CHAPTER 24 Spinal Cord Injury Laura V. Miller Rosanne DiZazzo-Miller “ … of the many forms of disability which can beset mankind, a severe injury or disease of the spinal cord undoubtedly constitutes one of the most devastating calamities in human life ” (Guttmann, 1976). —Sir Ludwig Guttmann, pioneer in 20th-century management of spinal cord injury “The future lies in our own hands, and if a challenge should enter our life, it is important to remember we have tremendous strength, courage, and ability to overcome any obstacle. ” —Douglas Heir, Esq., Attorney-at-Law (personal communication, December 1994) KEY TERMS Autonomic dysreflexia (hyperreflexia) Catheterization Cauda equina Credé’s maneuver Decubitus ulcers Deep vein thrombosis Heterotopic ossification Peristalsis Reflex arc Spina bifida Spinal shock The full impact of the preceding quotes may not strike the reader unless the whole story is known. The latter author, Doug Heir, sustained a spinal cord injury (SCI) at age 18. He dove into a pool to save a boy who appeared to be drowning. The boy was only playing, but Doug’s injury resulted in tetraplegia. Decades later, Doug has become known for being many things, among them an author, US ambassador to the Soviet Union, cover athlete for Wheaties cereal, associate legal editor of the National Trial Lawyer, and a gold medalist in the 1988 Olympics in Seoul, South Korea—an impressive list of accomplishments for someone who sustained “one of the most devastating calamities in human life!”The goals of the health care team should include empowering clients to take charge of their futures. To accomplish this, the health professional must understand the complexities of the diagnosis. This chapter explores the ramifications of spinal cord injuries, beginning with a brief overview of the central nervous system (CNS) and surrounding structures. Description and Definitions Overview of CNS and Related Structures The brain and spinal cord make up the CNS. The spinal cord receives sensory (afferent) information from the peripheral nervous system and transmits this information to higher structures (i.e., the thalamus, cerebellum, cerebral cortex) in the CNS. Descending motor (efferent) information, originating from the cortex, is also transmitted by the spinal cord back to the peripheral nervous system. The consistency of the spinal cord has been compared to a ripe banana, and it is fortunate that the spinal cord and cerebral cortex are protected by bony structures. Whereas the skull protects the brain, the vertebral column protects the spinal cord. The vertebral column is composed of 33 vertebrae, with 7 cervical vertebrae in the neck region (C1 through C7); 12 thoracic vertebrae in the chest region (T1 through T12); 5 lumbar vertebrae in the midback region (L1 through L5); 5 sacral vertebrae (S1 through S5), which are actually fused in the lower back and pelvic region; and 4 fused coccygeal vertebrae that make up the coccyx, or tail bone (Fig. 24.1). There are 31 pairs of spinal nerves, which exit from the spinal cord and branch to form the peripheral nervous system. The nerves exit through the openings formed between each two vertebrae. The spinal nerves are named according to the vertebrae above or below the point of exit. Note that spinal nerves C1 through C7 exit above the corresponding vertebrae, whereas the remaining spinal nerves (C8 through S5) exit below the corresponding vertebrae. Thus, although there are seven cervical vertebrae, there are eight cervical spinal nerves. The actual spinal cord ends just below the L1 vertebra. However, some spinal nerves continue and exit beyond the point where the spinal cord ends. Because of their visual resemblance, this bundle of nerves is referred to as the cauda equina, which is Latin for horse’s tail (Grundy, Tromans, & Jamil, 2002). The meningeal covering of the spinal cord, which contains the cerebrospinal fluid (CSF) that bathes the structures of the CNS, also extends past the end of the spinal cord to the L4 vertebral level. The CSFfilled meningeal space between L2 and L4, referred to as the lumbar cistern, is the site where diagnostic or therapeutic lumbar punctures, that is, spinal taps, are performed, because the spinal cord is not present, yet CSF is accessible. Sensory and Motor Tracts The terms tract, pathway, lemniscus, and fasciculus all refer to bundles of nerve fibers that have a similar function and travel through the spinal cord in a particular area. It is important to know the names, locations, and functions of these tracts to understand the possible outcomes of an SCI at a given level. Figure 24.2 shows the location of major tracts within a cross section of the spinal cord. Figure 24.2 Cross section of cervical spinal cord, shown in relation to surrounding vertebral structures. (From Cohen, B. J. (2012). Memmler's structure and function of the human body (10th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.) A. Spinal cord vertebral level and innervation. B. Spinal cord cross-section diagram. C. Spinal cord crosssection image Two basic types of nerve tissue make up the spinal cord. Gray matter is located centrally and resembles a butterfly in cross sections of the cord. Gray matter is composed of cell bodies and synapses. White matter encompasses most of the periphery of the cord and contains the ascending and descending pathways. Table 24.1 provides a more detailed description of the functions of the various sensory and motor pathways that travel through the white matter of the spinal cord. It may be helpful to remember that many pathways are named according to their origin and the location of their final synapse (e.g., spinocerebellar, corticospinal). TABLE 24.1 Noninclusive Listing of Ascending and Descending Pathways aCalled the posterior column. Each pair of spinal nerves carries specific motor and sensory information. In general, the cervical nerves (C1 through C8) carry afferent and efferent impulses for the head, neck, diaphragm, arms, and hands. The thoracic spinal nerves (T1 through T12) serve the chest and upper abdominal musculature. The lumbar spinal nerves (L1 through L5) carry information to and from the legs and a portion of the foot, and the sacral spinal nerves (S1 through S5) carry impulses for the remaining foot musculature, bowel, bladder, and the muscles involved in sexual functioning. Table 24.2 and Figure 24.3 present a more detailed outline of muscles innervated by each level of the spinal cord and a dermatomal segmentation (sensory map) of the body. Etiology Historically, many demographic sources attempted to count the number of people who have sustained SCIs. Since 1973, the National Spinal Cord Injury Database has been in existence, making strides in collecting comprehensive data on a national level. In 1985, the Centers for Disease Control and Prevention (CDC) began promoting surveillance mechanisms at state and national levels for the collection and reporting of these data. Prior to this time, data related to etiology and incidence of SCI in this country were inconsistently collected and lacked uniformity; advancements are continuing to be made in this area. The leading cause of SCI in the United States is motor vehicle accidents, followed by falls and acts of violence (Fig. 24.5). Sports-related injuries account for most of the remaining SCIs, with diving being historically the most common (and preventable) cause (Table 24.3). Understanding the different contexts in which SCI occurs is critical throughout the course of occupational therapy evaluation and intervention. For example, inner-city populations in particular comprise more SCI secondary to violence than in other environmental contexts. In fact, in the United States, gunshot wounds (GSW) are the third most common cause of SCI (Mayo Clinic, 2011; National Institute of Neurological Disorders and Stroke, 2013). Occupational therapists need to be aware of the culture of violence, environmental influences, and challenges with access to resources that are often unsupportive of individuals with SCI secondary to GSW (DiZazzo-Miller, 2015). Occupations take place throughout the dynamic union of client factors, performance skills, and performance patterns (AOTA, 2014) and are unique to each and every person with an SCI. Analyzing the etiology of SCIs helps target prevention programs. Public awareness of the effects of using substances while operating a vehicle is certainly heightened. Tougher penalties for driving under the influence of cognitive altering substances have been enacted, and many states have adopted seat belt, child restraint, and “distracted” driving legislation. All of these efforts have the potential to reduce the leading cause of SCI. Grant monies have even been awarded to hospital-based programs that evaluate the home environments of senior citizens for safety. Their recommendations may reduce the risk of falls—a major cause of SCI in the elderly. An innovative effort sponsored by the University of Michigan Health System involves airing public service announcements on the prevention of diving injuries before the “coming attractions trailers” at popular movies for teens during the summer months. Although much of the literature focuses on trauma, there are many nontraumatic causes of spinal cord damage. Developmental conditions, such as spina bifida, which is a congenital neural tube dysfunction resulting in an incomplete closing of the vertebral column and spinal cord agenesis, may yield many of the same clinical signs as traumatic SCI. Acquired conditions, such as bacterial or viral infections, benign or malignant growths, embolisms, thromboses, and hemorrhages— even radiation or vaccinations—can also lead to damage of spinal cord tissue. Incidence and Prevalence Incidence rates for SCI in the United States are estimated at 40 cases/million population/year, excluding those who die at the scene of an accident (The National SCI Statistical Center [NSCISC], 2013). This translates to about 12,000 new cases of SCI every year. The statistics indicate that over 80% of people who sustain spinal cord injuries are male; notably, the mean age at time of injury has increased from 28.7 years in the 1970s to the present mean age of 34.7 years (NSCISC, 2014). Seasonal sports cause fluctuations in etiology and incidence statistics throughout a given year, and some urban hospitals are reporting that a disproportionate number of their SCI cases are caused by acts of violence (NSCISC, 2014). In the United States, of the spinal cord injuries reported to the national database since 2010, 63% of individuals were identified as White, 24% Black, 2% Asian, and 10% Hispanic (NSCISC, 2014). One may be tempted to conclude from these statistics that Caucasians are at higher risk for sustaining spinal cord injuries—but this would be erroneous. When compared to the composition of the general population, spinal cord injuries have a higher incidence among non-Whites—specifically among Blacks where the general population is 12% compared to 24% who acquire SCI Signs and Symptoms Sensory Functions The two major classifications of SCI are complete and incomplete. A complete SCI occurs with a complete transection of the cord. In this case, all ascending and descending pathways are interrupted, and there is a total loss of motor and sensory function below the level of injury. The injury also may be referred to as an upper motor neuron (UMN) injury, if the reflex arcs are intact below the level of injury but are no longer mediated by the brain. UMN lesions are characterized by (a) a loss of voluntary function below the level of the injury Complete injuries below the level of the conus medullaris (Fig. 24.1) are referred to as lower motor neuron (LMN) injuries, because the injury has affected the spinal nerves after they exit from the cord. In fact, injuries involving spinal nerves after they exit the cord at any level are referred to as LMN injuries. In these injuries, the reflex arc cannot occur, because impulses cannot enter the cord to synapse. As a result, LMN injuries are characterized by (a) a loss of voluntary function below the level of the injury, (b) flaccid paralysis, (c) muscle atrophy, and (d) absence of reflexes. UMN and LMN injuries may be complete or incomplete. There also may be a mixture of UMN and LMN signs after an incomplete lesion in the lower thoracic/upper lumbar region. The following section discusses incomplete injuries in greater detail. Incomplete Injuries If damage to the spinal cord does not cause a total transection, there will still be some degree of voluntary movement or sensation below the level of injury. This is known as an incomplete injury, which may be further categorized according to the area of the spinal cord that was damaged and the clinical signs that are present. Anterior Cord Syndrome This syndrome results from damage to the anterior spinal artery or indirect damage to anterior spinal cord tissue (Fig. 24.7). Clinical signs include loss of motor function below the level of injury and loss of thermal, pain, and tactile sensation below the level of injury. Light touch and proprioceptive awareness are generally unaffected (Hayes, Hsieh, Wolfe, Potter, & Delaney, 2000). Brown-Séquard’s Syndrome This syndrome occurs when only one side of the spinal cord is damaged (Fig. 24.8). A hemisection of this nature frequently is the result of a penetrating (e.g., stab, gunshot) wound. The clinical signs of BrownSéquard’s syndrome generally include Ipsilateral reduction of deep touch and proprioceptive awareness. (There is a reduction rather than loss as many of these nerve fibers cross.) Contralateral loss of pain, temperature, and touch. Clinically, a major challenge presented by Brown-Séquard’s syndrome is that the extremities with the greatest motor function have the poorest sensation. Central Cervical Cord Syndrome In this lesion, the neural fibers serving the upper extremities are more impaired than those of the lower extremities (Fig. 24.9). This occurs because the fibers that innervate the upper extremities travel more centrally in the cord and, as the name of the syndrome implies, the central structures are the ones that are damaged (Fig. 24.2). Injury to the central portion of of the spinal cord is often seen, along with structural changes in the vertebrae. Most commonly, hyperextension of the neck, combined with a narrowing of the spinal canal, results in this type of injury. Because arthritic changes can lead to spinal canal narrowing, this syndrome is more prevalent in aging populations. The signs of central cord syndrome often include: Improvements in intrinsic hand function are generally evidenced last, if at all (Ackerman, Foy, & Tefertiller, 2013). A potential for flaccid paralysis of the upper extremities, as the anterior horn cells in the cervical spinal cord may be damaged. Because these are synapse sites for the motor pathways, an LMN injury may result. Cauda Equina Injuries Cauda equina injuries do not involve damage to the spinal cord itself but rather to the spinal nerves that extend below the end of the spinal cord (Fig. 24.1). Injuries to the nerve roots and spinal nerves that constitute the cauda equina are generally incomplete. Because this type of injury actually involves structures of the peripheral nervous system (exiting spinal nerves), there is some chance for nerve regeneration and recovery of function if the roots are not too severely damaged or divided. These injuries are usually the result of direct trauma from fracture dislocations of the lower thoracic or upper lumbar vertebrae. Clinical signs of cauda equina injuries include Loss of motor function and sensation below the level of injury. Absence of a reflex arc, as the transmission of impulses through the spinal nerves to their synapse point is interrupted. Motor paralysis is of the LMN type, with flaccidity and muscle atrophy seen below the level of injury. Bowel and bladder function are also areflexic (American Spinal Injury Association, 2008). Conus Medullaris Injuries Conus medullaris injuries are similar to cauda equina injuries. In many cases, it is very difficult to distinguish between these two types of injuries. They can both cause similar signs and symptoms such as local, referred, and radicular pain, loss of sphincter control, and gluteal and lower extremity sensation and weakness (Byrne, Benzel, & Waxman, 2000). Clinical signs of conus medullaris injuries include the following: Loss of motor function and sensation below the level of injury, although typically not severe. Absence of a reflex arc, as the transmission of impulses through the spinal nerves to their synapse point is interrupted. Motor paralysis is of the LMN type, with flaccidity and muscle atrophy seen below the level of injury. Bowel and bladder incontinence and sexual dysfunction are typically more severe than cauda equina injuries (Byrne et al., 2000). Complete Versus Incomplete Injuries In both complete and incomplete injuries, the terms quadriplegia, tetraplegia, and paraplegia may be used to further describe the impact of the injury. Quadriplegia refers to lost or limited function of all extremities as a result of damage to cervical cord segments. The American Spinal Injury Association (ASIA) advocates the term tetraplegia over quadriplegia. Tetraplegia refers to impairment or loss of motor or sensory function in the cervical segments of the spinal cord that is the result of damage of neural elements within the spinal canal. Tetraplegia causes impairment of function in the arms as well as in the trunk, legs, and pelvic organs. It does not include brachial plexus lesions or injury to peripheral nerves outside the neural canal (American Spinal Injury Association/International Medical Society of Paraplegia, 2013). Paraplegia, which refers to lost or limited function in the lower extremities and trunk depending on the level of injury, occurs after lesions to thoracic, lumbar, or sacral cord segments. Spinal cord injuries are frequently classified further, based on the ASIA Impairment Scale (American Spinal Injury Association/International Spinal Cord Society, 2013), which contains the following levels: Level A Complete; no motor or sensory function is preserved in the sacral segments S4 through S5. Level B Sensory incomplete; sensory but not motor function is preserved below the neurological level and extends through the sacral segments S4 through S5. Level C Motor incomplete; motor function is preserved below the neurological level, and the majority of key muscles below the neurological level have a muscle grade
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