Postural Orthostatic Tachycardia Syndrome (POTS) is characterized by a malfunction of the autonomic nervous system, which controls involuntary body functions like heart rate and blood pressure. This dysfunction causes an abnormal increase in heart rate—typically 30 beats per minute or more—when moving from a lying or sitting position to standing. The body struggles to maintain adequate blood flow to the brain and upper body, leading to orthostatic intolerance. Many people with POTS experience episodes involving a sudden loss of consciousness or uncontrolled movements, leading to the question of whether POTS can cause seizures. This exploration clarifies the distinction between true epileptic seizures and the seizure-like activity often seen in this syndrome.
The Relationship Between POTS and True Seizures
POTS itself does not typically cause true epileptic seizures, which are defined by abnormal, excessive electrical discharges in the brain. Epilepsy is a neurological disorder, whereas POTS is a disorder of the autonomic nervous system, primarily affecting circulation. While the two conditions are distinct, patients with POTS can sometimes be misdiagnosed with epilepsy due to the similarity of certain symptoms.
It is possible for a patient to have both POTS and epilepsy. However, the severe cerebral hypoperfusion—the dramatic lack of blood flow to the brain—that occurs during a POTS-related faint can, in rare cases, trigger a true epileptic seizure in a highly susceptible individual. This is not a common occurrence but represents a neurological event spurred by a cardiovascular crisis.
Understanding Convulsive Syncope
The most frequent reason people with POTS report “seizures” is the occurrence of convulsive syncope. Syncope, or fainting, results from a temporary, sudden drop in the blood supply to the brain. In POTS, this is often due to profound blood pooling in the lower body upon standing, which starves the brain of oxygen and nutrients.
When the brain experiences this rapid oxygen deprivation, it can trigger a brief, protective motor response in the form of uncontrolled muscle movements. These movements are typically myoclonic jerks—brief, rhythmic twitching or rigidity—that can be mistaken for a generalized seizure. These movements are not caused by the abnormal electrical activity characteristic of epilepsy, but rather by the brainstem’s response to anoxia.
Convulsive syncope usually involves a very brief loss of consciousness, often lasting only a few seconds. The individual regains full awareness quickly once they become horizontal. The jerking motions are short, generally lasting less than 20 seconds, and cease once blood flow to the brain is restored.
Diagnostic Methods to Differentiate Episodes
Differentiating between true epileptic seizures and POTS-related convulsive syncope is necessary for appropriate treatment. Medical professionals rely on the Head-Up Tilt Table Test (HUTT) to reproduce the syncopal event under controlled medical supervision.
During the HUTT, the patient is tilted upright while heart rate and blood pressure are continuously monitored. If the patient experiences a syncopal episode, simultaneous monitoring with an Electroencephalogram (EEG) is often performed. The EEG records the brain’s electrical activity, and in a true epileptic seizure, it captures the characteristic abnormal electrical discharge patterns.
If the episode is convulsive syncope, the EEG typically shows diffuse slowing of brain waves, reflecting the temporary lack of blood flow. It does not show the epileptiform activity seen in true seizures. The combination of the tilt table test and the EEG offers a clear way to distinguish a cardiovascular-driven faint from a primary neurological event.
Strategies for Reducing Seizure-Like Events
Since convulsive syncope is a direct result of the body’s inability to manage blood flow, reducing the frequency of syncopal and pre-syncopal episodes is the main management strategy. A primary intervention is volume expansion, achieved through increased fluid and salt intake. Patients are advised to consume between two and three liters of fluid daily and liberalize sodium intake, often to 5 to 10 grams per day, to retain water in the bloodstream.
Physical counter-maneuvers can also be employed when a person feels the onset of pre-syncope. These involve quickly engaging large muscle groups, such as crossing the legs and clenching the leg and abdominal muscles, which helps to temporarily push blood back toward the heart and brain. Wearing medical-grade compression garments, such as stockings that extend up to the waist or thigh, and using abdominal binders, helps mechanically reduce venous pooling in the lower extremities. This comprehensive approach directly lowers the risk of the cerebral hypoperfusion that leads to convulsive syncope.