The relationship between the heart and the brain is complex, and a problem in one system can manifest with symptoms in the other. The heart can cause events that look exactly like a seizure, and it can also cause true seizures through an indirect pathway. Understanding the difference between a seizure-mimicking event and a genuine seizure is fundamental to receiving the correct diagnosis and treatment. Cardiovascular issues are a recognized cause of transient loss of consciousness, and the resulting symptoms can easily be mistaken for a neurological event.
Differentiating Cardiogenic Syncope from Epileptic Seizures
The most common way a heart problem appears to cause a seizure is through syncope, or fainting. Syncope is a transient, self-limited loss of consciousness caused by a temporary drop in blood flow to the brain (global cerebral hypoperfusion). When this lack of blood flow is severe, it can induce brief, involuntary muscle movements, termed convulsive syncope.
These seizure-like movements are not true epileptic seizures, which result from abnormal electrical discharge within the brain. The myoclonic jerks or brief tonic posturing seen in convulsive syncope are thought to result from the brain’s temporary lack of oxygen, causing cortical disinhibition. The movements are generally short-lived, typically consisting of fewer than ten non-rhythmic jerks, distinguishing them from the sustained, rhythmic convulsions of a true seizure.
A primary difference between the two events is the post-event state. Following syncope, consciousness is typically regained quickly, and the person returns to full mental status promptly. In contrast, a true epileptic seizure is often followed by a postictal phase—a period of confusion, drowsiness, or fatigue that can last for minutes or even hours. Syncope is also frequently preceded by warning signs such as lightheadedness, nausea, or “tunnel vision,” while true seizures may begin abruptly or with a distinct aura.
Cardiogenic syncope results from a severe mechanical or electrical issue in the heart that drastically reduces cardiac output. A syncopal episode rarely lasts more than a minute, and recovery is spontaneous once the person is horizontal and blood flow to the brain is restored. If an event lasts longer than a few minutes, it is unlikely to be syncope and suggests a neurological process.
Specific Cardiovascular Conditions That Impair Cerebral Perfusion
Specific heart conditions can cause the sudden, severe reduction in cardiac output necessary to trigger cardiogenic syncope. Problems with the heart’s electrical system, known as arrhythmias, are a major cause. A heart rate that is either excessively slow (severe bradycardia) or excessively fast (ventricular tachycardia) prevents the heart chambers from filling or pumping effectively.
For instance, a heart rate below 30 to 35 beats per minute or above 150 to 180 beats per minute can drastically decrease the volume of blood the heart pushes out, leading to insufficient cerebral blood flow. These sudden electrical malfunctions can cause a loss of consciousness with little to no warning.
Structural heart disease can also physically obstruct the flow of blood leaving the heart. Conditions like severe aortic stenosis (a narrowing of the aortic valve) or hypertrophic cardiomyopathy (an abnormal thickening of the heart muscle) impede the outflow of blood, especially during physical exertion. This outflow obstruction causes a sharp drop in systemic blood pressure, which starves the brain of oxygen and induces syncope.
A separate, indirect pathway exists where heart problems cause true secondary seizures through a stroke. Conditions like Atrial Fibrillation (AFib) cause the upper chambers of the heart to quiver chaotically, allowing blood to pool and form clots. If a clot dislodges and travels to the brain, it causes an ischemic stroke.
The resulting brain tissue injury creates an area of abnormal electrical excitability, leading to new-onset seizures months or even years after the initial event. A Patent Foramen Ovale (PFO), a small opening between the heart’s upper chambers, can permit a paradoxical embolism. This occurs when a clot originating in the venous system crosses the PFO into the arterial circulation, travels to the brain, and causes a stroke, setting the stage for a true epileptic seizure.
Diagnostic Testing to Determine Seizure Origin
Determining whether a loss of consciousness is cardiac or neurological is paramount and requires collaboration between cardiologists and neurologists. The initial diagnostic workup involves tests designed to assess the electrical activity of both the heart and the brain.
To investigate a potential neurological cause, an Electroencephalogram (EEG) records the brain’s electrical activity. An EEG can capture the abnormal electrical discharges characteristic of epilepsy or show the generalized slowing associated with cerebral hypoperfusion during syncope.
Conversely, the heart’s function is assessed using an Electrocardiogram (ECG or EKG) to check for underlying rhythm disturbances or signs of structural disease. For infrequent events, a Holter monitor or an implantable cardiac monitor tracks the heart rhythm over days or years to capture a transient arrhythmia.
A Tilt Table Test is a specialized procedure often used when syncope is suspected. This test involves changing the patient’s body position while continuously monitoring heart rate and blood pressure, attempting to provoke a syncopal episode in a controlled setting. In complex cases, combining the Tilt Table Test with simultaneous video-EEG monitoring allows clinicians to correlate the patient’s symptoms with heart rhythm, blood pressure, and brain activity, providing the clearest picture of the event’s origin.