% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Perlova:1050024,
author = {Perlova, Ksenia and Schmidt, Claudia C. and Fink, Gereon R.
and Weiss-Blankenhorn, Peter},
title = {{T}he role of the left primary motor cortex in apraxia},
journal = {Neurological research and practice},
volume = {7},
number = {1},
issn = {2524-3489},
address = {[London]},
publisher = {BioMed Central},
reportid = {FZJ-2025-05738},
pages = {2},
year = {2025},
note = {FundingOpen Access funding enabled and organized by Projekt
DEAL. Funded by the German Research Foundation
(DFG)—Project-ID 431549029 (CRC/SFB 1451).},
abstract = {Background: Apraxia is a motor-cognitive disorder that
primary sensorimotor deficits cannot solely explain.
Previous research in stroke patients has focused on damage
to the fronto-parietal praxis networks in the left
hemisphere (LH) as the cause of apraxic deficits. In
contrast, the potential role of the (left) primary motor
cortex (M1) has largely been neglected. However, recent
brain stimulation and lesion-mapping studies suggest an
involvement of left M1 in motor cognitive processes-over and
above its role in motor execution. Therefore, this study
explored whether the left M1 plays a specific role in
apraxia.Methods: We identified 157 right-handed patients
with first-ever unilateral LH stroke in the sub-acute phase
(< 90 days post-stroke), for whom apraxia assessments
performed with the ipsilesional left hand and lesion maps
were available. Utilizing the maximum probability map of
Brodmann area 4 (representing M1) provided by the JuBrain
Anatomy Toolbox in SPM, patients were subdivided into two
groups depending on whether their lesions involved (n = 40)
or spared (n = 117) left M1. We applied a mixed model ANCOVA
with repeated measures to compare apraxic deficits between
the two patient groups, considering the factors "body part"
and "gesture meaning". Furthermore, we explored potential
differential effects of the anterior (4a) and posterior (4p)
parts of Brodmann area 4 by correlation analyses.Results:
Patients with and without M1 involvement did not differ in
age and time post-stroke but in lesion size. When
controlling for lesion size, the total apraxia scores did
not differ significantly between groups. However, the mixed
model ANCOVA showed that LH stroke patients with lesions
involving left M1 performed differentially worse when
imitating meaningless finger gestures. This effect was
primarily driven by lesions affecting Brodmann area
4p.Conclusions: Even though many current definitions of
apraxia disregard a relevant role of (left) M1, the observed
differential effect of M1 lesions, specifically involving
subarea 4p, on the imitation of meaningless finger gestures
in the current sample of LH stroke patients suggests a
specific role of left M1 in imitation when high amounts of
(motor) attention and sensorimotor integration are
required.Keywords: Body-part specificity; Finger gestures;
Gesture meaning; Imitation; Limb-kinetic apraxia; Motor
cognition},
cin = {INM-3},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406},
pnm = {5251 - Multilevel Brain Organization and Variability
(POF4-525) / DFG project G:(GEPRIS)431549029 - SFB 1451:
Schlüsselmechanismen normaler und krankheitsbedingt
gestörter motorischer Kontrolle (431549029)},
pid = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029},
typ = {PUB:(DE-HGF)16},
doi = {10.1186/s42466-024-00359-8},
url = {https://juser.fz-juelich.de/record/1050024},
}