Distinguishing Pseudoseizures from True Epileptic Seizures
A detailed history focusing on specific clinical features usually suffices to distinguish psychogenic non-epileptic seizures (PNES) from true epileptic seizures, with video-EEG monitoring serving as the gold standard when clinical diagnosis remains uncertain. 1
Key Clinical Features for Recognition
Timing and Duration of Events
Duration of unconsciousness is the single most discriminating feature:
- PNES: Episodes lasting >5 minutes strongly suggest PNES, sometimes extending 10-30 minutes 2, 3
- True epileptic seizures: Unconsciousness typically lasts <30 seconds to 90 seconds total 2, 3
- Syncope (another mimic): Loss of consciousness <30 seconds 2
Movement Characteristics
The relationship between movements and loss of consciousness is critical:
In PNES:
- Movements begin after apparent loss of consciousness 2, 3
- Asynchronous, side-to-side thrashing movements that cannot be counted 2
- Repeated waxing and waning in intensity with changes in movement nature 2
- Pelvic thrusting (highly characteristic, though rarely seen in frontal lobe seizures) 2
In true epileptic seizures:
- Movements begin at the exact moment of loss of consciousness or before the fall 2, 3
- Symmetrical and synchronous movements 2
- Stiff "keeling over" during tonic phase 2
- Hemilateral clonic movements 2
Eye Position During Unconsciousness
This is one of the most reliable distinguishing features:
- PNES: Eyes closed during unconsciousness (highly characteristic) 2
- True epileptic seizures: Eyes remain open 2
- Syncope: Eyes typically open except in shallow, short-lasting episodes 2
Pre-Event Features
Before PNES:
Before true epileptic seizures:
- Rising epigastric sensation, unusual unpleasant smell or taste, déjà vu/jamais vu 2
- Ictal cry or shout at onset 2
- Triggers include flashing lights and sleep deprivation 2
Before syncope (another important mimic):
- Nausea, sweating, pallor, lightheadedness, blurred vision 2
- Triggered by fear, pain, prolonged standing, warm environments 2
Post-Event Features
After PNES:
- Variable recovery pattern 2
- High rates of psychiatric comorbidities (depression, anxiety, PTSD, history of childhood trauma) 4
After true epileptic seizures:
- Prolonged confusion (post-ictal phase) 2
- Aching muscles, headache, sleepiness 2
- Elevation of creatinine kinase and prolactin (though not reliable for differentiation) 2
After syncope:
Features That Do NOT Differentiate
Common pitfalls to avoid:
- Tongue biting does not differentiate PNES from epilepsy (though lateral tongue biting is highly specific for epilepsy) 2
- Urinary incontinence occurs in both PNES and epileptic seizures 2
- Biomarkers (neuron-specific enolase, prolactin, creatine kinase) are unreliable 2, 4
Diagnostic Approach
Initial Clinical Assessment
When uncertain about the diagnosis, it is better to postpone diagnosis than to falsely diagnose epilepsy, given the significant treatment and psychosocial implications. 5
Focus your history on:
- Exact timing of movement onset relative to loss of consciousness 2, 3
- Duration of the episode 2, 3
- Eye position during unconsciousness 2
- Nature of movements (synchronous vs. asynchronous) 2
- Pre-event symptoms (aura vs. autonomic symptoms) 2
- Post-event recovery pattern 2
Diagnostic Testing Algorithm
When clinical diagnosis remains uncertain:
Video-EEG monitoring is the gold standard for PNES diagnosis 3, 4, 6, 7
Tilt-table testing with simultaneous EEG and hemodynamic monitoring can be useful when syncope vs. seizure differentiation is unclear 1, 3
- Can establish psychogenic pseudosyncope diagnosis: apparent unconsciousness with normal hemodynamics 3
Routine EEG is NOT recommended in the absence of specific neurological features suggestive of seizure 1
Critical warning: About 20-30% of patients with refractory "seizures" at epilepsy centers have been misdiagnosed, often due to overinterpretation of EEGs (misreading phase reversals as abnormalities). 6, 8
Important Diagnostic Pitfalls
Be aware of conditions that can mimic PNES:
- Frontal lobe seizures may present with similar characteristics to PNES 4
- NMDA receptor autoimmune encephalitis can present with posturing and rhythmic movements without epileptiform findings on EEG 9
- 10-30% of patients referred to epilepsy centers have PNES, and many have received wrong diagnosis of epilepsy 4, 8
- Comorbidity between epilepsy and PNES ("dual diagnosis") occurs and is a serious challenge 8
Management Approach
Initial Management Steps
Clearly communicate the PNES diagnosis to the patient 4
- This is essential but challenging, as the mean latency between manifestations and diagnosis is 7 years 4
Psychiatric evaluation is indicated 1
Ongoing Management
Neurologist involvement remains essential even after diagnosis 4
- Continue follow-up to monitor for development of true epileptic seizures (prevalence of epilepsy in PNES patients is higher than general population) 4
- Coordinate with psychiatry for treatment of comorbidities 4
Realistic expectations:
- Even after correct diagnosis, a high proportion of PNES patients continue to have seizures and serious disability 4
- Nearly half who become seizure-free remain unproductive 4
- Many continue to have symptoms of psychopathology including somatoform, depressive, and anxiety disorders 4
Treatment of Acute Events
If true epileptic seizures or status epilepticus:
- Benzodiazepines as first-line treatment 1, 3
- Followed by fosphenytoin, levetiracetam, or valproic acid 1, 3
- Sodium valproate, levetiracetam, phenytoin, propofol, or barbiturates for ongoing seizures 1
- Myoclonus is particularly difficult to treat; phenytoin is often ineffective 1
- Propofol is effective for post-anoxic myoclonus 1