Evidence map›Paper›PMID 25642354›Full record

ArticleJournal of neurology & neurophysiology2014

Perfusion and Diffusion Abnormalities of Multiple Sclerosis Lesions and Relevance of Classified Lesions to Disease Status.

Lian Li, Michael Chopp, Siamak P Nejad-Davarani, Kourosh Jafari-Khouzani, Suresh C Patel, John Budaj, Mei Lu, Stanton B Elias, Mirela Cerghet, Quan Jiang

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

Article in Journal of neurology & neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. What Have We Learned from Perfusion MRI in Multiple Sclerosis?AJNR. American journal of neuroradiology · 2018
    Review
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

10 authors at 1 institution in 1 country.

Lian LiDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Michael ChoppDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA ; Department of Physics, Oakland University, Rochester, Michigan, USA.
Siamak P Nejad-DavaraniDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Kourosh Jafari-KhouzaniDepartment of Radiology, Henry Ford Hospital, Detroit, Michigan, USA.
Suresh C PatelDepartment of Radiology, Henry Ford Hospital, Detroit, Michigan, USA.
John BudajDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Mei LuDepartment of Biostatistics and Research Epidemiology, Henry Ford Hospital, Detroit, Michigan, USA.
Stanton B EliasDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Mirela CerghetDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA.
Quan JiangDepartment of Neurology, Henry Ford Hospital, Detroit, Michigan, USA ; Department of Physics, Oakland University, Rochester, Michigan, USA.
Henry Ford Hospital · US

Funding

Imaging Cell Based Treatment of Traumatic Brain InjuryR01NS064134 · NINDS · HENRY FORD HEALTH SYSTEM · PI JIANG, QUAN · 2011 to 2014
$1.3M
NINDS NIH HHS R01 NS064134
6 · The paper itself

Abstract

objectiveHemodynamic abnormality and disruption of white matter (WM) integrity are significant components in the pathophysiology of multiple sclerosis (MS) lesions. However, the roles of stratified lesions with distinct degrees of hemodynamic and structural injury in disease states remain to be explored. We tested the hypothesis that hemodynamic and structural impairment, as assessed by cerebral blood volume (CBV) and fractional anisotropy (FA), respectively, characterizes the extent of tissue injury, and the load of lesion with substantial tissue destruction would reflect the disease status and therefore, would be related to clinical disability.

methodsSeven relapsing-remitting MS patients and seven healthy controls underwent perfusion, diffusion and conventional MRI scans. Based on T2-FLAIR and T1-weighted image, WM plaques were classified. After image coregistration, values of CBV and FA were estimated in three distinct lesion types (active, T1-hypointense and T1-isointense lesion) and compared with those obtained in WM from controls. A total of 1135 lesions were evaluated. Brain volumetric measurement and correlative analysis between brain atrophy, lesion volume and clinical disability were also performed.

resultsCompared with normal WM, significantly reduced CBV and FA were present in the T1-hypointense lesion, while insignificant changes in both parameters were exhibited in the T1-isointense lesion. However, increased CBV but significantly decreased FA was detected in the active lesion. A close spatial relationship between active and T1-hypointense lesion was observed. Lesion load represented by T1-hypointense plus active lesion volume significantly correlated with brain atrophy, which, in turn, significantly correlated with the severity of clinical disability.

conclusionA distinct combination of CBV and FA characterizes the status of a specific lesion type. A severe structural impairment does not solely occur in the T1-hypointense lesion, but is also associated with the active lesion. The burden of the lesion with extensive structural damage provides an image index, indicative of disease status.

Indexed as

Brain atrophyCerebral blood volumeClinical disabilityFractional anisotropyLesion loadMRIMultiple sclerosis

Identifiers

PMID25642354
PMCPMC4309012
OpenAlexW2317513491

What OpenQuestion holds

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LicenceCC BY
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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.