Evidence map›Paper›PMID 38923784›Full record

ArticleEuropean journal of neurology2024

Imbalanced optimal feedback motor control system in spinocerebellar ataxia type 3.

Leinian Li, Hui Chen, LiHua Deng, YongHua Huang, YuHan Zhang, YueYuan Luo, PeiLing Ou, LinFeng Shi, LiMeng Dai, Wei Chen and 3 more

Abstract read
In one paragraph

Article in European journal of neurology, 2024. 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
–field-weighted citation impact
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.

  1. Article
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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

13 authors.

Leinian Li7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Hui Chen7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
LiHua Deng7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
YongHua Huang7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
YuHan Zhang7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
YueYuan Luo7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
PeiLing Ou7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
LinFeng Shi7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
LiMeng DaiDepartment of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.
Wei ChenMR Research Collaboration Team, Siemens Healthineers Ltd., Wuhan, China.
HuaFu Chen7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Jian Wang7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Chen Liu7T Magnetic Resonance Translational Medicine Research Center, Department of Radiology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.ORCID 0000-0001-5149-2496

Funding

Chongqing Young and Middle-aged High-end Medical Talents Expert StudioChongqing Young and Middle-aged Medical Talents Project 414Z395National Natural Science Foundation of China 81601478National Natural Science Foundation of China 82071910
6 · The paper itself

Abstract

background and purposeHuman motor planning and control depend highly on optimal feedback control systems, such as the neocortex-cerebellum circuit. Here, diffusion tensor imaging was used to verify the disruption of the neocortex-cerebellum circuit in spinocerebellar ataxia type 3 (SCA3), and the circuit's disruption correlation with SCA3 motor dysfunction was investigated.

methodsThis study included 45 patients with familial SCA3, aged 17-67 years, and 49 age- and sex-matched healthy controls, aged 21-64 years. Tract-based spatial statistics and probabilistic tractography was conducted using magnetic resonance images of the patients and controls. The correlation between the local probability of probabilistic tractography traced from the cerebellum and clinical symptoms measured using specified symptom scales was also calculated.

resultsThe cerebellum-originated probabilistic tractography analysis showed that structural connectivity, mainly in the subcortical cerebellar-thalamo-cortical tract, was significantly reduced and the cortico-ponto-cerebellar tract was significantly stronger in the SCA3 group than in the control group. The enhanced tract was extended to the right lateral parietal region and the right primary motor cortex. The enhanced neocortex-cerebellum connections were highly associated with disease progression, including duration and symptomatic deterioration. Tractography probabilities from the cerebellar to parietal and sensorimotor areas were significantly negatively correlated with motor abilities in patients with SCA3.

conclusionTo our knowledge, this study is the first to reveal that disrupting the neocortex-cerebellum loop can cause SCA3-induced motor dysfunctions. The specific interaction between the cerebellar-thalamo-cortical and cortico-ponto-cerebellar pathways in patients with SCA3 and its relationship with ataxia symptoms provides a new direction for future research.

Indexed as

CerebellumFeedback, SensoryMachado-Joseph DiseaseNeocortexAdolescentAdultAgedDiffusion Tensor ImagingFemaleHumansMaleMiddle AgedYoung Adultcerebellummagnetic resonance imagingoptimal feedback controlspinocerebellar ataxia type 3structural connectivity

Identifiers

PMID38923784
PMCPMC11295168

What OpenQuestion holds

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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.