Evidence map›Paper›PMID 29592888›Full record

ArticleNeurology2018

Dorsal and ventral horn atrophy is associated with clinical outcome after spinal cord injury.

Eveline Huber, Gergely David, Alan J Thompson, Nikolaus Weiskopf, Siawoosh Mohammadi, Patrick Freund

Open access · hybridAbstract read
In one paragraph

Article in Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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 4 institutions in 3 countries.

Eveline HuberFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany.
Gergely DavidFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany.
Alan J ThompsonFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany.
Nikolaus WeiskopfFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany.
Siawoosh MohammadiFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany.
Patrick FreundFrom the Spinal Cord Injury Center (E.H., G.D., P.F.), Balgrist University Hospital, Zurich, Switzerland; Department of Brain Repair and Rehabilitation (A.J.T., P.F.) and Wellcome Trust Centre for Neuroimaging (N.W., S.M., P.F.), UCL Institute of Neurology, University College London, UK; Department of Neurophysics (N.W., P.F.), Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany; and Department of Systems Neuroscience (S.M.), University Medical Center Hamburg-Eppendorf, Germany. patrick.freund@balgrist.ch.
Universitätsklinik Balgrist · CHWellcome Centre for Human Neuroimaging · GBMax Planck Institute for Human Cognitive and Brain Sciences · DEUniversity College London · GB

Funding

Medical Research Council MC_PC_12024Wellcome Trust
6 · The paper itself

Abstract

objectiveTo investigate whether gray matter pathology above the level of injury, alongside white matter changes, also contributes to sensorimotor impairments after spinal cord injury.

methodsA 3T MRI protocol was acquired in 17 tetraplegic patients and 21 controls. A sagittal T2-weighted sequence was used to characterize lesion severity. At the C2-3 level, a high-resolution T2*-weighted sequence was used to assess cross-sectional areas of gray and white matter, including their subcompartments; a diffusion-weighted sequence was used to compute voxel-based diffusion indices. Regression models determined associations between lesion severity and tissue-specific neurodegeneration and associations between the latter with neurophysiologic and clinical outcome.

resultsNeurodegeneration was evident within the dorsal and ventral horns and white matter above the level of injury. Tract-specific neurodegeneration was associated with prolonged conduction of appropriate electrophysiologic recordings. Dorsal horn atrophy was associated with sensory outcome, while ventral horn atrophy was associated with motor outcome. White matter integrity of dorsal columns and corticospinal tracts was associated with daily-life independence.

conclusionOur results suggest that, next to anterograde and retrograde degeneration of white matter tracts, neuronal circuits within the spinal cord far above the level of injury undergo transsynaptic neurodegeneration, resulting in specific gray matter changes. Such improved understanding of tissue-specific cord pathology offers potential biomarkers with more efficient targeting and monitoring of neuroregenerative (i.e., white matter) and neuroprotective (i.e., gray matter) agents.

Indexed as

AdolescentAdultAgedAtrophyEvoked PotentialsFemaleHot TemperatureHumansImaging, Three-DimensionalMagnetic Resonance ImagingMaleMiddle AgedPhysical StimulationPyramidal TractsRetrospective StudiesSeverity of Illness Index

Identifiers

PMID29592888
PMCPMC5921039
OpenAlexW2794597110

What OpenQuestion holds

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LicenceCC BY
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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.