The knee joint plays a significant role in ground clearness, which is a crucial subtask of normal walking and avoiding falls. While post-stroke survivors are often faced with muscle weakness during walking, which leads to inadequate knee flexion. The lack of ground clearance caused by inadequate knee flexion will severely impede walking, increase metabolic exertion, and increase the risk of falls. A compliant exoskeleton robot possesses more favorable edges than other rigid ones in lightweight, safety, sense of comfort, and so on. We developed a new type of soft exoskeleton robot to assist the knee joint to achieve desired movements with Bowden cable transmitting force and torque. With the agonist–antagonist driving method, like a group of muscles working, we have explored dual-motors structure to realize the knee flexion function. It has built a standard dynamic model to analyze stability and realize the control law. We have conducted simulation and prototype experiments to verify the feasibility and usefulness of our method. The results show that the device can compensate for the lack of the knee joint driving force and realize the reference movement. Finally, we concluded that our method is a desirable way, and the scheme could improve the knee flexion ability and clearing ground.

Background: Both the lesion location hypothesis and the vascular depression hypothesis have been proposed to explain the high incidence of depression in stroke patients. However, research studying both hypotheses in a single cohort is, at present, scarce.

Objective: To test the independent effects of lesion location (left hemisphere, anterior region) and of co-occurring generalized vascular damage on the development of depression in the first year after ischemic stroke, while other risk factors for depression are controlled for.

Methods: One hundred and ninety consecutive patients with a first-ever, supratentorial infarct were followed up for one year. CT was performed in the acute phase of stroke, while in 75 patients an additional MRI scan was also available. Depression was assessed at 1, 3, 6, 9, and 12 months after stroke using self-rating scales as screening tools and the SCID-I to diagnose depression according to DSM-IV criteria.

Results: Separate analyses of the lesion location hypothesis and the vascular depression hypothesis failed to reveal significant support for either of these biological models of post-stroke depression. Similar negative results appeared from one overall, multivariate analysis including variables of both focal and generalized vascular brain damage, as well as other non-cerebral risk factors. In addition, level of handicap and neuroticism were independent predictors of depression in this cohort, as has been reported previously.

Conclusion: This study supports neither the lesion location nor the vascular depression hypothesis of post-stroke depression. A biopsychosocial model including both premorbid (prior to stroke) vulnerability factors, such as neuroticism and (family) history of depression, as well as post-stroke stressors, such as level of handicap, may be more appropriate and deserves further study.