Evidence map›Paper›PMID 35504222›Full record

ArticleNeuroImage. Clinical2022

Specific structuro-metabolic pattern of thalamic subnuclei in fatal familial insomnia: A PET/MRI imaging study.

Kexin Xie, Yaojing Chen, Min Chu, Yue Cui, Zhongyun Chen, Jing Zhang, Li Liu, Donglai Jing, Chunlei Cui, Zhigang Liang and 5 more

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

Article in NeuroImage. Clinical, 2022. 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
0.7field-weighted citation impact, top 37% 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, 7 citations in OpenAlex.

  1. Frontiers in neuroscience · 2026
    Article
  2. Difference of Resting State Functional Connectivity between Depressive Patients with and without Clinically Significant Insomnia.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article
  3. Article
  4. 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

15 authors at 6 institutions in 3 countries.

Kexin XieDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Yaojing ChenState Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing 100875, China.
Min ChuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Yue CuiDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Zhongyun ChenDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Jing ZhangDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Li LiuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China; Department of Neurology, Shenyang Fifth People Hospital, Shenyang, Liaoning 110023, China.
Donglai JingDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China; Department of Neurology, Rongcheng People's Hospital, Baoding, Hebei 071700, China.
Chunlei CuiDepartment of Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Zhigang LiangDepartment of Nuclear Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Liankun RenDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Pedro Rosa-NetoMcGill University Research Centre for Studies in Aging, Montreal, QC H3G 1Y6, Canada.
Imad GhorayebUniversité de Bordeaux, Institut de Neurosciences Cognitives et Intégratives d'Aquitaine, UMR 5287, F-33076 Bordeaux, France; CNRS, Institut de Neurosciences Cognitives et Intégratives d'Aquitaine, UMR 5287, F-33076 Bordeaux, France; Département de Neurophysiologie Clinique, Pôle Neurosciences Cliniques, CHU de Bordeaux, F-33076 Bordeaux, France.
Zhanjun ZhangState Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing 100875, China. Electronic address: zhang_rzs@bnu.edu.cn.
Liyong WuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China; National Clinical Research Center for Geriatric Diseases, Beijing 100053, China. Electronic address: wmywly@hotmail.com.
Capital Medical University · CNBeijing Normal University · CNCentre National de la Recherche Scientifique · FRMcGill University · CANational Clinical Research Center for Digestive Diseases · CNShenyang Fifth People Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysfunction of the thalamus has been proposed as a core mechanism of fatal familial insomnia. However, detailed metabolic and structural alterations in thalamic subnuclei are not well documented. We aimed to address the multimodal structuro-metabolic pattern at the level of the thalamic nuclei in fatal familial insomnia patients, and investigated the clinical presentation of primary thalamic alterations. MATERIALS AND

methodsFive fatal familial insomnia patients and 10 healthy controls were enrolled in this study. All participants underwent neuropsychological assessments, polysomnography, electroencephalogram, and cerebrospinal fluid tests. MRI and fluorodeoxyglucose PET were acquired on a hybrid PET/MRI system. Structural and metabolic changes were compared using voxel-based morphometry analyses and standardized uptake value ratio analyses, focusing on thalamic subnuclei region of interest analyses. Correlation analysis was conducted between gray matter volume and metabolic decrease ratios, and clinical features.

resultsThe whole-brain analysis showed that gray matter volume decline was confined to the bilateral thalamus and right middle temporal pole in fatal familial insomnia patients, whereas hypometabolism was observed in the bilateral thalamus, basal ganglia, and widespread cortices, mainly in the forebrain. In the regions of interest analysis, gray matter volume and metabolism decreases were prominent in bilateral medial dorsal nuclei, anterior nuclei, and the pulvinar, which is consistent with neuropathological and clinical findings. A positive correlation was found between gray matter volume and metabolic decrease ratios.

conclusionsOur study revealed specific structuro-metabolic pattern of fatal familial insomnia that demonstrated the essential roles of medial dorsal nuclei, anterior nuclei, and pulvinar, which may be a potential biomarker in diagnosis. Also, primary thalamic subnuclei alterations may be correlated with insomnia, neuropsychiatric, and autonomic symptoms sparing primary cortical involvement.

Indexed as

Insomnia, Fatal FamilialThalamusCase-Control StudiesHumansMagnetic Resonance ImagingPositron-Emission Tomography18F-FluorodeoxyglucoseFatal familial insomniaMagnetic resonance imagingPositron-Emission TomographyThalamic nuclei

Identifiers

PMID35504222
PMCPMC9065920
OpenAlexW4226430662

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.