Motor Stimulation

Clinical presentation

In 2013, 1.7% of the US population, or 5.4 million people, were living with paralysis. The leading causes of paralysis were stroke and spinal cord injury (SCI). Limitations brought on by any degree of paralysis significantly impact not only activity but also quality of life and emotional well-being. Patients with SCI and multiple sclerosis, another important cause of paralysis, are at 2.3 to 7.5 times greater risk of suicide than age-matched individuals in the general population. In this chapter, we will discuss the application of electrical stimulation to produce functional contractions of paralyzed or paretic muscles. These systems not only lead to functional improvement but, in some cases, can retrain the central nervous system to recover previously learned motor skills and alleviate pain.

Mechanism of motor peripheral nerve stimulation

The motor unit consists of the alpha motor nerve, or lower motor neuron, and the muscle fibers it innervates ( Fig. 41.1 ). Motor units vary in both size and fiber type, which allows the central nervous system to produce the precise movement appropriate for different circumstances, from fine eye and hand movements to explosive athletic compound movements. Disruption in signaling along this pathway, as occurs in stroke, SCI, multiple sclerosis, and so on, is a cause of significant disability and activity limitation, especially among older adults. Use of electrical stimulation to treat this type of disability spans more than 2000 years; however, the real wealth of information highlighting technological advances and the potential for rehabilitation began in the early 1960s. It was during the 1960s that the term “functional electrical stimulation” (FES) was coined to describe the use of neuromuscular electrical stimulation (NMES) applied to a paretic muscle to accomplish a functional task.

Researchers have developed a wide variety of prostheses to treat these deficits; however, nearly all of these prostheses work by electrically activating the muscle fibers of each motor unit served by a motor or mixed (motor/sensory) nerve. NMES, similar to most forms of electrical stimulation for pain, is delivered as a waveform characterized by stimulus frequency, amplitude, and pulse width. The amplitude and pulse width are the primary determinants of the number of muscle fibers that are activated. The mechanical response to repeated stimulation depends on the rate of the stimulation. Muscle, like other excitable tissues, has a period following its action potential during which the membrane will not respond to stimulation regardless of the strength. Therefore, a second pulse within that time span will not elicit any response. If, however, the pulses are sufficiently far apart, the muscle will be relaxing when the second pulse is given, and the tension will appear in waves in phase with the stimulation, causing an unfused tetanus. It is possible to stimulate the muscle at a frequency between these extremes so that the tension developed by the muscle remains constant. This latter type of contraction is called a fused tetanus, and the rate of stimulation that produces it is called the fusion frequency. Higher stimulus frequencies generate higher forces but can result in muscle fiber fatigue and rapid decrement in contractile force. An optimal NMES system utilizes the minimal stimulus frequency that produces a fused response. Stimulation frequencies that produce constant tension range from 12 to 16 Hz for upper-limb applications and 18 to 25 Hz for lower-limb applications (frequency range for NMES systems is 10–50 Hz).

The clinical application of NMES systems is complicated by the fact that the contractile force of muscle is highly nonlinear and variable over time, as well as by the differences in the recruitment pattern. An action potential produced by normal physiologic mechanisms initially recruits the smallest-diameter neurons prior to recruitment of larger-diameter fibers, while nerve fiber recruitment patterns mediated by NMES follow the principle of “reverse recruitment order.” Several stimulation techniques for selective activation of small fibers have been proposed, including high frequency block, anodic block, subthreshold-depolarizing prepulse, and single cathode. These techniques, however, require long-duration stimulation pulse (>500 microseconds) and large stimulation amplitudes. This leads to high charge injection at the electrode, which can cause corrosion. Furthermore, recent publications have suggested that NMES recruits in a nonselective, spatially fixed, and temporally synchronous pattern. Rather than attempt to reverse the recruitment order, researchers are now attempting to find parameters that delay fatigue of each motor unit regardless of when it is recruited.

Peripheral and central mechanisms of benefit

The rationale for use of motor stimulation is based on the physiological changes at muscle and spinal levels that occur over time. For example, repeated muscle contraction from peripheral nerve stimulation (PNS) increases the oxidative capacity of muscle, increases the number of microcapillaries, and leads to transformation of muscle fiber types. A small but expanding body of literature demonstrates that FES induces rapid plastic change in the sensorimotor regions of the cortex. This suggests that repetitive movements that are goal oriented and functionally relevant can facilitate relearning following stroke or brain injury. Motor relearning is defined as “the recovery of previously learned motor skills that have been lost following localized damage to the central nervous system.” It was hypothesized that the use of FES, which generates both an orthodromic and an antidromic impulse, may modulate activity in anterior horn cells via antidromic impulses. These impulses were thought to strengthen Hebbian-type synapses between pyramidal tract cells and the anterior horn cells, contributing to restoration of voluntary control. However, it is now largely accepted that the recovery is due to plastic changes in the sensorimotor cortex due to unmasking of latent horizontal connections, activation of silent synapses, modulation of activity-dependent synaptic plasticity, and generalized changes in the excitability of postsynaptic neurons.

Effects on cortical perfusion were recently studied in combination with FES in chronic stroke patients. This study found that the sensory motor integration due to FES may facilitate perfusion of the ipsilesional sensory motor cortex and result in functional improvement of hemiparetic upper extremity. After FES treatment, only patients who showed improved perfusion to the ipsilesional sensory motor cortex perfusion showed functional improvement of upper extremity. This further supports the idea that recovery of paretic limbs due to upper motor neuron lesions is largely the result of reorganization of the sensorimotor cortex, but that FES can help to facilitate this process. This neuroplasticity may also drive the alleviation of pain symptoms experienced by patients with motor stimulation.