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Keywords:

  • spinal cord;
  • neurotrauma;
  • neuroscience;
  • vertebral column;
  • surgery;
  • anatomy

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

The primary cause of spinal cord injury (SCI) is automobile collisions, followed by violence, falls, and injuries in sporting events. The patient is most frequently a young male. Regardless of cause and age, SCI is a potentially catastrophic injury. The unique anatomical relationship of the spinal cord, being enclosed in the dural sac within the bony vertebral column, make it venerable to a wide range of traumatic insults. SCI is classified as complete or incomplete with several subclasses arranged under each of these respective headings. The probability of recovery to a functional state is usually better for patients with incomplete injuries. Treatment for SCI involves initially immobilizing the injured vertebral column, medications to prevent secondary injury, and potential surgery to release pressure on the spinal cord and restore stability to the vertebral column. Postsurgical care is directed toward prevention and treatment of secondary complications of SCI such as respiratory failure, deep venous thrombosis, and decubitus ulcers. Advances in these areas are providing patients with a greater probability of recovery, a longer life, and a better quality of life. Research in the clinical and basic sciences is opening new avenues of hope for the spinal cord injury patient. Anat Rec (Part B: New Anat) 271BB:41–48, 2003. © 2003 Wiley-Liss, Inc.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Despite advances in the field of medicine, injury to the spinal cord remains a devastating problem. The annual incidence rate of spinal cord injury (SCI) in the United States has been estimated at 32–50 per million; with prehospital fatalities included, the estimated incidence rate increase to a range of 43 to 55 per million annually. The death rate from SCI approaches 50% with nearly one in five patients who survive the initial injury ultimately succumbing in the hospital (Sekhon and Fehlings, 2001). Morbidity is high and those that survive usually require lengthy stays in hospitals and rehabilitation facilities. Although the emotional toll from SCI on the patient and family is tremendous, the financial burden to, not only the patient and family, but to society as a whole is staggering.

Although the emotional toll from SCI on the patient and family is tremendous, the financial burden to, not only the patient and family, but to society as a whole is staggering.

Despite the relative low incidence of SCI, it was estimated in 1990 that the cost of caring for Americans with SCI was $4 billion annually (Stripling, 1990).

HISTORY

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Recordings of SCI in history date to the oldest known surgical document, the Edwin Smith Papyrus, which dates approximately 5,000 years ago. SCI was referred to as “an ailment not to be treated” (Elsberg, 1931). Hippocrates initially attempted treatment with large amounts of liquid, preferably milk from a donkey, mixed with honey along with Egyptian white wine (Vidus, 1544). He later developed a traction table that attempted to place the injured person in extension and reduce any fracture to the spine with a wooden plank. The first recorded surgery for SCI involving the removal of crushed bony elements occurred in the seventh century. Scholars later compared this surgical intervention with the extension bench of Hippocrates and found there to be no difference in the outcome. Thus, thoughts returned back to the Edwin Smith Papyrus and conservative management was chosen. This premise prevailed into the 20th century when basic science research and aggressive surgical intervention began to accelerate. The outlook for SCI has remained grim until recently. The advent of new pharmacologic strategies and the boom of stem cell research have given hope to those with the “ailment not to be treated.” See Collins (1995) and especially Greenblatt et al. (1997) for excellent historical perspectives.

ANATOMY

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

The spinal cord is a soft, delicate structure that exits the base of the skull, where it adjoins the brainstem, to run most of the length of the vertebral column to the lower back where it ends by giving off nerves traveling to the lower extremities. In children, the spinal cord ends at approximately the level of the second lumbar vertebrae. As the child grows, the spinal cord does not keep pace with the growth of the rest of vertebral column and, thus, ascends so that in the normal adult the conus medullaris lies opposite the first lumbar vertebrae. Both the brain and spinal cord are housed in the meninges, in which cerebrospinal fluid flows, providing some nutrients and serving as a protective cushion. Throughout its length, the spinal cord and dural sac are surrounded by the bony vertebral column that protects it from injury. Not only bone, but also ligaments, cartilage, muscle, and intervertebral discs hold the vertebral column together. Disruption of any of these structures surrounding the spinal cord may result in SCI.

In younger victims, SCI is usually secondary to a forceful trauma such as a motor vehicle collision or fall from a significant height. In the elderly, diseases such as osteoporosis, arthritis, or loss of muscle mass, can weaken the vertebral column, leading to a fall with resultant injury to the spinal cord itself. The pathophysiology of traumatic cords is usually a result of rapid cord compression secondary to a fracture and dislocation of the adjacent bony structures. It is believed that this primary injury to the spinal cord then initiates a cascade of events that leads to secondary injuries. These include (1) disruption of the normal blood flow to the cord leading to poor oxygenation or ischemia, (2) inflammation, (3) swelling of the cord, (4) release by the damaged cord of substrates that further damage the cord itself, and (5) activation of programmed cell death, known as apoptosis. These processes are believed to begin within the first few hours of injury. There recently has been a tremendous amount of basic science research leading to exciting discoveries and ultimately to the optimism in the treatment of SCI today (reviewed in Boyd et al., 2003; see also Jones, 2003).

When referring to SCI, there are two general types of lesions, based on location, that give rise to a predictable set of deficits. These are commonly called upper motor neuron (UMN) lesions (also called supranuclear lesions) and lower motor neuron (LMN) lesions. Upper motor neuron cell bodies are located at some supraspinal site, for example, motor cortex, red nucleus, reticular formation, and send their axons down the spinal cord to influence the activity of motor neurons in the spinal cord gray matter. Damage to upper motor neurons gives rise to UMN signs that include (1) muscles that are initially weak but may become spastic, (2) effects on groups of muscles not an individual muscle, (3) hypertonia, and (4) hyperreflexia (the Babinski sign, dorsiflexion of the great toe, is an example). Lower motor neuron cell bodies are located in the spinal cord gray matter (or cranial nerve motor nuclei); their axons directly innervate skeletal muscle. Damage to lower motor neurons gives rise to LMN signs that include (1) muscles that are weak and with time will atrophy, (2) muscles that involuntarily twitch (fasciculations), (3) hypotonia, and (4) hyporeflexia or areflexia. Depending on a variety of variables, as will be discussed below, UMN or LMN signs, or a combination of these, may be seen in the SCI patient.

The way in which one moves and perceives sensations is based on electricity. For example, after touching your thumb to a hot stove, receptors in the thumb convert this mechanical stimulus into electrical information that is relayed up nerves in the upper extremity to the spinal cord and into the brain. Here, through complex circuitry, the information is transported to the sensory cortex of the brain, which ultimately influences the motor cortex. The motor cortex houses the nerve cell bodies that, by means of corticospinal axons, influence motor neurons in the spinal cord. In this example, movement of the arm, forearm, hand, and thumb is seen in response to sensory input.

The spinal cord receives its blood supply from the anterior spinal (branch of the vertebral artery) and posterior spinal (branch of the posterior inferior cerebellar artery) arteries (Figure 1). Throughout their course, the spinal arteries receive small branches from segmental arteries at various levels to supplement the blood supply to the spinal cord; these are sometimes referred to as anterior and posterior spinal medullary arteries (Figure 1). These supplemental vessels anastomose with the arterial vasocorona on the surface of the spinal cord.

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Figure 1. Diagrammatic cross-section of half of the spinal cord at a cervical level showing the position of the main vessels, the territories they serve and the three main pathways discussed in the text (corticospinal tract, posterior columns, anterolateral system). L, lower extremity; T, trunk; A, upper extremity (Reprinted from Haines, 2002. Fundamental neuroscience. 2nd ed. p. 142. Churchill Livingston, with permission from Elsevier Science.)

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The anatomy of the spinal cord is complex. Like the brain, the spinal cord consists of a white matter comprising tracts and a central gray matter made up of numerous neuron cell bodies (including lower motor neurons) along with their supportive (glial) cells. The posterior horn is related to sensory input and the anterior horn to motor outflow. Fibers that influence lower motor neurons course through the corticospinal tract. The organization of fibers in this tract, as pertains to the upper and lower extremities, are important (Figure 1). Motor fibers from the upper extremity area of the motor cortex are located medially, whereas those from the lower extremity area of the motor cortex are more lateral. There are different types of sensations carried in separate tracts. Pain and temperature information is transported through the anterolateral system, whereas vibratory and position sense are carried in the posterior column system of the spinal cord (Figure 1). There are many other tracts that carry information related to motor and sensory function, although damage to the aforementioned tracts are most specifically related to the signs and symptoms seen in the SCI patient.

CLASSIFICATION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

The American Spinal Injury Association has established a standardized method for assessing neurologic status and classifying a spinal injury (International Standards for Neurological Classification of SCI; Anonymous, 2000). According to these standards, an SCI is classified as tetraplegia (quadriplegia) if it involves a cervical spinal segment or paraplegia if it involves a thoracic, lumbar, or sacral spinal segment. An SCI is further identified as being complete (absence of all motor or sensory function at the lowest sacral level) or incomplete (at lease some preservation of motor or sensory function below the level of the injury, including the lowest sacral level). Accordingly, trauma to the sixth cervical segment resulting in loss of all motor and sensory function below that level would be defined as complete tetraplegia. Likewise, an injury involving the conus with some preservation of perianal sensation or voluntary anal sphincter contraction would be defined as incomplete paraplegia. The classification scheme further outlines a method for quantifying both motor and sensory function that results in a motor score and independent sensory scores for light touch and pin prick sensation. Finally, a scale is included that quantifies the degree of impairment the patient experiences as a result of the injury.

A systematic examination of the myotomes and dermatomes of a spinal cord patient using The International Standards for Neurological Classification of SCI provides data that can be readily interpreted by any clinician, although it may have been generated by another examiner. The data can also be used for standardized data analysis among different institutions. Spinal injuries often show some improvement over time so the outcome measures (ASIA motor score, sensory scores, and impairment scale) accurately quantify changes in spinal function. Finally, the accumulation of data from a large number of SCI patients over time can be used to generate prognostic statistics.

When the spinal cord is injured, it is very slow to recover, if at all, particularly for complete spinal injuries. Although many patients with complete SCI will recover root function at or adjacent to the level of injury, the prognosis for significant long tract recovery is poor. The acutely injured patient often wants to know if the spinal cord is “severed” assuming that a cord that is not severed has a better chance for recovery. Unfortunately, in most cases of complete SCI, the cord is crushed or contused but not anatomically transected (Figure 2). Complete SCI is a functional transection of the spinal cord in which electrical impulses of sensory information going up to the brain, as well as, motor information coming down from the brain are disrupted. It is the complete loss of neural communication across the injury level evidenced by the neurologic examination that establishes a poor prognosis of recovery.

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Figure 2. A sagittal T2 weighted magnetic resonance image showing the appearance of a spinal cord contusion at the C5 levels. The C5 vertebral body is crushed and displaced posteriorly with resulting spinal cord compression. Note that the spinal cord is severely injured but not anatomically transected.

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Incomplete spinal cord injuries cover the spectrum from patients that have minimal preservation of distal sacral function to those that are practically normal. Even the more severe incomplete injuries have a significantly better prognosis than a complete SCI. The old saying is that if an acute spinal cord injured patient “can wiggle a toe they can eventually walk.” There are several subtypes of incomplete SCI, although all present with some residual function in the lowest sacral level.

In the central cord syndrome, the patient's upper extremities are neurologically impaired, particularly the hands, but the lower extremities are relatively spared. If mild, the patient may present ambulatory but with numb, clumsy, and painful hands. If severe, the patient may appear to have a complete loss of neurologic function below the level of the injury but maintain bowel and bladder control. Individuals with central cord syndrome commonly suffer hyperextension of the neck in the presence of degenerative arthritic changes of the vertebral column, especially anterior to the spinal cord. The forces causing the cord injury can be violent such as ejection from a car during a wreck or trivial as in a fall from a barstool. The central portion of the cord (gray matter) and medial portion of the corticospinal tracts are involved. The precise physiology behind this syndrome is debated, although it is believed to be related to the blood supply to the spinal cord (Figure 1). The unpaired anterior spinal artery and two posterior spinal arteries supply the spinal cord. End arteries fan out over the surface of the spinal cord (vasocorona) forming a centripetal system, whereas other end arteries enter the center of the cord through the midline sulci, forming a centrifugal system (Figure 1). There is no direct anastomosis between the centripetal and centrifugal systems, resulting in a watershed zone in the region of the gray–white interface. This area is the region believed to give rise to the symptoms of central cord syndrome. Overall, these individuals have a fair prognosis for spontaneous recovery (Bosch et al., 1971). Although many people make a rapid recovery, many are left with significant impairment of their hands.

In anterior spinal syndrome the patient is weak in all four extremities with loss of pain and temperature sensation in all extremities; however, vibration and position sense (posterior columns) remain intact. It is thought to be the result of inadequate blood supply from the anterior spinal artery, either occlusion through compression or embolization. The anterior spinal artery supplies approximately the anterior two thirds of the cord, including the lateral columns and central gray (Figure 1). The posterior columns are spared, because this area is supplied by the paired posterior spinal arteries. Prognosis after this type of injury is poor, because ischemia can rarely be reversed before infarction of the cord occurs.

When referring to SCI, there are two general types of lesions, based on location, that give rise to a predictable set of deficits.

In 1850, Brown-Sequard described a functional hemisection of the cord that now bears his name, the Brown-Sequard syndrome. Clinically, it is characterized by weakness ipsilateral to the injury and contralateral loss of pain and temperature. The anatomic basis for these neurologic findings is that postsynaptic pain and temperature fibers cross in the spinal cord near their point of origin, whereas motor fibers cross in the brainstem. Lesions of one side of the spinal cord interrupt ipsilateral descending motor pathways and contralateral ascending pathways conveying pain and thermal sensations. In trauma, the Brown-Sequard classically results from penetrating injuries such as a stab wound but it is seen most commonly as a result of nontraumatic demyelinating disorders such as multiple sclerosis. The prognosis is variable and dependent on the cause. A person with a compressive lesion has a more favorable outlook than one with a penetrating injury.

The adult spinal cord usually ends in the region of the first lumbar vertebrae. This ending is the conus medullaris. From the lumbosacral cord arise the nerves, collectively known as the cauda equina, which supply the legs as well as bowel, bladder, and sexual function. This transition from central nervous system (cord) to peripheral nervous system (roots) coincides with a transition from the relatively immobile thoracic spinal column to the highly flexible lumbar spine. This bony transition is prone to fracture, resulting in injury to the conus medullaris and cauda equina. The clinical presentation is lower extremity weakness and numbness with associated bowel/bladder deficiencies, but the neurologic findings pose a diagnostic dilemma. SCI above the level of the conus medullaris produces predominantly upper motor neuron damage. Paradoxically, SCI patients present initially with flaccid paralysis but gradually become hyperreflexic and spastic as they recover from spinal shock. Cauda equina injuries are lower motor neuron injuries that present with flaccid paralysis and remain that way. Trauma to the thoracolumbar junction may injure the conus medullaris, the cauda equina, or both, but the clinical examination for each situation cannot be differentiated. For this reason, although root injuries have a better prognosis than cord injuries, the prognosis is indeterminate after injuries in this region.

Children incur a unique entity known as SCIWORA, Spinal Cord Injury Without Radiographic Abnormality (Greenberg, 2001). X-rays and other imaging studies are normal, and the injury is presumed because of the laxity to spinal ligaments and muscles of the child. These are rarely complete injuries, and prognosis is mostly favorable.

EPIDEMIOLOGY AND ETIOLOGY

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

It has been estimated that there are 9,000 to 14,000 new SCI cases requiring hospitalization each year in the United States. Based on perhaps the most accurate state-wide surveillance system in the country, Mississippi reports an average of almost 200 SCI per year, which represents a higher per capita rate than the rest of the United States (Surkin et al., 1998, 2000). These differences may be explained by several factors, including predominance of rural highways, low rate of safety belt usage, and completeness of data collection. In Mississippi as elsewhere, SCI is a primarily a disease of the young males, with the highest occurrence among men 20–24 years of age (Surkin et al., 2000). The leading cause of SCI is motor vehicle collisions followed by violence (such as gunshot wounds) and falls (Surkin et al., 2000). Among persons sustaining SCI from vehicular collisions, at least 75% were determined to be unrestrained by safety belts and alcohol consumption is frequently associated (Surkin et al., 2000). Approximately half of patients surviving with SCI are quadriplegic and half paraplegic (Surkin et al., 2000).

TREATMENT

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Contemporary management of the SCI patient has centered on supportive care and stabilization of the spine. When found at the scene, all trauma patients undergo an “ABC” evaluation to assess airway, breathing, and circulation status. The eight cervical nerves (C1–C8) supply not only the upper extremities, but also other more vital functions such as breathing. Specifically, the phrenic nerve, which supplies the diaphragm (the major muscle of respiration), originates mainly from cervical nerves 3, 4, and 5. High cervical SCI may impair respiratory effort to such a degree that the patient may need to be placed on a respirator. Frequently, these patients with high cervical injury require a tracheostomy, and some even require permanent use of a respirator. Patients with SCI frequently exhibit signs of neurogenic shock early in their course. A drop in both blood pressure and heart rate characterizes this phenomenon. Although neurogenic shock is only transient, it can put the newly injured patient in grave danger and even lead to death through inadequate perfusion of vital organs. Hypotension may also lead to secondary SCI through ischemia to edematous spinal cord tissue. Treatment of neurogenic shock consists of fluid resuscitation, mechanical compression of distal veins, and vasopressor medications (Marshall et al., 1990).

Numerous pharmacologic therapies have been evaluated in the treatment of SCI, although none have met with significant success. High-dose corticosteroids have been shown to increase blood flow to the injured spinal cord and decrease the amount of swelling (Nockels and Young, 1992). These corticosteroids, given within the first 8 h of injury and continued for 24 to 48 h, have been the standard treatment (Bracken et al., 1990, 1992, 1997, 1998). Recently, the results of the initial studies showing the efficacy of corticosteroids in SCI have come under scrutiny, and presently, there are several studies reassessing this drug in a more controlled manner (Coleman et al., 2000; Hurlbert, 2000). Unfortunately, several other drugs, including GM-1 ganglioside, holding great promise in the pharmacologic treatment of SCI, have had limited clinical success (Geisler et al., 1991, 2001a–c).

After arriving at a treatment facility, an initial physical/neurologic examination can suggest the level of injury. Plain x-rays are obtained of the vertebral column to look for fractures and overall alignment. When SCI is suspected, further imaging with either computed tomography (CT) or magnetic resonance imaging (MRI) is usually warranted. CT provides excellent visualization of the bones of the spine, whereas the MRI provides superior images of soft tissue such as spinal cord, discs, ligaments, and muscle.

Patients found to have dislocations in the cervical spine should undergo reduction. This procedure is frequently accomplished with skeletal traction in an effort to reduce dislocated bones to their normal alignment. Dislocations in other portions of the spine usually are not reduced until the time of surgery, as these are technically very difficult. Once a fracture and/or dislocation has been identified, these areas are immobilized before surgical repair. This immobilization may be accomplished through skeletal traction, a rigid external brace or simply bed rest. A halo brace provides the most rigid form of external immobilization for the cervical spine. The brace consists of a ring that is bolted to the head with screws and then connected to a vest. This device is usually worn for 2 to 3 months.

SURGERY

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Once a decision has been made to operate on a patient with a SCI, the goal is to remove any tissue compressing the spinal cord, mechanically stabilize the spine, and foster a bony fusion. This procedure does not involve manipulation of the spinal cord per se. Surgery is done merely to release pressure on the spinal cord and then strengthen and support the surrounding bone, muscles, and ligaments. Management of the SCI patient has changed dramatically over the past 2 decades. The advent of CT and MRI has allowed rapid detection of injuries. With today's technologies and advances in nursing care, early surgery is routinely and safely performed. However, when a patient has concomitant injuries such as bruised lungs and head injuries, surgery to the spine is usually postponed until the patient is more stable.

Surgery on the cervical spinal column usually involves removal of the damaged structure with placement of a bone graft to permit fusion, followed by internal stabilization. Because of the ease of exposure, this operation has traditionally been undertaken from an anterior approach. The damaged disc and/or vertebral body may be easily removed, or drilled away, followed by placement of a strut graft and hardware (Figure 3). This strategy permits direct decompression of the vertebral spinal canal. Occasionally, in severe cervical injuries, both an anterior and posterior fusion may be required. When the injury involves the upper cervical spinal cord, fixation to the posterior skull can be required.

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Figure 3. A postsurgical lateral cervical spine x-ray. The C6 vertebral body has been partially removed to decompress the spinal cord. A bone graft has been inserted and is held in place by a metal plate secured by screws into the C5 and C7 vertebral bodies.

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Anterior approaches to the thoracic and lumbar spinal cord are technically more difficult because of the heart and lungs in the chest and intestines and other organs in the abdomen. Because of this, some spine surgeons believe an indirect decompression through a posterior approach is safer. Here, the bony posterior elements are removed, allowing access to the spinal canal. This approach does provide some exposure to damaged elements ventral to the spinal cord; however, the spinal cord is often quite swollen and the dural sac lacerated with resultant egress of cerebrospinal fluid. After decompression of the injured spinal cord, the surrounding damaged bone is usually fused above and below with bone and reinforced with metal hardware for support. A different approach involves removing the damaged bony area anteriorly or laterally with direct decompression of the spinal canal. Again, after removal of damaged bone, a strut is placed followed by hardware to internally brace this area (Figure 4). Anterior approaches allow removal of the damaged bony segment with reconstruction and eventual renewal of normal alignment to the spine. This approach also permits fusion over a shorter distance, thereby preserving more normally moving segments in the spine.

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Figure 4. A postsurgical thoracolumbar spine x-ray. The L1 vertebral body has been partially removed to decompress the conus medullaris and cauda equina. A metal cage containing a bone graft has been inserted and is held in place by a metal plate and secured by screws into the T12 and L2 vertebral bodies. Metal rods secured by hooks to the laminae of T12 and L2 supplement the stabilization.

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POSTINJURY CARE

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

In addition to injuries to the vertebral column and spinal cord, other organ systems are frequently involved. It has been estimated that of patients with an SCI, 42% had an injury missed at diagnosis with over half of these injuries being nonspinal (Ryan et al., 1993). The incidence of associated injuries is 12% with cervical SCI, 46% with thoracic SCI, and 22% with lumbar SCI (Ducker and Saul, 1982). If missed, these other injuries can be lethal. Bleeding into the chest or abdomen in these patients frequently leads to shock and death if not promptly treated.

The new SCI patient is prone to develop blood clots, known as a deep venous thrombosis (DVT), in veins of the legs. This condition is multifactorial in origin and related to decreased blood pressure, change in vasculature tone, and immobilization of the legs by paralysis. A DVT clot can dislodge from the leg and migrate to the lungs potentially blocking a major vessel within the lung itself. This is known as a pulmonary embolism and can lead to rapid demise. Symptoms include chest pain, shortness of breath, and cough. When a DVT is diagnosed, treatment consists of anticoagulating with blood thinners and, at times, dissolving the clots with “clot busting” drugs. Up to 80% of patients with SCI develop DVTs with 2–16% suffering a fatal pulmonary embolism (Green, 1991). DVT is most common in the first 2 weeks after injury, and for this reason, it is recommended to treat these patients prophylactically with anticoagulants. Because other injuries might exist, such as bruised organs, or surgery to the spine may need to be performed, blood thinners are not used as the first line of defense but rather are used once a DVT has been diagnosed. Also, once diagnosed, a special filter may be placed in the large vein within the abdomen leading from the legs to catch any clot that may become dislodged and is traveling toward the lung.

Ventalatory inspiration is primarily the function of the diaphragm, innervated by C3–C5 spinal segments, and intercostal muscles, innervated by the 12 thoracic nerves. Very high cervical SCI may result in the complete loss of inspiratory capacity, thereby necessitating mechanical ventilation to sustain life. Mid to lower cervical injuries spare diaphragmic function but impair intercostal function. These patients are still able to breath adequately at the outset but may subsequently develop respiratory failure (Kocan, 1990). This failure is due, in part, to decreased inspiratory capability, but also to an inability to cough. Normal ventilatory expiration is passive, but a cough requires forceful contraction of abdominal muscles, which are impaired in SCI patients. Prevention of secondary respiratory failure after cervical or high thoracic SCI is paramount. This success can be achieved with vigorous pulmonary hygiene consisting primarily of lung volume expansion and assisted cough.

Not only do limbs become paralyzed, but initially the bowels slow too. This slowing can lead to marked electrolyte imbalances and constipation. The new SCI patient has a tube passed into the stomach to help remove fluids that are not passing through the intestinal tract. Stool softeners are also begun once the bowels begin to move. Maintenance of a high-fiber diet with appropriate fluid intake and regular timing of meals becomes paramount in the long-term management of the SCI bowel. With time, these patients can “train” their bowels so that bowel movements occur upon awakening in the morning.

Loss of bladder control can lead to devastating problems if not managed appropriately. At the turn of the past century, up to 80% of SCI mortality was secondary to urologic complications (Selzmann and Hampel, 1991). A great deal of these deaths were related to delayed kidney failure. However, with early bladder catheterization and bladder training, this rate has improved dramatically. Initially, a patient should have an indwelling bladder catheter. Once stabilized and during rehabilitation, the patient is taught to intermittently self-catheterize three to four times daily. This catheterization must be done cleanly as bladder/urinary tract infections can lead to the same urologic demise as overdistention of the bladder.

Because of lack of sensation, sores can develop over pressure points (known as decubitus ulcers). One third of patients will develop a decubitus ulcer during their initial hospitalization (Mawson et al., 1993). This is another source of significant morbidity and even mortality for these debilitated patients. Once again, prevention is the best cure. Rolling the newly injured patient from side to side or instructing them to shift positions every 2 h is vital. Braces and wheelchairs must be assessed to ensure proper fit. Once diagnosed, these pressure sores must be kept clean and dry. More extensive lesions, especially those involving underlying muscle or bone, may require extensive surgical excision and sometimes a complex repair.

The advent of regional SCI treatment centers in the early 1970s hailed the concept of modern interdisciplinary management. These centers house all available specialists and treatment modalities available today. These centers are dedicated to the initial management and surgical stabilization along with rehabilatory services afterward. This coordination is best accomplished by a team committed to SCI treatment, including spinal surgeons and physiatrists (rehabilitation physicians) along with physical and occupational therapists, respiratory and speech therapists, psychologists, social workers, and dietitians. This cadre of health care professionals is needed to help the patient learn to cope and use the newly paralyzed body.

COST OF SCI

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

The cost of SCI management is staggering secondary to surgical interventions and extensive physical and psychological therapy. This cost does not begin to approximate the expense to the patient's psyche and that of his/her family. Generally, the sooner a patient is admitted to a SCI center the shorter the stay (Heinemann et al., 1989). In 1974, the average stay including acute care and rehabilitation was 140 days. By 1995, this average had dropped to 64 days with the introduction of modern rehabilitation facilities. As expected, patients with complete SCI require longer stays (Heinemann et al., 1989). The average stay in an acute care hospital is 15.4 days if admitted within 24 h and 20 days thereafter, whereas the rehabilitation stay is 46 and 91 days, respectively.

Although survival rates continue to improve, SCI patients still have a life expectancy lower than that of their peers. Decades ago a quadriplegic was given little more than a few months of survival, but today, with appropriate care, can expect to live close to a normal life span. Survival is a function of level and degree of injury as well as age (Anonymous, 2001). As mentioned earlier, in the past, the leading cause of death was renal failure. Today's leading causes, however, are pneumonia and pulmonary embolism. The monetary cost of health care and living expenses varies greatly according to severity of injury, with more severe injuries associated with higher costs (Anonymous, 2001). When multiplied by the number of Americans living with SCI, this expenditure runs well into the billions of dollars annually.

PREVENTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Pasteur wrote, “When meditating over a disease, I never think of finding a remedy for it, but instead a means of preventing it” (Eyster and Watts, 1989). Although there are many programs aimed at preventing SCI that are proven effective, they will not prevent all SCIs. Knowledge, however, is a better form of treatment than any intervention after a SCI has occurred. The majority of traumatic injuries are preventable, with 70% of motor vehicle collisions the result of human error (Council on Scientific Affairs, 1983). In fact, seat belts and airbags reduce both injury and death by 50% (National Highway Traffic Safety Administration, 1988).

Conceived in 1990, the THINK FIRST program's main goal was to raise public awareness of brain and SCI. This program consists in part of neurosurgeons representing both major American Neurological Surgery Associations. The program is an educational effort aimed at both children and adolescents. It discusses risk-taking behaviors and their consequences. The incidence of SCI has dropped in areas where this program has been initiated (Shaw et al., 1984). Other programs exist, such as Feet First, whose goal is to teach children to test the depth of water before jumping in and always dive feet-first initially. Other countries have embarked on prevention programs finding that youths retained the information (Wigglesworth, 1988; Yeo et al., 1987).

CONCLUSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

SCIs afflict millions of individuals worldwide. The cost to the patient, family, and society is enormous both from a financial and emotional standpoint. In the past, these patients were given no hope of cure or return of function. However, exciting research points to at least improvement in function in the future. Patients today can expect to live a nearly normal life span. They can return to work, raise families, and make useful contributions to society. With continued advances in medicine it is expected that survival rates and quality of life for SCI victims will continue to improve.

With continued advances in medicine, it is expected that survival rates and quality of life for SCI victims will continue to improve.

Acknowledgements

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

The authors thank Ms. Lisa Boyd in the Department of Anatomy at The University of Mississippi Medical Center for typing the manuscript.

LITERATURE CITED

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information
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Biographical Information

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. HISTORY
  5. ANATOMY
  6. CLASSIFICATION
  7. EPIDEMIOLOGY AND ETIOLOGY
  8. TREATMENT
  9. SURGERY
  10. POSTINJURY CARE
  11. COST OF SCI
  12. PREVENTION
  13. CONCLUSION
  14. Acknowledgements
  15. LITERATURE CITED
  16. Biographical Information

Dr. Harkey is Professor of Neurosurgery at The University of Mississippi Medical Center. He has a special interest in surgery on the vertebral column and spinal cord injury and in the postinjury and postsurgical care of the SCI patient. Dr. White is a fourth-year Neurosurgery Resident at The University of Mississippi Medical Center. Dr. Tibbs is in private practice in Neurosurgery in Oklahoma, with a special interest in the treatment of spinal disorders. Dr. Haines is Professor and Chairman of the Department of Anatomy and Professor of Neurosurgery at The University of Mississippi Medical Center with a special interest in systems neuroscience.