Psychogenic Nonepileptic Seizures (PNES) are episodic events that can significantly impact a person’s life, often mimicking epileptic seizures but arising from psychological rather than neurological causes. For healthcare professionals, including neurologists and psychiatrists, PNES presents a considerable diagnostic challenge. Unlike epileptic seizures, PNES are not associated with abnormal electrical activity in the brain. Instead, these events are understood as manifestations of psychological distress. Accurate diagnosis is critical because misdiagnosis can lead to ineffective treatments and potentially harmful interventions, while delaying necessary psychological support. This article delves into understanding “What Is Pnes Diagnosis,” exploring the key differentiators from epileptic seizures, the diagnostic process, and the essential role of an interprofessional team in effective management.
Decoding PNES: Differentiating from Epilepsy
Nonepileptic episodic events, broadly termed, encompass a range of paroxysmal occurrences rooted in either physiological or psychogenic factors. These events manifest as alterations in behavior, sensations, experiences, or movement, often strikingly similar to epileptic seizures. The critical distinction lies in the underlying cause: epileptic seizures originate from excessive, synchronous electrical discharges in the brain, detectable via electroencephalogram (EEG). PNES, conversely, do not stem from this neurological abnormality and lack corresponding epileptiform changes on EEG.
While the term “nonepileptic episodic events” covers both physiological and psychogenic origins, “psychogenic nonepileptic seizures” (PNES) specifically highlights the psychological basis of these episodes. This terminology is crucial for clinicians, signaling a distinct diagnostic and management pathway compared to events of epileptic origin. It’s also important to note that PNES and epilepsy can coexist in a patient, further complicating diagnosis.
Confirming a PNES diagnosis often necessitates the expertise of an epilepsy specialist and access to an epilepsy monitoring unit (EMU). This specialized setting allows for comprehensive evaluation to differentiate PNES from epilepsy, preventing misdiagnosis and the associated risks of inappropriate treatments. This review aims to clarify the distinctions between epileptic seizures and PNES, outline a clear approach to diagnostic confirmation of “what is PNES diagnosis”, and guide the implementation of appropriate treatment strategies. Furthermore, it emphasizes the vital contributions of an interprofessional team in providing holistic care for patients with PNES.
Unpacking the Etiology of PNES
While historically viewed as purely psychological in origin, the understanding of PNES etiology is evolving towards a more integrated model. Current perspectives consider a complex interplay of genetic predispositions, environmental factors, individual temperament, and early life experiences in the development of PNES.[1, 2, 3, 4, 5] It is crucial to understand that PNES are involuntary responses to underlying psychological distress and are distinct from intentional acts like factitious disorder or malingering.
The outdated term “pseudoseizure” is problematic as it can be misinterpreted by both patients and healthcare providers as implying that the patient is consciously faking their symptoms. This misconception is detrimental and inaccurate. Similarly, terms like “hysterical seizures,” “functional seizures,” and “stress seizures” are no longer appropriate and should be avoided due to their stigmatizing and oversimplified connotations.
Differentiating PNES from epileptic seizures based solely on bedside observation or history can be exceptionally challenging, even for experienced clinicians.[6, 7] PNES diagnosis often resides at the intersection of neurology and psychiatry, requiring expertise from both fields.[8] Diagnostic delays for PNES are unfortunately common, often spanning several years.[9] The gold standard for confirming “what is PNES diagnosis” is video-electroencephalography (video-EEG) monitoring. This involves capturing a typical event while simultaneously recording EEG, demonstrating the absence of epileptiform activity during the episode in a patient with a history suggestive of PNES.[10] Studies in epilepsy monitoring units reveal that a significant proportion, between 20% and 40%, of patients referred for intractable seizures are ultimately diagnosed with PNES. A pediatric study reviewing 15 years of video-EEG data found PNES to be the final diagnosis in nearly 20% of monitored children, with almost 25% requiring discontinuation of initially prescribed antiseizure medications (ASMs) due to misdiagnosis.[11]
Accurate diagnosis is paramount for effective PNES management. However, misdiagnosis remains prevalent, particularly among primary care and emergency physicians. A recent study indicated that nearly two-thirds of these physicians believe video-EEG is unnecessary for diagnostic confirmation.[1] While a thorough history and physical examination are essential initial steps, neurological consultation is almost always beneficial, and admission to an epilepsy monitoring unit for video-EEG analysis is frequently necessary. Referral to a comprehensive epilepsy center may be warranted in complex or ambiguous cases.
Communicating the PNES diagnosis to the patient requires sensitivity and empathy. A poorly delivered diagnosis can lead to confusion, anger, and resentment, potentially exacerbating PNES symptoms. This is especially delicate for patients previously diagnosed with epilepsy or those with a history of trauma or abuse, who may be retraumatized by insensitive communication. Crucially, clinicians must emphasize that help is available, that the symptoms are real and distressing, and that they are recognized as a genuine source of suffering for the patient and their families.
Treatment for PNES differs significantly from epilepsy. Antiseizure medications (ASMs) are ineffective for PNES and may even be harmful. Unless ASMs are required for coexisting conditions like epilepsy, chronic pain, or mood disorders, they should be discontinued upon PNES diagnosis. Continuing ASMs after diagnosing PNES is linked to poorer patient outcomes.[12] Psychotherapy, conversely, has proven effective in reducing seizure frequency, improving psychosocial functioning, and enhancing health-related quality of life in individuals with PNES.
Risk Factors and Comorbidities Associated with PNES
PNES is often viewed as a manifestation of unresolved emotions and underlying psychological distress. The diverse ways PNES presents have hindered the development of a universal etiological model, although integrative cognitive models are increasingly proposed.[13]
Several factors are recognized to elevate the risk of PNES, including a history of trauma or exposure to acute stressors. Comorbid disorders that increase PNES risk include functional or dissociative disorders, post-traumatic stress disorder (PTSD), mood and personality disorders, co-occurring epilepsy, mild traumatic brain injury, cognitive or sleep problems, migraine, pain disorders, and even asthma.[14]
Conversion disorder has been traditionally considered the most common underlying psychiatric mechanism in PNES. However, this explanation is now being challenged by more complex theories emphasizing a multifactorial etiology encompassing biological, psychological, and social dimensions.[13] Conversion disorder, by definition, implies a lack of conscious awareness of the underlying psychological stressor and that the events are not intentionally feigned. The Diagnostic and Statistical Manual of Mental Disorders (fifth edition) (DSM-5-TR) categorizes PNES as a type of conversion disorder. In contrast, the 11th revision of the International Classification of Diseases (ICD-11) classifies PNES as a dissociative disorder. The International League Against Epilepsy (ILAE) recognizes PNES as one of the ten most critical neuropsychiatric conditions related to epilepsy.[8]
It is crucial to emphasize that a PNES diagnosis should never be based on isolated suggestive historical elements or seizure semiology. The interaction of various risk factors leading to PNES episodes remains poorly understood.[15] Reported psychological stressors that can precipitate or trigger PNES onset include parental conflicts and divorce in children, ongoing physical or sexual abuse, bereavement, and job or financial loss.[16]
Paroxysmal nonepileptic episodic events can also arise from physiological causes, which may be neurological or non-neurological. Neurological physiological antecedents include migraine, nonepileptic myoclonus, cerebrovascular ischemia or stroke, and parasomnias. Non-neurological causes encompass metabolic disturbances, cardiac arrhythmias, and syncope, especially when syncope is accompanied by tonic or clonic movements mimicking a “convulsive” syncope.
Epidemiological Insights into PNES
Recent systematic reviews provide valuable insights into the epidemiology of PNES. One review estimated the US incidence of PNES at 3.1 per 100,000 individuals, with a prevalence of 108.5 per 100,000.[1, 17] In outpatient epilepsy clinics, PNES is observed in 5% to 10% of patients, while in inpatient epilepsy monitoring units, the prevalence rises to 20% to 40%.[8] Interestingly, a study on generalized convulsive status epilepticus found that 10% of patients initially thought to have benzodiazepine-refractory status epilepticus, who received additional antiepileptic drugs after expert review, were ultimately diagnosed with PNES.[18]
Several risk factors are consistently associated with PNES. Female sex, psychiatric comorbidities such as depression, anxiety, and posttraumatic stress disorder, and a history of childhood sexual abuse are well-established risk factors. Other suggested risk factors include trauma, brain injury, surgical procedures, and learning disabilities.[8]
Pathophysiology: Unraveling the Mechanisms of PNES
The precise pathophysiology of PNES is still not fully elucidated. However, a growing consensus views PNES as a network disorder. This model suggests that a combination of genetic factors, emotional dysregulation, abnormal sensorimotor processing, and stress responses converge to produce PNES symptoms.[19]
Neuroimaging studies, both functional and structural, have provided some insights, revealing abnormalities in limbic system structures. These include the prefrontal, cingulate, and insular cortices, hippocampal and parahippocampal gyri, and the amygdala.[20] These areas are crucial for emotional processing, stress response, and motor control, suggesting their involvement in the manifestation of PNES.
History and Physical Examination: Clues to “What is PNES Diagnosis?”
Distinguishing PNES from epileptic seizures based solely on history and physical examination can be challenging. Early and accurate diagnosis is critical, as patients with PNES often experience significant delays in diagnosis and are frequently treated with inappropriate antiseizure medications and interventions, sometimes including intubation.
Table. Characteristics of Ictal Semiology That May Aid in Differentiating PNES From an Epileptic Seizure.
| Feature | Suggestive of PNES | Suggestive of Epileptic Seizure |
|---|---|---|
| Onset | Gradual, fluctuating | Sudden, stereotyped |
| Duration | Variable, often prolonged (>2 minutes) | Typically brief (seconds to minutes) |
| Frequency | Variable, may wax and wane | More predictable patterns |
| Triggers | Psychological stress, emotional triggers, light | Missed medication, sleep deprivation, hormonal changes |
| Ictal eye closure | Forced, resisted opening | Open, or may deviate |
| Head/body movements | Side-to-side, asynchronous, thrashing, pelvic thrusting | Rhythmic, tonic-clonic, stereotyped |
| Vocalization | Intelligible speech, crying out, screaming | Incoherent sounds, ictal cry |
| Responsiveness | Fluctuating, inconsistent | Loss of awareness, unresponsiveness |
| Postictal state | Rapid return to baseline, minimal confusion | Prolonged confusion, drowsiness, Todd’s paralysis |
| Injuries | Infrequent | More common (tongue bite, injuries from falls) |
References for Table: [8, 13]
Meta-analysis studies highlight that specific ictal semiology features can increase the probability of PNES. For instance, ictal eye closure and asynchronous limb movements have shown moderate to large effects on post-test probability of PNES. However, it is crucial to recognize that no single sign or symptom is definitively pathognomonic for distinguishing PNES from epileptic seizures.[21, 1, 21]
Auras, which are focal-onset seizures that can precede generalized tonic-clonic epileptic seizures (especially those originating in the temporal lobe), can also occur in PNES. This makes aura an unreliable differentiating feature. A prospective registry study comparing auras in PNES and epileptic seizures found similarities in their manifestation. Headache and dizziness/vertigo were frequently reported auras in PNES, suggesting they might lean “in favor” of PNES but are not diagnostically conclusive.[22]
Certain triggers and associated symptoms can offer clues. PNES events have been linked to light triggers, emotional stressors, pre-ictal and post-ictal headaches, post-ictal muscle soreness, and ictal sensory symptoms. In contrast, missed doses of antiseizure medications are a common trigger for epileptic seizures.[23]
It is essential to be aware of exceptions. For example, pelvic thrusting, bicycling movements, and abnormal posturing, often associated with PNES, can also occur in frontal lobe epilepsy, particularly with nocturnal onset.[24, 25]
The widespread availability of cell phone cameras has added a valuable tool in PNES diagnosis. Video recordings of events captured by witnesses can be analyzed by experts and have been shown to significantly aid in diagnosing nonepileptic seizures.[26]
Evaluation: Confirming “What is PNES Diagnosis”
The typical pattern of a generalized convulsive seizure involves an abrupt onset of tonic stiffening followed by synchronized clonic movements of the extremities, altered consciousness, and a postictal confusion phase. However, variations can occur, especially in focal impaired awareness seizures (previously known as complex partial seizures) originating in the frontal or temporal lobes. These seizures may present with unusual motor patterns or prolonged confusional states with subtle motor automatisms. When permitted by hospital policy and with appropriate patient consent, video recording of events can be invaluable for later analysis.
Noxious stimuli, such as ammonia capsules or painful stimuli (e.g., sternal rub), are sometimes inappropriately used to “wake up” patients suspected of feigning unresponsiveness or having nonepileptic spells. These methods should be avoided as they are not diagnostically helpful and can be harmful or traumatizing.
Accurate diagnosis is fundamental for effective PNES treatment. Misdiagnosis as epilepsy is common, leading to unnecessary prescriptions of multiple antiseizure medications. Neurology consultation is recommended in almost all cases of suspected PNES. The diagnostic gold standard for “what is PNES diagnosis” is capturing a typical event during video-EEG monitoring, combined with a history consistent with PNES.[1, 27] Video-EEG allows for simultaneous video and electrographic documentation of the event. In a seemingly unconscious patient, an alpha rhythm on EEG indicates underlying alertness. The absence of epileptiform activity on the EEG during an event strongly suggests a nonepileptic origin. However, caution is warranted as scalp electrodes may not capture all epileptic seizures, particularly those originating deep in the brain or with subtle surface manifestations.[1] Further investigation may be needed to differentiate PNES from a physiological nonepileptic event.[7] Short-term video EEG has been shown to be useful in diagnosing PNES in many cases.[28]
Laboratory tests have limited utility in PNES evaluation. Serum prolactin levels have been noted to increase after generalized convulsive seizures but typically not after PNES. Prolactin levels peak 10–20 minutes post-event and return to normal within an hour. While extensively discussed, prolactin levels have limited practical value in distinguishing PNES, as convulsive syncope can also elevate prolactin. Furthermore, prolactin levels do not reliably differentiate PNES from focal impaired awareness seizures or focal seizures with retained awareness.[29] A normal prolactin level does not rule out epilepsy or confirm PNES.[30] Prolactin is also unhelpful in distinguishing PNES from physiological nonepileptic events, although it can be elevated in convulsive syncope.[31] False positives can occur in individuals taking dopamine agonists or with breast stimulation, while false negatives can occur in frontal lobe epilepsy and even status epilepticus.[13]
Lactic acidosis is common after generalized convulsions. However, elevated lactate levels are not specific to epileptic seizures; elevations have also been observed in volunteers simulating generalized seizures.[32] A normal lactate level with high prolactin might suggest convulsive syncope.[31] Other biomarkers, such as white blood cell counts, neurotrophic factors, cortisol, and creatine kinase, have limited discriminative value and are not routinely used. Elevated creatine kinase levels have been observed after generalized convulsive status epilepticus but not psychogenic nonepileptic status epilepticus and may have some utility in distinguishing psychogenic status epilepticus from generalized convulsive status epilepticus.[33]
Neuroimaging is a standard part of the initial seizure workup, regardless of etiology. However, it lacks pathognomonic features to differentiate PNES from epileptic seizures. A study comparing individuals with PNES, major depressive disorder (MDD), and healthy controls revealed selective cortical thinning in the medial orbitofrontal cortex in PNES patients, while MDD patients showed wider regions of thinning. Somatoform dissociation was the only psychopathological assessment significantly different between PNES and MDD groups.[34]
Neuropsychological testing can offer helpful adjunctive information but should not be used to diagnose PNES in isolation. Following comprehensive clinical assessment and video-EEG, neuropsychological testing can guide further evaluation and is best utilized to integrate results into a treatment plan targeting the patient’s personality structure and cognitive strengths and weaknesses. Research into personality structure and psychiatric comorbidities in PNES indicates that patients with PNES more frequently exhibit isolated cluster B personality symptomatology compared to those with epileptic seizures. Structured personality inventories have demonstrated a statistically significant increased prevalence of borderline and depressive personality disorders in PNES patients.[35]
Treatment and Management Strategies for PNES
The initial and arguably most crucial step in PNES treatment is the manner in which the diagnosis is communicated to the patient. Empathy is paramount, emphasizing the “real” nature of the events and dispelling the misconception that “it’s all in your head.” It is vital to underscore that effective treatment options are available. Opinions vary regarding the preferred terminology – “seizure” or “event.” However, unless coexisting epilepsy is present, antiseizure medications are unnecessary and should be discontinued, a point that must be clearly communicated during diagnostic disclosure. If the PNES diagnosis is confirmed, ASMs should be withdrawn.[36, 37] A respectful and reassuring approach, highlighting the potential for supportive therapy to reduce or eliminate event frequency, is essential.
The optimal PNES treatment remains an area of ongoing research, often requiring individualized approaches. Addressing comorbid psychiatric conditions, such as PTSD and mood disorders, is a critical component of comprehensive care.
Supportive care should commence immediately following diagnostic disclosure. Some patients may initially resist the diagnosis and seek alternative opinions. Emphasizing the benefits of regular follow-up appointments for long-term outcomes is crucial. The neurologist who delivers the diagnosis should remain involved in the patient’s care to minimize feelings of abandonment, which can negatively impact treatment engagement.
Cognitive behavioral therapy (CBT) is widely recognized as the most effective treatment for PNES. A multicenter randomized clinical trial demonstrated seizure frequency reductions exceeding 50% with CBT alone and nearly 60% when CBT was combined with an antidepressant (sertraline). The trial also reported significant improvements in overall quality of life, mood, and global functioning.[13]
Differential Diagnosis: Ruling Out Other Conditions
Psychogenic nonepileptic seizures are essentially a diagnosis of exclusion. A wide range of paroxysmal events can mimic seizures or PNES, including syncope, arrhythmias, functional movement disorders, and other episodic conditions. Once other paroxysmal events are excluded, differentiating PNES from epileptic seizures remains a significant diagnostic challenge, even for experienced clinicians. The differential diagnosis for PNES includes:
- Convulsive syncope
- Sleep disorders, particularly arousal disorders and parasomnias
- Functional movement disorders
- Factitious disorder
- Malingering
Prognosis and Long-Term Outcomes
The long-term prognosis for patients with PNES is variable. Accurate identification of events and PNES diagnosis, coupled with treatment of psychiatric comorbidities and psychotherapy, can lead to a reduction in event frequency. Cognitive-behavioral therapy-informed psychotherapy shows promise in improving outcomes. Patient acceptance of the PNES diagnosis is also considered a positive prognostic factor.[10] However, despite these interventions, patients with PNES still face a significantly elevated mortality risk, more than double that of the general population. Mortality rates in PNES are comparable to those in drug-resistant epilepsy, with suicide accounting for as many as 20% of deaths in individuals with PNES.[38] Furthermore, PNES is associated with reduced quality of life, increased unemployment, and disability.[16]
Complications of Misdiagnosis and Inappropriate Treatment
Potential complications arising from the erroneous treatment of PNES as generalized status epilepticus include adverse drug reactions from antiseizure medications. One study reported cases where misdiagnosed PNES patients received massive doses of ASMs, leading to impaired consciousness or respiratory failure.[39] Unnecessary endotracheal intubations with iatrogenic complications have also been documented.[40, 41]
The Role of Consultations and Interprofessional Care
Neurology consultation, ideally with an epileptologist experienced in EMU settings, is virtually mandatory in all but the most obvious PNES presentations. A multidisciplinary care team, including primary care practitioners, social workers, psychiatrists, and psychotherapists skilled in CBT and other relevant therapies, is essential and should be involved promptly after diagnosis. Psychotherapeutic approaches, such as novel integrative psychotherapy, eye movement desensitization and reprocessing (EMDR) therapy, or mindfulness-based therapy, warrant further investigation in large-scale clinical trials.
Deterrence and Patient Education: Empowering Patients
Accurate PNES diagnosis is crucial for guiding appropriate interventions. Patient and family education about the psychological basis of the events and the withdrawal of antiseizure medications are beneficial in reducing event frequency. Patients should be counseled on the importance of attending follow-up appointments with both neurology and behavioral health teams to maximize the likelihood of reducing event frequency and improving overall quality of life.
Key Pearls and Considerations for PNES
Essential points to remember regarding PNES:
- PNES events are involuntary manifestations of psychological distress. Patients often feel unjustly accused of “faking” their events. If events are intentional, malingering or factitious disorder should be considered instead.
- No single sign or symptom definitively distinguishes PNES from epileptic seizures.
- Video-EEG monitoring capturing a typical event is crucial for PNES diagnosis in most cases, demonstrating no electrographic correlation during the “ictus.”
- A multidisciplinary team approach, with cognitive behavioral therapy as the primary treatment modality, provides the most effective patient care.
Enhancing Healthcare Team Outcomes through Collaboration
Optimal management of PNES necessitates a collaborative interprofessional healthcare team. This team includes emergency medicine and primary care clinicians, specialists (neurologists, psychiatrists, psychotherapists), nursing staff, pharmacists, and mental health support professionals. Effective communication and collaboration across disciplinary boundaries are crucial for achieving optimal patient outcomes. Consistent communication with the patient and family is essential. Neurologic evaluation and timely referral to appropriate psychiatric or counseling resources are vital steps in the care pathway.
Review Questions
(Link to review questions from original article)
References
(References from original article)
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