TITLE:
Motor Control Network Effective Connectivity in Regulating Muscle Force Output
AUTHORS:
Soha Saleh, Zhiguo Jiang, Guang H. Yue
KEYWORDS:
Sensorimotor System, Force Regulation, Effective Connectivity, Motor Control
JOURNAL NAME:
Natural Science,
Vol.13 No.2,
February
20,
2021
ABSTRACT: Objective of the study:
This study aimed at characterizing output features of the higher-order motor
control centers (hoMCCs), including secondary (premotor cortex [Pre] and
supplementary motor area [SMA]) and association (prefrontal cortex [PFC]) motor
regions to the primary motor cortex (M1) during graded force tasks. It is well
known that one of the major roles of the primary motor cortex (M1) is
controlling motor output such as muscle force. However, it is unclear how the
hoMCCs interact with M1 in regulating voluntary muscle contractions. Methods:
fMRI data was acquired during graded force tasks and fMRI-based effective
connectivity (EC) and muscle force analyses were performed to study the
relationship between hoMCCs-M1 effective connectivity and voluntarily exerted
handgrip force. Results: The results show that there is a consistent
information flow from the hoMCCs to M1 under all force conditions, suggesting a
hierarchical control mechanism in the brain in regulating voluntary muscle
force. Only the premotor cortex exhibited a significant role in mediating the
level of force production through its EC with M1 but that role diminished when
the exerted force was high, suggesting perhaps a ceiling and/or fatigue effect
on the EC. A flip in the direction of EC from the primary sensory cortex (S1) to
the hoMCCs (PFC, SMA, and Pre) at lower force levels while at higher forces EC
was observed from the hoMCCs to S1. Conclusion: The hoMCCs regulate M1 output
to produce desired voluntary muscle force. Only the Pre-to-M1 connectivity
strength directly correlates with the force level especially from low to
moderate levels. The hoMCCs are involved in modulating higher force production
likely by strengthening M1 output and downgrading inhibition from
S1 to M1.