Evidence map›Paper›PMID 36199368›Full record

ArticleInternational journal of clinical and health psychology : IJCHP

Association of Mu opioid receptor (A118G) and BDNF (G196A) polymorphisms with rehabilitation-induced cortical inhibition and analgesic response in chronic osteoarthritis pain.

Fernanda de Toledo Gonçalves, Kevin Pacheco-Barrios, Ingrid Rebello-Sanchez, Luis Castelo-Branco, Paulo S de Melo, Joao Parente, Alejandra Cardenas-Rojas, Isabela Firigato, Anne Victorio Pessotto, Marta Imamura and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of clinical and health psychology : IJCHP. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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  10. A Preliminary Prospective Study on the Association of Polymorphisms inCancer control : journal of the Moffitt Cancer Center
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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

13 authors at 4 institutions in 3 countries.

Fernanda de Toledo GonçalvesDepartamento de Medicina Legal, Ética Médica e Medicina Social e do Trabalho, Laboratório de Imunohematologia e Hematologia Forense (LIM40), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC da FMUSP), São Paulo, Brazil.
Kevin Pacheco-BarriosNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Ingrid Rebello-SanchezNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Luis Castelo-BrancoNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Paulo S de MeloNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Joao ParenteNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Alejandra Cardenas-RojasNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Isabela FirigatoDepartamento de Medicina Legal, Ética Médica e Medicina Social e do Trabalho, Laboratório de Imunohematologia e Hematologia Forense (LIM40), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC da FMUSP), São Paulo, Brazil.
Anne Victorio PessottoDepartamento de Medicina Legal, Ética Médica e Medicina Social e do Trabalho, Laboratório de Imunohematologia e Hematologia Forense (LIM40), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC da FMUSP), São Paulo, Brazil.
Marta ImamuraInstituto de Medicina Física e Reabilitação, Hospital das Clinicas HCFMUSP, Universidade de São Paulo, São Paulo, Brazil.
Marcel SimisInstituto de Medicina Física e Reabilitação, Hospital das Clinicas HCFMUSP, Universidade de São Paulo, São Paulo, Brazil.
Linamara BattistellaInstituto de Medicina Física e Reabilitação, Hospital das Clinicas HCFMUSP, Universidade de São Paulo, São Paulo, Brazil.
Felipe FregniNeuromodulation Center and Center for Clinical Research Learning, Spaulding Rehabilitation Hospital and Massachusetts General Hospital, Harvard Medical School, Boston, USA.
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRMassachusetts General Hospital · USSpaulding Rehabilitation Hospital · USUniversidad San Ignacio de Loyola · PE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/objective: Chronic pain due to osteoarthritis (OA) is a prevalent cause of global disability. New biomarkers are needed to improve treatment allocation, and genetic polymorphisms are promising candidates. Method: We aimed to assess the association of OPRM1 (A118G and C17T) and brain-derived neurotrophic factor (BDNF [G196A]) polymorphisms with pain-related outcomes and motor cortex excitability metrics (measured by transcranial magnetic stimulation) in 113 knee OA patients with chronic pain. We performed adjusted multivariate regression analyses to compare carriers versus non-carriers in terms of clinical and neurophysiological characteristics at baseline, and treatment response (pain reduction and increased cortical inhibitory tonus) after rehabilitation. Results: Compared to non-carriers, participants with polymorphisms on both OPRM1 (A118G) and BDNF (G196A) genes were less likely to improve pain after rehabilitation (85 and 72% fewer odds of improvement, respectively). Likewise, both carriers of OPRM1 polymorphisms (A118G and C17T) were also less likely to improve cortical inhibition (short intracortical inhibition [SICI], and intracortical facilitation [ICF], respectively). While pain and cortical inhibition improvement did not correlate in the total sample, the presence of OPRM1 (A118G) and BDNF (G196A) polymorphisms moderated this relationship. Conclusions: These results underscore the promising role of combining genetic and neurophysiological markers to endotype the treatment response in this population.

Indexed as

Chronic painCortical excitabilityOsteoarthritisPolymorphism

Identifiers

PMID36199368
PMCPMC9508345
OpenAlexW4297422704

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.