The founder of modern neurology, Charcot became a resident doctor at the Salpêtrière, a Parisian hospice for indigent patients, in 1862 and founded its neurology clinic in 1882, becoming the first professor of neurology in the same year. Among the diseases he described that still belong to the diagnoses used by contemporary neurologists were multiple sclerosis, ALS (initially dubbed Charcot’s disease, only later Lou Gehrig’s disease), Charcot-Marie-Tooth disease (a hereditary neuropathy of the feet and legs currently thought to be associated with changes in the myelin gene PMP-22), and Charcot joint (a progressive degeneration of the foot joints due to peripheral neuropathy that was associated with syphilis in Charcot’s day, diabetes in our own). He was involved in the elucidation of two neurological disorders, Parkinson’s disease and Tourette’s syndrome, that he proposed be named after his students, demonstrated the importance of the small arteries in cerebral hemorrhage, and made important discoveries concerning the related mechanisms of peripheral arterial disease such as intermittent claudication. Additional discoveries outside of the realm of neurology included Charcot's triad, the combination of fever, jaundice and upper abdominal pain associated with infection of the common bile duct; and Charcot-Leyden crystals, the needle-shaped phosphate crystals still considered a characteristic pathological finding in asthma. As Joseph Babinski, after whom the famous plantar reflex was named, put it, “to take away from neurology all the discoveries made by Charcot would be to render it unrecognizable.”
Charcot was clearly one of the virtuoso practitioners of nineteenth-century positivist empiricism. Prior to becoming a professor of neurology, he had served as a professor of anatomical pathology, deploying the clinical-anatomical method developed by the seventeenth-century Italian pathologist Giovanni Morgagni and refined by the French clinician Rene Laennec to correlate the clinical symptoms observed in patients with anatomic lesions discovered at the time of autopsy. He was among the founders of the field of neuroanatomy that remains centrally important to brain science today. For all its fruitfulness, however, Charcot’s method required no major technological innovation: the methods of gross anatomical pathology he employed in the elucidation of neurological disorders had already been developed by the eighteenth century, and Virchow had created the field of microscopic pathology earlier in the nineteenth. Even Charcot’s interest in photography was adopted from his mentor, Guillaume Duchenne. Indeed, it was where Charcot introduced new methods, experimenting with paramedical technologies of his day such as electromagnetism, that he caused the greatest damage to his reputation.
Eighteenth-century anatomical wax model in Museo La Specola, Florence. By this period, the methods of gross pathology were already in place.
Known to the fashionable crowds who gathered to see his Tuesday lectures as the “Napoleon of the Neuroses,” Charcot has sometimes been credited as the founder of psychopathology. His primary contribution to the field was his revival of the diagnosis of hysteria, which he regarded not as a form of malingering, as it had come to be regarded, but as a hereditary neurological disorder, focusing on symptoms such as motor paralysis, sensory loss, convulsions and amnesia. Many contemporary neurologists show a similar interest in rescuing conversion and catatonia as movement disorders. Charcot constructed maps of what he termed "hysterogenic zones" that are strikingly similar to contemporary diagrams of fibromyalgia points. He was never able to associate hysteria with any anatomical lesion, acknowledging that it could not be accounted for within the parameters of the anatomico-clinico method and was what would nowadays be termed a “functional disorder.” Still, he performed careful clinical experiments that demonstrated the physiological differences between hysteria (the muscular contractures of which he observed to be smooth), and malingering (in which such contractures were accompanied by muscle fatigue and progressively labored breathing). As Freud famously put it, Charcot threw “the whole weight of his authority on the side of the genuineness and objectivity of hysterical phenomena," defending the hysteric against charges that she was no more than a fake. The great American psychologist William James concurred, observing that "amongst all the many victims of medical ignorance clad in authority, the poor hysteric has hitherto fared the worst; and her gradual rehabilitation and rescue will count among the philanthropic conquests of our generation." More recently, the feminist psychiatrist Judith Herman has pointed to the paternalistic nature of this rescue attempt, observing that feminists a generation later would come to criticize Charcot for his "vivisection of women under the pretext of studying a disease" -- a charge weighted with some irony, since Charcot, a lover of animals, had banned all experiments that used vivisection at the Salpetriere.
Contemporary diagram of fibromyalgia points.
Although he gave the “nomadic uterus” and its fixation by what seem now like barbaric methods such as the uterine compression belt a central role in the treatment of hysteria, Charcot was famous for his insistence that hysteria was by no means specific to the female sex. Regarding male hysteria as underdiagnosed, he maintained that it was "not at all rare," occurring in men of all ages and social classes, even in those “without an effeminate exterior,” and relating it to traumas including railroad accidents and industrial work injuries. He saw the clinical presentation of male hysteria as similar to (although "less dynamic" than) the female version, with more static symptoms such as tunnel vision, hemianesthesia, and muscular contractures. "Little by little," he told his students, "you will acquire the habit of speaking of hysteria in men without thinking in any way of the uterus." Charcot thus did a great deal to establish a diagnosis that was to become extremely important with the appearance of shell shock during World War I, becoming the object of study of psychologists as diverse as William Rivers and Freud (and ultimately featuring in Walter Benjamin’s diagnosis of shock and the literature of modernity in poets such as Baudelaire).
Douglas Gordon, "10ms-1," a 1994 video installation with looped footage of a shell-shocked World War I soldier on infinite repeat
While the neurologist Christopher Goetz has proposed that Charcot “faltered...in attempting to impose on hysteria the clinico-anatomic strategy he had used previously with success," it would perhaps be more accurate to say that he was forced in the case of hysteria to depart from this method, with scandalous results. Goetz suggests that Charcot's work on hysteria can be divided into two phases, a descriptive phase prior to 1877 in which he was concerned to categorize the symptoms and isolate the patterns and phases of hysteria, and an etiological phase after 1877, in which he began his experiments in the auditorium in search of a cause. In the first phase, he worked with the graphic illustrator Paul Richer, seated at the table in Brouillet's iconic 1887 painting "A Clinical Lesson at the Salpêtrière" (a lithograph of which Freud kept in his study throughout his career) and later professor of artistic anatomy at the Ecole des Beaux-Arts, using medical illustration as a means of delineating the clinical features of the diagnosis. Later, he amplified this project by making additional use of photography under the direction of Albert Londe, the medical photographer of the Salpêtrière who later became an expert in x-ray photography. In the second phase, Charcot developed the hypnotic experiments that he conducted in the amphitheatre before an admiring public, noting, for example, that hysterical contractures could be removed if a patient passed into a lethargic state and made to persist if she became cataleptic.
At the Salpêtrière, Charcot thus discovered the existence of a “new disorder” that was not to be named after him, but which he termed “hystero-epilepsy." An account of the phases of the hystero-epileptic attack is found in his 1887 treatise authored with Richer, Les Démoniaques dans l’art. In this description, the attack began with a prodrome that often appeared several days in advance, in which the patient became taciturn and melancholic or suffered from over-excitement, often vomiting or losing her appetite. This phase was sometimes accompanied by visual hallucinations (such as visions of animals), cramps or trembling limbs and a jerking body along with vertigo. Just prior to attack, there was an hysterical aura, followed by loss of consciousness as the attack proper began. The initial epileptoid phase mimicked a seizure and could, Charcot noted, easily "be mistaken” for one, lasting 1-3 mins. and consisting of three phases. The tonic phase was described as starting with a momentary arrest of inspiration and pallor, followed by flushing and facial distortion, including protrusion of the tongue. It ended with a tetanous immobilization that frequently involved extension of the trunk and limbs, followed by the clonic phase, a large generalized seizure accompanied by grimacing. This was followed by the phase of resolution, in which the eyes were closed and the muscles completely relaxed. These phases lasted about a minute each, the resolution phase 2-3 minutes.
The second phase of the attack was described as the “period of clownism.” After a moment of calm, it was characterized by contorsions and “grand movements,” phenomena that Charcot saw as linked by “an exaggerated discharge of muscular force.” It was in this phase that the famous arc-en-cercle, or arching of the back, took place. At this point, the patient was capable of displaying “a suppleness and agility, a muscular strength that may astonish the spectator.” With delicate discernment of gender differences, Charcot noted that women might significantly exceed the physical strength expected of their age and sex, whereas “in men, this period sometimes achieves a degree of violence that exceeds anything one can imagine.” It was also this phase that Charcot linked to the demoniacal possession of religious ecstasy examined in Les Demoniaques dans l'art. The third phase was described as a phase of "plastic poses" or what he termed "passionate attitudes," lasting from 5-15 minutes, in which the patient displayed happy, sad or frightened affect, often speaking or shouting. In the terminal phase, similar to the epileptic's post-ictal state, the patient at least partly regained consciousness, although she might remain delirious for periods of up to an hour.
As Goetz points out, Charcot never liked the term "hystero-epilepsy," with its implication that hysteria could be classified as a form of epilepsy. Although he noted that the hystero-epileptic attack resembled true epilepsy, and also that the latter sometimes occurred in conjunction with hysteria, he regarded the two disorders as distinct. "We are dealing always and exclusively with hysteria," he declared, "but hysteria taking on the appearance of epilepsy" (italics mine). Hystero-epilepsy was not a separate diagnosis, but one of many possible manifestations of hysteria. "It is likely that hysteria in the guise of epilepsy is only an exaggerated form," he insisted, "the highest development of this tonic variety of ordinary hysteria."
In the end, it was hysterico-epilepsy that led the Napoleon of the Neuroses to his
This version of Charcot's career is reiterated in influential histories of psychiatry and psychoanalysis such as Henri Ellenberger’s The Discovery of the Unconscious. The basic elements of Babinski’s and Munthe’s critique are also adopted in Didi-Huberman’s Invention of Hysteria. (see also Baer) Indeed, it is common among the media theorists who have focused on the visual regimes governing Charcot’s conception of hysteria to assume that he “invented” a disorder that no longer exists. Friedrich Kittler, for example, observes that "the 'great hysterical arc' can no longer be found in the lecture halls of today's medical schools," arguing that Charcot’s hystero-epilepsy should be understood as an effect of filmic technologies that "disappears from nosology of the world shortly after its storage on film.”
By comparison, psychiatrists continue to believe that what Charcot termed hysteria continues to exist. Guillain, a biographer of Charcot who served as a psychiatrist at the Salpêtrière in the 1960's, compared the percentage of cases diagnosed as hysteria by Charcot with those he himself later diagnosed at the same institution, finding that "the patients have not changed since Charcot's times, but the terminology applied to them has." While one well-known study has shown that the misdiagnosis of conversion disorder has decreased since the dramatic advances in neurology's use of diagnostic imaging (with 50% of cases initially diagnosed as conversion in 1965 later found to have neurological disease, whereas misdiagnosis is now thought to constitute between 4 and 10% of cases), it is still estimated to constitute 1-4% of diagnoses in Western hospitals. "The symptoms themselves have never changed," Patrik Veilleumier, a neurologist at the
Neither the media historians nor the psychiatrists appear entirely correct. While hysteria was not the invention of Charcot’s nineteenth-century positivism and it did not disappear with decline of filmic technologies for the recording of clinical presentations, hysteria has been changed by its contemporary incarnation as conversion disorder. In what follows, I will attempt to examine the evolution in the visual economies of hysteria that has occurred between Charcot and the present day.
In the DSM-III in 1980, psychogenic conversion was definitively stripped of all association with the uterus when "hysterical neurosis, conversion type," was renamed "conversion disorder," now defined as the production of quasi-neurologic symptoms such as blindness, paralysis and seizure. In the New York Times, William E. Narrow, associate director of the research division of the American Psychiatric Association, remarked that "hysteria, to me, has always been a pejorative term, because of its association with women. I think the fact we got rid of that word is a good thing." He could, perhaps, have been more precise, since the word he presumably meant to 'get rid of' was the uterus, never more than a metonymy for woman as such, and really more the etiological misattribution of a symptom to an unsubstantiated underlying anatomical defect. Ultimately, the new nomenclature was the culmination of Charcot's insistence that his students "should acquire the habit of speaking of hysteria ... without thinking in any way of the uterus." Indeed, the contemporary criteria for conversion disorder enumerated in DSM-IV bear such remarkable similarities to Charcot's view that one might argue that they constitute a re-neurologization of hysteria, the ultimate effect of which is the elision of any psychoanalytic explanation of hysterical symptoms on the level of unconscious desire.
The most basic criteria for the diagnosis of conversion disorder is the presence of "one or more symptoms or deficits affecting voluntary motor or sensory functioning that suggest a neurological or other general medical condition." As with many diagnoses in the DSM, conversion disorder requires that the symptom not be "fully" (the term is generally "better") explained 'by a general medical condition or as the direct effects of a substance,' thus acknowledging that conversion, while it suggests a neurological condition, lacks an organic lesion and thus eludes the clinico-anatomic method still encapsulated in the neurologist's demand to "localize the lesion." Considerable care is nonetheless taken to differentiate conversion from two DSM diagnoses characterized by the voluntary production of somatic symptoms, namely malingering (in which both the production and the motivation of symptoms are voluntary) and, more subtly, factitious disorder (in which the production of the symptoms may be voluntary, but their motivation remains obscure to the patient and occurs on the level of primary gain). Medical science thus remains torn between continuing to defend the hysteric's honor against charges of faking and the more troubling realization that conversion continues, whatever the patient's intention may be, to present the false appearance of a neurological disorder. Conversion has still not been rid of its dangerous capacity for representation-as-dissimulation and, worse still, for making a fool of the physician.
The second major criterion, which falls short of offering an etiological account of conversion, is the judgment that psychological factors are present since 'the initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors.' Charcot's patient Augustine, who maintained, like many other female hysterics in the Salpêtrière, that she had been raped (in her case by her employer at razor point at the age of 13), would fit both criteria, since her seizures were both manifestly neurological in appearance and had a psychological stressor as their immediate precipitant: "A few days [after the rape and the subsequent onset of bleeding, mistaken for her first menses], [she] was lying in her room and became frightened when she saw the green eyes of a cat looking at her; when she cried out, her mother arrived to find her utterly terrified and bleeding from her nose. Then the attacks broke out..." The basic phenomena that interested Charcot (motor contractures, opthalmological symptoms, and the notorious hystero-epilepsy) remain largely unchanged in the four subtypes of conversion disorder, 'with motor symptom or deficit,' 'with sensory symptom or deficit,' 'with seizures or convulsions' (with which Augustine would presumably have been diagnosed) and 'with mixed presentation.' Perhaps the major departure is the stipulation that the symptom cannot be explained 'as a culturally sanctioned behavior or experience,' a common gesture in the DSM that in this case serves to exclude the intimate association between hysteria and female religious experience that interested Charcot so much.
Interestingly, the misdiagnosis of conversion disorder is thought to have decreased since the dramatic advances in neurology's use of diagnostic imaging tools: in 1965, 50% of cases initially diagnosed as conversion were later found to have neurological disease, whereas misdiagnosis is now thought to constitute between 4 and 10% of cases. It is estimated to constitute 1-4% of diagnoses in Western hospitals. Goetz observes that Guillain, a biographer of Charcot who served as a psychiatrist at the Salpêtrière in the 1960's, compared the percentage of cases diagnosed as hysteria by Charcot with those "he himself diagnosed at the same institution over a comparable period in our century," finding that "the patients have not changed since Charcot's times, but the terminology applied to them has." "The symptoms themselves have never changed," Patrik Veilleumier, a neurologist at the
So what has become of what Charcot termed hystero-epilepsy? It, too, survives largely intact as the disorder currently known as PNES, or "psychogenic non-epileptic seizures." Once again, a fair amount of ideological position-taking is wrapped up in a name. Thus, from a summary of the literature on PNES for use by clinicians: "the terms 'hysterical' seizure or 'hysteroepilepsy' are now discouraged as both pejorative and oversimplified, failing to capture the broad range of psychopathology ... The term 'pseudoseizures' is also discouraged, since the root 'pseudo' or false invalidates the genuine, even if psychogenic, disorder that a patient experiences." As with conversion disorder, any reference to the uterus is to be avoided as much because it is regarded as disparaging or belittling as because it has been shown to be inaccurate, although in this case a concern is also expressed that it implies a single etiology that belies the considerable variety of underlying psychopathology. The term 'pseudoseizures' is similarly problematic because it implies that psychogenic seizures are disingenuous, thus perpetuating the clinician's chivalrous defense of the hysterical patient's honor. Still, the word 'mimicry' continues to feature prominently in the definition of psychogenic seizures, defined as "events that clinically mimic epileptic seizures but are not associated with physiological CNS dysfunction and are instead psychogenically determined." PNES thus constitutes a case of genuine mimicry, which is to say that it moves the production of mimetic symptoms onto the level of the unconscious (or, in the more neutral language of neurology, the involuntary) without denying that the nature of these symptoms is the production of false appearances.
While the patient's intention thus represents a crucial moral issue in the diagnosis of PNES, the production of false appearances continues to constitute the central challenge for the neurologist, whose primary goal is to accurately differentiate between psychogenic and epileptic seizures. The costs of missing a diagnosis of PNES are presented primarily in terms of the dangers of unnecessary treatment with antiepileptics, with the associated risk of drug toxicity, a consideration that is not insignificant given the association of these drugs with major side-effects such as congenital birth defects and Stevens-Johnson syndrome. The concern is presented as especially serious in the case of the psychogenic production of status epilepticus (seizures lasting more than 30 minutes), in which protocols call for the administration of toxic levels of antiepileptics as well as invasive procedures such as intubation and iatrogenically-induced coma. This may be a particularly significant consideration since one of the characteristics of psychogenic seizures is that they tend to be of longer duration than epileptic seizures, which typically last less than a minute. It is also pointed out that anti-epileptics administered during pregnancy carry significant risk of birth defects, a particularly relevant issue given that the female predominance of PNES is estimated to be between 65 and 90%, with the most common onset in the third decade of life, i.e. during the child-bearing years. Still, one wonders whether the increasingly widespread use of antiepileptics by psychiatrists for their mood stabilization properties reduces the force of this objection. In the rather chilling language of medical cost-benefit analysis, an additional reason given for the need for an accurate diagnosis is that it precludes unnecessary ER visits and hospitalizations, which "place a cost burden on the healthcare system." How great the societal burden of hysteria really is or how it compares, for example, to the use of xx remains unexplored. Finally, it is stated that an accurate diagnosis is required in order for the patient to receive necessary psychiatric treatment, despite the fact that the results of such treatments (which include individual psychotherapy, group therapy, and family education) are acknowledged to be mixed, none holding out hope for a reliable resolution of symptoms.
Such concerns are reiterated in the context of the common procedure of provoking seizures in patients who do not produce them spontaneously when admitted on an inpatient basis for EEG monitoring, the gold standard both for the diagnosis of epileptic seizures and for their differentiation from PNES. When PNES is suspected, this is frequently done by administering a placebo in the form of IV saline or rubbing alcohol on the skin. Indicating the special power of suggestion in psychogenic seizures, "67-90% of patients with [this disorder] will have a typical event" when informed that such treatments are likely to produce an episode, whereas the occurrence of epileptic events is considerably lower. "While facilitating diagnosis, the inherent deceit in this approach may jeopardize the physician-patient relationship and impede future treatment efforts," the authors concede. "However, many experts believe that these considerations are outweighed by the benefits of making an accurate diagnosis and avoiding future morbidity associated with inappropriate treatments." The neurologist is presumably less concerned than other members of the treatment team with the consequences of such an approach because his goal once an accurate diagnosis has been established is to withdraw unnecessary treatment and transfer care to an appropriate psychiatrist.
As it turns out, the differentiation between psychogenic and epileptic seizures has not been as greatly clarified by the use of diagnostic imaging as might be expected. While video EEG, which allows for a comparison of clinical and electrographic features, is considered the gold standard, "caution is required for interpretation" since "failure to see an electrographic seizure does not exclude epilepsy." Thus, while the majority of generalized tonic-clonic seizures show signs of ictal activity on EEG, only 15-33% of simple partial seizures or seizure auras will do so, either because they involve limited brain area or because they are not of superficial origin. In turn, 10-18% of PNES patients will demonstrate intraictal epileptiform abnormalities, despite the fact that they are generally characteristic of epilepsy. A highly specific EEG finding for PNES is "preictal pseudosleep," the clinical appearance of sleep with an EEG that demonstrates wakefulness, although failure to obtain this finding does not rule out PNES. The diagnosis of PNES thus requires a careful comparison of clinical events with EEG changes that may constitute an art as much as a science.
Moreover, there is no single clinical feature that is either sensitive (i.e. a criterion for ruling in) or specific (a criterion for ruling out) for PNES, so that a total clinical picture is required to support the diagnosis. The feature that is described as most characteristic of PNES is the frequent occurrence of episodes in front of a witness, with occurrence in a doctor's waiting room or exam room estimated to have a 75% predictive value for the disorder. Unlike epileptic seizures, psychogenic seizures also do not tend to occur during physiologic sleep (although a phenomenon of xx is considered consistent with PNES), and they are, somewhat surprisingly, less likely to be precipitated by stress or around the time of menstruation. The description of the ictal period in the two disorders is quite distinct. Whereas the ictus of an epileptic seizure is usually brief, lasting less than 1-2 minutes, a psychogenic seizure may last considerably longer, with 78% reporting an episode that qualifies as status epilepticus. While psychogenic seizures are characterized by unresponsive behavior accompanied by motor manifestations that most often mimic either a generalized tonic-clonic or a complex partial seizure, including elements such as tonic posturing and synchronized convulsion (mimicry of atonic, absence or simple partial seizures is considered less common), the patient's eyes are usually open during a generalized tonic-clonic seizure, whereas they may be forced shut during a psychogenic seizure, suggesting the retention of consciousness (in general, incomplete loss of consciousness is considered suggestive of PNES). Whereas motor activity during an epileptic seizure is described as stereotyped, synchronized and progressive, with consistent lateralization, in psychogenic seizures it is more likely to be asynchronous and variable, with a waxing and waning course. Specific movements suggestive of psychogenic seizures include writhing, thrashing, pelvic thrusting, opisthotonus (the famous arched back or arc-en-cercle) and jactitation (rolling from side to side). Vocalization, weeping and icteral stuttering all occur more commonly during psychogenic than epileptic seizures, whereas tongue-biting (especially xx), incontinence and self-injury are more characteristic of epileptic seizures, along with autonomic symptoms such as cyanosis and tachycardia. Finally, the post-ictal period is also distinct: whereas there may be a period of confusion and drowsiness accompanied by headache after an epileptic seizure, headaches are rare following psychogenic seizures, with the patient more likely to reawaken and reorient rapidly and to demonstrate shallow, rapid respirations suggestive of hyperventilation. Interestingly, the symptomatology of PNES is considered most closely related to frontal lobe seizures, although the latter is more likely if seizures are of short duration, they occur during sleep, motor manifestations are stereotyped and the patient's eyes remain open during ictus, whereas a lack of reduction in seizure frequency with antiepileptic drugs or failure to respond to protocols for status epilepticus suggest psychogenic seizure.
We can recognize in this clinical description a number of the key features of Charcot's staging of hysteroepilepsy worked out during the initial nosological phase of his study of hysteria. Although Charcot draws a distinction between an epileptoid phase lasting 1-3 mins. and a clownism phase of similar length that are not differentiated here, the "bizarre posturing" of the hysteric so copiously illustrated in Richer's drawings is clearing recognizable in the writhing, thrashing, pelvic thrusting, opisthotonus and jactitation described as features of the psychogenic ictal phase. The frequent weeping, vocalizations and icteral stuttering that also distinguish PNES correspond to Charcot's emotional phase, in which the patient may display a variety of emotions as well as speaking or crying out. Features of autonomic instability such as incontinence, cyanosis and tachycardia considered more commonly associated with epileptic seizures are not described in hysteroepilepsy. Although the postictal phase is characterized somewhat differently, Charcot speaking of a partial reacquisition of consciousness with a prolonged period of delirium, whereas PNES is thought to have a more rapid postictal reawakening and reorientation, it is emphasized that the latter does not always differentiate the disorder from epilepsy. Friedrich Kittler's observation that "the 'great hysterical arc' can no longer be found in the lecture halls of today's medical schools" (and his concomitant proposal that the invention of hystero-epilepsy should be understood as an effect of filmic technologies that "disappears from nosology or the world shortly after its storage on film") thus seems spectacularly wrong.
If Charcot stumbled in his attempt to provide an etiological explanation for hysteroepilepsy, modern neurology is considerably more circumspect in its willingness to venture an explanation for the disorder's causes. Thus it is only possible to speak of a number of psychiatric disorders that "commonly coexist" with psychogenic seizures, including depression, anxiety, somatoform disorder, borderline or other personality disorders, dissociative disorder, and PTSD. By comparison, schizophrenia and depression with major psychosis are relatively rare associations. 33-50% of patients have a history of physical or sexual abuse, which in the latter case carries with it the risk of a clinically more severe condition that is more likely to resemble epileptic seizures. Dysfunctional family relationships are common. Psychosocial stressors that may precipitate the emergence of PNES include bereavement; unwanted pregnancy; physical, verbal or sexual abuse; lawsuits; financial difficulties; job pressures; impending divorce; domestic conflicts and assault. In children, precipitants include separation anxiety, school avoidance and parental conflicts. A history of neurological insults such as prior head trauma is present in 33-44%, and neurological developmental disabilities are relatively common. Still, the authors warn that it is "impossible to distinguish comorbid from etiologic psychiatric conditions at the present time." Moreover, it is "unproven whether dissociative disorders and somatoform/conversion disorders underlie PNES."
The most provocative hint towards an explanation for the mechanism, if not the etiology, of psychogenic seizures is provided by a recent SPECT study. Demonstrating the continued significance of affective dysregulation in the production of the motor symptoms of conversion, the study demonstrated that conversion disorders may occur when primary motor cortex is overriden by parts of the brain involved in emotion such as the right orbitofrontal and right anterior cingulate cortex.
