Evidence map›Paper›PMID 33618681›Full record

ArticleBMC neurology2021

Intravenous methadone causes acute toxic and delayed inflammatory encephalopathy with persistent neurocognitive impairments.

Jonathan Repple, Svea Haessner, Andreas Johnen, Nils C Landmeyer, Andreas Schulte-Mecklenbeck, Marc Pawlitzki, Heinz Wiendl, Gerd Meyer Zu Hörste

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors at 2 institutions in 1 country.

Jonathan Repple *Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Svea Haessner *Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany. svea.haessner@ukmuenster.de.
Andreas JohnenDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Nils C LandmeyerDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Andreas Schulte-MecklenbeckDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Marc PawlitzkiDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Heinz WiendlDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
Gerd Meyer Zu HörsteDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, A1, 48149, Münster, Germany.
University Hospital Münster · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mu-opioid agonist methadone is administered orally and used in opioid detoxification and in the treatment of moderate-to-severe pain. Acute oral methadone-use and -abuse have been associated with inflammatory and toxic central nervous system (CNS) damage in some cases and cognitive deficits can develop in long-term methadone users. In contrast, reports of intravenous methadone adverse effects are rare. CASE PRESENTATION: Here, we report a patient who developed acute bilateral hearing loss, ataxia and paraparesis subsequently to intravenous methadone-abuse. While the patient gradually recovered from these deficits, widespread magnetic resonance imaging changes progressed and delayed-onset encephalopathy with signs of cortical dysfunction persisted. This was associated with changes in the composition of monocyte and natural killer cell subsets in the cerebrospinal fluid.

conclusionThis case suggests a potential bi-phasic primary toxic and secondary inflammatory CNS damage induced by intravenous methadone.

Indexed as

Substance Abuse, IntravenousAdministration, IntravenousAnalgesics, OpioidAtaxiaBrainBrain DiseasesBrain EdemaCognitive DysfunctionDiffusion Magnetic Resonance ImagingHearing Loss, BilateralHumansInflammationKiller Cells, NaturalMagnetic Resonance ImagingMaleMethadoneAnalgesics, OpioidMethadoneCase reportCognitionEncephalopathyFlow cytometryMethadone

Identifiers

PMID33618681
PMCPMC7898738
OpenAlexW3131146625

What OpenQuestion holds

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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.