Neurogenic Shock: Definition and Pathophysiology
Neurogenic shock is a distributive form of circulatory shock caused by loss of sympathetic nervous system control following spinal cord injury (SCI), resulting in profound hypotension and bradycardia due to unopposed parasympathetic (vagal) activity. 1, 2
Core Pathophysiologic Mechanism
Neurogenic shock occurs when traumatic spinal cord injury disrupts descending sympathetic pathways from central control centers to spinal sympathetic neurons in the intermediolateral nuclei of T1-L2 cord segments. 1, 2 This disruption produces:
- Loss of supraspinal control over the sympathetic nervous system below the injury level 1, 2
- Reduced overall sympathetic activity below the lesion 1, 2
- Unopposed parasympathetic outflow through the intact vagal nerve 1, 2
The result is a characteristic hemodynamic profile distinct from other shock states, though the specific mechanisms can vary between patients 3.
Clinical Presentation
Hemodynamic Criteria
Neurogenic shock manifests as severe arterial hypotension (systolic BP < 90 mmHg) combined with bradycardia—a combination that distinguishes it from hypovolemic shock, which typically presents with tachycardia. 1, 2, 4
The hemodynamic disturbance results from multiple mechanisms 3:
- Decreased peripheral vascular resistance (33% of cases) 3
- Loss of vascular capacitance (22% of cases) 3
- Mixed peripheral resistance and capacitance abnormalities (33% of cases) 3
- Purely cardiac mechanisms (11% of cases) 3
Temporal Context: Spinal Shock vs. Neurogenic Shock
Neurogenic shock is a component of the broader syndrome of spinal shock, which occurs during the acute phase following SCI and represents a transitory suspension of function and reflexes below the injury level. 1, 2 Spinal shock encompasses both neurologic and hemodynamic manifestations, whereas neurogenic shock specifically refers to the cardiovascular instability (severe hypotension and bradycardia) 1, 2.
Injury Level and Risk
Neurogenic shock predominantly occurs with cervical or high thoracic spinal cord injuries, particularly those above T5-T6 (the splanchnic sympathetic outflow level). 1, 2 The reported incidence varies significantly depending on diagnostic criteria used, with one rigorous study finding a 29% incidence in cervical SCI when appropriate hemodynamic and laboratory criteria were applied 5.
Clinical Course and Natural History
Blood pressure characteristically declines further during the first week post-injury, and current fluid management strategies often maintain patients at net zero or negative fluid balance. 5 This finding highlights that hypovolemia is frequently a confounding factor in the diagnosis and management of neurogenic shock 5.
Critical Distinguishing Features from Other Shock Types
Unlike cardiogenic shock (which shows elevated filling pressures and systemic vascular resistance) 6, 7 or hypovolemic shock (which presents with tachycardia and low filling pressures) 6, 7, neurogenic shock is characterized by:
- Low systemic vascular resistance 6, 3
- Bradycardia rather than tachycardia 1, 2, 4
- Hypotension despite adequate or even excessive fluid resuscitation 5, 4
- Loss of sympathetic tone below the injury level 1, 2
Clinical Significance and Complications
Neurogenic shock is life-threatening and aggravates the underlying neurological deficit by compromising spinal cord perfusion. 4 Cardiovascular disturbances represent the leading causes of morbidity and mortality in both acute and chronic stages of SCI 1, 2.
Additional cardiovascular complications include 1:
- Orthostatic hypotension (both acute and chronic phases) 1
- Deep vein thrombosis 1
- Long-term increased risk for coronary heart disease and systemic atherosclerosis 1
- Cardiac dysrhythmias, including rare cardiac arrest 2
Diagnostic Pitfalls
The reported incidence of neurogenic shock varies dramatically (from very low to very high) depending on which clinical definition is applied, with hypovolemia being the primary confounding factor responsible for inconsistent incidence reports between studies. 5 Accurate diagnosis requires combining hemodynamic criteria (hypotension with bradycardia) with laboratory markers and exclusion of hypovolemia 5.