Pathophysiology of Decreased Sympathetic Tone in Acute Spinal Cord Injury

Anatomical Basis

Cervical and high thoracic spinal cord injuries cause loss of supraspinal control over spinal sympathetic neurons, resulting in decreased overall sympathetic activity below the injury level and unopposed parasympathetic outflow through the intact vagus nerve 1, 2
When spinal cord injury occurs at or above T6, it disrupts the descending pathways from central control centers to these spinal sympathetic neurons 1

Unopposed parasympathetic activity occurs with sympathetic tone diminished, the vagus nerve exerts unopposed parasympathetic influence on the heart and cardiovascular system 3, 4
Spinal shock phenomenon occurs during the acute phase, with temporary loss or depression of all spinal reflex activity below the injury level, including autonomic reflexes 5

Profound hypotension occurs due to loss of cardiovascular sympathetic innervation, leading to severe hypotension, which compounds the ischemic insult to the already injured spinal cord 1, 2
Severe bradycardia occurs due to unopposed parasympathetic stimulation, causing severe sinus bradycardia that is common in the acute recovery phase 3, 4, 6
Cardiac arrest risk occurs in 16% of patients with severe cervical spinal injury during the first 2-4 weeks after injury, often from sinus arrest and asystole 3, 4, 6

Bradycardia episodes are often triggered by tracheal suctioning and turning the patient, and can be persistent and refractory to atropine and other adrenergic drugs 3, 4

Immune paralysis occurs due to loss of sympathetic innervation to lymphatic organs, inducing secondary immunodeficiency and increasing susceptibility to infections 1, 2
Inadequate vasoconstriction occurs due to functional impairment, preventing adequate increase in peripheral resistance upon postural changes 7
Chronotropic incompetence occurs due to inability to appropriately increase heart rate in response to physiologic demands 7