independent cohorts.
We used data of 262 participants from the Netherlands Study of Depression and Anxiety (NESDA) (mean age 37 years, 32% male) and 636 participants from the SMART-Medea study (mean age 61 years, 81% male). In both studies a 12-month diagnosis of MDD and CM were assessed using a diagnostic interview. Hippocampal volume was measured in NESDA using FreeSurfer software on 3-T magnetic resonance (MR) images and in SMART it was manually outlined on 1.5-T MR images. With analysis of covariance adjusted for intracranial volume, age, gender and lifestyle factors we estimated the effects of MDD and CM on hippocampal volume.
In both cohorts CM was not significantly associated with hippocampal volume. After pooling the data MDD was associated with smaller hippocampal volume (B = −138.90 mm3, p = 0.05) and the interaction between MDD and CM reached significance (p = 0.04); in participants with CM, MDD was related to smaller hippocampal volume (NESDA: B = −316.8 mm3, p = 0.02; SMART: B = −407.6, p = 0.046), but not in participants without CM (p > 0.05).
Our study shows that in two independent cohorts, particularly in individuals with CM, a diagnosis of MDD is related to smaller hippocampal volume. Prospective studies are needed to further determine through which mechanism CM may amplify the relationship between MDD and hippocampal volume.
Depressive symptoms and cognitive impairment often co-occur, but their interactive relationship is complex and the direction of causation is still a topic of research. We examined the influence of cognitive performance on the course of depressive symptoms during 7 years of follow-up in patients with vascular disease.
Within the SMART-MR study, 736 patients (mean age 62 ± 10 years) had neuropsychological assessment on four cognitive domains at baseline [memory (MEM), working memory (WMEM), executive functioning (EXEC), and information processing speed (SPEED)]. Depressive symptoms were assessed with the Patient Health Questionnaire-9 (PHQ-9) at baseline and every 6 months during 7 years of follow-up. Generalized Estimating Equation (GEE) models were used to assess the association between cognitive performance with depressive symptoms at multiple time points during follow-up. Interaction terms between the respective cognitive domains and time was included to examine if the course of depressive symptoms differed according to baseline cognitive performance.
The GEE analyses showed no significant interactions between the respective cognitive domains and time indicating no different course of depressive symptoms according to baseline cognitive performance. Lower MEM, EXEC or SPEED, but not WMEM performance, was significantly associated with more depressive symptoms during follow-up per z score decrease: MEM [B = 0.70, 95% confidence interval (CI) 0.35–1.05]; EXEC (B = 0.88, 95% CI 0.41–1.36), and SPEED (B = 0.57, 95% CI 0.21–0.92).
Poorer cognitive performance on the domains MEM, EXEC and SPEED, but not WMEM, was associated with higher levels of depressive symptoms over 7 years of follow-up, but not with a different course of depressive symptoms over time.
The ‘vascular depression’ hypothesis states that brain changes located in frontal-subcortical pathways increase vulnerability for specific depressive symptom profiles, but studies examining locations of small-vessel and degenerative changes with individual symptoms are scarce. We examined whether location and progression of white-matter lesions (WMLs), lacunar infarcts and atrophy were associated with motivational and mood symptoms in patients with symptomatic atherosclerotic disease.
In 578 patients [63 (s.d.=8) years] of the Second Manifestations of ARTerial disease (SMART)-Medea study, volumes of WMLs and atrophy and visually rated infarcts were obtained with 1.5 T magnetic resonance imaging at baseline and after 3.9 (s.d.=0.4) years' follow-up. Depressive symptoms were assessed with Patient Health Questionnaire-9 at follow-up and categorized into motivational and mood symptoms.
Regression analyses adjusted for age, gender, education, Mini-Mental State Examination, physical functioning, antidepressant use and vascular risk factors showed that location in mainly deep white-matter tracts and progression of WMLs were associated with symptoms of anhedonia, concentration problems, psychomotor retardation and appetite disturbance. Lacunar infarcts in deep white matter were associated with greater motivational [Incidence rate ratio (IRR) 1.7, 95% confidence interval (CI) 1.2–2.4] and mood (IRR 1.7, 95% CI 1.1–2.6) sumscores, and with symptoms of psychomotor retardation, energy loss and depressed mood; lacunar infarcts in the thalamus were associated with psychomotor retardation only. Cortical atrophy was associated with symptoms of anhedonia and appetite disturbance. Excluding patients with major depression did not materially change the results.
Our findings suggest that disruption of frontal-subcortical pathways by small-vessel lesions leads to a symptom profile that is mainly characteristic of motivational problems, also in the absence of major depression.
We report on the status of the R&D for a digital Time Projection Chamber based on Micromegas detectors using the CMOS chip TimePix as a direct readout anode protected by highly resistive a-Si:H layer. A small chamber was built as a demonstrator of the 2-D and 3-D imaging capabilities of this technique. We illustrate the new capabilities of this detector for x-ray observation with data taken from radioactive sources. This small TPC is a very useful tool both for studying gas properties thanks to its good efficiency for single electrons, and for reconstructing photoelectron direction for use as a soft x-ray polarimeter.
It has recently been proposed that major depression disorder (MDD) may, in a heterogeneous population-based cohort, be interpreted in terms of a random-mood model. Mood fluctuations are thought to result from stressors that occur randomly in time. We have investigated whether this concept also holds for more homogeneous groups, defined by known determinants for MDD, and whether the model's parameters, susceptibility (Z) and relaxation time (T), may be evaluated and used to differentiate between subcohorts.
From a large epidemiological survey, the Netherlands Mental Health Survey and Incidence Study (NEMESIS), data on the duration of MDD were obtained for subcohorts, based on gender, severity of depression, recurrence and co-morbidity with dysthymia, anxiety and somatic disorder, and were compared with random-mood simulation calculations.
Susceptibility, Z, is empirically found to be proportional to incidence and may be identified with a risk ratio. A second scaling rule states the proportionality of mean duration with the product of Z and T. This Z–T classification proves to be more sensitive than conventional significance tests. Notably for men/women and for co-morbid anxiety, differences are seen that have previously gone unnoticed.
Depression may be conceptualized as a disorder resulting from random-mood fluctuations, the response to which is influenced by a large variety of determinants or risk factors. The model's parameters can be evaluated and may be used in differentiating between risk factor-defined subgroups.
Previous reports on the incidence of schizophrenia in immigrant groups to The Netherlands were based on hospital data.
To compare the incidence of psychotic disorders in the immigrant groups to that in natives.
Two-year first-contact incidence study in The Hague.
The risks of schizophrenia, schizophreniform or schizoaffective disorder (DSM–IV criteria) were increased for subjects born in Morocco (gender and age-adjusted relative risk=4.5; 95% CI 1.4–8.5), Surinam (relative risk=3.2; 1.8–5.7), The Netherlands Antilles (relative risk=2.9; 0.9–9.5) and other non-Western countries (relative risk=2.4; 1.3–4.7). This risk was also increased for Moroccans (relative risk=8.0; 2.6–24.5) and Surinamese (relative risk=5.5; 2.5–11.9) of the second generation. The risks for Turkish immigrants, first or second generation, and for immigrants from Western countries were not significantly increased.
This study indicates that the incidence of schizophrenia is increased in several, but not all, immigrant groups to The Netherlands. It is possible that factors associated with a process of rapid westernisation precipitate schizophrenia in people who are genetically at risk.
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