Evidence map›Paper›PMID 28265119›Full record

Trial reportMolecular psychiatry2018

Evidence for neuroplastic compensation in the cerebral cortex of persons with depressive illness.

R Bansal, D J Hellerstein, B S Peterson

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
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  5. Pretreatment and early-treatment cortical thickness is associated with SSRI treatment response in major depressive disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Trial
  6. Review
  7. Article
  8. Female chronic social defeat stress (Frontiers in systems biology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Neural plasticity and depression treatment.IBRO neuroscience reports · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

3 authors at 3 institutions in 1 country.

R BansalInstitute for the Developing Mind, Children's Hospital, Los Angeles, Los Angeles, CA, USA.
D J HellersteinDepression Evaluation Service, Division of Clinical Therapeutics, New York State Psychiatric Institute, New York, NY, USA.
B S PetersonInstitute for the Developing Mind, Children's Hospital, Los Angeles, Los Angeles, CA, USA.
Children's Hospital of Los Angeles · USNew York Psychoanalytic Society and Institute · USUniversity of Southern California · US

Funding

MRI IN CHILDHOOD NEUROPSYCHIATRIC DISORDERSK02MH074677 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PETERSON, BRADLEY S · 2005 to 2009
$614k
NIMH NIH HHS K02 MH074677
6 · The paper itself

Abstract

We yoked anatomical brain magnetic resonance imaging to a randomized, double-blind, placebo-controlled trial (RCT) of antidepressant medication for 10-week's duration in patients with dysthymia. The RCT study design mitigated ascertainment bias by randomizing patients to receive either duloxetine or placebo, and it supported true causal inferences about treatment effects on the brain by controlling treatment assignment experimentally. We acquired 121 anatomical scans: at baseline and end point in 41 patients and once in 39 healthy controls. At baseline, patients had diffusely thicker cortices than did healthy participants, and patients who had thicker cortices had proportionately less severe symptoms. During the trial, symptoms improved significantly more in medication-compared with placebo-treated patients; concurrently, thicknesses in medication-treated patients declined toward values in healthy controls, but they increased slightly, away from control values, in placebo-treated patients. Changes in symptom severity during the trial mediated the association of treatment assignment with the change in thickness, suggesting that the beneficial effects of medication on symptom severity were at least partially responsible for normalizing cortical thickness. Together our findings suggest that baseline cortical hypertrophy in medication-free patients likely represented a compensatory, neuroplastic response that attenuated symptom severity. Medication then reduced symptoms and lessened the need for compensation, thereby normalizing thickness. This is to the best of our knowledge the first study to report within an RCT a differential change in cortical morphology during medication treatment for depressive illness and the first to provide within an RCT in vivo evidence for the presence of neuroanatomical plasticity in humans.

Indexed as

AdultAntidepressive AgentsBrainCerebral CortexDepressive DisorderDouble-Blind MethodDuloxetine HydrochlorideDysthymic DisorderFemaleHumansMagnetic Resonance ImagingMajor Depressive DisorderMaleMiddle AgedNeuroimagingNeuronal PlasticityAntidepressive AgentsDuloxetine Hydrochloride

Identifiers

PMID28265119
PMCPMC5589468
OpenAlexW2592641565

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.