eMedicine Specialties > Emergency Medicine > Neurology

Spinal Cord Injuries

Author: Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Contributor Information and Disclosures

Updated: Apr 8, 2009

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.
  • 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 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:
  • Neurogenic shock occurs only in the presence of acute SCI above T6. Hypotension and/or 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 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:
  • 0 - No contraction or movement
  • 1 - Minimal movement
  • 2 - Active movement, but not against gravity
  • 3 - Active movement against gravity
  • 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:
  • Loss of ventilatory muscle function from denervation and/or associated chest wall injury
  • Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion
  • 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.
  • With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent.
  • With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and 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:
  • Agitation, anxiety, or restlessness
  • Poor chest wall expansion
  • Decreased air entry
  • Rales, rhonchi
  • Pallor, cyanosis
  • Increased heart rate
  • Paradoxic movement of the chest wall
  • Increased accessory muscle use
  • 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:
  • Upper limb
    • Biceps C5
    • Wrist extensors C6
    • Triceps C7
    • Long finger flexors C8
    • Small finger abductors T1
  • Lower limb
    • 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:
  • Perineal sensation to light touch and pinprick
  • Bulbocavernous reflex (S3 or S4)
  • Anal wink (S5)
  • Rectal tone
  • Urine retention or incontinence
  • 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

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