Syncope, commonly known as fainting or passing out, is a sudden, temporary loss of consciousness and postural tone. This transient event occurs because of a brief, insufficient supply of blood flow to the brain, medically termed transient global cerebral hypoperfusion. While the brain is directly affected by the lack of blood, syncope is generally classified as a symptom rooted in a cardiovascular or circulatory malfunction, rather than being a primary neurological disorder itself. The core issue is the delivery system—the heart and blood vessels—failing to maintain adequate pressure, not a disease originating within the brain’s structure or electrical activity.
Understanding Syncope and Its Classification
The confusion about syncope’s classification stems from the fact that its ultimate manifestation—unconsciousness—is a neurological event. Syncope is defined by its rapid onset, short duration, and complete, spontaneous recovery, which typically happens once the person falls to a horizontal position, restoring blood flow to the head. The classification of syncope focuses on the underlying cause that leads to the circulatory failure. In the vast majority of cases, the malfunction originates outside of the central nervous system, involving the heart or the body’s blood pressure regulation mechanisms. Therefore, syncope is considered a symptom of an underlying condition, such as a heart rhythm problem or a reflex gone wrong, rather than an independent neurological disease like epilepsy or stroke.
The Primary Drivers of Syncope: Circulatory Causes
The causes of syncope are broadly categorized into three types, all primarily reflecting a failure of the body’s circulation.
Reflex Syncope
The most common is Reflex Syncope, also known as vasovagal or neurocardiogenic syncope, which accounts for nearly half of all cases. This type is triggered by an exaggerated response from the autonomic nervous system to stimuli like emotional distress, pain, or prolonged standing. The reflex causes a sudden withdrawal of sympathetic tone, leading to widespread vasodilation and often a drop in heart rate, which collectively reduces blood pressure and cerebral perfusion.
Orthostatic Hypotension
A second major cause is Orthostatic Hypotension, which occurs when blood pressure drops excessively upon standing up. Normally, the body compensates for gravitational pooling of blood in the lower extremities by increasing heart rate and constricting blood vessels. When this compensatory mechanism fails, often due to dehydration, certain medications, or autonomic nervous system dysfunction, the resulting hypotension leads to inadequate blood flow to the brain and syncope.
Cardiac Syncope
Cardiac Syncope, while less frequent, is the most serious category because it is often linked to an increased risk of sudden cardiac death. This type is caused by underlying heart or blood vessel issues, such as structural heart disease, valve problems, or, most commonly, cardiac arrhythmias. For instance, an abnormally slow (bradyarrhythmia) or fast (tachyarrhythmia) heart rate prevents the heart from pumping sufficient blood volume to the brain, causing the loss of consciousness.
Syncope Mimics and Secondary Neurological Effects
While syncope is generally not a neurological disorder, it is often confused with conditions that are. These “syncope mimics” include epileptic seizures, which result from abnormal electrical discharges in the brain, and psychogenic pseudosyncope, a non-epileptic event caused by psychological factors. A seizure can usually be distinguished from syncope by features such as a longer duration of unconsciousness, post-event confusion, or the presence of tonic-clonic activity. Transient Ischemic Attacks (TIAs), or “mini-strokes,” are also neurological events sometimes confused with syncope, but they typically cause focal neurological deficits like weakness or speech difficulty rather than a generalized loss of consciousness.
Despite its circulatory origin, a prolonged syncopal event can have secondary neurological consequences. However, the spontaneous recovery mechanism of syncope usually prevents this by returning the person to a horizontal position, which quickly restores blood flow. The neurological signs during syncope, such as myoclonic jerks or brief convulsive movements, are not indicative of a seizure disorder but are instead a temporary effect of the brain’s response to low oxygen.
Diagnostic Evaluation and Warning Signs
Diagnosing the cause of syncope begins with a detailed medical history and a thorough physical examination, as this initial assessment can often identify the underlying trigger. Clinicians ask about the events leading up to the episode, including posture, activity, and any preceding symptoms like nausea or lightheadedness, known as a prodrome. Measuring blood pressure in both lying and standing positions is a standard part of the physical exam to check for orthostatic hypotension.
A 12-lead electrocardiogram (EKG) is a routine initial test for all syncope patients to detect electrical problems of the heart, such as arrhythmias or signs of structural heart disease. Further tests may include prolonged heart rhythm monitoring, such as a Holter monitor or implantable loop recorder, to catch transient arrhythmias. A tilt-table test may be ordered to reproduce reflex syncope or orthostatic hypotension by monitoring heart rate and blood pressure while the patient is moved from a lying to an upright position.
Warning Signs
Certain warning signs indicate that syncope is likely serious and requires immediate medical consultation. Syncope that occurs during or immediately after physical exertion is a strong indicator of a cardiac cause, often due to an arrhythmia or structural issue. A lack of a prodrome, where the person faints without any warning symptoms, also points toward a potentially dangerous abrupt cardiac event. A personal or family history of structural heart disease or sudden unexplained death suggests a higher risk and necessitates a comprehensive cardiac evaluation.