Postural Orthostatic Tachycardia Syndrome (POTS) and episodes resembling seizures present a complex clinical question. POTS involves autonomic dysfunction, while non-epileptic seizures (NES) are paroxysmal events that mimic epilepsy. Understanding their overlap requires distinguishing between true epileptic activity and seizure-like episodes arising from systemic causes. This article explores the mechanisms through which the physiological effects of POTS may trigger non-epileptic events.
Understanding Postural Orthostatic Tachycardia Syndrome (POTS)
POTS is a disorder classified under dysautonomia, signifying a malfunction of the autonomic nervous system (ANS) that controls involuntary bodily functions like heart rate, blood pressure, and digestion. The defining characteristic is orthostatic intolerance, meaning symptoms worsen when standing upright and improve when lying down. The formal diagnostic criteria for adults require a sustained increase in heart rate of at least 30 beats per minute within the first ten minutes of moving from a lying to a standing position.
This heart rate increase must occur without significant orthostatic hypotension. The physiological problem involves poor regulation of blood flow, leading to venous pooling in the lower body upon standing. The heart compensates for this lack of blood return to the upper body and brain by accelerating its pace, resulting in characteristic tachycardia.
Common symptoms include lightheadedness, chronic fatigue, and heart palpitations. Other complaints are cognitive impairment, often described as “brain fog,” and tremulousness. These manifestations are chronic and can significantly impair a person’s quality of life.
The underlying cause of POTS can be heterogeneous, ranging from neuropathic issues to hyperadrenergic states involving excessive release of the stress hormone norepinephrine. The core challenge is the body’s inability to maintain stable circulation, particularly to the brain, when upright. This failure of blood flow regulation sets the stage for secondary symptoms, including those that may be mistaken for seizure activity.
Defining Non-Epileptic Seizures (NES)
Non-Epileptic Seizures (NES) are episodes that outwardly resemble the convulsions or altered awareness of epileptic seizures but do not stem from abnormal electrical discharges in the brain. This distinction is crucial for diagnosis and treatment, as NES do not respond to anti-seizure medications. The gold standard for confirming NES and differentiating them from true epilepsy is video-electroencephalographic (video-EEG) monitoring.
NES can be broadly divided into two main categories based on their underlying cause. The first type is physiological NES, which are triggered by a systemic physical condition. Examples include seizure-like events caused by metabolic disturbances, such as severely low blood sugar, or circulatory problems, such as syncope, a brief loss of consciousness due to temporary cerebral hypoperfusion.
The second subtype is Psychogenic Non-Epileptic Seizures (PNES), classified as a functional neurological disorder. PNES episodes are involuntary physical reactions linked to psychological factors, such as significant emotional distress, trauma, or chronic stress. They represent a complex manifestation of the mind-body connection.
Symptoms of NES can vary widely, sometimes mimicking a generalized tonic-clonic seizure with convulsions and unresponsiveness. Other presentations may resemble partial seizures, involving repetitive movements, staring, or changes in sensation. The underlying trigger, whether physiological or psychological, determines the specific nature of the episode and guides the necessary treatment approach.
The Underlying Mechanisms Linking POTS and NES
POTS creates an environment of systemic instability that can directly trigger seizure-like events or indirectly predispose an individual to them. The link involves a convergence of physiological and psychological stress pathways. The most direct pathway involves the physical consequence of poor blood flow regulation, a core feature of POTS.
Cerebral Hypoperfusion
The primary physiological mechanism linking POTS to NES is transient global cerebral hypoperfusion, a temporary reduction in blood flow to the brain. When a person with POTS stands up, the impaired autonomic control can lead to a significant drop in the volume of blood reaching the brain. This lack of oxygen and nutrients can be severe enough to cause a transient loss of consciousness, known as syncope, or a near-fainting episode called pre-syncope.
In some cases, this profound cerebral hypoperfusion can provoke a brief, involuntary motor response known as convulsive syncope. These episodes involve jerking or stiffening movements that closely resemble an epileptic seizure. They are due to the brain’s temporary deprivation of blood flow, not abnormal electrical activity. Functional imaging studies support this link, showing that individuals with POTS often have reduced cerebral blood flow velocity when upright.
Autonomic Overload and Stress
A second, more indirect mechanism involves the chronic stress and autonomic overload associated with living with POTS, which can predispose individuals to Psychogenic Non-Epileptic Seizures (PNES). The hyperadrenergic state seen in a significant subset of POTS patients means they live in a near-constant state of heightened sympathetic nervous system activation, often described as “fight or flight.” This chronic physiological stress can amplify emotional and psychological vulnerability.
The persistent symptoms of POTS, such as chronic pain, fatigue, and cognitive dysfunction, contribute to psychological distress. This chronic emotional burden serves as a potent predisposing factor for the development of PNES, as these episodes are often reactions to unmanaged stress or trauma. The chronic physical illness acts as a major source of the psychological strain that triggers PNES.
Diagnostic Precision and Targeted Management
Because the symptoms of POTS and NES can mimic each other or coexist, accurate diagnosis is necessary. Differentiation between true epilepsy, physiological NES (like convulsive syncope), and PNES requires a specialized approach. The Tilt Table Test remains the primary tool for diagnosing POTS, as it directly assesses the heart rate and blood pressure response to upright posture.
To definitively rule out epilepsy and classify a seizure-like event, Video-EEG monitoring is necessary. This test simultaneously records the patient’s physical movements and brain’s electrical activity during an episode, confirming the absence of epileptic discharges. Identifying the origin is crucial because anti-seizure medications are ineffective for NES and may cause unnecessary side effects.
Management must be integrated to address both the underlying dysautonomia and the specific trigger for the non-epileptic events. Treatment for POTS typically focuses on increasing blood volume through high fluid and salt intake, wearing compression garments, and targeted medications to manage heart rate and vasoconstriction. Addressing the physiological cause of convulsive syncope through optimal POTS management often resolves these episodes.
For individuals whose episodes are classified as PNES, management is primarily psychological, involving therapy such as cognitive behavioral therapy (CBT) and psychotherapy to address underlying emotional triggers and coping mechanisms. An integrated approach stabilizes the autonomic instability of POTS while simultaneously treating the psychological factors contributing to PNES.