Neuromuscular electrical stimulation (NMES) is commonly used in clinical settings to activate skeletal muscle in an effort to mimic voluntary contractions and enhance the rehabilitation of human skeletal muscles. It is also used as a tool in research to assess muscle performance and/or neuromuscular activation levels. However, there are fundamental differences between voluntary- and artificial-activation of motor units that need to be appreciated before NMES protocol design can be most effective. The unique effects of NMES have been attributed to several mechanisms, most notably, a reversal of the voluntary recruitment pattern that is known to occur during voluntary muscle contractions. This review outlines the assertion that electrical stimulation recruits motor units in a nonselective, spatially fixed, and temporally synchronous pattern. Additionally, it synthesizes the evidence that supports the contention that this recruitment pattern contributes to increased muscle fatigue when compared with voluntary actions and provides some commentary on the parameters of electrical stimulation as well as emerging technologies being developed to facilitate NMES implementation. A greater understanding of how electrical stimulation recruits motor units, as well as the benefits and limitations of its use, is highly relevant when using this tool for testing and training in rehabilitation, exercise, and/or research.

We tested how lateral stability affects gait as a function of age. A simple computational model suggests that walking is laterally unstable and that age-related decreases in motor and sensory function may be treated as noise-like perturbations to the body. Step width variability may be affected by active control of foot placement subject to noise. We hypothesized that age-related deficits may lead to increased step width variability. A possible compensation would be to walk with wider steps to reduce the lateral instability. The addition of external stabilization, through elastic cords acting laterally on the body during treadmill walking, would be expected to yield reduced step width variability and/or reduced average step width. We measured step width, its variability (defined as standard deviation), and metabolic energy expenditure in eight adult human subjects aged less than 30 years (Young) and ten subjects aged at least 65 years (Old). Subjects walked with and without external stabilization, each at a self-selected step width as well as a prescribed step width of zero. In normal walking, Old subjects preferred 41% wider steps than Young, and expended 26% more net energy (P < 0.05). External stabilization caused both groups to prefer 58% narrower steps. In the prescribed zero step width condition, Old subjects walked with 52% more step width variability and at 20% higher energetic cost. External stabilization resulted in reduced step width variability and 16% decreased energetic cost. Although there was no significant statistical interaction between age group and stabilization, Old and Young subjects walked with similar energetic costs in the stabilized, prescribed step width condition. Age-related changes appear to affect lateral balance, and the resulting compensations explain much of the increased energetic cost of walking in older adults.

Intermittent stimulation of the vagus nerve in four patients resulted in complete seizure control in two, a 40% reduction of seizure frequency in one, and no change in seizure frequency in the other. Side effects (hoarseness, stimulation sensation in the neck, and hiccups) were transient and occurred concomitantly with stimulation. All patients tolerated increasing stimulation parameters well. The results, however, are inconclusive because of the brief duration (6-12 months) of follow-up. Vagal stimulation represents a novel approach for seizure control in patients who have intractable epilepsy, but additional studies are needed to clarify the efficacy and safety of the procedure and to define selection criteria for patients.

Stability is an important concern during human walking and can limit mobility in clinical populations. Mediolateral stability can be efficiently controlled through appropriate foot placement, although the underlying neuromechanical strategy is unclear. We hypothesized that humans control mediolateral foot placement through swing leg muscle activity, basing this control on the mechanical state of the contralateral stance leg. Participants walked under Unperturbed and Perturbed conditions, in which foot placement was intermittently perturbed by moving the right leg medially or laterally during the swing phase (by ∼50-100 mm). We quantified mediolateral foot placement, electromyographic activity of frontal-plane hip muscles, and stance leg mechanical state. During Unperturbed walking, greater swing-phase gluteus medius (GM) activity was associated with more lateral foot placement. Increases in GM activity were most strongly predicted by increased mediolateral displacement between the center of mass (CoM) and the contralateral stance foot. The Perturbed walking results indicated a causal relationship between stance leg mechanics and swing-phase GM activity. Perturbations that reduced the mediolateral CoM displacement from the stance foot caused reductions in swing-phase GM activity and more medial foot placement. Conversely, increases in mediolateral CoM displacement caused increased swing-phase GM activity and more lateral foot placement. Under both Unperturbed and Perturbed conditions, humans controlled their mediolateral foot placement by modulating swing-phase muscle activity in response to the mechanical state of the contralateral leg. This strategy may be disrupted in clinical populations with a reduced ability to modulate muscle activity or sense their body's mechanical state.

Consciousness is determined both by level (e.g., being awake versus being anesthetized) and content (i.e., the qualitative aspects of experience). Subcortical areas are known to play a causal role in regulating the level of consciousness [1-9], but the role of the cortex is less well understood. Clinical and correlative data have been used both to support and refute a role for prefrontal and posterior cortices in the level of consciousness [10-22]. The prefrontal cortex has extensive reciprocal connections to wake-promoting centers in the brainstem and diencephalon [23, 24], and hence is in a unique position to modulate level of consciousness. Furthermore, a recent study suggested that the prefrontal cortex might be important in regulating level of consciousness [25] but causal evidence, and a comparison with more posterior cortical sites, is lacking. Therefore, to test the hypothesis that prefrontal cortex plays a role in regulating level of consciousness, we attempted to reverse sevoflurane anesthesia by cholinergic or noradrenergic stimulation of the prefrontal prelimbic cortex and two areas of parietal cortex in rat. General anesthesia was defined by loss of the righting reflex, a widely used surrogate measure in rodents. We demonstrate that cholinergic stimulation of prefrontal cortex, but not parietal cortex, restored wake-like behavior, despite continuous exposure to clinically relevant concentrations of sevoflurane anesthesia. Noradrenergic stimulation of the prefrontal and parietal areas resulted in electroencephalographic activation but failed to produce any signs of wake-like behavior. We conclude that cholinergic mechanisms in prefrontal cortex can regulate the level of consciousness.

Neuromuscular electrical stimulation can generate contractions through peripheral and central mechanisms. Direct activation of motor axons (peripheral mechanism) recruits motor units in an unnatural order, with fatigable muscle fibers often activated early in contractions. The activation of sensory axons can produce contractions through a central mechanism, providing excitatory synaptic input to spinal neurons that recruit motor units in the natural order. Presently, we quantified the effect of stimulation frequency (10-100 Hz), duration (0.25-2 s of high-frequency bursts, or 20 s of constant-frequency stimulation), and intensity [1-5% maximal voluntary contraction (MVC) torque generated by a brief 100-Hz train] on the torque generated centrally. Electrical stimulation (1-ms pulses) was delivered over the triceps surae in eight subjects, and plantar flexion torque was recorded. Stimulation frequency, duration, and intensity all influenced the magnitude of the central contribution to torque. Central torque did not develop at frequencies < or = 20 Hz, and it was maximal at frequencies > or = 80 Hz. Increasing the duration of high-frequency stimulation increased the central contribution to torque, as central torque developed over 11 s. Central torque was greatest at a relatively low contraction intensity. The largest amount of central torque was produced by a 20-s, 100-Hz train (10.7 +/- 5.5 %MVC) and by repeated 2-s bursts of 80- or 100-Hz stimulation (9.2 +/- 4.8 and 10.2 +/- 8.1% MVC, respectively). Therefore, central torque was maximized by applying high-frequency, long-duration stimulation while avoiding antidromic block by stimulating at a relatively low intensity. If, as hypothesized, the central mechanism primarily activates fatigue-resistant muscle fibers, generating muscle contractions through this pathway may improve rehabilitation applications.

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