Muscle weakness, or the inability to generate normal levels of force, has clinically been recognized as one of the limiting factors in the motor rehabilitation of patients following stroke [1, 2]. In the lower limbs, this muscle weakness can be attributed to disuse atrophy  and/or the disruption in descending neural pathways leading to inadequate recruitment of motorneuron pools [1, 4–6]. It has also been reported that weakness following stroke may be the result of co-contraction of antagonistic muscles [7–9]. Spasticity has also been proposed as an alternative explanation for lower limb impairments in hemiparetic stroke [10, 11], but more recent studies have found that spasticity may not play a significant role in gait abnormalities [12, 13].
A well documented factor limiting the motor rehabilitation of patients following stroke is the presence of abnormal muscle activation patterns. Following stroke, some patients lose independent control over select muscle groups, resulting in coupled joint movements that are often inappropriate for the desired task [14, 15]. These coupled movements are known as synergies and, for the lower limb, have been grouped into the extension synergy (internal rotation, adduction, and extension of the hip, extension of the knee and extension and inversion of the ankle) and the flexion synergy (external rotation, abduction, and flexion of the hip, flexion of the knee, and flexion and eversion of the ankle) [16, 17] with varying levels of completeness  and dominance .
Much of the literature attempting to quantify these abnormal muscle synergies is focused on the paretic upper limb of stroke patients. In isometric conditions, it has been shown that stroke patients have a limited number of upper limb synergies available to them due to abnormal muscle coactivation patterns . In dynamic tasks, abnormal synergy patterns exist in the paretic upper limb between shoulder abduction with elbow flexion as well as shoulder adduction with elbow extension . These, and other inappropriate upper limb muscle synergy patterns were attributed to abnormal torque generation about joints secondary to the intended, or primary, joint axis during maximal voluntary isometric contractions .
This analysis technique of quantifying torques at joints secondary to the intended joint axis was applied to the lower limbs of cerebral palsy patients in a seated position, where abnormal secondary joint torques were expressed during maximal hip and knee extension . However, it has been shown that gravity can influence the control of limb movements by affecting sensory input  and altering task mechanics [25, 26]. When acute (<6 weeks post-injury) stroke subjects were placed in a functionally relevant weight-bearing anti-gravity standing position, no such abnormal secondary joint torque patterns during maximal voluntary isometric contractions were found, even though primary joint torques deficits were observed .
The goal of this study was to quantify lower limb weakness and coordination in chronic (> 1 year post-injury) stroke patients in a functionally relevant standing position. Subjects were asked to generate maximum isometric contractions about a given joint while torques at joints secondary to the desired exertion were simultaneously calculated and recorded. This allowed us to quantify weakness as a torque deficit and coordination as the generation of any synergy patterns in the lower limbs of hemiparetic stroke patients. Additionally, EMG activity of relevant muscles was simultaneously recorded to quantify the presence of abnormal muscle activation patterns.