Multiple Sclerosis (MS) is a chronic condition where the immune system attacks the protective myelin sheath surrounding nerve fibers in the brain and spinal cord. While MS is widely recognized for causing issues with mobility, vision, and sensation, its impact extends beyond these motor and sensory functions. As a disease of the central nervous system, MS can disrupt involuntary bodily processes, including the mechanisms that regulate blood pressure. This disruption leads to unexpected fluctuations and cardiovascular symptoms. The link between MS and blood pressure abnormalities is neurological, arising directly from damage to specific areas of the nervous system.
The Autonomic Nervous System and MS
The link between Multiple Sclerosis and blood pressure control is rooted in the Autonomic Nervous System (ANS), which oversees all involuntary bodily functions. This system operates without conscious thought, managing processes like heart rate, breathing, digestion, and the constriction or dilation of blood vessels to maintain stable blood pressure. The ANS is divided into two main branches: the sympathetic nervous system, which prepares the body for activity or stress by raising blood pressure, and the parasympathetic nervous system, which promotes rest and recovery by lowering blood pressure.
When MS-related inflammation and demyelination occur in certain regions of the central nervous system, this delicate balance is compromised, a condition known as dysautonomia. Lesions in areas like the brainstem, which contains the medulla oblongata responsible for cardiovascular control, can sever the communication lines of the ANS. Damage to the spinal cord can also interrupt the descending neural pathways that carry sympathetic signals to the heart and blood vessels. This interruption means the body’s automatic, rapid response to changes in posture or activity becomes sluggish or ineffective.
Lesions in the brainstem and spinal cord block the signals that regulate blood vessel constriction or heart rate. This results in faulty communication between the brain’s regulatory centers and the peripheral circulatory system. This ANS dysfunction is a consequence of neurological damage to the control centers, directly impacting the body’s ability to adjust blood flow, particularly when gravity is involved.
How MS Damage Affects Blood Pressure Regulation
The neurological damage caused by MS lesions manifests as two primary and opposing forms of blood pressure dysregulation, both stemming from the inability of the ANS to adapt quickly. The most common manifestation is Orthostatic Hypotension (OH), a condition defined by a significant drop in blood pressure when a person stands up from a sitting or lying position. This drop is typically measured as a decrease of at least 20 mm Hg in systolic pressure or 10 mm Hg in diastolic pressure within three minutes of standing. Symptoms often include dizziness, lightheadedness, blurred vision, or even fainting, collectively termed orthostatic intolerance.
Orthostatic Hypotension occurs because the sympathetic nervous system fails to trigger reflexive vasoconstriction in the lower body’s blood vessels upon standing. Normally, sympathetic nerves release norepinephrine to constrict vessels and push blood back toward the brain when gravity pulls blood downward. In MS patients with dysautonomia, this response is impaired, leading to blood pooling in the lower extremities and a temporary lack of blood flow to the brain. Cardiovascular autonomic dysfunction is reported to affect up to two-thirds of people with MS.
Conversely, MS can also contribute to sustained high blood pressure, known as hypertension. Damage to central regulatory areas can interfere with the long-term balance of blood pressure control. Blood pressure variability—the degree to which pressure swings between readings—is often altered in people with progressive forms of MS, indicating broader instability in the ANS. This dysregulation and the presence of hypertension are associated with an increased risk of long-term brain injury and disability progression.
Secondary Factors Contributing to Blood Pressure Changes
Several secondary factors related to living with MS can influence blood pressure levels beyond the direct neurological impact of lesions. Physical inactivity and a sedentary lifestyle are highly prevalent due to mobility impairment and fatigue, which directly contribute to hypertension. Reduced physical activity leads to poor cardiovascular fitness, increasing blood vessel stiffness and raising systemic blood pressure. People with MS often spend many hours per day sitting, which is a leading contributor to hypertension regardless of the primary neurological disease.
Certain medications used to manage MS symptoms or modify the disease course can also cause side effects that alter blood pressure. Disease-modifying therapies (DMTs), such as fingolimod, are known to temporarily lower the heart rate and can interfere with blood pressure regulation, sometimes causing or exacerbating orthostatic hypotension. Conversely, corticosteroids used to treat acute relapses are well-known to cause fluid retention and elevated blood pressure, which can temporarily induce or worsen hypertension. Managing these medication side effects requires careful monitoring and often necessitates adjustments to the treatment regimen.
Systemic inflammation in MS is another factor that contributes to vascular changes. Chronic inflammation affects the lining of blood vessels, leading to arterial stiffness and dysfunction over time. This process accelerates the development of hypertension, which acts as a separate comorbidity contributing to poor health outcomes and faster MS disease progression. The interplay between the inflammatory state of MS and traditional cardiovascular risk factors creates a complex challenge for maintaining stable blood pressure.
Monitoring and Clinical Management
Addressing blood pressure issues in MS requires specialized monitoring and a multi-pronged approach to management. To diagnose Orthostatic Hypotension (OH), the healthcare team must evaluate the body’s postural response beyond simple seated blood pressure checks. The active standing test involves measuring blood pressure and heart rate while the patient is lying down, immediately upon standing, and again after three minutes, looking for a characteristic pressure drop. For complex cases, a tilt table test may be used, where the patient is secured on a table that slowly tilts them upright while continuous monitoring is performed.
Treatment for OH typically begins with non-pharmacological interventions aimed at stabilizing blood volume and improving venous return. These strategies include:
- Significantly increasing daily fluid and salt intake to expand blood volume.
- Wearing medical-grade compression stockings or abdominal binders to prevent blood pooling in the lower extremities.
- Avoiding sudden position changes.
- Sleeping with the head of the bed slightly elevated to reduce morning symptoms.
If lifestyle modifications prove insufficient, pharmacological agents are available to manage symptomatic OH. Midodrine is an oral medication that acts as a peripheral alpha-1 adrenergic agonist, directly constricting blood vessels to raise blood pressure upon standing. Fludrocortisone is another option, a mineralocorticoid that promotes sodium and water retention, increasing blood volume to sustain blood pressure. For patients with hypertension, management follows standard medical guidelines using drugs like ACE inhibitors or beta-blockers, but this must be carefully coordinated with the MS neurologist to avoid interactions.