Да простят меня за передирание статьи полностью, но формат у них несносный.
Tibor Hortobágyi, Ph.D.
East Carolina University
Greenville, NC 27858
Phone: (919) 757 - 4688
Electrical muscle stimulation has a long history, that is, the history of electricity and medicine combined. In 2600 B.C., Egyptians utilized the galvanizing nature of some animals for medical purposes. Scribonius Largus, a physician in the Roman empire, reported first on the use of electricity for pain relief in 47 A.D. He described a case when a live torpedo fish was used for the relief of headache and gout pain. Useful but not very convenient as a therapeutic approach, some 1,700 years later the torpedo fish was replaced with the Leyden Jar, invented in 1745 by a Dutch mathematician, Pieter van Musschenbroek (1692-1761). The Leyden Jar is a simple device that can store electric charge, i.e., electric force. Two gold foil leaves are suspended in a glass jar. The leaves are connected to an outside metal ball wired to the metal jacket on the outside of the glass jar. When electricity is introduced from the outside into the jar, the charge is stored between the gold leaves in the form of repulsive force that separates the leaves. Though rudimentary, the Leyden Jar, modified for the purposes of electrotherapy by John Wesley in 1760, was used to shock patients suffering from paralysis or convulsive seizure and to abolish pain from headache, angina, and sciatica.
These early attempts, experimental, if not accidental, were reformed by Luigi Galvani's (1737-1798) 1791 observation that muscles and nerves were truly excitable, even though Galvani wrongly assumed that muscle contraction was caused by the discharge of "animal electricity". In 1793, Alessandro Volta (1745-1827) discovered that muscle contraction occurred if a piece of metal (the "bi-metallic rod") was placed on the surface of a spinal motor nerve and on the muscle it innervates. This electrical responsiveness of the tissues was seen to be pervasive in biological systems and to be responsible for a broad range of biological activities in nerves and muscles. Volta's experiments demonstrated that electrical muscle stimulation could overcome interruptions in the pathways from neurons to muscles. Could paralyzed muscles then be externally electrically stimulated to re-establish functional movement lost due to accidents and injuries? To answer this question, rehabilitation researchers and therapists had to achieve great advances to completely free spinal cord injured patients from their wheelchairs.
Skeletal muscle is excitable tissue. To the muscle, there is not much difference between a normal neural impulse or one generated artificially. So when a muscle is stimulated, either directly or through its nerve, it contracts. Furthermore, the contractile force response to electrical stimulation is influenced by many factors. One important consideration is the means of transmission of the electric current to the motor nerve. Cloth-covered electrodes placed on the skin surface were used as early as 1833 by Duchenne de Boulogne.
Today, however, stimulating current is passed onto the motor nerve via intramuscular or over-the-skin electrodes of different size and material. With experience, researchers also noted that, peculiarly, it was easier to elicit a muscle contraction if the electrodes were placed at a discrete location on the skin over a particular muscle. Mapped for all accessible muscles of the body, these sites were termed "motor points", the greatest concentration of muscle-nerve junctions in the superficial layer of muscles. Even if stimulated exactly above the motor point, a muscle's force production varies according to stimulus parameters such as the type, size, placement, and configuration of electrodes and whether voltage or current is controlled. The manipulation of the stimulus wave-form (rectangular, sinusoidal, triangle, symmetric, asymmetric, etc.) and its duration, amplitude, and frequency are all factors to consider for the reproduction of the physiological coupling of muscles with nerves.
Indeed, electrical muscle stimulation is far from natural even in the hands of the most experienced therapists with the best intentions. Skeletal muscle's force response to stimulation depends on stimulation intensity and frequency. One single shock to a muscle results in a muscle twitch of some 200 milliseconds in duration. If the stimulation frequency is increased to 10 or 20 pulses per second (i.e., 10 or 20 Hz, low frequency stimulation), muscle contraction becomes ragged or twitch-like because the force production fluctuates according to the on-off periods of the stimulus. On the contrary, if a muscle is stimulated at higher frequencies, the contraction is smooth and force production peaks (tetanus), but the muscle fatigues rapidly.
On the other hand, natural force production by the motoneuron-stimulated muscles is different and more sophisticated (1). Under natural conditions, motoneurons (i.e., the nerves that innervate the muscle fibers) fire asynchronously, whereas the artificial electrical muscle stimulation signals are synchronous. When stimulated naturally, motor units (i.e., the motoneuron plus the muscle fibers it innervates) produce muscle force by hierarchically calling in the smaller units first at low forces followed by the larger units at high forces. In addition to this so-called orderly recruitment of motor units, a second natural mode of force regulation is the increase in firing rates of the motor units at higher contraction levels.
However, in case of electrical muscle stimulation motor units are recruited in a reversed order: because of their lower resistance, the larger motor units are recruited first, an observation made by Blair and Erlanger as early as 1933. Physiologically, the large motor units are made up of fast-contracting and rapidly fatiguing muscle fibers, whereas the small motor units contain slow-contracting fatigue-resistant muscle fibers. Hence, artificial electrical muscle stimulation that aims for high force production must use high frequency stimulation, but unavoidably will result in muscle fatigue.
To overcome fatigue, researchers and therapists vary stimulation parameters (i.e., pulse amplitude, pulse duration, frequency, rest period). Still, muscle force production is submaximal and poorly controlled. Since 1975, several research groups have tried to simulate natural events of muscle contraction using artificial stimulation. Solomonow and his co-workers used a four-electrode set-up. High frequency stimulation was injected through one electrode pair to a nerve bundle. This high frequency stimulus was used to block large axons from firing initially. The researchers then simultaneously applied low frequency stimulation and, with computer control of the high frequency stimulus, achieved a natural recruitment order of motor units.
Therapeutical electrical muscle stimulation, as used today, has probably evolved from experience with artificial cardiac pacemakers. In the early 1950s, a patient suffering for some 20 minutes from Adam-Stokes syndrome, a stoppage of heart beat, was treated by placing a set of stimulating electrodes of a pacemaker on his chest. Upon stimulation, the patient's heart started to beat and he was resuscitated.
Since its inception, over-the-skin electrical muscle stimulation has been used as a clinical modality and research tool. Electrical muscle stimulation has been employed to re-educate skeletal muscles, hasten recovery from knee ligament surgery and from chondromalacia patellae, reduce exaggerated muscle tone (spasticity) and range of motion (contractures), ameliorate pain, prevent deep vein thrombosis, assess fatigability, and evaluate plasticity of the neuromuscular system in human and animal research models. However, the primary areas of application include muscle strengthening and restoration of functional capacities.
Today, muscle strengthening by means of electrical stimulation is a routine procedure in rehabilitation clinics (2). It is now well accepted that muscles become stronger and larger at a faster rate if subjected to exercise with heavy loads. That is why the magnitude of tetanic force, in comparison to the maximal voluntary force, is important. Because electrical muscle stimulation brings in the large high-force motor units first, muscles get stronger and bigger even if trained with electrical stimulation intensities corresponding to below-maximal voluntary intensities.
Accordingly, some researchers also noted that strengthening of atrophied muscles of meniscectomy patients is more easily achieved with electrical stimulation than with voluntary exercise training. Research studies suggest that electrical stimulation of the knee extensor muscles can improve the isometric strength (i.e., exertion without apparent change in muscle length) up to 50 per cent. Unfortunately, other muscle groups have not been extensively studied for potential strength gains in response to electrical muscle stimulation. Ultimately, the success of a training program depends on the stimulation frequency and intensity that can be tolerated by the patient (low frequency is more fatiguing but the force response is lower) and the duration of the sessions and the entire program.
When normal muscles are trained with electrical stimulation, the initial rate of strength gains is rapid and without change in muscle volume. This suggests that the adaptive mechanisms are neural in nature. One possible mechanism is the increased activation of the spinal motoneuron pool. These motoneurons regulate force production due to the stimulation of the sensory (afferent) neurons. Long-term potentiation has also been implicated, involving an increased sensitivity of synapses due to the stimulation of the afferent nerve fibers. Therefore, strength gains can be maintained for some weeks even if training is discontinued--hence long-term potentiation. Grouped or synchronized firing of the motor units is also a potential mechanism for strength gains. The beneficial effects of muscle strengthening with electrical stimulation are unequivocal in muscles weakened by disuse. For example, when the leg is casted for three weeks, the muscles of the thigh atrophy by 20%. But if electrical stimulation is applied to the immobilized muscles, initial muscle size is maintained. These beneficial effects of electrical muscle stimulation are accompanied by increased blood flow inside the muscles and in the surrounding soft-walled veins, thus enhancing the pumping action of the muscles.
While electrical muscle stimulation for the purpose of strengthening a single muscle group is a relatively simple procedure, the restoration of daily function using electrical stimulation is a much more difficult task. For example, a stimulation paradigm that allows a person with paraplegia (spinal cord damage in the thoracic or lumbar region causing paralysis of the legs and the lower body) to stand up from the wheelchair and walk across the street requires the coordinated contraction of some 30 muscles. Impossible as it sounds, the effort would be well worth it from a humane and financial standpoint to the patients. The societal impact of the approximately 10,000 patients with spinal cord injury admitted to hospitals yearly is substantial: their average age is about 30 years and the projected life span is 70 to 80 years with an estimated health care cost of about two million dollars per patient per lifetime (4). Usually a person with spinal cord injury is confined to wheelchair, a mode of "therapy" and lifestyle. Despite the revolutionary changes anticipated due to the 1990 passage of the Americans with Disabilities Act, these patients continue to suffer from physical and psychological setbacks: access to facilities and buildings, pressure ulcers due to long-term sitting, and the unavoidable feeling of dependence. One viable alternative to wheelchairs is the restoration of muscle function using electrical stimulation.
By understanding the basic anatomical, motor control, and engineering principles, a ground-breaking experiment was carried out in 1961. Liberson and his colleagues engineered an electrical stimulator that allowed the stimulation of the peroneal nerve in synchrony with the swing phase of gait to avoid foot drop in a patient with hemiplegia (paralysis of one side of the body). Likewise, Kantrowitz and his colleagues used electrical stimulation in a patient with paraplegia who, upon electrical stimulation of the knee extensors and gluteus muscles, was able to stand erect freely for a few minutes. These early successes opened up new opportunities in electro-muscle therapy, appropriately coined "functional electrical muscle stimulation". The goal of functional electrical muscle stimulation is to restore functional capacity of muscles (i.e., breathing, sitting, standing, walking, reaching, grasping) following a debilitating trauma. Primary candidates for functional electrical muscle stimulation include persons with paraplegia, hemiplegia, and quadriplegia (spinal cord damage in the cervical area causing paralysis of all four limbs), individuals with spinal cord injury or patients suffering from an impairment of the central nervous system (e.g., multiple sclerosis, head injury, or children with cerebral palsy).
In contrast to the electrically evoked contractions for muscle strengthening during which muscle contraction forces are gradually increased, held for several seconds and repeated several times, the procedures of functional electrical muscle stimulation use short trains of impulses to achieve target levels of force with a rapid rise. A person with paraplegia with disabilitated dorsiflexors (i.e., muscles that bend the foot upward), could clear a threshold only if the tibialis anterior was stimulated with a brief, high frequency train, producing a rapidly rising and high force. In person with paraplegia and quadriplegia the best hope to date for some recovery of lost functions is electrical muscle stimulation. In these patients, stimulation is targeted at the portion of the motoneuron that remains intact below the level of spinal cord damage.
However, researchers in Europe and the United States have encountered several problems in aiding patients with movement deficits. For instance, the extent and speed of movement is directly related to fatigue, electrode positioning, the interaction between electrodes and the skin surface, muscle temperature, and many other factors. In addition, following spinal cord injury or stroke, muscles atrophy, strength declines to a fraction of its initial level, and disuse seriously impairs cardiovascular and respiratory functions (e.g., blood volume is reduced).
Because resistive exercise with electrical stimulation is not the best way to improve cardiovascular function, many researchers have opted for exercise bicycle ergometer combined with computer controlled electrical stimulation of the paralyzed patients' leg muscles. The bicycle is equipped with special sensors to monitor crank position and speed. This information is then fed into a computer to regulate the timing and pattern of the electrical stimulation of the muscles. Results using this technique in the 1980s showed that paraplegic and quadriplegic patients who suffer from low blood pressure, were able to increase resting blood pressure and heart rate. Cardiovascular responses to exercise were also favorable. Thus, the patients achieved not only cardiovascular improvements, but their muscles got stronger as well. These are fundamental prerequisites for changing body position (e.g., from sitting to standing) without fainting due to poor circulation, or for standing and walking (muscle strength, fatigue).
The ultimate goal for patients with spinal cord injury is to ambulate (4). Even after some level of cardiovascular stability is achieved and muscular strength is recovered, muscle fatigue and subsequent falls represent major challenges to patients and researchers. During gait, muscles are stimulated in the swing phase to advance the limb. Muscles are also stimulated during the stance phase so the patient can remain in the upright position. Despite the momentary recovery periods between swing and stance phases of one leg, due to the activation of the fatigue-prone fast motor units by the stimulation, fatigue sets in rapidly and muscles can simply fail. Fatigue may also prevail because the disruptions of the spinal cord promote the conversion of slow fatigue-resistant to fast fatigable muscle fibers, particularly in the weight-bearing muscles that cross single joints. Further, postural instability may cause falls. This instability is related to the small number of muscles stimulated, compared to the total number of muscles that would normally require stimulation.
Due to equipment limitations and accessibility to the muscles, at present an "all-muscle" stimulation paradigm is not possible. Patients are therefore provided with orthoses of different complexities to compensate for the ruggedness of gait controlled by electrical stimulation. Because sensory feedback from muscles, joints, and skin to the motor centers is a key element of controlled movement and such feedback may or may not be intact in spinal cord injured patients, future research efforts on electrical muscle stimulation will probably focus on the addition of the sensory segment of the system.
Restoration of movement with electrical stimulation in stroke paralysis has been historically unsuccessful. In patients who have suffered a stroke, spontaneous recovery of lost motor function occurs one to three months after stroke, with little, if any, further recovery beyond one year. In contrast to functional electrical muscle stimulation, patterned electrical muscle stimulation applies the template of the firing pattern recorded in the healthy limb to the paralyzed muscles of the other limb (3). For example, the intact biceps and the triceps muscles' activity pattern is detected and recorded during the flexion of the straight arm. Then the timing and amplitude parameters of these electromyographic activities (the synergy patterns) are analyzed. Using a mathematical model, the activity patterns are reconstructed and applied via an electrical muscle stimulator to the impaired muscle pair. When the impaired muscles contract, a sensory stimulus pattern ascends to the brain where, in way thus far unidentified, a new motor template is generated. Once the new motor template is available, voluntary movement may be possible. Patterned electrical stimulation has been employed with some success in stroke-paralyzed patients' arm and lower leg muscles. And when a patient with paralysis is enabled to move a finger or flex a toe with the aid of electrical muscle stimulation therapy, we all know that the effort was well worth it: a pinnacle of achievement in the history of electricity and medicine.
1. Bach-y-Rita, P. (Editor) Recovery of Function: Theoretical Considerations for Brain Injury Rehabilitation. University Park Press, Baltimore, MD, 1980.
2. Kralj, A. and T, Bajd. Functional Electrical Stimulation: Standing and Walking after Spinal Cord Injury. CRC Press, Boca Raton, FL, 1989.
3. Kilmer, W., W. Kroll, V. Congdon. An EMG-level muscle model for a fast arm movement to target. Biological Cybernetics 44:17-26, 1982.
4. Phillips, C.A. Functional Electrical Rehabilitation. Springer-Verlag, New York, NY, 1991.