The spinal (or vertebral) column is composed of 33 bony rings or vertebrae, named for the region of the spine in which they are located and numbered cephalad to caudal: 7 cervical vertebrae (C1-7), 12 thoracic vertebrae (T1-12), 5 lumbar vertebrae (L1-5), 5 vertebrae fused as the sacrum (S1-5), and 4 coccygeal vertebrae.

     The first cervical vertebra, C1, articulates with the skull. The last vertebrae, in the sacrum, form the posterior wall of the pelvis. Between the vertebrae are cartilaginous disks for cushioning. Along the length of the spinal column are ligaments for support. Openings between each bony segment, called foramina, allow the nerve roots to exit the spinal canal.

     The spinal cord extends from the base of the brain through the spinal canal to the second lumbar vertebra (L2), with nerves exiting the cord between each pair of vertebrae and continuing through the spinal canal as the cauda equina. The spinal cord segments are numbered for the level at which the nerve root exits the spinal column.

     During an injury, the spinal column and the spinal cord can be injured anywhere along their length. The majority of the damage to the spinal cord occurs at the time of injury, but further damage can be caused by improper handling of the unstable spine and by the disruption of the blood supply, which can cause hypoxia and necrosis.

     Immediately following SCI, spinal shock occurs in the portion of the spinal cord that is injured and results in a complete loss of all motor, sensory, reflex, and autonomic function below the level of the injury. This loss is manifested in loss of bowel and bladder tone and peripheral vascular tone, which result in bladder distention, paralytic ileus, flaccid paralysis, and hypotension.

     After a period that varies from hours to months, but which usually lasts for 1 to 6 weeks, the spinal neurons gradually regain their excitability and the period of spinal shock ends. The earliest indication is the return of the perianal reflexes. The bulbocavernous reflex has returned if a slight muscle contraction follows squeezing of the glans penis or pulling the indwelling catheter. The anal flex has returned if there a puckering of the anal sphincter following a digital examination of the rectum, insertion of a rectal thermometer, or a scratching of the skin around the anal area. The flaccid paralysis during spinal shock is replaced by spastic paralysis during recovery.

     The degree of neuron excitability that returns can be greater than before the injury. Depending on the degree of spinal shock and the completeness of the injury, either:

  • Transmission of impulses will resume, along with motor, sensory, reflex, and autonomic activity below the level of the injury, or,
  • The isolated cord segment will develop its own reflex activity: minimal reflex activity, flexor spasm activity, alternating flexor and extensor spasm activities, and predominent extensor spasm activity

Spinal shock recovery can, therefore, be accompanied by complications such as autonomic hyperreflexia, and sexual, bladder, and autonomic dysfunctions.

     Neurogenic shock is the temporary loss or disruption of autonomic nervous system innervation below the level of injury, which can cause orthostatic hypotension, bradycardia, lower than normal body temperature, and loss of the ability to perspire. Orthostatic hypotension is the rapid drop in blood pressure when an erect position is assumed, due to inadequate blood supply to the brain, which can result in brain damage or death. The systolic pressure can drop as low as 40 mm Hg, the diastolic pressure can decrease to 0 mm Hg, and pooling of blood in the abdomen and lower extremities can occur. Orthostatic hypotension is commonly seen in patients with lesions above T7, and can result from even a slight raising of the head of the bed for a patient with tetraplegia.

The PoinTIS Spinal Cord Nursing site of the SCI Manual for Providers is based on information in Hickey JV. The Clinical Practice of Neurological and Neurosurgical Nursing, 4th ed., Philadelphia: Lippincott, 1997; Chin PA, et al. Rehabilitation Nursing Practice, N.Y.: McGraw-Hill, 1998; and Wirtz KM, Managing chronic spinal cord injury: issues in critical care, Critical Care Nurse 1996 16(4):24-35 Aug., except for information where other papers are cited.