Evidence map›Paper›PMID 36388611›Full record

ArticleRadiology case reports2023

Subcortical signal alteration of corticospinal tracts. A radiologic manifestation of ARIA: A case report.

Houman Sotoudeh, Mohammadreza Alizadeh, Ramin Shahidi, Parnian Shobeiri, Natelson Love, Aparna Singhal

Open access · goldAbstract readCase Reports
In one paragraph

Article in Radiology case reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
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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 2 countries.

Houman SotoudehDepartment of Radiology and Neurology, University of Alabama at Birmingham (UAB), JTN 333, 619 19th St S, Birmingham, AL 35294, USA.
Mohammadreza AlizadehPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Ramin ShahidiSchool of Medicine, Bushehr university of medical sciences, Bushehr, Iran.
Parnian ShobeiriSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Natelson LoveDepartment of Neurology, University of Alabama at Birmingham (UAB), Birmingham, AL, USA.
Aparna SinghalDepartment of Radiology, University of Alabama at Birmingham (UAB), Birmingham, AL, USA.
University of Alabama at Birmingham · USBushehr University of Medical Sciences · IRIran University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with Alzheimer's disease who have been given monoclonal antibodies targeting amyloid-β (Aβ) (eg, gantenerumab, donanemab, lecanemab, and aducanumab) for scientific purposes may have a spectrum of imaging findings known as amyloid-related imaging abnormalities (ARIA), shown on brain magnetic resonance imaging (MRI) scans. These neuroimaging abnormalities are caused by antibody-mediated destruction of accumulated Aβ aggregates in cerebral blood vessels and brain parenchyma. ARIA may demonstrate as brain edema or sulcal effusion (ARIA-E) or as hemosiderin deposits caused by brain parenchymal or pial hemorrhage (ARIA-H). The current study explores 2 cases with interval development of FLAIR hyper signal intensity along the bilateral corticospinal tracts in the motor cortex/precentral gyri after treatment by aducanumab. We believe this manifestation is a subtype of ARIA-A that has not been explored earlier. Our first case was a 72-year-old woman with a history of HTN and kidney transplant (polycystic kidney) who presented with mild cognitive impairment with clinical findings consistent with early Alzheimer's disease. After receiving 3 doses of aducunumab and experiencing cognition improvement, she underwent a brain MRI because of dizziness and vertigo. The brain MRI demonstrated new FLAIR hyper signal intensity in subcortical regions of precentral gyri (motor cortex) symmetrically as well as trace subarachnoid hemorrhage at the vertex compatible with ARIA-E and ARIA-H. Our second case was an 85-year-old woman with a history of small lymphocytic leukemia which was treated 20 years earlier. After orthopedic surgery 2 years ago, she developed dementia with anterograde amnesia. Since then, Aricept and Namenda have been started, but there have been no improvements in her subjective condition. The initial Amyloid PET/MR imaging showed diffuse cerebral Amyloid deposition. After tolerating 6 doses of aducanumab a safety MRI revealed new bilateral symmetric FLAIR hyper signal intensity in the subcortical motor cortex. Results of our study suggest that the subcortical corticospinal tract is another hotspot for ARIA findings. Hence, these regions might be an unknown site for both the action and adverse effects of aducanumab on amyloid plaques with secondary inflammation. In addition, radiologists must take this phenomenon into the account, and be cognizant that the FLAIR hyper signal intensities should not be misinterpreted as motor neuron disease (eg, amyotrophic lateral sclerosis).

Indexed as

AD, Alzheimer's diseaseaducanumabAlzheimer DiseaseAmyloid-related imaging abnormalitiesARIA, amyloid-related imaging abnormalitiesAβ, amyloid-beta peptideMagnetic Resonance ImagingMRI, magnetic resonance imaging

Identifiers

PMID36388611
PMCPMC9647162
OpenAlexW4308319542

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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.