Psychiatric Annals

CME Article 

Diagnosis and Treatment of Pseudoseizures

Elizabeth S. Bowman, MD; Omkar N. Markand, MD

Abstract

Pseudoseizures (PS) are a form of conversion disorder that resemble organically based seizures but are not due to physiologic dysfunction of the nervous system. They usually are diagnosed by neurologists and subsequently treated by psychiatrists or other mental health professionals. They occur commonly, cause considerable disability, and often are misdiagnosed as epilepsy for extended periods. In this article, we discuss a practical approach to diagnosing and treating PS, presenting this diagnosis to patients, and exploring psychological origins.

The behavioral characteristics displayed during PS reflect the mental image or knowledge the patient has regarding epileptic seizures. A wide variety of symptoms may characterize an individual psychogenic event, which may mimic generalized tonic-clonic (GTCS), complex partial (CPS), simple partial (SPS), or absence seizures. Rarely is the resemblance perfect.

Meierkort et al.1 and Leis et al.2 divided the majority of psychogenic events into two categories. One is dominated by excessive motor activity mimicking GTCS. The other is characterized by unresponsiveness without significant motor manifestations. Both types may occur in the same patient during different episodes or simultaneously during a single event.

Motor movements in PS range from quivering of one extremity to uncontrolled forceful flailing of all extremities. Patients may assume opisthotonic posture, including the classic “arc en circle.” Movements in PS tended to be disorganized, asynchronous, and even chaotic. The out-of-phase movements of the limbs (ie, movements in arms and legs in opposite directions) may not be present in all PS events.3 Pelvic thrusting is common in women with PS. The repetitive pattern of movements in PS may be regular, in contrast to epileptic seizures which are associated with sudden, jerking movements.

Vocalization occurs commonly in PS and may include yelling, screaming, crying, sobbing, and verbal expressions of obscenities. Emotionally charged vocalizations (eg, crying or weeping) are rare with epileptic seizures but common during or after PS.

Purposeful or semi purposeful coordinated motor behavior simulating CPS (eg, labio-lingual movements, rapid eye flutter, fumbling with clothes) may occur during PS.1,4 Patients with PS may exhibit combative or violent behavior including biting, striking, kicking, pushing, obscene gesturing, or directed rage.4,5 Autonomic changes that may accompany PS include hyperventilation, difficulty breathing, coughing, choking, color changes (dusky or flushed face), paresthesiae, dizziness or lightheadedness, headaches, dilated reactive pupils, tachycardia, or palpitations.

Leis et al.2 reported unresponsiveness without motor manifestation as the single most common ictal characteristic in their PS patients. Such patients may “swoon” or exhibit prolonged unresponsiveness in bed with a motionless “limp” body and closed eyes. They may squeeze their eyelids on attempted opening. Pupils remain normal in size and respond normally to light. They often show avoidance response to a passively elevated arm dropped on their face. Touching their eyelashes usually elicits blinking. The normal response to cotton wool testing of the cornea remains preserved. After PS, responsiveness often returns gradually but may return promptly.

The state of the eyes may be a significant differentiating feature. The eyes are usually open (“staring”) during an epileptic seizure, whereas eyes are usually kept closed during a PS. Flugel et al.6 reported that 90% of their patients with PS had closed eyes during the episodes; the 10% with open eyes had a higher incidence of co-existing epileptic seizures.

Significant injuries during paroxysmal events often are considered supportive evidence for epileptic seizures. However, tongue biting, urinary or fecal incontinence, and self-injury all can occur during PS. As many as one-third of PS patients may report self-injury during PS, a finding more commonly seen in patients who previously had attempted suicide.1,7 Burns, fractures or laceration of the tongue are rare, but mild injuries are commonly reported. Urinary or…

Pseudoseizures (PS) are a form of conversion disorder that resemble organically based seizures but are not due to physiologic dysfunction of the nervous system. They usually are diagnosed by neurologists and subsequently treated by psychiatrists or other mental health professionals. They occur commonly, cause considerable disability, and often are misdiagnosed as epilepsy for extended periods. In this article, we discuss a practical approach to diagnosing and treating PS, presenting this diagnosis to patients, and exploring psychological origins.

Clinical Presentation and Differential Diagnosis

The behavioral characteristics displayed during PS reflect the mental image or knowledge the patient has regarding epileptic seizures. A wide variety of symptoms may characterize an individual psychogenic event, which may mimic generalized tonic-clonic (GTCS), complex partial (CPS), simple partial (SPS), or absence seizures. Rarely is the resemblance perfect.

Meierkort et al.1 and Leis et al.2 divided the majority of psychogenic events into two categories. One is dominated by excessive motor activity mimicking GTCS. The other is characterized by unresponsiveness without significant motor manifestations. Both types may occur in the same patient during different episodes or simultaneously during a single event.

General Characteristics of PS

Motor movements in PS range from quivering of one extremity to uncontrolled forceful flailing of all extremities. Patients may assume opisthotonic posture, including the classic “arc en circle.” Movements in PS tended to be disorganized, asynchronous, and even chaotic. The out-of-phase movements of the limbs (ie, movements in arms and legs in opposite directions) may not be present in all PS events.3 Pelvic thrusting is common in women with PS. The repetitive pattern of movements in PS may be regular, in contrast to epileptic seizures which are associated with sudden, jerking movements.

Vocalization occurs commonly in PS and may include yelling, screaming, crying, sobbing, and verbal expressions of obscenities. Emotionally charged vocalizations (eg, crying or weeping) are rare with epileptic seizures but common during or after PS.

Purposeful or semi purposeful coordinated motor behavior simulating CPS (eg, labio-lingual movements, rapid eye flutter, fumbling with clothes) may occur during PS.1,4 Patients with PS may exhibit combative or violent behavior including biting, striking, kicking, pushing, obscene gesturing, or directed rage.4,5 Autonomic changes that may accompany PS include hyperventilation, difficulty breathing, coughing, choking, color changes (dusky or flushed face), paresthesiae, dizziness or lightheadedness, headaches, dilated reactive pupils, tachycardia, or palpitations.

Leis et al.2 reported unresponsiveness without motor manifestation as the single most common ictal characteristic in their PS patients. Such patients may “swoon” or exhibit prolonged unresponsiveness in bed with a motionless “limp” body and closed eyes. They may squeeze their eyelids on attempted opening. Pupils remain normal in size and respond normally to light. They often show avoidance response to a passively elevated arm dropped on their face. Touching their eyelashes usually elicits blinking. The normal response to cotton wool testing of the cornea remains preserved. After PS, responsiveness often returns gradually but may return promptly.

The state of the eyes may be a significant differentiating feature. The eyes are usually open (“staring”) during an epileptic seizure, whereas eyes are usually kept closed during a PS. Flugel et al.6 reported that 90% of their patients with PS had closed eyes during the episodes; the 10% with open eyes had a higher incidence of co-existing epileptic seizures.

Significant injuries during paroxysmal events often are considered supportive evidence for epileptic seizures. However, tongue biting, urinary or fecal incontinence, and self-injury all can occur during PS. As many as one-third of PS patients may report self-injury during PS, a finding more commonly seen in patients who previously had attempted suicide.1,7 Burns, fractures or laceration of the tongue are rare, but mild injuries are commonly reported. Urinary or fecal incontinence, or both, have been reported in about 20% of PS patients.1,5,7 These features demonstrate the capacity of some patients to tolerate self-inflicted pain through the mechanism of dissociation.

Contrary to expectations that it occurs only during wakefulness, PS occurs during apparent “sleep,” a finding likely to be misinterpreted as evidence of epileptic seizures.8 However, when evaluated by video electroencephalogram (EEG), such patients show findings consistent with wakefulness (alpha rhythm) before the start of a PS. In addition, PS tend to be longer than epileptic seizures.1,2,9 Gates et al.9 found the mean duration of GTCS to be 69 seconds (range of 50 to 92 seconds), whereas PS mimicking generalized convulsions had a mean duration of 134 seconds (range of 20 to 805 seconds). Paroxysmal events characterized by excessive generalized motor activity lasting longer than 2 minutes should raise suspicion for PS.

Although PS more commonly are assumed to be precipitated by emotional stress than epileptic seizures, this is not reliable. Most epileptic patients report increased likelihood of having an epileptic seizure under mental stress, whereas patients with PS are more likely to deny a connection between their episodes and emotional stress, consistent with alexithymia and because the episode itself serves to keep psychic discomfort out of conscious awareness.

Some patients with PS may be diagnosed and treated for status epilepticus. Such patients with “pseudo-status epilepticus” may present with many of the features described above. Surprisingly, they allow themselves to be intubated, paralyzed, or treated with intravenous anti-convulsants with a high potential for serious and life-threatening complications.

The phenomenologic differences between PS and GTCS are summarized in Table 1 (see page 308). Although clinical features are helpful, none are specific or confirmatory. Instead, one needs to consider the entire symptom picture and sequence of events. The typical tonic-clonic sequence and the progression of clonic jerks from fast, small-amplitude to slow, large-amplitude movement and the rapid contraction followed by slow relaxation during the clonic phase in GTCS are not observed in PS.1

Distinguishing Features of ‘Convulsive’ PS and Generalized Tonic-Clonic Epileptic Seizures (GTCS)

Table 1:

Distinguishing Features of ‘Convulsive’ PS and Generalized Tonic-Clonic Epileptic Seizures (GTCS)

Stereotypic manifestations during paroxysmal events are more characteristic of epileptic seizures, whereas variable intensity and features characterize most PS. However, patients with focal epilepsies may have simple partial, complex partial, and secondarily generalized seizures on different occasions, which may be misinterpreted as PS-like variability in types of episodes.

A detailed neurological assessment demonstrating the presence of responsiveness, reactivity to painful stimulation, and preservation of avoidance reflexes are suggestive of PS that are characterized by “apparent” unconsciousness. Similarly, precipitation of the episode and its prompt termination by suggestion are highly indicative of PS.10

It is more challenging to differentiate PS from frontal lobe complex partial seizures (FLCPS) because of the often bizarre presentation of FLCPS (Table 2).11 Motor phenomena during FLCPS may include thrashing or kicking, unilateral or bilateral tonic posturing, sexual gestures, and vocalization with fragmented and variable preservation of responsiveness during the seizure and prompt return to baseline without postictal confusion. Furthermore, the EEG in many patients with FLCPS may show no interictal epileptiform abnormalities, or the ictal EEG pattern may be obscured by artifacts generated by vigorous ictal motor activity, not unlike the electrographic findings in PS.11,12 The most important discriminating characteristics of FLCPS are their stereotypic character, very brief duration (less than 1 minute), and occurrence during sleep. Finally, various nonepileptic physiologic events, such as syncope, breath holding spells, complicated migraine, transient ischemic attacks, movement disorders, and cardiac arrhythmias, also need to be differentiated from PS.

Distinguishing Featur8s of Frontal Lobe Complex Partial Seizures (FLCPS) and PS.**

Table 2:

Distinguishing Featur8s of Frontal Lobe Complex Partial Seizures (FLCPS) and PS.

Diagnostic Evaluation

The importance of differentiating nonepileptic events from epileptic seizures cannot be overemphasized because consequences of misdiagnosis are far reaching. Labeling a patient as epileptic has profound psychosocial implications, especially for driving and employment, and misdiagnosed patients may fail to obtain treatment for underlying psychopathology. Chronic use of anticonvulsants results in side effects, including potential teratogenic effects during pregnancy; in addition, potentially hazardous iatrogenic complications can occur as a result of misdiagnosing status epilepticus. Misdiagnosis also places an unnecessary drain on limited health resources and can cause difficulties in rehabilitation when the proper diagnosis is delayed. Hence, any patient with medically refractory seizures with unusual or atypical manifestations must undergo thorough evaluation.

Even though clinical features may be highly suggestive of PS, unequivocal confirmation requires further diagnostic evaluation. Alsaadi et al.13 found as many as 29 of 121 patients (24%) referred to an epilepsy monitoring unit had been misdiagnosed. Twenty-two patients previously diagnosed with epileptic seizures had PS, and four previously diagnosed with PS turned out to have epileptic seizures.

Serum prolactin measured after a suspected seizure has been used as a method to differentiate PS from epileptic seizures.14 Neurologic excitation during an epileptic seizure inhibits dopamine release, which results in a pulse of prolactin released into the serum. Serum prolactin increases at the onset of an epileptic seizure, peaks at 15 to 30 minutes, and declines to baseline value by 60 minutes after the seizure. Prolactin increases consistently (90% of cases) and most prominently following GTCS, less consistently (70%) with CPS, and least (9%) with SPS.14 A postictal (drawn 15 to 30 minutes after a seizure) elevation of at least twice baseline (baseline drawn at least 60 minutes after the seizure) is suggestive of an epileptic seizure.

However, many factors can increase baseline serum prolactin (eg, antipsychotics). Hence, use of paired serum prolactin levels is mandatory to preclude falsely labeling an event as an epileptic seizure simply because of an elevated baseline prolactin. Occurrence of both false positives and false negatives (particularly in SPS and CPS) limits the utility of prolactin for diagnosing PS. Nevertheless, a negative prolactin test after an episode of bilateral (generalized) motor activity of a few minutes duration is highly suggestive of a psychogenic event.

Routine electroencephalography (EEG) usually is of limited value in the differentiation between PS and epileptic seizures. Although interictal epilepti-form abnormalities in a routine EEG suggest an epileptogenic basis, the yield of a single routine EEG in epileptics is only 30% to 55%.15 EEG may show nonspecific abnormalities such as focal or generalized slowing due to unrelated causes such as encephalopathy, medication effect, or a cerebral lesion. Artifacts or benign epileptiform variants may be confused with abnormal epileptiform discharges. Interictal epileptiform abnormalities have been reported in 1.5% to 4% of neurologically intact subjects without paroxysmal events, and the incidence of such epileptiform abnormalities may even be higher in patients with PS.16,17 Hence, the presence of epileptiform discharges in a routine EEG may be incidental or supportive of epileptic seizures but cannot exclude the concomitant diagnosis of PS. Similarly, the absence of such abnormalities cannot exclude an epileptic basis for paroxysmal events. Nonetheless, recording several normal EEGs (including during sleep or following sleep deprivation) in a patient with very frequent episodes that remain refractory to anticonvulsant medication provides strong support for the diagnosis of PS.

The hallmark of an epileptic seizure is the occurrence of an abnormal and excessive electrical discharge in the brain concurrent with altered behavior, whereas a psychogenic event will not demonstrate such an ictal pattern. Establishing an unequivocal diagnosis, therefore, requires recording characteristic episodes during simultaneously recorded EEG. Prolonged video EEG monitoring has been used extensively to obtain combined electro-clinical correlation. This procedure has become a “gold standard” in evaluating patients suspected of having PS.

To be most effective, video EEG requires detailed and frequent intervention by an EEG technologist or nurse. During and immediately following a paroxysmal event, the patient is assessed for any changes in awareness, responsiveness, difficulty with speech, comprehension, alteration in muscle tone and strength, and changes in pupillary and plantar reflexes. Verbal cues are spoken aloud repeatedly to determine if the patient is able to recall these items at the conclusion of the event. Elevating the patient's arm and releasing it above the face may be performed repeatedly to determine if the patient consistently avoids hitting her or his eyes. Painful stimuli may be delivered to determine the degree of responsiveness.

All efforts are made during video EEG monitoring to capture the patient's habitual episodes. If precipitating factors are known, these are appropriately exploited, in addition to the commonly used activating procedures such as hyperventilation, intermittent photic stimulation, sleep activation, and sleep deprivation. Video EEG monitoring also provides an extended EEG recording during wakefulness and sleep which aids in detecting previously undetected interictal epileptiform abnormalities.

The absence of a characteristic ictal pattern and continuation of a normal EEG recording during an episode are findings highly suggestive of PS but with several caveats; concomitant ictal change may be absent in scalp recordings during a SPS because the neuronal discharge may be either deeply situated in the brain or may involve only a small neuronal pool; an ictal EEG change may be obscured by movement artifacts accompanying a genuine epileptic seizure, a common occurrence during FLCPS;12 movement artifacts accompanying PS may be misinterpreted as a cerebral discharge; certain nonepileptic paroxysmal events may be associated with EEG changes (eg, attenuation followed by diffuse slowing with syncope and breath holding spells); episodes captured during the video EEG study must be similar to the habitual episodes of the patient.

Despite the above caveats, several EEG findings are diagnostic of a psychogenic episode: an episode of bilateral motor activity associated with unresponsiveness and amnesia but without any changes in the EEG immediately before, during or after the episode; an episode of apparent motor flaccidity and unconsciousness associated with continuing alpha rhythm characteristic of wakefulness; or absence of interictal epileptiform abnormalities during extended video EEG recording.

Because paroxysmal events may not necessarily occur spontaneously during video EEG monitoring, techniques to induce episodes based on direct or indirect suggestions commonly are employed to shorten monitoring time. Instructions are given to the patient that the procedure to be performed commonly precipitates seizures in susceptible individuals. Different induction protocols use verbal suggestions, often coupled with photic stimulation, hyperventilation or various placebos (eg, injecting saline).18,19

In a recent survey, nearly 40% of physicians reported using provocative tests routinely to diagnose nonepileptic seizures.19 Although there are no studies comparing the efficacy of different induction procedures, there appears to be little difference in sensitivities (approximately 75%).19 Although patients with epilepsy usually are not inducible, Walczak et al.20 reported 3 of 40 patients with PS and 3 of 20 patients with epilepsy had atypical episodes induced by IV saline. Two of the patients with epilepsy had their typical epileptic seizures induced by placebo.

In summary, induction techniques elicit typical psychogenic events in most patients with PS but atypical events and even epileptic seizures may occur and lead to an incorrect diagnosis. Any induced episodes must be confirmed by reliable witnesses to resemble the patient's habitual episodes before the diagnosis of PS is considered. Furthermore, recording a spontaneous or induced PS does not exclude co-existing epileptic seizures.

Provocative techniques, particularly IV infusions, raise ethical issues and may compromise patient-physician relationships, leaving patients feeling deceived and unwilling to accept subsequent psychiatric treatment. Some physicians deplore the practice of placebo induction, but others have considered it useful and ethical in establishing the diagnosis sooner and permitting early institution of appropriate psychiatric management.4,8,19

Considering the above ethical issues, we suggest the following stepwise approach for the clinician. Initially, use only verbal suggestions. Reduce anti-convulsant medication before video EEG monitoring or withhold it the day of the study, and inform the patient that this is being done to facilitate the occurrence of seizures. Video EEG recordings may then be started, during wakefulness and sleep, to detect spontaneous interictal epileptiform abnormalities. If spontaneous episodes are not observed, hyperventilation and photic stimulation are used. Inform the patient that these activating techniques precipitate seizures in patients with epilepsy, a true statement.

Parra et al.21 have shown that spontaneous events can be expected to occur after a mean interval of 15 hours of video EEG monitoring in patients with PS. By 48 hours, almost all have had their episodes spontaneously. Hence, it is reasonable to wait 15 to 24 hours before applying inducing procedures. Verbal suggestions coupled with hyperventilation and photic stimulation provoke episodes in more than 70% of patients with PS who failed to have spontaneous episodes.21 If all of the above attempts fail to yield positive results, consider provocative techniques.

Diagnosis of co-existing PS and epileptic seizures is firmly established only if both epileptic seizures and PS are recorded during one or more video EEG monitoring sessions. If a patient has had only psychogenic events during video EEG but also demonstrated unequivocal interictal abnormalities in the EEG, the diagnosis of concomitant epilepsy is probable. Recent video EEG studies using strict diagnostic criteria, showed that only 5% to 10% of patients with PS have concurrent epileptic seizures.22,23 Therefore, if only PS are recorded in the absence of interictal epileptiform discharges during prolonged video EEG, a concomitant diagnosis of epileptic seizures should be avoided to ensure participation of patients and families in subsequent psychiatric management and tapering of anticonvulsant drugs.

Psychiatric Evaluation and Management

People diagnosed with conversion symptoms often are confused, frightened, or shamed by the diagnosis. Their initial psychological management can be divided into explaining, exploring, and treating.24

Explaining Conversion and PS

To begin psychiatric treatment of patients with PS, it is important to explain the diagnosis in ways that educate the patient, provide a cognitive framework of understanding, reduce shame, and motivate willingness to undertake treatment. The first meeting with a mental health professional is critical. To accomplish these objectives, we recommend first using techniques to reduce shame and second providing a cognitive framework by using concrete metaphors for understanding conversion symptoms. To reduce shame and facilitate rapport, it is important initially to address anxiety about being perceived as weak or “crazy,” the role of stress, coping responses, and underlying emotions.

We recommend including the family in this discussion. Family disagreements over the meaning of symptoms are ameliorated when patient and family hear the same explanation. When family tension or conflict is a factor in the conversion symptom, these tensions and dynamics are readily observable in the interview and can be discussed later with the patient.25,26

Conversion symptoms are generated unconsciously and express unconscious emotions and conflict. Conversion disorder patients have alexithymia, or difficulty recognizing and verbally expressing emotions, and therefore experience their symptoms as involuntary and uncontrollable. As a result, it is important to provide a cognitive framework for understanding conversion that emphasizes the possibility of gaining control over symptoms. We have found simple metaphors are helpful in explaining these abstract concepts related to PS and are easily adapted for other conversion symptoms. For example, emotions stemming from life stresses or trauma can be compared with steam in a pressure cooker, with “seizures” acting as a safety valve. Another useful metaphor compares conversion symptoms with a coded message — a symbolic message in somatic language that could be understood if translated or decoded through therapy.

A third useful metaphor was suggested by Griffith et al.25 after they observed videotaped interviews in which patients with PS nearly always were the most silent members of their families. The authors identified “unspeakable dilemmas” that the patients were expressing somatically. In nearly half the cases, the dilemma was a realistic threat of physical or sexual assault to someone in the family. In other cases, the family tacitly silenced emotional expression via shame or guilt. These patients were in an unspeakable bind; to express their dilemma verbally might be dangerous to themselves or others. To escape would pose even greater emotional pain to them and might endanger someone else.

Most patients identify with some aspect of these metaphors. Common resistances include denial of stresses, family dilemmas or “double binds,” or unexpressed emotions. Denial is best handled with a calm suggestion to discuss more of the patient's life history. Inevitably, a number of stresses or conflicts emerge. Resistance to the concept of overcontrol of emotions can be handled gradually by noting when the patient answers questions about affect with a statement of cognition, or verbally noting when inappropriate smiling (la belle indifférence) recurrently accompanies discussion of emotionally painful topics. Clinicians should confront inappropriate smiling gently, persistently, and promptly. This increases the patients' awareness of their alexithymia and often elicits more appropriate affect.

Conversion disorder patients actually need to be reminded of the names of broad categories of emotions (eg, mad, sad, bad, glad, hurt, scared) and encouraged to express emotions verbally. A common resistance is disbelief that the mind could cause these somatic symptoms. We remind patients that their unconscious mind has been controlling their breathing, heart rate, and other body functions during the interview, and that automatic physical responses to sudden fright (eg, increased heart rate) are normal.

We find that denial of the psychological nature of conversion symptoms is a poor prognostic factor, especially when the family colludes with or is the proponent of this denial. In these cases, we recommend the clinician allow that “we can agree to disagree” but insist that treatment be undertaken until “we are both sure” what causes the symptoms. Conflict can be reduced by reminding patients that conversion is a “good news” diagnosis because PS are potentially 100% treatable and the patient could be weaned from anticonvulsants (if concomitant epilepsy is not present).27

The empathetic explanation of PS as an automatic outlet for intolerable affect is a powerful therapeutic tool. The cognitive framework of a metaphor helps patients feel less helpless and controlled by the symptoms. The explanation alone helps some patients immediately reduce their frequency of PS.

Exploring the Causes of PS

The second step in psychiatric management of PS is exploration of their cause in an individual patient. Psychoanalytic theory holds that conversion expresses internal conflict and denial of forbidden unconscious impulses or wishes that are converted to somatic expression. Janet linked conversion to trauma and dissociative mechanisms.28 Freud initially understood conversion (“hysteria”) to be a consequence of childhood sexual seduction, but later repudiated that understanding.29 We now understand conversion to be related to a wider array of conflicts and emotions.30–32 The conflicts that produce symptoms are wide ranging but fall into distinct categories that can be explored systematically.33–35

The lives of most conversion patients have been painful or traumatic.30,33,34,36,37 Their difficulties often begin in childhood and encompass multiple stresses and traumas. Symptom onset is a response to “last straw” stresses after years of heavy emotional burdens.35

Table 3 lists four common life-event and emotional patterns in a series of intensely studied patients with PS.34,35 These patterns can assist in understanding most patients with PS. In addition to looking at life-event patterns, physicians should assess the most common comorbid diagnoses found in studies of PS patients, including dissociative disorders, posttraumatic stress disorder (PTSD), major depression, and generalized anxiety disorder.38 Some patients have panic attacks that are mistaken for PS.38

Patterns of Life Events and Emotions That Contribute to Pseudoseizures34,35

Table 3:

Patterns of Life Events and Emotions That Contribute to Pseudoseizures34,35

Patients with PS often experience other conversion symptoms and somatoform disorders. Psychosis, malingering, and factitious disorders occur in patients with apparent PS but are uncommon.

Numerous authors have noted the association of PS with sexual trauma, incest, rape, physical abuse, and domestic violence.28–30,33,34,36,37,39,40 Not all people with PS have experienced abuse, but approximately 85% report trauma, often with corroboration from family members.33,39 Adequate evaluation of the cause of PS therefore requires open-ended, nonleading questions about trauma or abuse. We find the most common life pattern associated with PS is childhood physical, sexual, or severe emotional abuse that is dissociated and brought near consciousness by adulthood trauma or other reminders of the abuse.34 Reminders of past abuse may be symbolic (eg, genital pain after childbirth or gynecologic surgery in a rape or sexual abuse survivor), obvious (eg, moving near the place of one's child abuse, encountering a former abuser, death of a parental abuser) or subtle (eg, children reaching the age at which the patient was at onset of his or her abuse). These reminders reduce dissociative barriers.

Dissociated emotions and memories threaten to emerge in consciousness. PTSD symptoms and dissociative episodes increase, and may be expressed as re-experiencing trauma in flashbacks or amnestic episodes that resemble seizures.34,39 At times, dissociated alter ego states or personality states emerge in response to reminders of trauma and re-enact assaults during PS. This life pattern can be ascertained by taking a detailed history of the person's life, noting amnesia for substantial portions of childhood, or for episodes of time loss in adult domestic abuse or in current life.

These patients should be evaluated for PTSD, depression, and for dissociative amnesia and dissociative identity disorder. Their trauma is often chronic, varied, and extensive. Their families may deny trauma, punish discussion of it, or blame and shame the patient. Ordinary stresses also may add to tension. Not all trauma is abuse; severe accidents, crime victimization, nondomestic trauma, combat trauma, and traumatic bereavement may be relevant.

Treatment focuses on identifying the emotions that these events raise and exploring the trauma. If possible, exploration should be conducted through a number of sessions after the patient's supports and defenses have been stabilized.41,42 This is not always possible in the seizure clinic but should be the norm in ongoing outpatient psychiatric treatment. Interviewers should avoid leading or suggestive interview techniques when inquiring about trauma or events underlying childhood amnesia.43

A second life event pattern of unexpressed anger is seen in about 25% of PS patients, more in men than in women.34 These patients often report verbally or physically abusive families of origin where expression of anger by the patient is discouraged or even punished. These families typically either avoid anger and conflict or express anger violently. Patients from such families conclude that anger is either too dangerous to acknowledge or is expressed only through violence, so they suppress awareness of it. Commonly, they describe a critical family, cruel school teasing from peers, or childhood or adulthood physical battering or threats.

These patients often describe aggravating or enraging life situations with la belle indifférence or an inappropriate smile. They deny sensing or expressing anger, saying, “I don't get angry.” They endorse cognitive distortions about anger; only blind rage is recognized as anger, and it is feared as destructive. They minimize all other irritation as “frustration, not anger.”

These patients also express anxiety about psychological or physical harm if they disagreed with or became angry at abusive parents or spouses. They avoid conflict in nondangerous life situations. Their faces or their general musculature show tension or anger of which they are blithely unaware.

In a third life pattern, the PS of patients express overwhelming grief and sadness at multiple losses or an unresolvable bereavement.44 Some patients describe multiple deaths, or losses of jobs, marriages, relationships, homes, finances, and so on. They may have relatively intact emotional expression or may have cultural or personal inhibitions about crying or grieving (especially true of male patients).

Major depression often is present and adds to their emotional burden. Some have PTSD symptoms from traumatic losses (accidental or combat deaths). The death of abusive parents is difficult for victims and may trigger the onset or cessation of PS. Some patients benefit from visiting the gravesite or discussing ambivalence about the deceased before their seizures resolve. Patients may display unexpected emotional blandness about losses. Patients with multiple losses also should be screened for depression and PTSD.

Approximately 10% to 15% of patients with PS deny trauma or multiple losses and do not have obviously anger-engendering families. Their PS —often accompanied by other conversion symptoms such as muteness, dysphonic, weakness, numbness, or fainting — are an expression of family conflicts that are experienced as “double binds.” Even if they consciously perceive the family conflict, they see no emotionally acceptable answer to it and believe verbalization of it is also unacceptable. Emotional tension rises and depression or anxiety mount until a dissociative escape via conversion symptoms is their only solution. This focuses the family on the symptoms and eventually on discussion of the conflict after the patient verbalizes it in psychotherapy. These conflicts often involve duties, guilt, and family norms of interactions.

PS usually decrease sharply after the conflict is verbalized in individual psychotherapy and the patient is assisted in discussing it in family therapy. If the conflict centers on family secrets (such as incest), the trauma also must be addressed to resolve conversion symptoms.

These four life patterns associated with PS deal with life events associated with conversion but not its underlying mechanism of dissociation.34,45 Psychological dissociation is disconnection of mental processes from each other or from consciousness. Somatoform dissociation (another name for conversion) is disconnection of somatic (motor or sensory) control from conscious control.45,46

Many PS episodes represent dissociative detachment from the self and the environment in trance states or limp collapse with amnesia.47 These PS are simply staring episodes of autogenic trance states of dissociation that appear to be like absence epilepsy. During the evaluations of PS patients, they often can be observed to enter trance states (eg, staring, looking clouded or blank, even becoming unresponsive). A dynamic formulation of the cause of the seizures can be inferred by noting which topics or emotions elicit this dissociative response.

We advise interrupting the patients' entry into a trance by breaking their staring gaze, advising them to move their bodies and alert themselves. Patients can be taught to recognize their entry into trance, which often precedes their conversion symptoms, and how to avoid such entry. This may be their first experience of gaining some control over symptom occurrence. When a pattern of association between trances and emotional themes is discerned, the patient can learn that trances and seizures are defensive patterns related to specific issues.

The International Statistical Classification of Diseases and Related Health Problems, 10th edition,48 classifies conversion as a dissociative disorder, substituting the word “dissociative” for “conversion.” Dissociation is nearly ubiquitous in PS patients but often is overlooked and not formally diagnosed. When a validated diagnostic instrument for dissociative disorders under criteria from the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV)49 — the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D) — was used systematically, 90% of PS patients were found to have a dissociative disorder, usually dissociative amnesia.28,50 Dissociative amnesia is extremely common during PS, occuring in about 80% of patients at times other than during seizure spells.39 When systematic inquiry is undertaken, up to half of PS patients are found to have a dissociated ego state that will admit to causing the seizures.39 PS patients dissociate affect and often dissociate behaviors (flashbacks) and memories. We recommend screening all PS patients for dissociative symptoms and disorders such as amnesia, depersonalization, derealization, and identity alteration. The screening questions of the SCID-D are useful for diagnosing dissociative disorders.50

In a significant minority of patients, PS are dissociative re-enactments of sexual or physical trauma by dissociated ego states or personalities in patients with dissociative disorder – not otherwise specified, dissociative identity disorder, or complex PTSD. This situation is unlikely to be addressed in treatment unless a formal evaluation of dissociation has been conducted. Evaluations should be completed over several sessions to avoid flooding patients with panic from rapid awareness of having dissociative lapses. We screen all PS patients with the self-report Dissociative Experiences Scale (DES) and carefully screen for complex dissociative disorders when DES scores are higher than 30.51,52 All PS patients who report significant trauma should be screened for PTSD in addition to dissociative disorders.

In summary, patients with PS should be evaluated for a variety of life stresses and traumas in childhood and adulthood, for the presence of unexpressed painful emotions, and for cognitive and defensive patterns that inhibit verbal and affective expression of their distress. In addition, clinicians should screen for the common comorbid illnesses of dissociative disorders, PTSD, major depression, panic disorder, generalized anxiety disorder, and family relationship binds.

Treatment of Pseudoseizures

Treatment of PS depends entirely on the underlying cause in each patient and on associated psychiatric diagnoses. This field is hampered by a lack of controlled treatment outcome studies. Our recommendations are based on clinical experience with more than 800 patients. Psychotherapy is the mainstay of treatment but should be individualized. Underlying comorbid disorders require treatment to stabilize the patient and reduce anxiety and depression that may contribute to PS.

Psychopharmacologic Treatment

We recommend using antidepressants for comorbid PTSD, panic, and major depression and have found selective serotonin reuptake inhibitors to be effective. Some patients with overwhelming anxiety may require initial treatment with anxiolytics until their anxiety or trauma are resolved in psychotherapy. A few PS patients have psychotic symptoms that can be treated with second-generation antipsychotic medications.

We recommend psychiatrists work with treating neurologists to enable patients without co-existing epilepsy or bipolar disorder to wean safely from anticonvulsant medications. Care should be exercised to minimize drug-drug interactions between anticonvulsants and psychotropic medications. We have found minimal interactions with anti-convulsants when using citalopram, sertraline, and escitalopram.

Psychotherapeutic Treatment

The primary principles of therapy are a nonjudgemental, supportive, and educative approach that addresses alexithymia and encourages verbal expression, problem-solving skills, and resolution of trauma. We believe patients do not respond well to more neutral approaches, such as classical psychoanalysis. It is important to first address depression, anxiety, and PTSD with anti-depressants and cognitive-behavior or supportive-expressive therapy. Patients should focus on their symptoms, their dissociative defenses, and the stresses or emotions that trigger PS. Clinicians should emphasize hope, the ability to gain control of symptoms, and the need to identify and verbalize emotions. Hypnosis is useful in helping patients percieve dissociated affect related to their PS. We also recommend teaching patients to recognize and stop entry into dissociative trances. This may be accomplished with or without hypnosis.

To address alexithymia, we recommend confronting inappropriate smiling and teaching patients to name and focus on emotions. Patients with PS associated with rape, incest, or child abuse do well in appropriately paced therapies that address their trauma and dissociation. Ignoring trauma does not resolve it, but exploring trauma prematurely also creates a negative outcome.

Most patients require individual psychotherapy to overcome PS, but some require marital and family therapy in addition to resolve dysfunctional dynamics or to safely exit from abusive marriages or families. With motivation, understanding of the causes of PS, and targeted psychotherapy and pharmacotherapy, most patients with PS of less than 2 years' duration do well and attain remission.3,53,54 This is a treatable disorder if properly diagnosed and carefully managed.

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Distinguishing Features of ‘Convulsive’ PS and Generalized Tonic-Clonic Epileptic Seizures (GTCS)

FeaturePS (Pseudoseizures)GTCS
   OccurrenceUsually awake.Awake and asleep.
   SuggestibilityCommon.Very rare.
   DurationLonger, 2 to many minutes.Usually brief; less than 2 minutes.
   StereotypedUncommon.Usual.
   Symptom pictureVariable and bizzare motor activity. Fluctuating intensity and severity in longer seizures.Classical sequence of tonic followed by clonic activity. Clonus fast-small amplitude to slow-large amplitude.
   AwarenessPartly preserved.Absent.
   Motor activitiesTrembling, thrashing, flailing, synchronous (out of phase) limb movements.Synchronous (in phase) limb movements during convulsive activity.
   Pelvic thrustingCommonly forward.Rare.
   Head movementRhythmic, side to side.Sustained tonic deviation.
   Emotional display, combative behavior, directed rage, verbal obscenitiesCommon.Very rare.
   Severe bodily injury (burn, fracture)Rare. More common with suicidality history.Common.
   EyesUsually closed (90%).Usually open (staring).
   CyanosisUnusual but does occur.Common.
   Tongue bitingSelf injury in one third.Common.
   Urinary incontinenceIn one-fifth.Common.
   Resistance to passive eye openingCommon.Absent.
   Responsiveness to painful stimuliCommon.Absent
   Allows hand falling on faceRare.Common.
   Postictal confusionUsually absent or very brief.Common
Ictal EEG *Normal.Characteristic ictal pattern.
  Postictal EEGNormal.Usually abnormal (slow).
  Prolactin levelNormal, even with prolonged motor activity.Increased after 90% of GTCS.

Distinguishing Featur8s of Frontal Lobe Complex Partial Seizures (FLCPS) and PS.**

FeaturePS (Pseudoseizures)FLCPS (Frontal lobe epilepsy)
OccurrenceUsually wakefulness.Sleep.
DurationSeveral minutes.Less than 1 minute.
SemiologyVariable and bizzare.Sterotypic.
PosturingOpisthotonus (arc en circle).Arms in abduction;Turning to prone position. Unilateral or bilateral tonus.
ThrashingSide to side movements of head and trunk.Leg movements are most common.
VocalizationMore frequently with emotional content. Crying, screaming.Monotonous and without emotional content.
Postictal confusionUsually absent or very brief.Sometimes brief or absent.
AwarenessVariable: preserved to amnestic.Minimal loss.

Patterns of Life Events and Emotions That Contribute to Pseudoseizures34,35

Life Event PatternEmotion Expressed by PSCommon Psychiatric Diagnoses
  1. Old trauma, recent reminderFear, anxietyPTSD, dissociation, panic, generalized anxiety disorder
  2. Enraging families or situationsAngerDissociation, depression, intermittent explosive disorder
  3. Grief, multiple lossesSadness, griefDepression, anxiety, dissociation, PTSD
  4. Double binds in familiesGuilt, shame, angerDepression, anxiety, dissociation, PTSD

Educational Objectives

  1. Describe the gold standard for diagnosing pseudoseizures.

  2. Explain pseudoseizures to a patient using a metaphor that reduces shame.

  3. List the primary causes of and treatments for conversion seizures.

Authors

Dr. Bowman is a psychiatrist in private practice and adjunct professor of neurology, Department of Neurology, Indiana University School of Medicine, Indianapolis, IN.Dr. Markand is professor emeritus of neurology and director, Indiana University Epilepsy Clinic, Department of Neurology, Indiana University School of Medicine.

Address reprint requests to: Elizabeth S. Bowman, MD, 10585 N.Meridian St., Suite 340, Indianapolis, IN 46290.

The authors have no industry relationships to disclose.

10.3928/00485713-20050401-05

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