Shock is characterized by inadequate blood flow to the body’s tissues, leading to a lack of oxygen delivery to vital organs. Neurogenic shock is a distinct form arising specifically from damage to the central nervous system. This particular type of shock is not caused by blood loss, but by the body’s inability to properly regulate the circulatory system due to nervous system dysfunction. Understanding the circumstances of this neurological insult helps explain when this serious complication is likely to occur.
Understanding the Nature of Neurogenic Shock
Neurogenic shock is classified as a type of distributive shock, defined by a problem with the distribution of blood flow rather than a lack of blood volume. The total volume of blood in the body remains normal, but the size of the vascular system expands significantly. This causes the available blood to not be enough to fill the vastly enlarged vessels, leading to a sudden drop in pressure.
This condition is a failure of the Autonomic Nervous System (ANS), which controls involuntary bodily functions like heart rate and blood vessel tone. The loss of control results in widespread dilation of blood vessels throughout the body. Distributive shock differs from hypovolemic shock, where the issue is a direct loss of blood or plasma volume; in neurogenic shock, the container is too large for the fluid.
Specific Injuries That Trigger Neurogenic Shock
Neurogenic shock occurs when significant injury to the central nervous system disrupts the pathways controlling circulation. The most common cause is traumatic damage to the spinal cord, particularly in the upper segments. This condition is most frequently observed following injury at or above the sixth thoracic vertebra (T6) level of the spine.
The spinal cord contains the nerve tracts responsible for sympathetic outflow, which is why damage in the neck (cervical spine) or upper back (thoracic spine) is particularly dangerous. Injuries below T6 are less likely to cause true neurogenic shock because the sympathetic pathways controlling the upper body and heart often remain intact.
Other, though rarer, causes include severe traumatic brain injury, complications from high spinal anesthesia, and neurological diseases such as transverse myelitis. The severity of the shock is often correlated with how high and how complete the spinal cord injury is. A complete lesion above T6 carries a much higher risk of developing the condition.
The Underlying Mechanism of Onset
The physiological onset of neurogenic shock begins with the abrupt disruption of the sympathetic nervous system pathways. These pathways normally maintain sympathetic tone, a low-level tension that keeps blood vessels slightly constricted. This tone is essential for maintaining normal blood pressure and ensuring blood returns effectively to the heart.
When a severe injury occurs above T6, these descending sympathetic signals are blocked from reaching the blood vessels below the level of the injury. The immediate loss of this vasomotor tone causes widespread vasodilation, meaning the blood vessels suddenly relax and widen significantly. This massive expansion allows blood to pool in the periphery, effectively removing it from the central circulation.
Compounding the problem is the simultaneous, unopposed action of the parasympathetic nervous system, which remains intact and is primarily mediated by the vagus nerve. This imbalance causes a reflex slowing of the heart rate, known as bradycardia. The combination of widespread vasodilation and a slow heart rate severely compromises the heart’s ability to move blood effectively, leading to profound organ tissue under-perfusion.
Immediate Clinical Manifestations
The breakdown of autonomic control results in a unique set of observable symptoms that distinguish neurogenic shock from other forms of shock. The most telling sign is severe hypotension, or abnormally low blood pressure, resulting from the loss of vascular resistance due to widespread vessel dilation. A systolic blood pressure below 90 mmHg is a common finding.
Paradoxically, the patient typically presents with profound bradycardia, an abnormally slow heart rate, which is the direct result of the unopposed vagus nerve activity. In contrast, most other types of shock cause the heart rate to speed up (tachycardia) as the body attempts to compensate for low blood pressure.
Another characteristic sign is warm, dry, and flushed skin below the level of injury, rather than the cool, clammy skin seen in other forms of shock. This warm skin occurs because the blood vessels, without sympathetic input, cannot constrict to conserve heat and instead remain dilated.