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- Abé, Christoph, et al.
(author)
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Cortical thickness, volume and surface area in patients with bipolar disorder types I and II.
- 2016
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In: Journal of psychiatry & neuroscience : JPN. - : CMA Joule Inc.. - 1488-2434 .- 1180-4882. ; 41:4, s. 240-50
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Journal article (peer-reviewed)abstract
- Bipolar disorder (BD) is a common chronic psychiatric disorder mainly characterized by episodes of mania, hypomania and depression. The disorder is associated with cognitive impairments and structural brain abnormalities, such as lower cortical volumes in primarily frontal brain regions than healthy controls. Although bipolar disorder types I (BDI) and II (BDII) exhibit different symptoms and severity, previous studies have focused on BDI. Furthermore, the most frequently investigated measure in this population is cortical volume. The aim of our study was to investigate abnormalities in patients with BDI and BDII by simultaneously analyzing cortical volume, thickness and surface area, which yields more information about disease- and symptom-related neurobiology.
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| 3. |
- Abé, Christoph, et al.
(author)
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Longitudinal Cortical Thickness Changes in Bipolar Disorder and the Relationship to Genetic Risk, Mania, and Lithium Use.
- 2020
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In: Biological psychiatry. - : Elsevier BV. - 1873-2402 .- 0006-3223. ; 87:3, s. 271-281
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Journal article (peer-reviewed)abstract
- Bipolar disorder (BD) is a highly heritable psychiatric disorder characterized by episodes of manic and depressed mood states and associated with cortical brain abnormalities. Although the course of BD is often progressive, longitudinal brain imaging studies are scarce. It remains unknown whether brain abnormalities are static traits of BD or result from pathological changes over time. Moreover, the genetic effect on implicated brain regions remains unknown.Patients with BD and healthy control (HC) subjects underwent structural magnetic resonance imaging at baseline (123 patients, 83 HC subjects) and after 6 years (90 patients, 61 HC subjects). Cortical thickness maps were generated using FreeSurfer. Using linear mixed effects models, we compared longitudinal changes in cortical thickness between patients with BD and HC subjects across the whole brain. We related our findings to genetic risk for BD and tested for effects of demographic and clinical variables.Patients showed abnormal cortical thinning of temporal cortices and thickness increases in visual/somatosensory brain areas. Thickness increases were related to genetic risk and lithium use. Patients who experienced hypomanic or manic episodes between time points showed abnormal thinning in inferior frontal cortices. Cortical changes did not differ between diagnostic BD subtypes I and II.In the largest longitudinal BD study to date, we detected abnormal cortical changes with high anatomical resolution. We delineated regional effects of clinical symptoms, genetic factors, and medication that may explain progressive brain changes in BD. Our study yields important insights into disease mechanisms and suggests that neuroprogression plays a role in BD.
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| 4. |
- Abé, Christoph, et al.
(author)
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Manic episodes are related to changes in frontal cortex: a longitudinal neuroimaging study of bipolar disorder 1.
- 2015
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In: Brain : a journal of neurology. - : Oxford University Press (OUP). - 1460-2156. ; 138:Pt 11, s. 3440-8
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Journal article (peer-reviewed)abstract
- Higher numbers of manic episodes in bipolar patients has, in cross-sectional studies, been associated with less grey matter volume in prefrontal brain areas. Longitudinal studies are needed to determine if manic episodes set off progressive cortical changes, or if the association is better explained by premorbid brain conditions that increase risk for mania. We followed patients with bipolar disorder type 1 for 6 years. Structural brain magnetic resonance imaging scans were performed at baseline and follow-up. We compared patients who had at least one manic episode between baseline and follow-up (Mania group, n = 13) with those who had no manic episodes (No-Mania group, n = 18). We used measures of cortical volume, thickness, and area to assess grey matter changes between baseline and follow-up. We found significantly decreased frontal cortical volume (dorsolateral prefrontal and inferior frontal cortex) in the Mania group, but no volume changes in the No-Mania group. Our results indicate that volume decrease in frontal brain regions can be attributed to the incidence of manic episodes.
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| 6. |
- Balter, Leonie J. T., et al.
(author)
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Experimental Sleep Deprivation Results in Diminished Perceptual Stability Independently of Psychosis Proneness
- 2022
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In: Brain Sciences. - : MDPI AG. - 2076-3425. ; 12:10
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Journal article (peer-reviewed)abstract
- Psychotic disorders as well as psychosis proneness in the general population have been associated with perceptual instability, suggesting weakened predictive processing. Sleep disturbances play a prominent role in psychosis and schizophrenia, but it is unclear whether perceptual stability diminishes with sleep deprivation, and whether the effects of sleep deprivation differ as a function of psychosis proneness. In the current study, we aimed to clarify this matter. In this preregistered study, 146 participants successfully completed an intermittent version of the random dot kinematogram (RDK) task and the 21-item Peters Delusion Inventory (PDI-21) to assess perceptual stability and psychosis proneness, respectively. Participants were randomized to sleep either as normal (8 to 9 h in bed) (n = 72; Mage = 24.7, SD = 6.2, 41 women) or to stay awake through the night (n = 74; Mage = 24.8, SD = 5.1, 44 women). Sleep deprivation resulted in diminished perceptual stability, as well as in decreases in perceptual stability over the course of the task. However, we did not observe any association between perceptual stability and PDI-21 scores, nor a tendency for individuals with higher PDI-21 scores to be more vulnerable to sleep-deprivation-induced decreases in perceptual stability. The present study suggests a compromised predictive processing system in the brain after sleep deprivation, but variation in psychosis trait is not related to greater vulnerability to sleep deprivation in our dataset. Further studies in risk groups and patients with psychosis are needed to evaluate whether sleep loss plays a role in the occurrence of objectively measured perceptual-related clinical symptoms.
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| 7. |
- Balter, Leonie J. T., et al.
(author)
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Intelligence predicts better cognitive performance after normal sleep but larger vulnerability to sleep deprivation
- 2023
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In: Journal of Sleep Research. - : John Wiley & Sons. - 0962-1105 .- 1365-2869. ; 32:4
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Journal article (peer-reviewed)abstract
- Fluid intelligence is seen as a beneficial attribute, protecting against stress and ill-health. Whether intelligence provides resilience to the cognitive effects of insufficient sleep was tested in the current pre-registered experimental study. Participants (N = 182) completed the Raven's test (measuring fluid intelligence) and a normal night of sleep or a night of total sleep deprivation. Sleepiness and four cognitive tests were completed at 22:30 hours (baseline), and the following day after sleep manipulation. At baseline, higher fluid intelligence was associated with faster and more accurate arithmetic calculations, and better episodic memory, but not with spatial working memory, simple attention or sleepiness. Those with higher fluid intelligence were more, not less, impacted by sleep deprivation, evident for arithmetic ability, episodic memory and spatial working memory. We need to establish a more nuanced picture of the benefits of intelligence, where intelligence is not related to cognitive advantages in all situations.
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| 8. |
- Bayard, Frida, et al.
(author)
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Emotional Instability Relates to Ventral Striatum Activity During Reward Anticipation in Females
- 2020
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In: Frontiers in Behavioral Neuroscience. - : Frontiers Media S.A.. - 1662-5153. ; 14
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Journal article (peer-reviewed)abstract
- Both non-emotional symptoms, such as inattention, and symptoms of emotional instability (EI) are partially co-varying and normally distributed in the general population. Attention Deficit Hyperactivity Disorder (ADHD), which is associated with both inattention and emotional instability, has been related to lower reward anticipation activation in the ventral striatum. However, it is not known whether non-emotional dysregulation, such as inattention, or EI-or both-are associated with this effect. We hypothesized that altered reward processing relates specifically to EI. To test this, 29 healthy participants were recruited to this functional MRI study (n= 15 females). Reward processing was studied using a modified version of the Monetary Incentive Delay (MID) task. Brown Attention-Deficit Disorder Scales questionnaire was used to assess EI and inattention symptoms on a trait level. We observed less ventral striatal activation during reward anticipation related to the EI trait in females, also when controlling for the inattention trait, but not in the whole sample or males only. Our study suggests the existence of sex differences in the relationship between reward processing and EI/inattention traits.
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| 9. |
- Bejerot, Susanne, 1955-, et al.
(author)
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Study protocol for a randomized controlled trial with rituximab for psychotic disorder in adults (RCT-Rits)
- 2023
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In: BMC Psychiatry. - : BioMed Central (BMC). - 1471-244X. ; 23:1
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Journal article (peer-reviewed)abstract
- BACKGROUND: The role of inflammation in the aetiology of schizophrenia has gained wide attention and research on the association shows an exponential growth in the last 15 years. Autoimmune diseases and severe infections are risk factors for the later development of schizophrenia, elevated inflammatory markers in childhood or adolescence are associated with a greater risk of schizophrenia in adulthood, individuals with schizophrenia have increased levels of pro-inflammatory cytokines compared to healthy controls, and autoimmune diseases are overrepresented in schizophrenia. However, treatments with anti-inflammatory agents are so far of doubtful clinical relevance. The primary objective of this study is to test whether the monoclonal antibody rituximab, directed against the B-cell antigen CD20 ameliorates psychotic symptoms in adults with schizophrenia or schizoaffective disorder and to examine potential mechanisms. A secondary objective is to examine characteristics of inflammation-associated psychosis and to identify pre-treatment biochemical characteristics of rituximab responders. A third objective is to interview a subset of patients and informants on their experiences of the trial to obtain insights that rating scales may not capture.METHODS: A proof-of-concept study employing a randomised, parallel-group, double-blind, placebo-controlled design testing the effect of B-cell depletion in patients with psychosis. 120 participants with a diagnosis of schizophrenia spectrum disorders (SSD) (ICD-10 codes F20, F25) will receive either one intravenous infusion of rituximab (1000 mg) or saline. Psychiatric measures and blood samples will be collected at baseline, week 12, and week 24 post-infusion. Brief assessments will also be made in weeks 2 and 7. Neuroimaging and lumbar puncture, both optional, will be performed at baseline and endpoints. Approximately 40 of the patients and their informants will be interviewed for qualitative analyses on the perceived changes in well-being and emotional qualities, in addition to their views on the research.DISCUSSION: This is the first RCT investigating add-on treatment with rituximab in unselected SSD patients. If the treatment is helpful, it may transform the treatment of patients with psychotic disorders. It may also heighten the awareness of immune-psychiatric disorders and reduce stigma.TRIAL REGISTRATION: NCT05622201, EudraCT-nr 2022-000220-37 version 2.1. registered 14th of October 2022.
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| 10. |
- Borg Skoglund, Lotta, et al.
(author)
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ADHD hos vuxna – historia, epidemiologi och neurobiologi : [ADHD in adults - history, epidemiology, and neuroscience]
- 2022
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In: Läkartidningen. - : Läkartidningen Förlag AB. - 0023-7205 .- 1652-7518. ; 119:8
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Journal article (peer-reviewed)abstract
- ADHD beskrivs i litteraturen från 1700-talet. Diagnosen har förändrats i takt med reviderade diagnossystem.ADHD är vanligt och förekommer hos 5–7 procent av ungdomar och 2–3 procent av vuxna.ADHD beror på en kombination av genetiska och miljömässiga faktorer.De strukturella och funktionella skillnader som påvisas i hjärnan vid ADHD används inte i diagnostiskt syfte.ADHD är en dimensionell diagnos, och även personer med »subtröskel-problematik« uppvisar symtom och funktionsnedsättning.Odiagnostiserad och obehandlad ADHD riskerar att ge allvarliga konsekvenser för individen och stora kostnader för samhället.ADHD kan behandlas säkert och effektivt hos de flesta vuxna.
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