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 LI 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 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 to light touch, proprioception, and vibration. Opposed to 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. In the anterior interomedial tract, higher spinal cord lesions cause increasing degrees of autonomic dysfunction.

Neurogenic shock is characterized by severe autonomic dysfunction, resulting in hypotension, relative bradycardia, peripheral vasodilation, and hypothermia. It usually does not occur with SCI below the level of T6. Shock associated with these lower thoracic SCIs should 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 SCI.

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.

SCIs may be primary or secondary. Primary SCIs arise from mechanical disruption, transection, extradural pathology, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary SCI may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary SCI. More commonly, displaced bony fragments cause penetrating spinal cord or segmental spinal nerve injuries. Extradural pathology may also cause a primary SCI. 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 SCI without spinal fracture or dislocation.

Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary SCI. Anoxic or hypoxic effects compound the extent of SCI.

SCI, 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 and acid-base balance is required to prevent worsening of the SCI.

Frequency:
 

• In the US: The incidence is approximately 50 patients per million population, or 10,000 patients, per year.

Sex: Male-to-female ratio is approximately 2.5-3.0:1.

Age:

• About 80% of males with SCIs are aged 18-25 years.

• SCI without radiologic abnormality occurs primarily in children. The spinal cord is tethered more securely than the vertebral column. 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

• 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 neurological 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. An SCI must be considered concurrently.

The clinical assessment of pulmonary function in acute SCI begins with careful history taking regarding respiratory complaints 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. ABG analysis and pulse oximetry are especially useful, since the bedside diagnosis of hypoxia or carbon dioxide retention may be difficult.

• The degree of respiratory dysfunction is ultimately dependent on the pre-existing pulmonary comorbidity, level of SCI, and 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 between the level of cord injury and the degree of respiratory dysfunction exists.

• 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:

• Decreased air entry

   

• Rales, rhonchi