TY - JOUR
T1 - Stratifying chronic stroke patients based on the influence of contralesional motor cortices
T2 - An inter-hemispheric inhibition study
AU - Lin, Yin Liang
AU - Potter-Baker, Kelsey A.
AU - Cunningham, David A.
AU - Li, Manshi
AU - Sankarasubramanian, Vishwanath
AU - Lee, John
AU - Jones, Stephen
AU - Sakaie, Ken
AU - Wang, Xiaofeng
AU - Machado, Andre G.
AU - Plow, Ela B.
N1 - Publisher Copyright:
© 2020 International Federation of Clinical Neurophysiology
PY - 2020/10
Y1 - 2020/10
N2 - Objective: A recent “bimodal-balance recovery” model suggests that contralesional influence varies based on the amount of ipsilesional reserve: inhibitory when there is a large reserve, but supportive when there is a low reserve. Here, we investigated the relationships between contralesional influence (inter-hemispheric inhibition, IHI) and ipsilesional reserve (corticospinal damage/impairment), and also defined a criterion separating subgroups based on the relationships. Methods: Twenty-four patients underwent assessment of IHI using Transcranial Magnetic Stimulation (ipsilateral silent period method), motor impairment using Upper Extremity Fugl-Meyer (UEFM), and corticospinal damage using Diffusion Tensor Imaging and active motor threshold. Assessments of UEFM and IHI were repeated after 5-week rehabilitation (n = 21). Results: Relationship between IHI and baseline UEFM was quadratic with criterion at UEFM 43 (95%conference interval: 40–46). Patients less impaired than UEFM = 43 showed stronger IHI with more impairment, whereas patients more impaired than UEFM = 43 showed lower IHI with more impairment. Of those made clinically-meaningful functional gains in rehabilitation (n = 14), more-impaired patients showed further IHI reduction. Conclusions: A criterion impairment-level can be derived to stratify patient-subgroups based on the bimodal influence of contralesional cortex. Contralesional influence also evolves differently across subgroups following rehabilitation. Significance: The criterion may be used to stratify patients to design targeted, precision treatments.
AB - Objective: A recent “bimodal-balance recovery” model suggests that contralesional influence varies based on the amount of ipsilesional reserve: inhibitory when there is a large reserve, but supportive when there is a low reserve. Here, we investigated the relationships between contralesional influence (inter-hemispheric inhibition, IHI) and ipsilesional reserve (corticospinal damage/impairment), and also defined a criterion separating subgroups based on the relationships. Methods: Twenty-four patients underwent assessment of IHI using Transcranial Magnetic Stimulation (ipsilateral silent period method), motor impairment using Upper Extremity Fugl-Meyer (UEFM), and corticospinal damage using Diffusion Tensor Imaging and active motor threshold. Assessments of UEFM and IHI were repeated after 5-week rehabilitation (n = 21). Results: Relationship between IHI and baseline UEFM was quadratic with criterion at UEFM 43 (95%conference interval: 40–46). Patients less impaired than UEFM = 43 showed stronger IHI with more impairment, whereas patients more impaired than UEFM = 43 showed lower IHI with more impairment. Of those made clinically-meaningful functional gains in rehabilitation (n = 14), more-impaired patients showed further IHI reduction. Conclusions: A criterion impairment-level can be derived to stratify patient-subgroups based on the bimodal influence of contralesional cortex. Contralesional influence also evolves differently across subgroups following rehabilitation. Significance: The criterion may be used to stratify patients to design targeted, precision treatments.
KW - Corticospinal
KW - Diffusion Tensor Imaging (DTI)
KW - Inter-Hemispheric Inhibition (IHI)
KW - Motor function
KW - Rehabilitation
KW - Stroke
KW - Transcranial Magnetic Stimulation (TMS)
KW - Upper limb
UR - http://www.scopus.com/inward/record.url?scp=85088391347&partnerID=8YFLogxK
U2 - 10.1016/j.clinph.2020.06.016
DO - 10.1016/j.clinph.2020.06.016
M3 - Article
C2 - 32712080
AN - SCOPUS:85088391347
SN - 1388-2457
VL - 131
SP - 2516
EP - 2525
JO - Clinical Neurophysiology
JF - Clinical Neurophysiology
IS - 10
ER -