Pathophysiological Mechanisms of Neurogenic Shock

Abstract

Neurogenic shock is caused by damage to the sympathetic nervous system. This can have negative outcomes in the patient, leading to excessive vasodilation, hypotension, and poor circulation. Spinal or brain damage usually continues. Disturbance in autonomous control, reduction in norepinephrine, inflammation, and excess nitrogen oxides are exacerbated. Compensation mechanisms often fail and highlight the need for improved treatment.

Keywords

neurogenic shock - hypotension - spinal cord injury - autonomic dysfunction - vasodilation - sympathetic nervous system - bradycardia - circulation failure - inflammation - nitric oxide

Introduction

The loss of blood pressure regulation through damage to the sympathetic nervous system and to the nervous system, in general, creates neurogenic shock.[1] [2] Shock occurs differently in the human body because blood vessels lose constriction ability rather than resulting from blood loss or infection. Spinal cord injuries (SCIs), traumatic brain injuries (TBIs), and specific brainstem disorders represent the main causes of neurogenic shock, according to the literature.[3] The body modifies both nerve functions and chemical signals as a result of neurogenic shock.[4]

Physiology

A central nervous system or SCI above T6 causes blood vessel control damage to the nervous system, resulting in neurogenic shock, which is mathematically termed circulatory failure.[5] [6] The nervous system injury results in blood pressure reduction called hypotension and bradycardia alongside diminished circulation (see [Fig. 1]). The review discusses the mechanism of neurogenic shock along with its physical impacts on the body and the natural homeostatic mechanisms at work. Knowledge about these mechanisms benefits efforts to improve the medical management of patients suffering from this condition.[7] [8]

Fig. 1 Physiology of neurogenic shock.

Disruption of the Autonomic Nervous System

Involuntary systems such as blood pressure and heart rate fall under autonomic nervous system control.[9] The sympathetic nervous system is based on spinal cord segments T1–L2 to operate blood vessels at a level that controls blood pressure. High-level spinal injuries disrupt involuntary blood vessel control pathways, which cause excessive relaxation of blood vessels. While the parasympathetic system stays active, the heart rate decreases.[9] The deteriorating blood pressure alongside the heart rate slowing down becomes severe because of this imbalance.[10]

Effects of Sympathetic Dysfunction on Blood Circulation

Blood vessels become too dilated after sympathetic control loss, which causes blood pressure drops and venous blood accumulation.[11] [12] Neurogenic shock produces the opposite effect from other shocks because the parasympathetic system overrides other systems, which normally produce elevated heart rates.[13] Organ oxygen supply decreases because the heart's blood output quantity and pump speed go down during this condition.[14] [15] The improper blood vessel adjustment results in an inadequate supply of blood to essential organs, including the kidneys and the digestive tract.[16]

Pathophysiology of Neurogenic Shock

The key processes that occur in neurogenic shock can disrupt the body's normal balance and lead to life-threatening complications ([Table 1]). A dysfunctional nervous system decreases norepinephrine and epinephrine output since these compounds help preserve blood pressure levels.[17] [18] Pressure sensor failure in the body results in disturbed blood pressure detection ability, thereby worsening the condition.[19] The process of inflammation triggers body cells to emit cytokines, which makes blood vessels leak more before fluid escapes and lowers blood pressure even more.[20] [21] The chemical nitric oxide, which develops as a result of inflammation, causes excessive blood vessel relaxation, which creates a worsening condition.[22] The changes may include the following:

Table 1 Pathophysiology of neurogenic shock

Pathophysiological aspect	Description
Primary cause	Disruption of the sympathetic nervous system due to spinal cord injury (above T6), brainstem trauma, or medication effects
Loss of sympathetic tone	Unopposed parasympathetic activity causes widespread vasodilation, bradycardia, and hypotension
Vascular changes	Peripheral vasodilation reduces systemic vascular resistance (SVR), causing blood pooling and reduced venous return to the heart
Cardiac effects	Decreased sympathetic input results in a slow heart rate (bradycardia), which reduces cardiac output
Hemodynamic consequences	Severe hypotension, reduced cardiac output, and poor organ perfusion
Autonomic dysregulation	Loss of body temperature control, leading to poikilothermia (inability to regulate body temperature)
Endothelial dysfunction	Increased blood vessel permeability leads to fluid loss and worsened hypotension
Systemic hypoperfusion	Reduced blood supply to major organs, increasing the risk of multi-organ failure
Compensatory mechanisms	The renin-angiotensin-aldosterone system (RAAS) is activated but insufficient to counteract vasodilation
Neurological consequences	Depending on injury level, it is associated with flaccid paralysis, loss of reflexes, and sensory deficits

• Chemical and inflammatory responses and lack of stress hormones: The damaged nervous system reduces the release of norepinephrine and epinephrine, which normally help keep blood pressure up.[17] [18]

• Faulty pressure sensors: Sensors in the body that normally detect low blood pressure and trigger a response fail to do their job, making the condition worse.[19]

• Inflammation: The body releases inflammatory chemicals like cytokines, which make blood vessels even more leaky, leading to fluid loss and further drops in blood pressure.[20] [21]

• Excess nitric oxide: This chemical, released in response to inflammation, further relaxes blood vessels, making the situation worse.[22]

Neurogenic shock varies in severity and can be categorized based on its clinical impact ([Table 2]). This classification helps health care providers assess the severity of neurogenic shock and tailor treatment accordingly.

Table 2 Classification of neurogenic shock based on severity

Type	Description	Clinical features	Hemodynamic impact
Mild	Partial sympathetic disruption with some compensatory mechanisms intact	Mild hypotension, bradycardia, preserved consciousness, minimal organ dysfunction	There was a slight decrease in systemic vascular resistance (SVR), a modest reduction in cardiac output (CO), and compensatory vasoconstriction in unaffected areas
Moderate	Significant autonomic dysfunction with pronounced hemodynamic instability	Severe hypotension, marked bradycardia, poikilothermia, decreased urine output, and early signs of organ hypoperfusion	A profound decrease in SVR significantly reduced CO, venous pooling, and impaired perfusion to vital organs
Severe	Complete autonomic failure with profound cardiovascular collapse	Refractory hypotension, extreme bradycardia (may require pacing), multi-organ failure, coma, and high mortality risk	Drastic drop in SVR, critical reduction in CO, and inability to restore perfusion without aggressive interventions (vasopressors, fluid resuscitation)

How the Body Tries to Compensate

Without sympathetic nerve signals, the kidney hormones renin and aldosterone become ineffective at increasing blood pressure.[23] The adrenal glands attempt to increase cortisol hormone production since it helps elevate blood pressure; however, the hormone release might be insufficient.[24] The adjustment of blood vessels eventually occurs as a way to handle long-lasting low blood pressure, yet it results in chronic circulation problems.[25]

Conclusion

Neurogenic shock can be a life-threatening condition and can lead to low blood pressure, slow heart rate, and poor circulation, and can be followed by irreversible damage to the nervous system. The main problem is the loss of nerve control over blood vessels, resulting in excessive relaxation and low resistance to blood flow. The body tries to compensate by releasing hormones, but these mechanisms are often not enough to restore normal function. Understanding these processes is key to developing better treatments and improving patient survival.

Conflict of Interest

None declared.

• References

• 1 Furlan JC, Fehlings MG. Cardiovascular complications after acute spinal cord injury: pathophysiology, diagnosis, and management. Neurosurg Focus 2008; 25 (05) E13
• 2 Taylor MP, Wrenn P, O'Donnell AD. Presentation of neurogenic shock within the emergency department. Emerg Med J 2017; 34 (03) 157-162
• 3 Guly HR, Bouamra O, Lecky FE. Trauma Audit and Research Network. The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergency department. Resuscitation 2008; 76 (01) 57-62
• 4 Walters BC, Hadley MN, Hurlbert RJ. et al; American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of acute cervical spine and spinal cord injuries: 2013 update. Neurosurgery 2013; 60 (CN_suppl_1): 82-91
• 5 Florez-Perdomo WA, Guillermo AC-C, García-Ballestas E. et al. Pathobiology of traumatic spinal cord injury: an overview. Egypt J Neurosurg 2024; 39 (01) 27
• 6 Moscote-Salazar LR, Misol D, Rubiano AM. Neurogenic shock: pathophysiology, diagnosis and treatment. Rev Traum Amér. 2016; 6: 27-30
• 7 Moscote-Salazar LR, Janjua T, Agrawal A. The clinical rules for the management of neurogenic shock. Indian J Neurotrauma 2025; (e-pub ahead of print).
• 8 Parra MW, Ordoñez CA, Mejia D. et al. Damage control approach to refractory neurogenic shock: a new proposal to a well-established algorithm. Colomb Med (Cali) 2021; 52 (02) e4164800
• 9 Adegeest CY, Ter Wengel PV, Peul WC. Traumatic spinal cord injury: acute phase treatment in critical care. Curr Opin Crit Care 2023; 29 (06) 659-665
• 10 Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord 2004; 42 (07) 383-395
• 11 Draghici AE, Taylor JA. The physiological basis and measurement of heart rate variability in humans. J Physiol Anthropol 2016; 35 (01) 22
• 12 West CR, Crawford MA, Poormasjedi-Meibod MS. et al. Passive hind-limb cycling improves cardiac function and reduces cardiovascular disease risk in experimental spinal cord injury. J Physiol 2014; 592 (08) 1771-1783
• 13 Claydon VE, Krassioukov AV. Clinical correlates of frequency analyses of cardiovascular control after spinal cord injury. Am J Physiol Heart Circ Physiol 2008; 294 (02) H668-H678
• 14 Karlsson AK. Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs. Prog Brain Res 2006; 152: 1-8
• 15 Soriano JE, Romac R, Squair JW. et al. Passive leg cycling increases activity of the cardiorespiratory system in people with tetraplegia. Appl Physiol Nutr Metab 2022; 47 (03) 269-277
• 16 Summers RL, Baker SD, Sterling SA, Porter JM, Jones AE. Characterization of the spectrum of hemodynamic profiles in trauma patients with acute neurogenic shock. J Crit Care 2013; 28 (04) 531.e1-531.e5
• 17 Krassioukov A, Warburton DE, Teasell R, Eng JJ. Spinal Cord Injury Rehabilitation Evidence Research Team. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil 2009; 90 (04) 682-695
• 18 Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil 2000; 81 (04) 506-516
• 19 Khan F, Amatya B, Bensmail D, Yelnik A. Non-pharmacological interventions for spasticity in adults: an overview of systematic reviews. Ann Phys Rehabil Med 2019; 62 (04) 265-273
• 20 Eldahan KC, Rabchevsky AG. Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management. Auton Neurosci 2018; 209: 59-70
• 21 Grossman RG, Frankowski RF, Burau KD. et al. Incidence and severity of acute complications after spinal cord injury. J Neurosurg Spine 2012; 17 (01) 119-128
• 22 Krassioukov A, Claydon VE. The clinical problems in cardiovascular control following spinal cord injury: an overview. Prog Brain Res 2006; 152: 223-229
• 23 Zhang Y, Al Mamun A, Yuan Y. et al. Acute spinal cord injury: pathophysiology and pharmacological intervention (review). Mol Med Rep 2021; 23 (06) 1-18
• 24 Lee BB, Cripps RA, Fitzharris M, Wing PC. The global map for traumatic spinal cord injury epidemiology: update 2011, global incidence rate. Spinal Cord 2014; 52 (02) 110-116
• 25 Sterner RC, Sterner RM. Immune response following traumatic spinal cord injury: pathophysiology and therapies. Front Immunol 2023; 13: 1084101

Publication History

Article published online:
21 April 2025