Open Access
CC BY 4.0 · Indian Journal of Neurotrauma
DOI: 10.1055/s-0045-1808077
Review Article

Pathophysiological Mechanisms of Neurogenic Shock

1   Department of Research, Colombian Clinical Research Group in Neurocritical Care, Bogotá, Colombia
2   Department of Research, AV Healthcare Innovators, LLC, Madison, Wisconsin, United States
3   Department of Research, International Consortium of Neurological Research, Minneapolis, United States
4   Department of Medicine, School of Medicine, University of Cartagena, Cartagena, Colombia
,
5   Department of Research, Aneuclose LLC, Eagan, Minnesota, United States
,
Willian Andres Florez-Perdomo
1   Department of Research, Colombian Clinical Research Group in Neurocritical Care, Bogotá, Colombia
,
Charushila Rukadikar
6   Department of Physiology, All India Institute of Medical Sciences, Gorakhpur, Uttar Pradesh, India
,
7   Department of Neurosurgery, All India Institute of Medical Sciences, Bhopal, Saket Nagar, Bhopal, Madhya Pradesh, India
› Author Affiliations

Funding None.
 

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.


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]

Zoom
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.


Address for correspondence

Luis Rafael Moscote-Salazar, MD
Department of Research, AV Healthcare Innovators
LLC, Madison, Wisconsin 53716
United States   

Publication History

Article published online:
21 April 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India


Zoom
Fig. 1 Physiology of neurogenic shock.