Spinal Cord Injuries-kyien

Transcript

Spinal cord injuries cause myelopathy or damage to nerve roots or myelinated fiber tracts that carry signals to and from the brain. [1][2] Depending on its classification and severity, this type of traumatic injury could also damage the gray matter in the central part of the cord, causing segmental losses of interneurons and motorneurons. Spinal cord injury can occur from many causes, including: • • • • • • • • Trauma such as automobile crashes, falls, gunshots, diving accidents, war injuries, etc. Tumor such as meningiomas, ependymomas, astrocytomas, and metastatic cancer. Ischemia resulting from occlusion of spinal blood vessels, including dissecting aortic aneurysms, emboli, arteriosclerosis. Developmental disorders, such as spina bifida, meningomyolcoele, and other. Neurodegenerative diseases, such as Friedreich's ataxia, spinocerebellar ataxia, etc. Demyelinative diseases, such as Multiple Sclerosis. Transverse myelitis, resulting from stroke, inflammation, or other causes. Vascular malformations, such as arteriovenous malformation (AVM), dural arteriovenous fistula (AVF), spinal hemangioma, cavernous angioma and aneurysm [edit] Classification The American Spinal Injury Association (ASIA) defined an international classification based on neurological responses, touch and pinprick sensations tested in each dermatome, and strength of ten key muscles on each side of the body, i.e. shoulder shrug (C4), elbow flexion (C5), wrist extension (C6), elbow extension (C7), hip flexion (L2). Traumatic spinal cord injury is classified into five categories by the American Spinal Injury Association and the International Spinal Cord Injury Classification System: • • • • • A indicates a "complete" spinal cord injury where no motor or sensory function is preserved in the sacral segments S4-S5. B indicates an "incomplete" spinal cord injury where sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5. This is typically a transient phase and if the person recovers any motor function below the neurological level, that person essentially becomes a motor incomplete, i.e. ASIA C or D. C indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade of less than 3, which indicates active movement with full range of motion against gravity. D indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more. E indicates "normal" where motor and sensory scores are normal. Note that it is possible to have spinal cord injury and neurological deficits with completely normal motor and sensory scores. In addition, there are several clinical syndromes associated with incomplete spinal cord injuries. • • • • • • The Central cord syndrome is associated with greater loss of upper limb function compared to lower limbs. The Brown-Séquard syndrome results from injury to one side with the spinal cord, causing weakness and loss of proprioception on the side of the injury and loss of pain and thermal sensation of the other side. The Anterior cord syndrome results from injury to the anterior part of the spinal cord, causing weakness and loss of pain and thermal sensations below the injury site but preservation of proprioception that is usually carried in the posterior part of the spinal cord. Tabes Dorsalis results from injury to the posterior part of the spinal cord, usually from infection diseases such as syphilis, causing loss of touch and proprioceptive sensation. Conus medullaris syndrome results from injury to the tip of the spinal cord, located at L1 vertebra. Cauda equina syndrome is, strictly speaking, not really spinal cord injury but injury to the spinal roots below the L1 vertebra Facts and Figures One can have spine injury without spinal cord injury. Many people suffer transient loss of function ("stingers") in sports accidents or pain in "whiplash" of the neck without neurological loss and relatively few of these suffer spinal cord injury sufficient to warrant hospitalization. In the United States, the incidence of spinal cord injury has been estimated to be about 40 cases per million per year.[3] In China, the incidence of spinal cord injury is approximately 60,000 per year. [4] The prevalence of spinal cord injury is not well known in many large countries. In some countries, such as Sweden and Iceland, registries are available. According to new data collected by the Christopher and Dana Reeve Foundation, in the US, there are currently 1.3 million individuals living with spinal cord injuries- a number five times that previously estimated in 2007. 61% of spinal cord injuries occur in males, and 39% in females. The average age for spinal cord injuries is 48 years old. There are many causes leading to spinal cord injuries. These include motor vehicle accidents (24%), work-related accidents (28%), sporting/recreation accidents (16%), and falls (9%). The consequences of a spinal cord injury may vary depending on the type, level, and severity of injury, but can be classified into two general categories: • In a complete injury, function below the "neurological" level is lost. Absence of motor and sensory function below a specific spinal level is considered a "complete injury". • Recent evidence suggests that less than 5% of people with "complete" spinal cord injuries recover locomotion. In an incomplete injury, some sensation and/or movement below the level of the injury is retained. The lowest spinal segment in humans is located at vertebral levels S4-5, corresponding to the anal sphincter and peri-anal sensation. The ability to contract the anal sphincter voluntarily or to feel peri-anal pinprick or touch, the injury is considered to be "incomplete". Recent evidence suggests that over 95% of people with "incomplete" spinal cord injuries recover some locomotor function. In addition to loss of sensation and motor function below the level of injury, individuals with spinal cord injuries will also often experience other complications: • • • • • • • • • • • Bowel and bladder function is regulated by the sacral region of the spine. In that regard, it is very common to experience dysfunction of the bowel and bladder, including infections of the bladder and anal incontinence, after traumatic injury. Sexual function is also associated with the sacral spinal segments, and is often affected after injury. During a psychogenic sexual experience, signals from the brain are sent to spinal levels T10-L2 and in case of men, are then relayed to the penis where they trigger an erection. A reflex erection, on the other hand, occurs as a result of direct physical contact to the penis or other erotic areas such as the ears, nipples or neck. A reflex erection is involuntary and can occur without sexually stimulating thoughts. The nerves that control a man’s ability to have a reflex erection are located in the sacral nerves (S2S4) of the spinal cord and could be affected after a spinal cord injury. [5] Injuries at the C-1/C-2 levels will often result in loss of breathing, necessitating mechanical ventilators or phrenic nerve pacing. Inability or reduced ability to regulate heart rate, blood pressure, sweating and hence body temperature. Spasticity (increased reflexes and stiffness of the limbs). Neuropathic pain. Autonomic dysreflexia or abnormal increases in blood pressure, sweating, and other autonomic responses to pain or sensory disturbances. Atrophy of muscle. Superior Mesenteric Artery Syndrome. Osteoporosis (loss of calcium) and bone degeneration. Gallbladder and renal stones. [edit] The Location of the Injury Determining the exact level of injury is critical in making accurate predictions about the specific parts of the body that may be affected by paralysis and loss of function. The symptoms observed after a spinal cord injury differ by location (refer to the spinal cord map on the right to determine location). Notably, while the prognosis of complete injuries are generally predictable, the symptoms of incomplete injuries span a variable range. Accordingly, it is difficult to make an accurate prognosis for these types of injuries. [edit] Cervical injuries Cervical (neck) injuries usually result in full or partial tetraplegia (Quadriplegia). However, depending on the specific location and severity of trauma, limited function may be retained. • • • • • C3 vertebrae and above : Typically results in loss of diaphragm function, necessitating the use of a ventilator for breathing. C4 : Results in significant loss of function at the biceps and shoulders. C5 : Results in potential loss of function at the shoulders and biceps, and complete loss of function at the wrists and hands. C6 : Results in limited wrist control, and complete loss of hand function. C7 and T1 : Results in lack of dexterity in the hands and fingers, but allows for limited use of arms. C7 is generally the threshold level for retaining functional independence. [edit] Thoracic injuries Injuries at or below the thoracic spinal levels result in paraplegia. Function of the hands, arms, neck, and breathing is usually not affected. • • T1 to T8 : Results in the inability to control the abdominal muscles. Accordingly, trunk stability is affected. The lower the level of injury, the less severe the effects. T9 to T12 : Results in partial loss of trunk and abdominal muscle control. [edit] Lumbar and Sacral injuries The effects of injuries to the lumbar or sacral regions of the spinal cord are decreased control of the legs and hips, urinary system, and anus. [edit] Central Cord and Other Syndromes Central cord syndrome (picture 1) is a form of incomplete spinal cord injury characterized by impairment in the arms and hands and, to a lesser extent, in the legs. This is also referred to as inverse paraplegia, because the hands and arms are paralyzed while the legs and lower extremities work correctly. Most often the damage is to the cervical or upper thoracic regions of the spinal cord, and characterized by weakness in the arms with relative sparing of the legs with variable sensory loss. This condition is associated with ischemia, hemorrhage, or necrosis involving the central portions of the spinal cord (the large nerve fibers that carry information directly from the cerebral cortex). Corticospinal fibers destined for the legs are spared due to their more external location in the spinal cord. This clinical pattern may emerge during recovery from spinal shock due to prolonged swelling around or near the vertebrae, causing pressures on the cord. The symptoms may be transient or permanent. Anterior cord syndrome (picture 2) is also an incomplete spinal cord injury. Below the injury, motor function, pain sensation, and temperature sensation is lost; touch, proprioception (sense of position in space), and vibration sense remain intact. Posterior cord syndrome (not pictured) can also occur, but is very rare. Brown-Séquard syndrome (picture 3) usually occurs when the spinal cord is hemisectioned or injured on the lateral side. On the ipsilateral side of the injury (same side), there is a loss of motor function, proprioception, vibration, and light touch. Contralaterally (opposite side of injury), there is a loss of pain, temperature, and deep touch sensations [edit] Treatment Treatment options for acute, traumatic non-penetrating spinal cord injuries include the administration of a high dose of an anti-inflammatory agent, methylprednisolone, within 8 hours of injury. This recommendation is primarily based on the National Acute Spinal Cord Injury Studies (NASCIS) I and II. However, in a third study, methylprednisolone failed to demonstrate an effect in comparison to placebo. Additionally, due to increased risk of infections, the use of this anti-inflammatory drug after spinal cord injuries is no longer recommended [6][7]. Presently, administration of cold saline acutely after injury is gaining popularity, but there is a paucity of empirical evidence for the beneficial effects of therapeutic hypothermia. Scientists are investigating many promising avenues for treatment of spinal cord injury. Numerous articles in the medical literature describe research, mostly in animal models, aimed at reducing the paralyzing effects of injury and promoting regrowth of functional nerve fibers. Despite the devastating effects of the condition, commercial funding for research investigating a cure after spinal cord injury is limited, partially due to the small size of the population of potential beneficiaries. Despite this limitation, a number of experimental treatments have reached controlled human trials[citation needed]. In addition, therapeutic strategies involving neuronal protection and regeneration are also being investigated in other neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, Amyotrophic Lateral Sclerosis and Multiple sclerosis. There are many similarities between these conditions of the CNS and spinal cord injuries, thus increasing the potential for discovery of a treatment after spinal cord injuries. Advances in identification of an effective therapeutic target after spinal cord injury have been newsworthy, and considerable media attention is often drawn towards new developments in this area. However, aside from methylprednisolone, none of these developments have reached even limited use in the clinical care of human spinal cord injury in the U.S.[citation needed]. Around the world, proprietary centers offering stem cell transplants and treatment with neuroregenerative substances are fueled by glowing testimonial reports of neurological improvement. Independent validation of the results of these treatments is lacking.[8] However, in January 2009, the Geron Corporation received FDA clearance to begin human safety testing of its stem cell treatment candidate, GRNOPC1, on newly injured patients with complete thoracic injury.[9] A diverse array of other treatments are being researched, including biomaterial solutions,[10] cell replacement therapies, and electronic stimulative devices References 1. ^ Spinal Cord Medicine: Principles and Practice (2002) Lin VWH, Cardenas DD, Cutter NC, Frost FS, Hammond MC. Demos Medical Publishing 2. ^ Spinal Cord Medicine (2001) Kirshblum S, Campagnolo D, Delisa J. Lippincott Williams & Wilkins 3. ^ http://www.fscip.org/facts.htm 4. ^ Qiu J (July 2009). "China Spinal Cord Injury Network: changes from within". Lancet Neurol 8 (7): 606–7. doi:10.1016/S1474-4422(09)70162-0. PMID 19539234. 5. ^ Klebin, Phil Sexual Function of Men with Spinal Cord Injury May 2007 6. ^ "UpToDate Inc.". http://www.uptodate.com/online/content/topic.do? topicKey=medneuro/10703&selectedTitle=3~150&source=search_result. 7. ^ "BestBets: Steroids in acute spinal cord injury". http://www.bestbets.org/bets/bet.php?id=105. 8. ^ Dobkin, BH.; Curt, A.; Guest, J. “Cellular transplants in China: observational study from the largest human experiment in chronic spinal cord injury.” Neurorehabilitation and Neural Repair, v. 20 issue 1, 2006, p. 5-13. 9. ^ Geron press release January 23 2009: Geron Receives FDA Clearance to Begin World's First Human Clinical Trial of Embryonic Stem Cell-Based Therapy 10.^ See for example Benton Martin, Eric Minner, Sherri Wiseman, Rebecca Klank, Ryan Gilbert, 2008, “Injectable agarose and methylcellulose hydrogel blends for nerve regeneration applications,” Journal of Neural Engineering, Vol. 5, No. 2, pp. 221-231. Retrieved from "http://en.wikipedia.org/wiki/Spinal_cord_injury" Introduction Background Patients with spinal cord injury (SCI) usually have permanent and often devastating neurologic deficits and disability. According to the National Institutes of Health, "among neurological disorders, the cost to society of automotive SCI is exceeded only by the cost of mental retardation." The goals for the emergency physician are to establish the diagnosis and initiate treatment to prevent further neurologic injury from either pathologic motion of the injured vertebrae or secondary injury from the deleterious effects of cardiovascular instability or respiratory insufficiency. Pathophysiology The spinal cord is divided into 31 segments, each with a pair of anterior (motor) and dorsal (sensory) spinal nerve roots. On each side, the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neuroforamina. The spinal cord extends from the base of the skull and terminates near the lower margin of the L1 vertebral body. Thereafter, the spinal canal contains the lumbar, sacral, and coccygeal spinal nerves that comprise the cauda equina. Therefore, injuries below L1 are not considered spinal cord injuries (SCIs) because they involve the segmental spinal nerves and/or cauda equina. Spinal injuries proximal to L1, above the termination of the spinal cord, often involve a combination of spinal cord lesions and segmental root or spinal nerve injuries. The spinal cord itself is organized into a series of tracts or neuropathways that carry motor (descending) and sensory (ascending) information. These tracts are organized anatomically within the spinal cord. The corticospinal tracts are descending motor pathways located anteriorly within the spinal cord. Axons extend from the cerebral cortex in the brain as far as the corresponding segment, where they form synapses with motor neurons in the anterior (ventral) horn. They decussate (cross over) in the medulla prior to entering the spinal cord. The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and vibration information to the sensory cortex. They do not decussate until they reach the medulla. The lateral spinothalamic tracts transmit pain and temperature sensation. These tracts usually decussate within 3 segments of their origin as they ascend. The anterior spinothalamic tract transmits light touch. Autonomic function traverses within the anterior interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1, while parasympathetic system pathways exit between S2 and S4. Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensation. Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation. Anterior cord injury causes paralysis and incomplete loss of light touch sensation. Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous system fibers exit from the spinal cord between C7 and L1. The parasympathetic system nerves exit between S2 and S4. Therefore, progressively higher spinal cord lesions or injury causes increasing degrees of autonomic dysfunction. Neurogenic shock is characterized by severe autonomic dysfunction, resulting in hypotension, relative bradycardia, peripheral vasodilation, and hypothermia. It does not usually occur with spinal cord injury below the level of T6. Shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from autonomic dysfunction and the interruption of sympathetic nervous system control in acute spinal cord injury. The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature sensation, and autonomic dysfunction. The posterior spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in the neck and descend from the base of the skull. Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow. The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. For example, a lower cervical spine fracture may result in disruption of the vertebral artery that ascends through the affected vertebra. The resulting vascular injury may cause an ischemic high cervical cord injury. At any given level of the spinal cord, the central part is a watershed area. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome. Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary spinal cord injury. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries. Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas or abscesses cause acute cord compression and injury. Spinal cord compression from metastatic disease is a common oncologic emergency. Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary spinal cord injury without spinal fracture or dislocation. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in SCIWORA. The term SCIWORA (spinal cord injury without radiologic abnormality) was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or CT evidence of fracture or dislocation. However with the advent of MRI, the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury. SCIWORA should now be more correctly renamed as "spinal cord injury without neuroimaging abnormality" and recognize that its prognosis is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury.1,2,3 Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or hypoxic effects compound the extent of spinal cord injury. One of the goals of the emergency physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete. A complete cord syndrome is characterized clinically as complete loss of motor and sensory function below the level of the traumatic lesion. Incomplete cord syndromes have variable neurologic findings with partial loss of sensory and/or motor function below the level of injury. Incomplete cord syndromes include the anterior cord syndrome, the Brown-Séquard syndrome, and the central cord syndrome. Other cord syndromes include the conus medullaris syndrome, the cauda equina syndrome, and spinal cord concussion. In most clinical scenarios, the emergency physician should use a best-fit model to classify the SCI syndrome. The incomplete SCI syndromes are further characterized clinically as follows: • • Anterior cord syndrome involves variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception. Brown-Séquard syndrome involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation. • Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities. The pattern of motor weakness shows greater distal involvement in the affected extremity than proximal muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in the upper extremities (eg, sensation of burning in the hands or arms), are common. Sacral sensory sparing usually exists. Other cord syndromes are clinically described as follows: • • • Conus medullaris syndrome is a sacral cord injury with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs. Motor and sensory loss in the lower limbs is variable. Cauda equina syndrome involves injury to the lumbosacral nerve roots and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true spinal cord injury (SCI), the affected limbs are areflexic. This injury is usually caused by a central lumbar disk herniation. A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage. Spinal cord injury, as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the spinal cord injury. Frequency United States The incidence of spinal cord injury is approximately 40 cases per million population, or about 12,000 patients, per year based on data in the National Spinal Cord Injury database. However, this estimate is based on older data from the 1970s as there has not been any new overall incidence studies completed. Mortality/Morbidity Originally the leading cause of death in patients with spinal cord injury who survived their initial injury was renal failure, but, currently, the leading causes of death are pneumonia, pulmonary embolism, or septicemia. Life expectancies for patients with spinal cord injury continues to increase but are still below the general population. Based on 2003 US Life Tables, a healthy 20-year-old would have a life expectancy of 78.4 years, whereas a quadriplegic who was injured at age 20 would have a life expectancy of only 60. Race A significant trend over time has been observed in the racial distribution of persons with spinal cord injury. Since 2000, 63% are Caucasian, 22.7% are African American, 11.8% are Hispanic, and fewer than 2% are Asian.4 Sex The male-to-female ratio is approximately 4:1.4 Age • • • Since 2005, the average age at injury is 39.5 years, reflecting the rise in the median age of the general population in the United States. About 50% of spinal cord injuries (SCIs) occurred between the ages of 16 and 30. Of SCIs, 3.5% occur in children aged ≤ 15 years, while there has been an increasing incidence of spinal cord injury in persons older than 60 years (11.5%). Clinical History • Clinical evaluation of a patient with suspected spinal cord injury (SCI) begins with careful history taking, focusing on symptoms related to the vertebral column (most commonly pain) and any motor or sensory deficits. Complete bilateral loss of sensation or motor function below a certain level indicates a complete SCI. Ascertaining the mechanism of injury is also important in identifying the potential for spinal injury. Hemorrhagic shock may be difficult to diagnose because the clinical findings may be affected by autonomic dysfunction. o Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure the emergency physician. Occult internal injuries with associated hemorrhage may be missed. In all patients with SCI and hypotension, a diligent search for sources of hemorrhage must be • • • o o • made before hypotension is attributed to neurogenic shock. In acute SCI, shock may be neurogenic, hemorrhagic, or both. The following clinical pearls are useful in distinguishing hemorrhagic shock from neurogenic shock: o Neurogenic shock occurs only in the presence of acute SCI above T6. Hypotension and/or o o shock with acute SCI at or below T6 is caused by hemorrhage. Hypotension with a spinal fracture alone, without any neurologic deficit or apparent SCI, is invariably due to hemorrhage. Patients with an SCI above T6 may not have the classic physical findings associated with hemorrhage (eg, tachycardia, peripheral vasoconstriction). This vital sign confusion attributed to autonomic dysfunction is common in SCI. The presence of vital sign confusion in acute SCI and a high incidence of associated injuries o • • • requires a diligent search for occult sources of hemorrhage. A careful neurologic assessment is required to establish the presence or absence of SCI and to classify the lesion according to a specific cord syndrome. Determine the level of injury and try to differentiate nerve root injury from SCI but recognize that both may be present. The American Spinal Injury Association has established pertinent definitions. The neurologic level of injury is the lowest (most caudal) level with normal sensory and motor function. For example, a patient with C5 quadriplegia has, by definition, abnormal motor and sensory function from C6 down. The American Spinal Injury Association recommends use of the following scale of findings for the assessment of motor strength in SCI: o 0 - No contraction or movement o 1 - Minimal movement o 2 - Active movement, but not against gravity o 3 - Active movement against gravity o o • • 4 - Active movement against resistance 5 - Active movement against full resistance Assessment of sensory function helps to identify the different pathways for light touch, proprioception, vibration, and pain. Use a pinprick to evaluate pain sensation. Differentiating a nerve root injury from SCI can be difficult. The presence of neurologic deficits that indicate multilevel involvement suggests SCI rather than a nerve root injury. In the absence of spinal shock, motor weakness with intact reflexes indicates SCI, while motor weakness with absent reflexes indicates a nerve root lesion. Physical As with all trauma patients, initial clinical evaluation begins with a primary survey. The primary survey focuses on life-threatening conditions. Assessment of airway, breathing, and circulation takes precedence. A spinal cord injury (SCI) must be considered concurrently.5,6,7 The clinical assessment of pulmonary function in acute spinal cord injury begins with careful history taking regarding respiratory symptoms and a review of underlying cardiopulmonary comorbidity such as chronic obstructive pulmonary disease or heart failure. Carefully evaluate respiratory rate, chest wall expansion, abdominal wall movement, cough, and chest wall and/or pulmonary injuries. Arterial blood gas (ABG) analysis and pulse oximetry are especially useful because the bedside diagnosis of hypoxia or carbon dioxide retention may be difficult. • The degree of respiratory dysfunction is ultimately dependent on preexisting pulmonary comorbidity, the level of SCI, and any associated chest wall or lung injury. Any or all of the following determinants of pulmonary function may be impaired in the setting of SCI: o Loss of ventilatory muscle function from denervation and/or associated chest wall injury o Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion o Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction. o With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent. o With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and • o o o • ineffective. With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak. With lower cord injuries, respiratory function improves. With injuries at T11, respiratory dysfunction is minimal. Vital capacity is essentially normal, and cough is strong. Other findings of respiratory disfunction include the following: o Agitation, anxiety, or restlessness o Poor chest wall expansion o Decreased air entry o Rales, rhonchi o Pallor, cyanosis o Increased heart rate o Paradoxic movement of the chest wall o Increased accessory muscle use o Moist cough In all patients, a complete detailed neurological assessment including motor function, sensory evaluation, deep tendon reflexes, and perineal evaluation is critical. The presence or absence of sacral sparing is a key prognostic indicator. In 1982, the American Spinal Injury Association (ASIA) first published standards for neurological classification of patients with spinal injury. Since then, further refinements have been made to definitions of neurological levels, key muscles and sensory points were identified corresponding to specific neurological levels, and the Frankel scale was validated. In 1992, the International Medical Society of paraplegia adopted these guidelines to create true international standards. Further refinements have been adopted. A standardized ASIA method for classifying spinal cord injury (SCI) by neurologic level has been developed and is included here to serve as a useful educational and reference tool. (See Media file 1.) • The key muscles that need to be tested to establish neurologic level are as follows: o Upper limb Biceps C5 Wrist extensors C6 Triceps C7 Long finger flexors C8 Small finger abductors T1 Lower limb           o • Hip flexors L2 Knee extensors L3 Ankle dorsiflexors L4 Extensor Hallucis L5 Ankle plantar flexors S1 The sacral roots may be evaluated by documenting the following: o Perineal sensation to light touch and pinprick o Bulbocavernous reflex (S3 or S4) o Anal wink (S5) o Rectal tone o Urine retention or incontinence o Priapism The axial skeleton should be examined to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. The posterior cervical spine and paraspinal tissues should be evaluated for pain, swelling, bruising, or possible malalignment. Logrolling the patient to systematically examine each spinous process of the entire axial skeleton from the occiput to the sacrum can help identify and localize injury. • Causes Since 2005, the most common causes of spinal cord injury (SCI) remain motor vehicle accidents (42%), falls (27.1%), interpersonal violence primary gunshot wounds(15.3%), and sports (7.4%).4 Treatment Prehospital Care • • Most prehospital care providers recognize the need to stabilize and immobilize the spine on the basis of mechanism of injury, pain in the vertebral column, or neurologic symptoms. Patients are usually transported to the ED with a cervical hard collar on a hard backboard. o Commercial devices are available to secure the patient to the board. o The patient should be secured so that in the event of emesis, the backboard may be rapidly rotated 90 degrees while the patient remains fully immobilized in a neutral position. Spinal immobilization protocols should be standard in all prehospital care systems. Emergency Department Care Most patients with spinal cord injuries (SCIs) have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation takes precedence. Airway management in the setting of spinal cord injury, with or without a cervical spine injury, is complex and difficult. The cervical spine must be maintained in neutral alignment at all times. Clearing of oral secretions and/or debris is essential to maintain airway patency and to prevent aspiration. The modified jaw thrust and insertion of an oral airway may be all that is required to maintain an airway in some cases. However, intubation may be required in others. Failure to intubate emergently when indicated because of concerns regarding the instability of the patient's cervical spine is a potential pitfall. Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury. Because of the vital sign confusion in acute spinal cord injury and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made. The most common causes of occult hemorrhage are chest, intra-abdominal, or retroperitoneal injuries and pelvic or long bone fractures. Appropriate investigations, including radiography or CT scanning, are required. In the unstable patient, diagnostic peritoneal lavage or bedside FAST (focused abdominal sonography for trauma) ultrasonographic study may be required to detect intra-abdominal hemorrhage. Once occult sources of hemorrhage have been excluded, initial treatment of neurogenic shock focuses on fluid resuscitation. Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 liters is the initial treatment of choice. Overzealous crystalloid administration may cause pulmonary edema because these patients are at risk for the acute respiratory distress syndrome. • The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters: o Systolic blood pressure (BP) should be 90-100 mm Hg. Systolic BPs in this range are typical for patients with complete cord lesions. The most important treatment consideration is to maintain adequate oxygenation and perfusion of the injured spinal cord. Compelling animal and human studies recommend maintenance of systolic blood pressure higher than 90 and prevent any hypotensive episodes.16,7 Heart rate should be 60-100 beats per minute in normal sinus rhythm. Hemodynamically significant bradycardia may be treated with atropine. Urine output should be more than 30 mL/h. Placement of a Foley catheter to monitor urine output is essential. Rarely, inotropic support with dopamine is required. It should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation. Usually, low doses of dopamine in the 2- to 5-mcg/kg/min range are sufficient. Prevent hypothermia. o o o o • • • • Associated head injury occurs in about 25% of patients with spinal cord injury. A careful neurologic assessment for associated head injury is compulsory. The presence of amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, and a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning. Ileus is common. Placement of a nasogastric tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function. Antiemetics should be used aggressively. The patient is best treated initially in the supine position. Occasionally, the patient may have been transported prone by the prehospital care providers. Logrolling the patient to the supine position is safe to facilitate diagnostic evaluation and treatment. Use analgesics appropriately and aggressively to maintain the patient's comfort if he or she has been lying on a hard backboard for an extended period. Prevent pressure sores. Denervated skin is particularly prone to pressure necrosis. Turn the patient every 1-2 hours. Pad all extensor surfaces. Undress the patient to remove belts and back pocket keys or wallets. Remove the spine board as soon as possible. Use of steroids in spinal cord injury • The National Acute Spinal Cord Injury Studies (NASCIS) II and III, a Cochrane Database of Systematic Reviews article of all randomized clinical trials and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete spinal cord injuries (SCIs) who were treated with high doses of methylprednisolone within 8 hours of injury.17,18 o The NASCIS II study evaluated methylprednisolone administered within 8 hours of injury. The NASCIS III study evaluated methylprednisolone 5.4 mg/kg/h for 24 or 48 hours versus tirilazad 2.5 mg/kg q6h for 48 hours. (Tirilazad is a potent lipid preoxidation inhibitor.) High doses of steroids or tirilazad are thought to minimize the secondary effects of acute spinal cord injury (SCI). In the NASCIS III trial, all patients (n = 499) received a 30-mg/kg bolus of methylprednisolone intravenously. The study found that, in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 hours was best. In patients treated 3-8 hours after injury, the use of methylprednisolone for 48 hours was best. Tirilazad was equivalent to methylprednisolone for 24 hours.18 Both NASCIS studies evaluated the patients' neurologic status at baseline on enrollment into o • • the study, at 6 weeks, and at 6 months. Absolutely no evidence from these studies suggests that giving the medication earlier (eg, in the first hour) provides more benefit than giving it later (eg, between hours 7 and 8). The authors only concluded that there was a benefit if given within 8 hours of injury following the NASCIS trials.18 The use of high-dose methylprednisolone in nonpenetrating acute spinal cord injury had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned the validity of the results.19 These authors cited concerns about the statistical analysis, randomization, and clinical endpoints used in the study. Even if the benefits of steroid therapy are valid, the clinical gains are questionable. Other reports have cited flaws in the study designs, trial conduct, and final presentation of the data. The risks of steroid therapy are not inconsequential. An increased incidence of infection and avascular necrosis has been documented. A number of professional organizations have therefore revised their recommendations pertaining to steroid therapy in spinal cord injury (SCI). The Canadian Association of Emergency Physicians is no longer recommending high-dose methylprednisolone as the standard of care. The Congress of Neurological Surgeons has stated that steroid therapy "should only be undertaken with the knowledge • • • • • • that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit."20 The American College of Surgeons has modified their Advanced Trauma Life Support guidelines to state that methylprednisolone is "a recommended treatment" rather than "the recommended treatment." In a recent survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids in spinal cord injury (SCI), but only 24% believed that they were of any clinical benefit.21 Note that the authors discovered that approximately 7% of spine surgeons do not recommend or use steroids at all in acute spinal cord injury. The authors reported that most centers were following the NASCIS II trial protocol. Overall, the benefit from steroids is considered modest at best, but for patients with complete or incomplete quadriplegia, a small improvement in motor strength in one or more muscles can provide important functional gains. The administration of steroids remains an institutional and physician preference in spinal cord injury. Nevertheless, the administration of high-dose steroids within 8 hours of injury for all patients with acute SCI is practiced by most physicians. The current recommendation is to treat all patients with SCI according to the local/regional protocol. If steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus. Local policy will also determine if the NASCIS II or NASCIS III protocol is to be followed. Two North American studies have addressed the administration of GM-1 ganglioside following acute spinal cord injury. The available medical evidence does not support a significant clinical benefit. It was evaluated as a treatment adjunct after the administration of methylprednisolone.22,16 Treatment of pulmonary complications and injury in spinal cord injury • • • Treatment of pulmonary complications and/or injury in patients with spinal cord injury (SCI) includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax. The ideal technique for emergent intubation in the setting of SCI is fiberoptic intubation with cervical spine control. This, however, has not been proven better than orotracheal with in-line immobilization. Furthermore, no definite reports of worsening neurologic injury with properly performed orotracheal intubation and in-line immobilization exist. If the necessary experience or equipment is lacking, blind nasotracheal or oral intubation with in-line immobilization is acceptable. Indications for intubation in SCI are acute respiratory failure, decreased level of consciousness (Glasgow score <9), increased respiratory rate with hypoxia, PCO2 more than 50, and vital capacity less than 10 mL/kg. In the presence of autonomic disruption from cervical or high thoracic spinal cord injury, intubation may cause severe bradyarrhythmias from unopposed vagal stimulation. Simple oral suctioning can also cause significant bradycardia. Preoxygenation with 100% oxygen may be preventive. Atropine may be required as an adjunct. Topical lidocaine spray can minimize or prevent this reaction. Consultations • • • Consultation with a neurosurgeon and/or an orthopedist is required, depending on local preferences. Because most patients with spinal cord injury have multiple associated injuries, consultation with a general surgeon or a trauma specialist may be required. Depending on the patient's associated injuries, other consultations may be required. Medication The goal of therapy is to improve motor function and sensation in patients with spinal cord injuries (SCIs). Glucocorticoids High-dose steroids are thought to reduce the secondary effects of acute spinal cord injury (SCI). Studies have shown limited but significant improvement in the neurologic outcome of patients treated within 8 h of injury. Methylprednisolone (Solu-Medrol) Used to reduce the secondary effects of acute SCI. • • • • Adult Dosing Interactions Contraindications Precautions 30 mg/kg IV bolus over 15 min, followed by 5.4 mg/kg/h over 23 h; begin IV infusion 45 min after conclusion of bolus Pediatric Administer as in adults • • • • • • • • • • • • Dosing Interactions Contraindications Precautions Dosing Interactions Contraindications Precautions Dosing Interactions Contraindications Precautions Definitions and Pathophysiology Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or permanent, in its normal motor, sensory, or autonomic function. The International Standards for Neurological and Functional Classification of Spinal Cord Injury is a widely accepted system describing the level and extent of injury based on a systematic motor and sensory examination of neurologic function.1,2 The following terminology has developed around the classification of SCI: • • Tetraplegia (replaces the term quadriplegia) - Injury to the spinal cord in the cervical region, with associated loss of muscle strength in all 4 extremities Paraplegia - Injury in the spinal cord in the thoracic, lumbar, or sacral segments, including the cauda equina and conus medullaris SCI can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage: • • • Destruction from direct trauma Compression by bone fragments, hematoma, or disk material Ischemia from damage or impingement on the spinal arteries Edema could ensue subsequent to any of these types of damage. The different clinical presentations of the above causes of tissue damage are explained further below. Spinal shock Spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions. An initial increase in blood pressure due to the release of catecholamines, followed by hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. These symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [MSR]). Neurogenic shock Neurogenic shock is manifested by the triad of hypotension, bradycardia, and hypothermia. Shock tends to occur more commonly in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance, with associated vascular dilatation. Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia. Autonomic dysreflexia See the article Autonomic Dysreflexia in Spinal Cord Injury. In a study showing a high incidence of autonomic dysfunction, including orthostatic hypotension and impaired cardiovascular control, following SCI, it was recommended that an assessment of autonomic function be routinely used, along with American Spinal Injury Association (ASIA) assessment, in the neurologic evaluation of patients with SCI.3 Motor strengths and sensory testing The extent of injury is defined by the ASIA Impairment Scale (modified from the Frankel classification), using the following categories1,2 : • • • • • A - Complete: No sensory or motor function is preserved in sacral segments S4-S5.4 B - Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5. C - Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade less than 3. D - Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade greater than or equal to 3. E - Normal: Sensory and motor functions are normal. Perform a rectal examination to check motor function or sensation at the anal mucocutaneous junction. The presence of either is considered sacral-sparing. Definitions of complete and incomplete SCI are based on the above ASIA definition with sacral-sparing.1,2,4 • • Complete - Absence of sensory and motor functions in the lowest sacral segments Incomplete - Preservation of sensory or motor function below the level of injury, including the lowest sacral segments Sacral-sparing is evidence of the physiologic continuity of spinal cord long tract fibers (with the sacral fibers located more at the periphery of the cord). Indication of the presence of sacral fibers is of significance in defining the completeness of the injury and the potential for some motor recovery. This finding tends to be repeated and better defined after the period of spinal shock. With the ASIA classification system, the terms paraparesis and quadriparesis now have become obsolete. The ASIA classification using the description of the neurologic level of injury is employed in defining the type of SCI (eg, C8 ASIA A with zone of partial preservation of pinprick to T2). Other classifications of SCI include the following: • • • • • Central cord syndrome often is associated with a cervical region injury and leads to greater weakness in the upper limbs than in the lower limbs, with sacral sensory sparing. Brown-Séquard syndrome, which often is associated with a hemisection lesion of the cord, causes a relatively greater ipsilateral proprioceptive and motor loss, with contralateral loss of sensitivity to pain and temperature. Anterior cord syndrome often is associated with a lesion causing variable loss of motor function and sensitivity to pain and temperature; proprioception is preserved. Conus medullaris syndrome is associated with injury to the sacral cord and lumbar nerve roots leading to areflexic bladder, bowel, and lower limbs, while the sacral segments occasionally may show preserved reflexes (eg, bulbocavernosus and micturition reflexes). Cauda equina syndrome is due to injury to the lumbosacral nerve roots in the spinal canal, leading to areflexic bladder, bowel, and lower limbs. Muscle strength is graded using the following Medical Research Council (MRC) scale of 0-5: • • • • 5 - Normal power 4+ - Submaximal movement against resistance 4 - Moderate movement against resistance 4- - Slight movement against resistance • • • • 3 - Movement against gravity but not against resistance 2 - Movement with gravity eliminated 1 - Flicker of movement 0 - No movement Muscle strength always should be graded according to the maximum strength attained, no matter how briefly that strength is maintained during the examination. The muscles are tested with the patient supine. The following key muscles are tested in patients with SCI, and the corresponding level of injury is indicated: • • • • • • • • • • C5 - Elbow flexors (biceps, brachialis) C6 - Wrist extensors (extensor carpi radialis longus and brevis) C7 - Elbow extensors (triceps) C8 - Finger flexors (flexor digitorum profundus) to the middle finger T1 - Small finger abductors (abductor digiti minimi) L2 - Hip flexors (iliopsoas) L3 - Knee extensors (quadriceps) L4 - Ankle dorsiflexors (tibialis anterior) L5 - Long toe extensors (extensors hallucis longus) S1 - Ankle plantar flexors (gastrocnemius, soleus) Sensory testing is performed at the following levels: • • • • • • • • • • • • • • • • • • • • • • • • • C2 - Occipital protuberance C3 - Supraclavicular fossa C4 - Top of the acromioclavicular joint C5 - Lateral side of antecubital fossa C6 - Thumb C7 - Middle finger C8 - Little finger T1 - Medial side of antecubital fossa T2 - Apex of axilla T3 - Third intercostal space (IS) T4 - Fourth IS at nipple line T5 - Fifth IS (midway between T4 and T6) T6 - Sixth IS at the level of the xiphisternum T7 - Seventh IS (midway between T6 and T8) T8 - Eighth IS (midway between T6 and T10) T9 - Ninth IS (midway between T8 and T10) T10 - 10th IS or umbilicus T11 - 11th IS (midway between T10 and T12) T12 - Midpoint of inguinal ligament L1 - Half the distance between T12 and L2 L2 - Midanterior thigh L3 - Medial femoral condyle L4 - Medial malleolus L5 - Dorsum of the foot at third metatarsophalangeal joint S1 - Lateral heel • • • S2 - Popliteal fossa in the midline S3 - Ischial tuberosity S4-5 - Perianal area (taken as 1 level) Sensory scoring is for light touch and pinprick, as follows: • • • 0 - Absent 1 - Impaired or hyperesthesia 2 - Intact A score of zero is given if the patient cannot differentiate between the point of a sharp pin and the dull edge. Motor level - Determined by the most caudal key muscles that have muscle strength of 3 or above while the segment above is normal (= 5) Motor index scoring - Using the 0-5 scoring of each key muscle, with total points being 25 per extremity and with the total possible score being 100 Sensory level - Most caudal dermatome with a normal score of 2/2 for pinprick and light touch Sensory index scoring - Total score from adding each dermatomal score with possible total score (= 112 each for pinprick and light touch) Neurologic level of injury - Most caudal level at which motor and sensory levels are intact, with motor level as defined above and sensory level defined by a sensory score of 2 Zone of partial preservation - All segments below the neurologic level of injury with preservation of motor or sensory findings (This index is used only when the injury is complete.) Skeletal level of injury - Level of the greatest vertebral damage on radiograph Lower extremities motor score (LEMS) - Uses the ASIA key muscles in both lower extremities, with a total possible score of 50 (ie, maximum score of 5 for each key muscle [L2, L3, L4, L5, and S1] per extremity). A LEMS of 20 or less indicates that the patient is likely to be a limited ambulator. A LEMS of 30 or more suggests that the individual is likely to be a community ambulator. Related eMedicine topics: Spinal Cord Injuries Spinal Cord, Topographical and Functional Anatomy Spinal Cord Trauma and Related Diseases Epidemiology Spinal cord injury (SCI) due to trauma is not a common condition, but it has major functional, medical, and financial effects on the injured person, as well as an important effect on the individual's psychosocial wellbeing.5,6,7 The most common causes of SCI include the following: • • • • Motor vehicle accidents (44.5%) - These are the major cause of traumatic SCI in the United States. Falls (18.1%) - These are most common in persons at or above age 45 years. Older females with osteoporosis have a propensity for vertebral fractures from falls with associated spinal cord injury. Violence (16.6%) - This is the most common cause of SCI in some urban settings in the United States, although a trend toward a slight decrease in violence-related SCI has been found. One study showed that among patients who had suffered an assault, SCI from a penetrating injury tended to be worse than that from a blunt injury.8 Sports injuries (12.7%) - Such injuries are responsible for many cases of SCI. The sport that most commonly leads to SCI is diving. Other causes of SCI include the following: • • • • • • • Vascular disorders Tumors9 Infectious conditions Spondylosis Iatrogenic injuries, especially after spinal injections and epidural catheter placement Vertebral fractures secondary to osteoporosis Developmental disorders No statistical/epidemiologic data have been compiled for the occurrence of nontraumatic SCI, but cancer alone may account for more SCI than does trauma. Spondylosis is also a common cause of SCI. Traumatic SCI is more common in persons younger than 40 years, while nontraumatic injury is more common in persons older than 40 years. The incidence of traumatic SCI in the United States is 30-60 new cases per million population, or 10,000 cases per year in the United States. Some sources cite 8 cases per 10,000 population per year. Figures on estimated prevalence vary from approximately 183,000 to 230,000 cases in the United States, the equivalent of 700-900 cases per million population. Race In the United States, the incidence of SCI among whites is higher than among African Americans, which in turn is higher than among Hispanics. Studies indicate that in the United States, 66.4% of SCIs occur in whites; 21.1%, in African Americans; 8.8%, in Hispanics; 1.6%, in Asians; 1.1%, in Native Americans; and 1% in other populations. Sex The male-to-female ratio of individuals with SCI in the United States is 4:1; ie, males constitute about 80% of persons with SCI. Age More than 50% of all cases of SCI occur in persons aged 16-30 years. The median age is 26.4 years, while the mean age is 31.8 years, and the mode age at injury is 19 years. Traumatic SCI is more common in persons younger than 40 years, while nontraumatic SCI is more common in persons older than 40 years. Greater mortality is reported in older patients with SCI. In a study on pediatric SCI by Vitale and colleagues, using information from the Kids' Inpatient Database (KID) and the National Trauma Database (NTDB), it was found that, with regard to the annual incidence rate of pediatric SCI, there were significant differences between patient populations (as stratified by race and sex).10 A significantly greater incidence of pediatric SCI was found in African Americans (1.53 cases per 100,000 children) than in Native Americans (1.0 case per 100,000 children) and Hispanics (0.87 case per 100,000 children). The frequency in Asians was significantly lower than that in all other races (0.36 per 100,000 children). Also, the likelihood that boys would suffer SCI was found to be more than twice that of girls (2.79 cases per 100,000 children vs 1.15 cases per 100,000 children, respectively). The overall incidence of pediatric SCI is 1.99 cases per 100,000 US children. As estimated from the above data, 1455 children are admitted to US hospitals annually for SCI treatment. Vitale and coauthors looked at the major causative factors of pediatric SCI as well, with the following incidences reported10 : • • • • Motor vehicle accidents - 56% Accidental falls - 14% Firearm injuries - 9% Sports injuries - 7% Among children in the study, 67.7% of those injured in a motor vehicle accident were not wearing a seatbelt. Alcohol and drugs were found to have played a role in 30% of all pediatric SCI cases. Associated injuries Other injuries are often associated with traumatic SCI, including bone fractures (29.3%), loss of consciousness (17.8%), and traumatic brain injury affecting emotional/cognitive functioning (11.5%). Marital status Single persons sustain SCIs more commonly than do married persons. Research has indicated that among persons with SCI whose injury is approximately 15 years old, one third will remain single 20 years postinjury. The marriage rate after SCI is annually about 59% below that of persons in the general population of comparable gender, age, and marital status. The divorce rate annually among individuals with SCI within the first 3 years following injury is approximately 2.5 times that of the general population, while the rate of marriages contracted after the injury is about 1.7 times that of the general population. Marriage is more likely if the patient is a college graduate, previously divorced, paraplegic (not tetraplegic), ambulatory, living in a private residence, and independent in the performance of activities of daily living (ADL). The divorce rate among persons with SCI who were married at the time of injury is higher if the patient is younger, female, African American, without children, nonambulatory, and previously divorced. The divorce rate among those who were married after the SCI is higher if the individual is male, has less than a college education, has a thoracic level injury, and was previously divorced. Educational status The rate of injury differs according to educational status, as follows: • • • • • • Less than a high school degree at 39.8% High school degree - 49.9% Associate degree - 1.6% Bachelors degree - 5.9% Masters or doctorate degree - 2.1% Other degree - 0.7%. Level and type of injury The most common levels of injury on admission are C4, C5 (the most common), and C6, while the level for paraplegia is the thoracolumbar junction (T12). The most common type of injury on admission is ASIA level A. Season SCIs occur most frequently in July and least commonly in February. The most common day on which SCIs occur is Saturday. SCIs occur more frequently during daylight hours, which may be due to the increased frequency of motor vehicle accidents and of diving and other recreational sporting accidents during the day. Substance abuse The rate of alcohol intoxication among individuals who sustain SCI is 17-49%. Injuries by ASIA classification • • • • Incomplete tetraplegia - 29.5% Complete paraplegia - 27.9% Incomplete paraplegia - 21.3% Complete tetraplegia - 18.5% The most common neurologic level of injury is C5. In paraplegia, T12 is the most common level. Employment Patients with SCI classified as ASIA D are more likely to be employed than individuals with ASIA A, B, and C. Persons employed tend to work full-time. Individuals who return to work within a year of injury tend to return to the same job. Those individuals who return to work after a year of injury tend to work for a different employer at a different job requiring retraining.11 The likelihood of employment after injury is greater in patients who are younger, male, and white and who have more formal education, higher reported intelligence quotient (IQ), greater functional capacity, and less severe injury. Patients with greater functional capacity, less severe injury, history of employment at the time of injury, greater motivation to return to work, nonviolent injury, and ability to drive are more likely to return to work, especially after more elapsed time following injury. Life expectancy Approximately 10-20% of patients who have sustained an SCI do not survive to reach acute hospitalization, while about 3% of patients die during acute hospitalization. Patients aged 20 years at the time they sustain an SCI have a life expectancy of approximately 33 years (patients with tetraplegia), 39 years (patients with low tetraplegia), or 44 years (patients with paraplegia). Individuals aged 60 years at the time of injury have a life expectancy of approximately 7 years (patients with tetraplegia), 9 years (patients with low tetraplegia), and 13 years (patients with paraplegia). The annual death rate for patients with acute SCI is 7501000 deaths per year in the United States. Studies have found that patients with SCI who suffer from pain have less life satisfaction than do patients in whom pain is well controlled; this may also affect the patients' general outlook on life.12,13 A 2006 study by Strauss and colleagues reported that among patients with SCI, during the critical first 2 years following injury, a 40% decline in mortality occurred between 1973 and 2004.14 The study also found that during that same 31year period, there had been only a small, statistically insignificant reduction in mortality in the post 2-year period for these patients. Leading cause of death The leading causes of death in patients following SCI are pneumonia and other respiratory conditions, followed by heart disease, subsequent trauma, and septicemia.15,16 Suicide and alcohol-related deaths are also major causes of death in patients with SCI.17,18 In persons with SCI, the suicide rate is higher among individuals who are younger than 25 years. Among patients with incomplete paraplegia, the leading causes of death are cancer and suicide (1:1 ratio), while among persons with complete paraplegia, the leading cause of death is suicide, followed by heart disease.