A seizure is a temporary disturbance in brain function caused by abnormal electrical activity in the brain’s nerve cells. Not all episodes that look like seizures are true epileptic events. These non-epileptic events can range from involuntary psychological reactions to conscious attempts at deception, making accurate diagnosis challenging. Physicians use detailed behavioral observation, medical history, and objective tests to determine the event’s origin. Differentiating a true epileptic seizure from a simulated or non-epileptic event is paramount for proper treatment.
Defining Intent: Malingering and Factitious Disorder
When a person consciously attempts to fake a seizure-like event, the motivation falls into two categories: malingering or factitious disorder. Malingering involves the deliberate production of false symptoms for a clear external benefit. This gain could include avoiding legal consequences, obtaining financial compensation, or seeking discharge from work. This behavior is intentional, and the motivation lies outside of the medical context.
Factitious disorder involves the conscious creation of symptoms, but the underlying motivation is internal. The primary goal is to assume the “sick role” and receive the care, attention, and sympathy associated with being a patient. The individual gains no external reward, as the desire for medical attention and psychological gratification is the main driver.
A third category is Psychogenic Non-Epileptic Seizures (PNES), which are events resembling epileptic seizures but are psychological in origin, often linked to emotional distress. Unlike malingering and factitious disorder, PNES are not consciously feigned; the person genuinely experiences the event, but it is not due to abnormal electrical activity in the brain. Understanding the intent—whether for external gain, to assume the sick role, or as an involuntary psychological reaction—is the first step in diagnosis.
Observable Differences in Simulated Episodes
Clinicians rely on specific physical signs, known as semiology, to differentiate true epileptic seizures from simulated events. One difference is the risk of injury, as true generalized tonic-clonic seizures often result in accidental falls, lacerations, or tongue biting. Simulated events rarely result in serious self-injury, with patients often exhibiting protective behaviors as they fall.
The timing and context of the event provide significant clues, as simulated episodes often occur only when the person knows they are being observed or during stressful situations. True epileptic seizures, caused by a spontaneous electrical discharge, are less likely to be triggered by an audience. Motor activity in a simulated event may appear disorganized, featuring asynchronous limb movements or pronounced pelvic thrusting, which is atypical of the rhythmic jerking seen in a generalized epileptic seizure.
Eye signs are another feature, as individuals experiencing a simulated or PNES event often exhibit forced eye closure, resisting attempts to open their eyelids. In contrast, the eyes of a person experiencing a true tonic-clonic seizure typically remain open, or the gaze may be fixed or deviated. The overall duration can also be suggestive, as psychogenic events often last longer than most true epileptic seizures, which usually resolve within a few minutes.
Clinical Verification Methods
The primary method for distinguishing between true epileptic seizures and simulated events is Video-EEG Monitoring (VEEG). VEEG is considered the gold standard and involves admitting the patient to an Epilepsy Monitoring Unit (EMU). Here, the brain’s electrical activity is recorded continuously by an electroencephalogram (EEG) synchronized with video and audio recording of their behavior. During a true epileptic seizure, the EEG captures abnormal electrical discharges that correlate precisely with the patient’s physical movements.
If the episode is simulated or psychogenic, the video shows seizure-like movements, but the simultaneous EEG recording remains normal. This lack of electrical correlation provides evidence that the event is not epileptic in nature. To increase diagnostic yield, clinicians may employ activation maneuvers such as sleep deprivation or hyperventilation to encourage the patient to have their typical event under controlled monitoring.
Another biological marker used for verification is the measurement of post-event serum prolactin levels, a hormone released by the pituitary gland. Following a true generalized tonic-clonic seizure, prolactin levels in the blood often rise significantly, peaking 10 to 20 minutes after the event concludes. A simulated event or a PNES episode will not cause this hormonal surge, resulting in normal prolactin levels. A negative prolactin test strongly supports the non-epileptic nature of a convulsive event when combined with VEEG results.