Evidence map›Paper›PMID 26645741›Full record

ArticleJournal of psychiatry & neuroscience : JPN2016

Cortical thickness, volume and surface area in patients with bipolar disorder types I and II.

Christoph Abé, Carl-Johan Ekman, Carl Sellgren, Predrag Petrovic, Martin Ingvar, Mikael Landén

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
10.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.

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  20. Lithium rescues dendritic abnormalities in Ank3 deficiency models through the synergic effects of GSK3β and cyclic AMP signaling pathways.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Christoph AbéFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
Carl-Johan EkmanFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
Carl SellgrenFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
Predrag PetrovicFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
Martin IngvarFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
Mikael LandénFrom the Departments of Clinical Neuroscience (Abé, Ekman, Petrovic, Ingvar, Landén), Physiology and Pharmacology (Sellgren), and Medical Epidemiology and Biostatistics (Landén), Karolinska Institutet, Stockholm, Sweden; and the Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the Gothenburg University, Gothenburg, Sweden (Landén).
University of Gothenburg · SECenter for Neurosciences · USKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBipolar 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.

methodsWe used MRI to measure cortical volume, thickness and area in patients with BDI and BDII as well as in healthy controls. The large study cohort enabled us to adjust for important confounding factors.

resultsWe included 81 patients with BDI, 59 with BDII and 85 controls in our analyses. Cortical volume, thickness and surface area abnormalities were present in frontal, temporal and medial occipital regions in patients with BD. Lithium and antiepileptic drug use had an effect on the observed differences in medial occipital regions. Patients with the subtypes BDI and BDII displayed common cortical abnormalities, such as lower volume, thickness and surface area than healthy controls in frontal brain regions but differed in temporal and medial prefrontal regions, where only those with BDI had abnormally low cortical volume and thickness. LIMITATIONS: The group differences can be explained by progressive changes, but also by premorbid conditions. They could also have been influenced by unknown factors, such as social, environmental or genetic factors.

conclusionOur findings suggest diagnosis-related neurobiological differences between the BD subtypes, which could explain distinct symptoms and point to potential biomarkers that could inform the subtype diagnosis of BD.

Indexed as

AdultAnticonvulsantsAntidepressive AgentsBipolar DisorderBrain DiseasesCase-Control StudiesCerebral CortexFemaleHumansLithium CompoundsMagnetic Resonance ImagingMaleOrgan SizeSex DistributionAnticonvulsantsAntidepressive AgentsLithium Compounds

Identifiers

PMID26645741
PMCPMC4915933
OpenAlexW2411759106

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.