Pathophysiology of Decreased Sympathetic Tone in Acute Spinal Cord Injury
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
Anatomical Basis
The sympathetic nervous system originates from the intermediolateral nuclei of the T1-L2 spinal cord segments 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, 3, 2. This anatomical disruption creates a functional segregation where critical spinal sympathetic neurons lose their supraspinal modulation 4.
Mechanism of Sympathetic Dysfunction
The pathophysiology unfolds through several interconnected mechanisms:
Loss of descending sympathetic control: The injury interrupts supraspinal control of sympathetic nervous system function, leading to reduced sympathetic activity below the level of injury 2, 5
Unopposed parasympathetic activity: With sympathetic tone diminished, the vagus nerve (which remains intact above the injury) exerts unopposed parasympathetic influence on the heart and cardiovascular system 1, 2
Spinal shock phenomenon: During the acute phase (within 48 hours to several weeks), there is temporary loss or depression of all spinal reflex activity below the injury level, including autonomic reflexes 1, 5
Cardiovascular Consequences
The loss of sympathetic tone produces profound hemodynamic effects:
Profound hypotension: Loss of cardiovascular sympathetic innervation leads to severe hypotension, which compounds the ischemic insult to the already injured spinal cord 1, 3
Severe bradycardia: The unopposed parasympathetic stimulation causes severe sinus bradycardia that is common in the acute recovery phase, with both incidence and severity related to the level and severity of injury 1
Cardiac arrest risk: During the first 2-4 weeks after injury, cardiac arrest (most often from sinus arrest and asystole) occurs in 16% of patients with severe cervical spinal injury 1
Clinical Triggers and Refractoriness
Bradycardia episodes are often triggered by tracheal suctioning and turning the patient, and can be persistent and refractory to atropine and other adrenergic drugs. 1 This refractoriness occurs because the primary abnormality is unopposed parasympathetic stimulation rather than simple sympathetic deficiency 1.
Secondary Complications
Beyond direct cardiovascular effects, decreased sympathetic tone contributes to:
Immune paralysis: Loss of sympathetic innervation to lymphatic organs (particularly the spleen) induces secondary immunodeficiency, increasing susceptibility to infections 1
Inadequate vasoconstriction: Functional impairment prevents adequate increase in peripheral resistance upon postural changes 1
Chronotropic incompetence: Inability to appropriately increase heart rate in response to physiologic demands 1
Important Clinical Caveat
The pressor response to adrenergic drugs, including phenylephrine, can be paradoxically increased in patients with autonomic dysfunction from spinal cord injuries, requiring careful titration of vasopressor therapy 6. This hypersensitivity occurs because peripheral vasculature becomes denervated and develops supersensitivity to circulating catecholamines.