Spinal cord injury (SCI) is often recognized for its impact on movement and sensation, but the most immediate and life-threatening consequence is frequently the loss of independent breathing. The spinal cord is the main communication highway between the brain and the body. When this pathway is damaged, the brain loses its ability to send signals to the muscles that control respiration. The severity of the injury directly correlates with the degree of breathing impairment, making respiratory care a central focus of treatment after an SCI.
The Neural Control of Respiration
Breathing is a complex process relying on specific muscle groups innervated by nerves originating along the spinal cord. The diaphragm is the primary muscle of inspiration, responsible for the majority of air drawn into the lungs. This large, dome-shaped muscle is controlled by the phrenic nerve, which originates high in the cervical spine from the C3, C4, and C5 spinal segments.
Secondary muscles of breathing play a role, particularly during physical exertion or when a forced breath is needed. These include the intercostal muscles, located between the ribs, and the abdominal muscles. The intercostal muscles (T1 to T11) assist in expanding the rib cage during inhalation and pulling it inward during exhalation. The abdominal muscles, controlled by nerves lower in the thoracic and lumbar spine, are crucial for forceful exhalation, such as coughing.
Damage to the spinal cord above the level where these respiratory nerves exit interrupts the communication pathway, resulting in muscle weakness or complete paralysis. Because the phrenic nerve originates high in the neck, injuries that do not cause total paralysis of the limbs can still severely compromise breathing.
How Injury Level Determines Severity
The location of a spinal cord injury determines which respiratory muscles are affected and the severity of breathing impairment. Injuries in the high cervical spine (C1 to C3 levels) are the most devastating to respiratory function. Since the phrenic nerve’s origin (C3-C5) is severed from the brain’s control centers, the diaphragm is completely paralyzed. Patients with injuries at this level require full-time mechanical ventilation to sustain life, as they cannot initiate a breath independently.
Injuries at the mid-to-low cervical levels (C4 through C8) often result in varying degrees of spared diaphragm function. An injury at C4 may leave the diaphragm partially functional, potentially allowing the person to breathe independently for periods of time. However, the nerves controlling the intercostal and abdominal muscles are compromised. This leads to a weakened chest wall and an inability to forcefully exhale, which reduces lung capacity and impairs the ability to clear the airways.
When the injury is in the thoracic spine (T1 level and below), the diaphragm is almost always spared because its controlling nerves exit higher up. While these individuals can breathe without ventilator support, the paralysis of the abdominal and intercostal muscles still causes significant respiratory inefficiency. The loss of these muscles reduces the force available for coughing and decreases overall respiratory endurance. Even with preserved diaphragm function, the ability to take a deep breath and exhale forcefully is diminished.
Secondary Respiratory Complications
Weakness of the respiratory muscles leads directly to secondary health risks. One significant problem is the inability to generate an effective cough, which is necessary to clear mucus and foreign particles from the lungs. Without the strong contraction of the abdominal and intercostal muscles, the expulsive force required for a productive cough is lost.
This ineffective cough results in the retention of secretions within the lungs, creating a breeding ground for bacteria and infection. Pneumonia is a frequent and serious complication, representing the leading cause of death in people with high-level SCI. The inability to take deep breaths also causes atelectasis, the partial or complete collapse of small sections of the lung. This collapse occurs because the air sacs are not fully inflated regularly, blocking proper oxygen exchange.
The reduction in the mechanical strength of the breathing muscles decreases the total volume of air moved in and out of the lungs, known as reduced vital capacity. For a person with a complete cervical injury, vital capacity can drop to 20% to 50% of the predicted normal value. This reduced capacity contributes to chronic respiratory compromise, increasing the effort required for quiet breathing and making the person more susceptible to respiratory failure during illness.
Managing Breathing Function After Injury
Management of breathing function after SCI focuses on immediate life support and long-term strategies to maximize remaining muscle strength. For those with high cervical injuries and complete diaphragm paralysis, mechanical ventilation is required to move air into and out of the lungs. However, many individuals with partial diaphragm function can be gradually weaned from the ventilator, transitioning to part-time use or full independence.
In cases where the phrenic nerve is intact but severed from the brain, phrenic nerve pacing may be considered. This surgical procedure involves implanting electrodes that send electrical impulses directly to the phrenic nerve or the diaphragm muscle. This mimics the brain’s signal and stimulates a contraction. Pacing can allow some patients to breathe without a ventilator for extended periods, improving quality of life.
Other management strategies focus on leveraging existing muscle function and providing mechanical assistance for airway clearance.
Airway Clearance and Support
Breathing exercises, such as glossopharyngeal breathing, teach individuals to use mouth and throat muscles to “gulp” air into the lungs, achieving deeper breaths. Assistive devices like mechanical insufflation-exsufflation machines (cough assist devices) force air into the lungs and then rapidly pull it out, simulating a powerful cough to mobilize secretions. Abdominal binders provide external support for the lax abdominal wall, which helps stabilize the diaphragm and improves breathing efficiency.