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Evidence-Based Reviews

Psychogenic or epileptic seizures? How to clinch the diagnosis

‘Pseudo’ seizure is misleading, as most patients do not feign symptoms

Vol. 3, No. 11 / November 2004

When you evaluate patients whose seizures could be epileptic or psychogenic, the evidence points to three useful diagnostic steps:

  • Step 1: Characterize the seizure by its triggers and presentation.
  • Step 2: Identify psychiatric comorbidity that might be precipitating psychogenic nonepileptic seizures (PNES). 1
  • Step 3: Obtain video EEG and blood tests for physiologic confirmation of epilepsy.

Using a case illustration, this article describes how to accomplish these steps by seeking clues in the patient’s seizure and psychiatric histories and choosing high-yield laboratory tests. When a PNES diagnosis becomes clear, we suggest an empathic approach that can help patients develop healthier responses to stress.


Psychiatric profile of patients with psychogenic seizures

Patients with psychogenic nonepileptic seizure (PNES)have high rates of repressed anger and life stressors. Psychodynamic interpretations postulate PNES as an unconscious conversion of emotional distress into physical symptoms, unlike factitious disorder’s intentionality. Repressed traumatic childhood sexual experience may be significant. 2

Family dynamics. PNES may be a maladaptive communication method by which an individual uses behavior to manipulate the environment to meet emotional needs or to compensate for an environment intolerant of direct verbal expression. 3

Characteristics. PNES patients are a heterogeneous group. They average a full-scale IQ of 92 in the lower quartile of intellectual capacity and neuropsychological functioning. PNES usually presents in the 20s but may occur at any age. PNES is more common in women than men (ratio 4:1). 4,5

Comorbidities. Up to 40% of patients treated at epilepsy centers are reported to have both epilepsy and PNES. 4,5 In a 1-year study at an EEG-video monitoring unit, however, only 9.4% of PNES patients had interictal epileptiform discharges to support a coexisting diagnosis of epilepsy. 4

PNES may be highly associated with somatoform disorder, mood disorder, anxiety disorder, brief reactive psychosis, or schizophreniform disorder. 6


Ms. X’s husband brought her to the emergency room after her third tonic-clonic convulsion within 1 week. He reported that her eyes suddenly rolled up and she became limp and fell down after they argued about money. She suffered a minor temple laceration, but this seizure—unlike past episodes—was not associated with mouth foaming or fecal or urinary incontinence.

Ms. X, age 35, has a history of seizure disorder and 5 years of unemployment when seizures were uncontrolled. Her seizures have been stabilized for 18 months with phenytoin, 300 mg bid. She has been hospitalized twice for major depressive disorder, most recently 2 years ago. Since then, her depression has been in remission with paroxetine, 20 mg once daily. She does not abuse drugs or alcohol. She has been married 8 years, has no children, and receives disability income.

Ms. X was stabilized and admitted for neurologic evaluation. CT and MRI were normal, EEG recordings were unremarkable, and blood workup revealed slightly elevated creatine kinase but normal prolactin. Her phenytoin serum level was 12 mcg/mL (therapeutic range, 5 to 20 mcg/mL). When video-EEG recording during one seizure revealed no abnormality, the neurologist requested psychiatric consultation.


Patients with PNES are a heterogeneous population (Box) 2-6 that appears repeatedly at emergency rooms, resulting in multiple investigations and treatment with antiepileptic medications. Those with both PNES and epileptic seizure disorders, such as Ms. X, present a particularly difficult clinical dilemma as:

  • discontinuing anticonvulsants may exacerbate epileptic seizures
  • increasing the medication in the mistaken belief that a seizure breakthrough has occurred could result in toxic serum levels.

Psychological stressors may precipitate PNES in a person who has never had a seizure or in someone with co-existing epilepsy. Patients with PNES frequently deny a correlation between emotional stress and their seizures, whereas the opposite usually holds for patients who have experienced an epileptic seizure. 7,8

PNES has been called “pseudoseizure” a term we believe is unfair to patients because the etiologic determinants are mostly subconscious. 9 Although one author has defended the term, 10 we agree with others that “pseudoseizure” can give a misleading impression that patients feign their symptoms. 9

Psychiatric comorbidity. When PNES is suspected, a careful history is essential to identify precipitating psychiatric comorbidity, such as somatoform, somatization, conversion, or dissociative disorder. PNES may also be precipitated by or coexist with mood and anxiety disorders, schizophrenia, malingering and factitious disorders, diffuse organic brain disease, and developmental disorders (Table 1). 11,12


Ms. X was admitted to the psychiatric unit. Her psychiatric history showed recurrent depressive disorder and excluded head injury. She was mildly depressed but expressed minimal cognitive and biological depressive symptoms in the mental status examination. She denied suicidal or homicidal thoughts. Perception, thought process, and cognition were normal.

With her consent, the psychiatrist obtained collateral information from her brother. He reported that his sister had received a diagnosis of “pseudoseizures” about 5 years before this presentation. The brother was unsure of any emotional precipitants.

Table 1

Psychiatric disorders that may precipitate or coexist with PNES



Somatoform disorders

Physical symptoms suggest a medical condition but are not the result of a medical condition, substance, or another mental disorder such as panic disorder or schizophrenia

Conversion disorder

Psychological symptoms expressed as neurologic symptoms—such as paralysis, blindness, or paresthesia—in the absence of a known medical or neurologic disorder

Dissociative disorder

Disruption in consciousness, memory, identity, or perception that may be sudden or gradual, transient or chronic

Depressive disorders

Mood or anxiety symptoms related to depressive, bipolar, panic, posttraumatic stress, or acute stress disorders may coexist with PNES

Psychotic disorders

Schizophrenia may be associated with seizure-like events in some patients 12

Factitious disorder

Seizure-like symptoms may be produced intentionally for secondary gain (as in malingering) or feigned to assume a sick role (as in factitious disorder)

Developmental disorders

In a patient with mental retardation, PNES may result from reinforced operant behavior patterns

Source: Diagnostic and statistical manual of mental disorders (4th ed., text rev). 11


Initial assessment of suspected PNES includes a medical, psychiatric, social, psychological, and substance abuse history, as well as a thorough physical examination.

In patients with suspected PNES, obtain collateral histories of seizure precipitants, abortants, childhood events, and family history. Ms. X, for example, has a history of depression and at least one past episode of probable PNES, as described by her brother. An argument with her husband apparently precipitated the most recent seizure episode.

Table 2

Psychogenic seizures PNES vs. epileptic seizures: Differences in presentation*

Clinical features

Psychogenic nonepileptic seizures (PNES)

Epileptic seizures



Short (20 to 70 seconds)






Paroxysmal, cluster




Occurs in presence of others



Occurs during sleep






Biting pattern

Tip of tongue, lips

Side of tongue, cheek


Bizarre, trashing, sexual movements



Infrequent, mild

Infrequent, severe

Pupillary reflex


Slow, nonreactive

Babinski’s reflex


Yes, if convulsion

Orientation afterwards



Postictal stupor



Serum prolactin


Elevated (>18 ng/mL in men; >30 ng/mL in nonpregnant women)



Abnormal or variable

* Apply loosely, as the spectrum of seizure types within epilepsy is very large.

Source: Adapted from reference 13.

PNES features. Clinical features (Table 2)13—although not definitive—can help differentiate PNES from epileptic seizure. 1 PNES features to look for include:

  • prolonged and bizarre prodrome
  • prominent out-of-phase ictal or postictal activity
  • clear-cut precipitants, especially in an emotionally charged atmosphere
  • lack of falls or injuries
  • fluctuating consciousness or vivid recall of details during ictal moments.

PNES’ physical symptoms are not voluntary. Patients often have out-of-phase upper- and lower-extremity movements and vocalization as the event starts, as opposed to about 20 seconds into the event when true tonic-clonic seizure makes the tonic-clonic transformation. Other common features are high-amplitude, forward pelvic thrusting, and lack of rigidity. Weeping during an apparent seizure strongly suggests a nonepileptic event. 14

Ictal duration can be useful in assessment. Events that resemble tonic-clonic seizure but continue for >70 seconds or <20 seconds raise suspicion of nonepileptic seizures, although status epilepticus is possible.

Prolactin elevation. Epileptic tonic-clonic and partial complex seizures increase serum prolactin and are most reliable approximately 20 minutes after event onset. Nipple manipulation can spuriously increase serum prolactin, so observe female patients for this behavior if a seizure occurs in your presence. Psychotropics such as chlorpromazine and haloperidol may also elevate serum prolactin.


Video EEG recording is available in most neurologic centers and is the investigation of choice. Epileptic seizure is characterized by recruitment of seizure activity in a physiologic distribution and postictal slowing, which would be difficult for a patient to imitate.

Unlike traditional EEG, video EEG shows evidence of electrographic paroxysmal changes immediately before, during, or after an epileptic seizure. 15 Seizure presentations without paroxysmal electrographic changes would be considered PNES.

Traditional EEG is not recommended for a PNES workup because seizure activity is not recorded and myogenic infarcts may obscure readings. Moreover, because interictal EEG changes may occur even in patients with PNES, these changes in isolation cannot be interpreted as evidence of epilepsy. 16

Laboratory testing includes full blood count, electrolytes, urea and creatinine, urine drug screen, and thyroid and liver function tests, as well as serum levels in patients taking anticonvulsants. These tests may exclude some seizure causes (such as hypokalemia or hypocalcemia with electrolyte disturbances) and provide baseline values for monitoring drug toxicity. Thyroid function testing will rule out hypo- or hyperthyroidism in patients with comorbid depressive or anxiety disorders. Urine drug screen reveals evidence of drug abuse—a possible organic seizure disorder precipitant.

Normal serum prolactin (men: 2 to 18 ng/mL; nonpregnant women: 3 to 30 ng/mL), cortisol (5 to 22 mcg/dL, morning blood specimen), and creatine kinase (50 to 200 U/L) rise substantially after an epileptic—but not psychogenic—seizure. 17 Note, however, that creatine kinase and prolactin may be as elevated in PNES as in an epileptic seizure if PNES presents with vigorous muscular activity. 18

Psychological testing may help distinguish PNES from epileptic seizure:

  • Minnesota Multiphasic Personality Inventory (MMPI) is fairly sensitive and shows statistically significant differences between PNES and epileptic seizures in hypochondriasis, depression, hysteria, and schizophrenia. 19
  • Washington Psychosocial Seizure Inventory helps identify etiologic subgroups among PNES patients. 9

Others. As in Ms. X’s case, CT and MRI for cerebral pathology may not help.20 Provocative techniques 21 based on suggestibility also may have little value because PNES can be provoked in patients with documented epileptic seizures. Hypnosis has been used in attempts to demonstrate the psychogenic component of nonepileptic seizures by reversing ictal and postictal amnesia. Patients with PNES seem to be more responsive to hypnosis than those with epileptic seizures. 22


The psychiatric team concluded that even though Ms. X has a seizure disorder, this particular episode was psychogenic. This conclusion was based on the emotional precipitant, her brother’s collateral history, video EEG recordings, and her history of depression.

The psychiatrist explained to Ms. X that PNES and seizure disorders can coexist and that a PNES diagnosis does not imply that a patient is lying. It simply means that some seizures are precipitated by psychoemotional events.

Unlike some patients with PNES, Ms. X accepted the diagnosis without anger. Because her epilepsy and depression were stable, the psychiatrist did not change her phenytoin or paroxetine dosages. She was discharged, with follow-up care by a psychiatrist and neurologist.


It is important to present a PNES diagnosis with care because some patients react with aggressive denial and suicidal behavior. A patient who believes he or she has been perceived as a liar or “fake” may feel humiliated,9 which is why we prefer the term “PNES” rather than “pseudoseizure.”

PNES treatment calls for collaboration among the neurologist, psychiatrist, psychologist, therapists, support workers, and family. When PNES is clearly the only cause of seizures, avoid treating with anticonvulsants. If PNES coexists with a treated seizure disorder, no change in anticonvulsant dosage is necessary, especially if blood levels are normal.

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