The reticulospinal tract was recently shown to have synaptic connections to the intrinsic muscles of the fingers in nonhuman primates, indicating it may contribute to hand function long thought to be controlled exclusively through corticospinal pathways. Our objective was to obtain evidence supporting the hypothesis that these same anatomical connections exist in humans. startReact, an involuntary release of a planned movement via the startle reflex, provides a noninvasive means to examine the reticulospinal tract in humans. We found that startReact was triggered during coordinated grasp but not individuated finger movements. This result suggests that the reticulospinal tract does have connections to the intrinsic muscles of the fingers in humans but its functional role is limited to coordinated movement of the whole hand. These results do not diminish the well-established role of corticospinal pathways in the control of hand movement. Indeed, they cement the significance of corticospinal pathways in individuated finger movement control. Still, these results point to an updated and expanded view of distal hand control where reticulospinal and corticospinal pathways work in parallel to generate a large repertoire of diverse, coordinated movement in the hand. Finally, the presence of reticulospinal pathways to the muscles of the hand makes this pathway an attractive therapeutic target for clinical populations where the corticospinal tract is absent or injured.

Following stroke, reaching movements are slow, segmented, and variable. It is unclear if these deficits result from a poorly constructed movement plan or an inability to voluntarily execute an appropriate plan. The acoustic startle reflex provides a means to initiate a motor plan involuntarily. In the presence of a movement plan, startling acoustic stimulus triggers non-voluntary early execution of planned movement, a phenomenon known as the startReact response. In unimpaired individuals, the startReact response is identical to a voluntarily initiated movement, except that it is elicited 30–40 ms. As the startReact response is thought to be mediated by brainstem pathways, we hypothesized that the startReact response is intact in stroke subjects. If startReact is intact, it may be possible to elicit more task-appropriate patterns of muscle activation than can be elicited voluntarily. We found that startReact responses were intact following stroke. Responses were initiated as rapidly as those in unimpaired subjects, and with muscle coordination patterns resembling those seen during unimpaired volitional movements. Results were striking for elbow flexion movements, which demonstrated no significant differences between the startReact responses elicited in our stroke and unimpaired subject groups. The results during planned extension movements were less straightforward for stroke subjects, since the startReact response exhibited task inappropriate activity in the flexors. This inappropriate activity diminished over time. This adaptation suggests that the inappropriate activity was transient in nature and not related to the underlying movement plan. We hypothesize that the task-inappropriate flexor activity during extension results from an inability to suppress the classic startle reflex, which primarily influences flexor muscles and adapts rapidly with successive stimuli. These results indicate that stroke subjects are capable of planning ballistic elbow movements, and that when these planned movements are involuntarily executed they can be as rapid and appropriate as those in unimpaired individuals.

The sensory and neural mechanisms underlying postural control have received much attention in recent decades but remain poorly understood. Our objectives were 1) to establish the decerebrate cat as an appropriate model for further research into the sensory mechanisms of postural control and 2) to observe what elements of the postural response can be generated by the brain stem and spinal cord. Ten animals were decerebrated using a modified premammillary technique, which consists of a premammillary decerebration that is modified with a vertical transection near the subthalamic nucleus to eliminate spontaneous locomotion. Horizontal support surface perturbations were applied to all four limbs and electromyographic recordings were collected from 14 muscles of the right hindlimb. Muscle activation was quantified with tuning curves, which compared increases and decreases in muscle activity to background and graphed the difference against perturbation direction. Parallels were drawn between these tuning curves, which were further quantified with a principal direction and breadth (range of directions of muscle activation), and data collected by other researchers from the intact animal. We found a strong similarity in the direction and breadth of the tuning curves generated in the decerebrate and intact cat. These results support our hypothesis that directionally specific tuning of muscles in response to support surface perturbations does not require the cortex, further indicating a strong role for the brain stem and spinal cord circuits in mediating directionally appropriate muscle activation patterns.

Long-latency responses elicited by postural perturbation are modulated by how a subject is instructed to respond to the perturbation, yet the neural pathways responsible for this modulation remain unclear. The goal of this study was to determine if instruction-dependent modulation is associated with activity in brainstem pathways contributing to startle. Our hypothesis was that elbow perturbations can evoked startle, indicated by activity in the sternocleidomastoid muscle (SCM). Perturbation responses were compared to those elicited by a loud acoustic stimulus, known to elicit startle. Postural perturbations and startling acoustic stimuli both evoked SCM activity, but only when a ballistic elbow extension movement was planned. Both stimuli triggered SCM activity with the same probability. When SCM activity was present, there was an associated early onset of triceps EMG, as required for the planned movement. This early EMG onset occurred at a time often attributed to long-latency stretch reflexes (75-100ms). The nature of the perturbation-triggered EMG (excitatory or inhibitory) was independent of the perturbation direction (flexion or extension) indicating that it was not a feedback response appropriate for returning the limb to its original position. The net EMG response to perturbations delivered after a movement had been planned could be explained as the sum of a stretch reflex opposing the perturbation and a startle-evoked response associated with the prepared movement. These results demonstrate that rapid perturbations can trigger early release of a planned ballistic movement, and that this release is associated with activity in the brainstem pathways contributing to startle reflexes.

Objective A startling loud acoustic stimulus can involuntarily elicit planned movements, a phenomenon referred to as startReact. Following stroke, startReact elbow flexion in stroke survivors are improved from voluntary movements. Specifically, startReact elbow flexion in unimpaired individuals is not statistically different from stroke survivors in terms of onset latency and muscle activation patterns. As hand movements are particularly impacted by stroke, our objective was to determine if startReact was intact in the hand following stroke. Methods Data were collected in 8 stroke survivors and 10 age-matched subjects performing hand extension following two non-startling acoustic stimuli representing “get ready” and “go” respectively. Randomly, the “go” was replaced with a startling acoustic stimulus. We hypothesized that 1) startReact would be intact during hand extension in stroke survivors and 2) that the latency of movement would be the same as in age-matched subjects. Results We found that startReact was intact in stroke subjects and further that the onset latency of these movements was not different from age-matched subjects. Conclusions We conclude that startReact is intact in the hand following stroke. Significance An intact startReact response indicates that this reflex may be an attractive therapeutic target for initiating hand extension in stroke survivors.

Falls are the most common and expensive medical complication in stroke survivors. There is remarkably little information about what factors lead to a fall in stroke survivors. With few exceptions, the falls literature in stroke has focused on relating metrics of static balance and impairment to fall outcomes in the acute care setting or in community. While informative, these studies provide little information about what specific impairments in a stroke-survivor’s response to dynamic balance challenges lead to a fall. We identified the key kinematic characteristics of stroke survivors’ stepping responses following a balance disturbance that are associated with a fall following dynamic balance challenges. Stroke survivors were exposed to posteriorly-directed translations of a treadmill belt that elicited a stepping response. Kinematics were compared between successful and failed recovery attempts (i.e. a fall). We found that the ability to arrest and reverse trunk flexion and the ability to perform an appropriate initial compensatory step were the most critical response contributors to a successful recovery. We also identified 2 compensatory strategies utilized by stroke survivors to avoid a fall. Despite significant post-stroke functional impairments, the biomechanical causes of trip-related falls by stroke survivors appear to be similar to those of unimpaired older adults and lower extremity amputees. However, compensatory strategies (pivot, hopping) were observed.

Objective The startle reflex elicits involuntary release of planned movements (startReact). Following stroke, startReact flexion movements are intact but startReact extension movements are impaired by task-inappropriate flexor activity impeding arm extension. Our objective was to quantify deficits in startReact elbow extension movements, particularly how these deficits are influenced by impairment. Methods Data were collected in 8 stroke survivors performing elbow extension following two non-startling acoustic stimuli representing “get ready” and “go” respectively. Randomly, the “go” was replaced with a startling acoustic stimulus. We hypothesized that task-inappropriate flexor activity originates from unsuppressed classic startle reflex. We expected that increasing damage to the cortex (increasing impairment) would relate to increasing task-inappropriate flexor activity causing poor elbow extension movement and target acquisition. Results Task-inappropriate flexor activity increased with impairment resulting in larger flexion deflections away from the subjects’ intended target corresponding to decreased target acquisition. Conclusions We conclude that the task-inappropriate flexor activity likely results from cortical or corticospinal damage leading to an unsuppressed or hypermetric classic startle reflex that interrupts startReact elbow extension. Significance Given startReact’s functional role in compensation during environmental disturbances, our results may have important implications for our understanding deficits in stroke survivor’s response to unexpected environmental disturbances.

Objective Modulation of the long-latency reflex (LLR) is important for sensorimotor control during interaction with different mechanical loads. Transcortical pathways usually contribute to LLR modulation, but the integrity of pathways projecting to the paretic and non-paretic arms of stroke survivors is compromised. We hypothesize that disruption of transcortical reflex pathways reduces the capacity for stroke survivors to appropriately regulate the LLR bilaterally. Methods Elbow perturbations were applied to the paretic and non-paretic arms of persons with stroke, and the dominant arm of age-matched controls as subjects interacted with Stiff or Compliant environments rendered by a linear actuator. Reflexes were quantified using surface electromyograms, recorded from biceps. Results LLR amplitude was significantly larger during interaction with the Compliant load compared to the Stiff load in controls. However, there was no significant change in LLR amplitude for the paretic or non-paretic arm of stroke survivors. Conclusions Modulation of the LLR is altered in the paretic and non-paretic arms after stroke. Significance Our results are indicative of bilateral sensorimotor impairments following stroke. The inability to regulate the LLR may contribute to bilateral deficits in tasks that require precise control of limb mechanics and stability.