Up to two thirds of individuals with chronic hemiparetic stroke suffer life-long residual impairments to their paretic hands, affecting their independence and quality of life. These impairments stem initially from losses of direct corticospinal projections that result in an increased reliance on indirect bulbospinal pathways. This reliance on the indirect pathways causes motor control deficits including weakness, loss of independent joint control (LIJC), and muscle hyperactivity. In addition to these neurologic impairments secondary musculoskeletal adaptations may occur that produce biomechanical changes increasing the passive joint torques in the paretic limb as compared to the non-paretic limb. Such biomechanical alterations within the hand would further contribute to hand impairments post stroke in addition to the neurological motor control deficits, yet quantitative data of these adaptations within the hand is lacking.

To gain a greater understanding of how altered passive joint biomechanics affects hand impairments post-stroke separate from the neurological impairments, both experimental and computer simulation methods were utilized. First, a dynamic computational musculoskeletal model of the finger was developed using a novel technique to incorporate the complex passive properties of the hand muscles. Next, to quantify how the passive torques adapt post-stroke within the hand, the passive torques about the wrist and four metacarpophalangeal joints were collected in 35 individuals with chronic hemiparetic stroke. Finally, to differentiate how the altered joint mechanics versus neurological deficits impair hand function, computational simulations were developed incorporating both the experimentally collected impaired biomechanics and neurological deficits.

In individuals with chronic hemiparetic stroke there were not substantial differences in torques between the paretic and non-paretic hands, unless the individual had received Botulinum Neurotoxin (BoNT) in their wrist and finger muscles at any point following their stroke. Currently BoNT is the preferred treatment for muscle hyperactivity however this work has found that BoNT may have residual long-term effects that substantially increase the stiffness of muscles that were injected with it. The computational simulations demonstrated these increases in muscles stiffness due to BoNT limits the ability to extend the fingers in individuals with severe and moderate hand impairments. However, the simulations also demonstrated that the flexion synergy and resulting increased involuntary flexor muscle drive is the primary driver of hand impairments following chronic hemiparetic stroke and overshadows the increases due to the biomechanical changes. The findings from this work indicates the use of BoNT for treatment of muscle hyperactivity following a stroke should be further evaluated and that future rehabilitation and pharmaceutical interventions developed for these individuals should focus on reducing the impact of the neural deficits following stroke to maximize hand function.