ABSTRACT
INTRODUCTIONSpinal cord injury (SCI) is a complex and devastating condition involving permanent disruption of signal transmission between the brain and the sensorimotor and autonomic systems below the injury level. This disruption is typically caused by vertebral bone and disc fragments, dislodged by fractures and dislocations, that puncture or rupture neural tissue and blood vessels [1].The American Spinal Injury Association (ASIA) has established a clinical diagnostic scale that divides SCI into five categories (ASIA A, B, C, D, and E), depending on the degree of neurological deficit [2]. The category descriptions are as follows: ASIA A: no sensory or motor function in the fourth and fifth sacral (S4, S5) spinal segments; ASIA B: preservation of sensory function below the level of injury, including the fourth and fifth sacral
spinal region, but absence of motor function more than three spinal levels below the injury; ASIA C and D: intact sensory function and motor function more than three spinal levels below the injury, the difference between them depending on the degree of motor activity that is present, which can range from palpable muscle contractions to either observable or functional limb movement; and ASIA E: complete recovery of motor and sensory function.It is estimated that in the United States alone, with an annual incidence of 40 cases per million, 240,000 to 337,000 people live with paralysis resulting from SCI [3-5]. The majority of these cases are caused by vehicular accidents (38%), falls (30%), violence (14%), and sport injuries (9%) [5]. Mortality rates associated with SCI have drastically decreased in the last 30 years due to improved emergency responsiveness, surgical stabilization, and early post-injury rehabilitation strategies [6]. Improved prevention and treatment of secondary complications (e.g., urologic infections, renal failure, and respiratory complications) has further reduced mortality rates and continues to drive the average life expectancy of SCI victims toward that of the general population [3, 7-9]. However, metabolic changes, autonomic dysfunction, and reduced physical exercise leading to loss of muscle mass and increased levels of adipose tissue increase the risk of cardiovascular complications for SCI survivors [10-13]. Thus, risk of premature death in SCI survivors continues to be higher than in individuals without SCI [14-16]. These health-related complications, combined with an estimated patient population cost of over $35 billion annually in the United States, highlight the importance of improving current therapies and restoring function lost as a result of SCI [5]. FUNCTIONAL ELECTRICAL STIMULATIONLimb movement as well as the autonomic functions of respiration, bladder, bowel, and sexual function receive inputs from higher brain centers, but are ultimately controlled by efferent neurons that originate within the grey matter of the spinal cord [17]. When transmission of brain signals to these efferent neurons are interrupted, permanent loss of motor and autonomic function
occurs below the lesion. However, the spinal circuitry both above and below the injury remains intact. These intact neuromuscular networks lay dormant but remain capable of evoking and coordinating limb movements when externally stimulated [18-22]. This can be achieved using functional electrical stimulation (FES), a form of therapy that applies electrical currents to various locations within the neuromuscular networks below the level of injury to evoke muscle contractions (Fig. 16.1) [23]. Electrical excitation of motor neurons leads to depolarization of skeletal muscle, followed by a cascade of events within the myocytes, which results in contraction of the muscle and thus a “functional” response (Fig. 16.2).
