Stroke is a leading cause of death and serious long-term disability in the United States [1, 2].
Individuals with hemiparesis due to stroke commonly demonstrate
difficulty bearing weight on the paretic lower extremity and
transferring weight from one leg to the other [3,4,5]. Reduced paretic limb weight bearing has been associated with functional deficits when rising from a chair [6], standing [7], and walking [8, 9]. The ability to transfer bodyweight between the lower limbs is related to impaired standing and stepping balance [10, 11] and gait performance [3, 12].
In particular, diminished weight transfer to the paretic limb
contributes to gait asymmetries, which commonly lead to greater energy
expenditure [13].
Previously we reported the ability to transfer weight laterally to the
paretic leg during single stance was associated with self-selected
walking speed and the capacity to increase walking speed [14].
This may indicate that weight transfer deficits negatively affect
forward progression. Indeed, forceful weight shift towards the paretic
limb enhanced paretic lower extremity kinetics and muscle activities
that contribute to forward progression [15].
Moreover, deficits in paretic limb weight-bearing contribute to lateral
and vertical balance instability and are associated with risk of
falling in individuals with chronic stroke [16].
These functional limitations can affect community participation and
quality of life. Consequently, restoring the capacity to load the
paretic limb is an important goal for rehabilitation post-stroke [17,18,19].
Despite considerable rehabilitation efforts aimed at improving weight transfer following a stroke [10, 20],
the impairments in neuromotor and biomechanical control underlying
weight transfer dysfunction remain poorly understood. Functional weight
transfer requires the coordination of multi-joint actions to absorb the
impact force and provide support to the body. In particular, the ankle
and knee joints are key contributors to shock absorption [21,22,23,24] and body weight support [25]. Increased stiffness in the paretic limb knee and ankle joints has been reported in persons with stroke [26, 27].
Inadequate lower limb joint flexion may disrupt impact force regulation
during weight acceptance and lead to instability that ultimately delays
and prolongs weight transfer timing during locomotion. Alternatively,
excessive ankle and knee joint flexion during loading may precipitate
limb collapse and destabilize balance during weight transfer. Thus, both
insufficient and excessive joint movement could affect weight transfer
processes. In addition to the amplitude of paretic ankle and knee joint
angular displacements, abnormalities in the relative timing of these
joint motions (i.e., inter-joint coordination) may also contribute to
impaired weight transfer following stroke.
Another key factor
affecting functional weight transfer is the ability to regulate the
center of pressure (COP) beneath the feet in relation to the body center
of mass (COM). During locomotion, effective neuromotor control of the
lower extremities contributes to regulating COM position and movement
relative to the base of support to maintain stability and prevent
falling. Compared with able-bodied adults, persons with chronic stroke
have a reduced capacity to rapidly shift their COP to the stance limb
during gait initiation [28],
reflecting abnormalities in balance control during weight transfer.
Because hip and ankle musculature regulates COM and COP movements [29],
difficulties in controlling hip kinematics and hip-ankle joint
coordination may contribute to delayed and reduced weight transfer after
a stroke.
To further address the foregoing issues, this study
examined the potential biomechanical factors that could affect lower
paretic limb weight bearing and weight transfer performance following
stroke. After stroke individuals often limit their use of the paretic
limb by favoring the use of the less affected leg during stance and gait
[30].
An approach that forces individuals to fully load the paretic limb is
warranted to reveal the performance capacity and assess the control of
weight bearing and weight transfer. Accordingly, we designed a novel
system that vertically displaces the support surface underneath one leg
and therefore imposes weight transfer. By unilaterally introducing a
perturbation that drops the standing support surface, this approach
forces a rapid alteration in inter-limb weight bearing distribution and
challenges medial–lateral balance control.
The primary purpose of
this study was to characterize the kinematics and kinetics of the
paretic lower extremity during an externally induced weight transfer
towards the paretic limb in chronic stroke compared to age-matched
controls. We hypothesized that, compared with able-bodied individuals,
those with chronic stroke would show reduced and uncoordinated paretic
limb joint angular displacements, and prolonged stabilization time of
the COP velocity following an externally induced weight transfer. In
addition, relationships between measurements during imposed weight
transfer, motor recovery assessment (i.e. Chedoke McMaster Stroke
Assessment leg and foot subscale), and clinical limb loading and balance
performance (i.e. Four-Square Step Test (FSST) and Step Test (ST)) were
explored. We expected that COP velocity stabilization time and CMSA
scores would be associated with FSST and ST scores.
