Corticospinal Tract Microstructure Correlates With Beta Oscillatory Activity in the Primary Motor Cortex After Stroke.


Journal

Stroke
ISSN: 1524-4628
Titre abrégé: Stroke
Pays: United States
ID NLM: 0235266

Informations de publication

Date de publication:
12 2021
Historique:
pubmed: 21 8 2021
medline: 7 1 2022
entrez: 20 8 2021
Statut: ppublish

Résumé

Cortical beta oscillations are reported to serve as robust measures of the integrity of the human motor system. Their alterations after stroke, such as reduced movement-related beta desynchronization in the primary motor cortex, have been repeatedly related to the level of impairment. However, there is only little data whether such measures of brain function might directly relate to structural brain changes after stroke. This multimodal study investigated 18 well-recovered patients with stroke (mean age 65 years, 12 males) by means of task-related EEG and diffusion-weighted structural MRI 3 months after stroke. Beta power at rest and movement-related beta desynchronization was assessed in 3 key motor areas of the ipsilesional hemisphere that are the primary motor cortex (M1), the ventral premotor area and the supplementary motor area. Template trajectories of corticospinal tracts (CST) originating from M1, premotor cortex, and supplementary motor area were used to quantify the microstructural state of CST subcomponents. Linear mixed-effects analyses were used to relate tract-related mean fractional anisotropy to EEG measures. In the present cohort, we detected statistically significant reductions in ipsilesional CST fractional anisotropy but no alterations in EEG measures when compared with healthy controls. However, in patients with stroke, there was a significant association between both beta power at rest ( These data suggest there might be a link connecting microstructure of the CST originating from M1 pyramidal neurons and beta oscillatory activity, measures which have already been related to motor impairment in patients with stroke by previous reports.

Sections du résumé

BACKGROUND AND PURPOSE
Cortical beta oscillations are reported to serve as robust measures of the integrity of the human motor system. Their alterations after stroke, such as reduced movement-related beta desynchronization in the primary motor cortex, have been repeatedly related to the level of impairment. However, there is only little data whether such measures of brain function might directly relate to structural brain changes after stroke.
METHODS
This multimodal study investigated 18 well-recovered patients with stroke (mean age 65 years, 12 males) by means of task-related EEG and diffusion-weighted structural MRI 3 months after stroke. Beta power at rest and movement-related beta desynchronization was assessed in 3 key motor areas of the ipsilesional hemisphere that are the primary motor cortex (M1), the ventral premotor area and the supplementary motor area. Template trajectories of corticospinal tracts (CST) originating from M1, premotor cortex, and supplementary motor area were used to quantify the microstructural state of CST subcomponents. Linear mixed-effects analyses were used to relate tract-related mean fractional anisotropy to EEG measures.
RESULTS
In the present cohort, we detected statistically significant reductions in ipsilesional CST fractional anisotropy but no alterations in EEG measures when compared with healthy controls. However, in patients with stroke, there was a significant association between both beta power at rest (
CONCLUSIONS
These data suggest there might be a link connecting microstructure of the CST originating from M1 pyramidal neurons and beta oscillatory activity, measures which have already been related to motor impairment in patients with stroke by previous reports.

Identifiants

pubmed: 34412514
doi: 10.1161/STROKEAHA.121.034344
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3839-3847

Auteurs

Robert Schulz (R)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Marlene Bönstrup (M)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).
Department of Neurology, University Medical Centre, Leipzig, Germany (M.B.).

Stephanie Guder (S)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Jingchun Liu (J)

Department of Radiology, Tianjin Medical University General Hospital, China (J.L.).

Benedikt Frey (B)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Fanny Quandt (F)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Lutz A Krawinkel (LA)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Bastian Cheng (B)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Götz Thomalla (G)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

Christian Gerloff (C)

Department of Neurology, University Medical Centre Hamburg-Eppendorf, Germany (R.S., M.B., S.G., B.F., F.Q., L.A.K., B.C., G.T., C.G.).

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