Biomedical Engineering Reference
In-Depth Information
walking), the control strategy appears to be mixed, and both mechanisms act in
opposite ways to maintain the postural control. During the standing position, the
generated moments at the various body kinetic chains are transmitted to the base of
support, seeing as a signal of the COP component.
Considering the COP behaviour as a measure of body dynamics, there is access
to a greater representation of the various neuromuscular components that act on
different joints. These neuromuscular components and their characteristics are
strongly dependent on the stimuli that control the postural stability [
76
]. Disorders in
stimuli processing, such as occurs in neurological disorders, lead to changes in COP
characteristics [
77
]. The standing posture is defined by mutual relations between
the body segments and the vertical orientation of the body in the gravitational field,
thus, this guidance (in conjunction with the small airfoil and body architecture)
determines the potential for postural instability [
78
].
2.4.1
Joint Stability
The joint stability results from motor control over the elements acting on each joint.
Thus, the effect of control over the active elements (neuromuscular) is associated
with the effect of passive elements (mechanical properties of joint materials) [
10
]
act simultaneously to produce an adequate stability. Joint stability should provide
adequate stiffness and resistance to external forces, when the objective is maintain
postural stability [
10
]. One of the key components of joint stability is related to
muscle stiffness. The concept of stiffness as an important factor in the stability
control was introduced in 1998 [
54
]. The key point of these arguments (based on
experimental evidence) was that the controlled variable (COM) was virtually in
phase with the controlling variable (COP) [
79
].
The role of the CNS in this postural control is to maintain a steady supply of
muscle tone, capable to support the gravitational load and shift the COP faster than
the COM, to maintain this position. In anterior-posterior direction, when a subject
is in the standing position, usually presents the COM about 5 cm below the ankle.
When an oscillation occurs, is necessary that the ankle muscles generate a tone
with sufficient stiffness to move the COP faster than COM. If the reactive control is
normal, the afferent and efferent latencies combined with biomechanical delays of
muscle recruitment, resulting in a delay of COP about 100 ms after the initial COM
movement [
80
]. In standing position the amount of gravitational COM movement,
increases linearly with the increase in ankle dorsal-flexion, but the frontal body
collapse is controlled by the ankle joint moment, produced by the activity of triceps
and soleus muscle [
81
]. The activation of this muscle generates an intrinsic joint
stiffness, causing a force moment in response to the instantaneous change in the
joint angle, without any intervention from the CNS. If the stiffness is less than the
gravitational movement, the COM is mechanically unstable, with need for neural
modulation of joint moment to produce stability [
71
].
It has been postulated that the CNS performs the modulation of joint stiffness to
control postural sway [
54
,
82
]. However the experimental results of another study
