Psychogenic non-epileptic seizures: so-called psychiatric comorbidity and underlying defense mechanisms

Abstract

Historical background

Historically, phenomena of functional etiology were of relevant interest in the context of phenomenological psychiatry and were described as hysterical phenomena, recognizing for as a specific psychopathological dimension.¹ Until the advent of dynamic psychiatry, epileptic seizures (ES) and psychogenic non-epileptic seizures (PNES) were considered nearly the same, since it was not possible to distinguish between them, either on the level of instrumental evidence, or on the phenomenological level of the symptom manifestations. PNES differ from ES for some clinical signs but in most cases, a clinical distinction is not possible (Table 1).

Only with the growth of magnetism works, came the first “scientific” distinction between ES and PNES. In 1870s, at the school of Salpêtrière, Charcot² seemed able to distinguish between ES and PNES, and the possibility to achieve the disappearance of the symptoms, or at least an improvement using hypnotic practice.

In France, Charcot² and later Babinski,³ focused their research on hysteria, stating that hysteria was a psychic state which made the subject capable of autosuggestion; therefore, hysterical symptoms may (unlike nervous system disorders) be triggered in the patient by suggestion (phenomena called “pithiatic”).

The traumatic origin was initially supported by Breuer and Freud’s “seduction theory”, but the same authors later considered PNES as complex issues in which biological thrusts and emotional factors were involved and connected.⁴ An instability of the ego (theory of Pierre Janet⁵), a strong predisposition of the female sex, the presence of a secondary benefit, and the so-called “belle indifference” were specific for the hysteria.

PNES are actually considered paroxysmal and involve involuntary attacks or behavioral changes characterized by sudden and temporary alteration of motor, sensory, autonomic, cognitive, and emotional control, whose critical content is similar to those observed during ES, but without electrical alterations or pathological modifications of the electroencephalography.⁶ The PNES are in fact a nonintentional expression of emotional distress.⁷ The semiology of these attacks is various: generalized movements, either tonic (stiffness), clonic or dystonic, absence of movement (aki nesia), falling, focal motor movements or experiential phenomena reported by the patients (fear, anxiety, dreamy state, paresthesia, etc); nevertheless, a universally accepted classification has not been done yet.

Due to their similarity to ES, those phenomena that were similar to ES but did not have the same electrophysiological etiology, were labeled simply as “non-epileptic seizures” without further investigation, and relegated to a care setting that was foreign to the neurologist and poorly understood by the psychiatrist, confined in a sort of “land of anyone”.

Concerning the nosography, after the transition from the Diagnostic and Statistical Manual of Mental Disorders (DSM)-II to DSM-III, the terms “neurosis” and “hysteria” disappeared. Symptoms were broken up to their individual phenotypes and deprived of their meaning into experience and history of the subject.⁸ After the publication of DSM-IV TR,⁸ the classification of PNES no longer has found a unique and proper place as they are distributed in different categories: conversion, dissociative, and somatization disorders. In a recent small study,⁹ 63% of patients were diagnosed with conversion disorder, 19% with somatization disorder, 7% with dissociative disorder not specified, 7% with post-traumatic stress disorder (PTSD), and 4% with undifferentiated somatoform disorder. PNES are likely to be confused with a framework which “could be epilepsy but is not”, and therefore be relegated to a lower level tagged as a comorbidity of something else. In the DSM-5,¹⁰ the theoretical point of view has changed a lot; the new classification of “somatic symptoms and related disorders” defines the major diagnosis on the basis of positive symptoms (distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response to these symptoms). However, unexplained medical symptoms remain a key feature in conversion disorder and PNES do not have the specific place where they are needed yet. Stone et al¹¹ supported the current DSM classification affirming that the arguments in favor of splitting off PNES from other neurological symptoms are not as strong as keeping them together (wherever they are placed in DSM-5).

The ICD-10¹² places the PNES in the dissociative disorders, although, unlike the DSM-5, it merges dissociative disorders and conversion disorders even if the underlying defense mechanisms are different.

The risk is to create a “cauldron” where every different manifestation, which is rarely understood in their clinical significance and symptomatic expressiveness, is likely to be found together.

The present work intends to assess, due to the current lack of literature, what are the clinical conditions that characterize the phenomena we call PNES could be, particularly in light of the so-called psychiatric comorbidity and the underlying defense mechanisms that are not taken into account in the other studies.

Psychiatric disorders and PNES: can we talk about comorbidity?

In the literature, the comorbidity between PNES and other psychiatric disorders is frequent^13,14 as, in a study conducted by Turner et al,¹⁵ all patients with PNES had a psychiatric diagnosis. A recent review estimates that the prevalence rate of depression in adults with PNES is between 21% and 60%.¹⁶ This rate is higher than in the general population^16,17 and in patients with ES.¹⁶ Depression is correlated with a lower level of functioning and to a worse quality of life,^17,18 although in patients with PNES the quality of life is lower than in patients with ES even without a diagnosis of depression.¹⁷ The type of depression symptoms seems to differ between PNES patients, who show more physiological symptoms of depression, and ES patients.¹⁹

The prevalence of anxiety disorders (especially for PTSD) is higher in PNES than in the general population and in drug-resistant epilepsy.^20,21 More specifically, many patients who have PNES have features of PTSD and 22%–100% of patients with PNES fulfill the DSM-5 criteria for PTSD.²² In the patients with comorbid PTSD, the hypomotor semiology seems to be predominant,²³ as well as in patients with PNES only than in patients with comorbid PNES and ES.²⁴ Depression and anxiety ratings are higher in the presence of trauma.²⁵ Data on psychosis are scarce, but the prevalence of psychosis in PNES seems to be the same²² or even lower²⁰ than in the drug-resistant epilepsy.

Personality disorder (especially of cluster B) seems to be correlated with PNES^16,26 even more than depression and anxiety.²⁷ Significant differences between patients with PNES and patients with ES and healthy controls were found in two recent cohort studies in cluster B personality disorders (but not in depression and anxiety disorders).^15,28

Two studies comparing the Personality Assessment Inventory (PAI) patients with PNES and patients with ES and healthy controls showed more disorders of the subscales related to somatization disorders and conversion disorders in patients with PNES.^29,30 Similarly, a significant difference was detected in somatic subscales with the Minnesota Multiphasic Personality Inventory (MMPI) between patients with PNES and patients with insomnia.³¹

All these findings are summarized in Table 2.

Defense mechanisms

Defense mechanisms are unconscious psychological tools that are useful in maintaining the intrapsychic balance of the subject, especially, though not exclusively, in situations with deep anxiety or stress. According to the structural model, defense mechanisms are totally unconscious processes activated by the ego under the pressure of anxiety to prevent the trauma recall and the emergence of instinctual wishes not satisfactory on a conscious level. In case of traumatic or hard-to-manage contents, the individual can develop a defense mechanism to avoid contact with this type of experiences that may reactivate painful sensations or memories; this is a normal psychological procedure, as it leads to the individual’s self-preservation and to a beneficial adaptation. However, if there is a separation between the affective and emotional content and the consciousness, a nonadaptive behavior can lead to the rise of pathological states.

The defense mechanisms in relation to the PNES

Patients with PNES are often related closely to subjects with “hysterical” type disorders (somatization and conversion), and are often correlated with anxious or depressive disorders. In these cases, the symbolic function is preserved, as patients use defensive mechanisms belonging to the neurotic register as repression, reactive formation, retroactive annulment, displacement, and affect isolation.³⁴ Defense mechanisms belonging to the so-called “Style 1” are not excluded and indicate a more regressive situation linked to the inability to integrate pulses, such as autistic withdrawal, acting out, inhibition, passive aggression, and projection.⁴³

The majority of patients with PNES have alexithymia traits, meaning that they had difficulties in feeling or perceiving emotions.^7,25,44,45 The role played by the bodily expression of the disorder, as well as the presence of a repression process that drives most disturbing elements in the unconscious (tendency to minimize the critical event and to focus attention more on the context), is undeniable.

Various studies that used conversational approach in the differential diagnosis between ES and PNES^46–48 showed that individuals with PNES are very vague, while people with ES are very precise in the description of seizures, with an attempt to overcome the gap, or interruption of the existential continuum. This further shows the “functionality” of this gap inside a defense mechanism, whose aim is to lead to a split, either vertical or horizontal. In the stories of individuals with PNES, the gap is maintained, even if they do not actually lose consciousness, their descriptive effort is directed fully to the context, which is addressed to their symptomatic and bodily message. By contrast, in patients with ES, even in front of a loss of consciousness, the effort is all about the story reconstruction, even imaginary, of the gap, because they experienced the seizure as intrusive and unexpected.⁴⁹

In subjects whose PNES are associated with a borderline personality structure, in which the symbolic function is lost or significantly damaged, the defense mechanisms are not only archaic in nature for mainly dissociation (which reconnects to primitive idealization), but also denial, omnipotence, devaluation, and the split.³⁴ According to Bond,⁴³ the defensive style of borderline structures could be defined as “Style 2”, which is characterized by an image distortion through splitting, primitive idealization, and almighty devaluation. As in the borderline personality disorder, the subject with PNES lives the separation and alternation, almost compartmental, between opposing states of their own experience (presence or absence of seizures) and appeals to denial when the traumatic reality (seizure) is disregarded inside the horizontal split. Even in this case, the narrative experience of not reconstructing the gap is understood.

Patients with PNES can also have different coping strategies. A high emotion-focused coping was seen in patients with underlying psychological symptoms that were not observed in other coping strategies. This information supports the relevance of assessing stress coping in patients with PNES because it allows the identification of useful behavioral targets for the psychotherapist.⁵⁰

For these reasons, PNES with different underlying defense mechanisms need usually a different treatment (pharmacological or psychological). The relationship between the type of PNES and defense mechanism involved has not been studied yet in the literature.

Discussion

In recent decades, the defense mechanisms are being increasingly considered in their clinical sense, not as mental operation, which have the function to protect from anxiety, but rather as structures specialized in the solution to psychic conflicts⁵¹ which mediate between desires, needs, feelings, and impulses of the individual, on the one hand, and internal prohibitions and external realities, on the other hand. They, therefore, constitute a creative synthesis, are relatively involuntary and unconscious, and can distort internal and/or external reality.⁵²

Bromberg⁵³ affirms that “Dissociation, such as repression, is a healthy and adaptive function of the human mind.” It is a basic process that allows individual states of the self to work in an optimal way (and not only in a simply defensive way), when we really need or want to have a full immersion in a single reality, a single strong affection, and a suspension of the auto-reflexive ability. In other words, the dissociation is, first and foremost, a means by which a human being keeps personal continuity, consistency, and integrity of the sense of self.⁵³

Patients with PNES displayed somatoform dissociation to a greater extent than those with ES, but this difference was not retained when statistically controlling for anxiety scores or demographic and seizure variables.⁵⁴ A recent study carried out by Kaplan et al⁴⁴ compared patients with ES and patients with PNES on their defensive style, using the response evaluation measure, and did not find any difference between the two groups.³⁷ In addition, different problems of emotion processing may predominate in the same patient at different points of their disorder.⁵⁴

As suggested by Brown et al⁵⁵ and Baslet,⁵⁶ at the basis of the etiopathogenic mechanism of PNES and some ES in its expression of “dissociation”, there could be the same disconnection of brain areas involved in different cognitive and emotional functions. When either an epileptic or a psychogenic event occurs, there is a “dissociation” of behavioral and attention systems with a “gap” between the usual systems and the symptoms that emerge during the seizure. According to Roberts and Reuber,⁵⁴ neural mechanisms underlying these processes have begun to be explored in PNES, and relevant models have been developed more fully in related states or conditions such as PTSD, dissociation and depersonalization, and borderline personality disorder.

When there is no organic correspondence explaining and justifying some physical states, we enter a field where the presented symptoms convey meanings that have to be interpreted and processed; this definition seems to recall vaguely the one that Freud used to describe the pathology of hysteria.

During the ES, there is a hyperactivation of a specific part of the brain, while the remaining is excluded; in case of complex partial epilepsy, dissociative symptoms may occur because patients during ictal and postictal phases may exhibit wandering or semifinalized behaviors resulting in amnesia; amnesia for the event or feelings of déjà vu, like in epilepsy of the temporal lobe, are also possible phenomena of denial of sensory data.

There is an element that connects the experience of any critical event, being of epileptic or psychogenic etiology (a “split”), between different states of mind awareness.

Both ES and PNES present a dysfunction in emotional processes or to gain from dissociation (in Bromberg meaning)⁵³ to cope with a traumatic event.

Not surprisingly, many studies have highlighted that the prevalence of severe traumatic events, such as child sexual or physical abuse, is present in patients with PNES in a percentage that goes from 32.4% to 88.0%. A history of trauma affects in a negative way alexithymia traits and adherence to psychotherapy.^7,45,57

There is an attempt to cope with a trauma, trying to depart from it, and not to be disintegrated by it; in the case of PNES, such an attempt is made using the body at a symbolic level. The affection that cannot be verbalized is shown in different ways: more advanced in the case of a neurotic structure and more archaic for the borderline one, where the symbolic level is more lacking.

In PNES, the body is only a vehicle, a medium; the trauma does not originate from the person and his or her manifestations, but from a previous emotional “engorgement” that materializes through the body.

Patients with PNES report more negative life events and they do not indicate them as triggers of their seizures. However, patients with epilepsy correlate more of their negative life events to seizures.^7,56 In PNES, traumatic experiences are also accompanied by dissociative phenomena, since many of these seizures represent a complete or partial loss of integration of mental functions such as identity, memory, consciousness, and environment perception. From this point of view, the split no longer belongs exclusively to the defense mechanisms, but arises as a process that distinguishes mental states that accompany the human experience, both in its healthy expressions and in its pathological ones, and thus becomes an experience of how the psychic apparatus is structured under certain circumstances.

At this point, we have to do with a framework with its own statute and dignity. PNES are the symptomatic expression of a psychiatric disorder itself, and we should talk about an underlying etiological diagnosis instead of psychiatric comorbidity. The PNES indicate a way to “convert” psychological distress on organic level by replacing the verbal with a representation of symptoms.

The most appropriate part of PNES definition is that of “psychogenic” seizures, as that term encompasses the variety and depth of the exhibited symptoms as well as the types of underlying defense mechanisms.

Following this trend, traits seem to emerge connected to a disease, apparently disappearing like hysteria, and, therefore, it is almost natural to recall Mattioli and Scalzone⁵⁸ who argued that

[…] the hysterical pathology will never disappear because it represents a specific state of mind, an operational mode, characterized by an psychodynamic organization made up of defense mechanisms, cognitive styles, memory functions, personality traits and psychological and somatic symptoms.⁵⁸

Conclusion

PNES are the result of differences in brain processes and that of defense mechanisms. Consequently, prognosis and different pharmacological or psychological treatment should be need. Thus, it appears superfluous to talk about psychiatric comorbidity, since PNES are a different symptomatic expression of specific psychiatric disorders.

Footnotes

References