Can Spinal Cord Compression Cause High Blood Pressure?

Spinal cord compression (SCC) occurs when material, such as a bone spur, disc fragment, or tumor, presses on the spinal cord, disrupting its normal function. This pressure interferes with signaling pathways between the brain and the body below the compression. Hypertension is a condition where the force of blood against the artery walls is consistently too high. SCC can cause high blood pressure, but only when the compression affects the nerve pathways responsible for involuntary body functions. This specific hypertensive response results from a severe imbalance in the body’s control systems.

The Spinal Cord’s Role in Blood Pressure Regulation

The body’s blood pressure is automatically managed by the Autonomic Nervous System (ANS), which controls involuntary functions like heart rate and blood vessel diameter. The ANS has two opposing branches: the sympathetic and the parasympathetic nervous systems. The sympathetic system initiates the “fight or flight” response, increasing heart rate and constricting blood vessels to raise blood pressure. Conversely, the parasympathetic system promotes “rest and digest,” slowing the heart and decreasing blood pressure.

The spinal cord acts as the main conduit for these ANS signals, relaying commands from the brain to the body’s organs and blood vessels. Sympathetic nerve fibers controlling vascular tone exit the spinal cord primarily from the thoracic and lumbar regions. These pathways regulate the constriction and dilation of blood vessels, directly influencing systemic blood pressure. The brain sends continuous regulatory signals down the spinal cord to modulate this sympathetic activity, maintaining a stable baseline blood pressure.

A healthy spinal cord ensures a balance between sympathetic and parasympathetic influences on the cardiovascular system. When this pathway is interrupted by compression, communication between the brain and the lower spinal cord is blocked. This disruption compromises the brain’s ability to exert inhibitory control over sympathetic reflexes below the damage. Consequently, the body loses its capacity to regulate blood pressure in response to stimuli, leading to a hypertensive event.

Autonomic Dysreflexia: The Mechanism Causing High Blood Pressure

The specific mechanism by which spinal cord issues cause high blood pressure is Autonomic Dysreflexia (AD), a potentially life-threatening syndrome. AD is characterized by an abrupt and severe surge in blood pressure. It typically affects individuals with compression at or above the sixth thoracic vertebral level (T6). This level is significant because it is above the major sympathetic outflow controlling the splanchnic vascular bed, a large network of blood vessels in the abdomen.

The episode begins with a painful or irritating stimulus below the level of compression, such as a full bladder, bowel impaction, or tight clothing. Sensory signals travel up peripheral nerves to the spinal cord, triggering a massive, uncontrolled reflex sympathetic discharge. This response causes widespread, intense vasoconstriction in the body below the compression, particularly in the splanchnic region.

The resulting extreme narrowing of blood vessels leads to a rapid and dangerous rise in blood pressure. The brain recognizes this crisis through intact baroreceptors in the neck and attempts to counteract it by sending inhibitory signals down the spinal cord. However, the compression prevents these descending signals from traveling past the affected T6 level to reach the site of the sympathetic surge. The sympathetic outflow remains unchecked, leading to sustained, severe systemic hypertension.

Recognizing and Addressing This Hypertensive Crisis

Recognizing the onset of Autonomic Dysreflexia is important because rapid blood pressure elevation can lead to stroke, seizure, or organ damage. The hallmark presentation is a sudden, severe, and often pounding headache, which directly results from the high blood pressure. Other distinct symptoms include profuse sweating and flushing of the skin, but only in areas above the level of compression.

Conversely, the skin below the level of compression may appear pale and cool due to severe, sympathetic-driven vasoconstriction. The affected person may also experience nasal congestion, blurred vision, or apprehension. Any patient with a spinal cord issue at or above T6 who complains of a sudden headache must have their blood pressure checked immediately, as a rise of 20 to 40 mmHg above their typical baseline suggests AD.

The immediate response to a suspected AD episode is to sit the individual upright, which helps lower blood pressure through gravity. The next step is to quickly identify and remove the provoking stimulus, as this is the fastest way to resolve the crisis. Bladder distension, often from a blocked catheter, is the most common cause and should be addressed first. If blood pressure does not return to a safe level quickly after the trigger is removed, rapid-acting pharmacological intervention is required. Medications such as nitroglycerine paste or nifedipine may be administered to rapidly lower the blood pressure and prevent complications.