Jean Martin Charcot Pseudoseizures

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Psychogenic pseudoseizures are paroxysmal events which mimic epileptic seizures. While patients suffering from these symptoms are referred to neurologists because they are mistakenly believed to have epilepsy, neurologists consider the underlying disorder to be of psychological aetiology. Our observations on the nature of pseudoseizures are based on a carefully studied sample of 100 patients with pseudo-seizures evaluated over a period of 5 years at the University of Michigan Medical Center. The patients were evaluated by intensive neurological, clinical psychological and/or neuropsychological investigations. Psychodynamic psychotherapy was performed in a portion of this group. The results of these efforts have provided us with insights into the psychopathology of the disorder (Kalogjera-Sackellares, 1995; Kalogjera-Sackellares and Sackellares, 1997«, b, 1999). In addition, we discovered evidence to suggest that neurological disturbances may play a role in the pathophysiology of the disorder (Kalogjera-Sackellares and Sackellares, 1999). A recurrent theme among our patients was trauma. This included physical as well as emotional trauma (Kalogjera-Sackellares, 1995; Kalogjera-Sackellares and Sackellares, 1999). The prevalence of trauma, as well as the post-traumatic character of many of the symptoms, do not fit with the current diagnostic framework of the somatoform disorders (Guggenheim and Smith, 1995) under which pseudoseizures are typically considered. The concept of somatoform disorders obscures the operative impact of both the emotional as well as physical trauma which are cornerstones of our approach to this disorder. Our own observations regarding the psychopathology as well as the possibility of neurological disturbance led us to an extensive review of the literature on pseudoseizures and hysteria.

Among the richest sources of information on the subject are the case descriptions by the nineteenth century clinical investigators, Paul Briquet (a psychiatrist) and Jean-Martin Charcot (a neurologist). Briquet wrote extensively on the subject of hysterical seizures (a historic term for pseudoseizures) in his classic book on hys teria (Briquet, 1859). Charcot's case descriptions as well as his comments on the subjects have been captured for posterity in the form of published lectures (Charcot, 1879; Goetz, 1987; Harris, 1991). These clinicians contributed much to the foundations of both neurology and psychiatry. As we came to learn from the review of their work, both believed that hysteria resulted from a neurological disorder, but failed to find neuroanatomical abnormalities to support this view. As a result, neurological investigations into this disorder all but ceased. The emphasis shifted to investigations into the psychopathology of the disorder. These psychiatric investigations occurred under the historic impact of the pioneering insights of Janet, Freud and others. Our analysis of the literature was aided considerably by the translation of Charcot by G. Siegerson (Charcot, 1879), as well as the more recent translations (Goetz, 1987; Harris, 1991). Analysis of Briquet, on the other hand, was largely based on direct translations (by DKS) ofhis text (Briquet, 1859) because no English translation ofhis work was available.

In this chapter, we will review the historical events that led to the commonly held view that pseudoseizures are solely grounded in psychopathology, in the absence of detectable neurological disorders. In reviewing the works of Charcot and Briquet, it is apparent that the importance of trauma in the development of hysteria was recognized by both Briquet (1859) and Charcot (1879; Harris, 1991). However, focusing on a series of well-described cases of Charcot, we find that it was emotional trauma, not physical trauma that he emphasized. Yet, we will provide ample evidence that, in Charcot's cases, physical trauma (particularly head injury) may have played an equally important role. In addition to our review of historical cases, we will discuss the results of recent studies supporting the concept that neurobiologi-cal disturbances interact with traumatic environmental stresses, leading to the development of psychogenic pseudoseizures.

Historically, psychogenic pseudoseizures have been considered to be a classic manifestation of hysteria. Until the emergence of the modern view of hysteria in the nineteenth century, hysteria was generally believed to result from disturbances in the reproductive system, specifically the uterus. Nineteenth century investigators, particularly Pierre Briquet, and Jean-Martin Charcot, rejected the aetiological role of the uterus. In addition to making this historic contribution, they furthermore hypothesized that hysteria arose from disturbances in the central nervous system (Briquet, 1859; Goetz, 1987; Harris, 1991). Thus, both of these clinical investigators believed hysteria to be a neurological disorder (although Briquet's contribution to the conceptualization of hysteria as a disorder of the central nervous system is rarely acknowledged and has only recently been discussed at some length in the context of the 'forgotten avantgarde of neuroscience' (Mai, 1982; Mai and Merskey, 1981). First Briquet (Mai, 1982; Mai and Merskey, 1981), and later Charcot, attempted to identify lesions in the nervous system to account for the symptoms of hysteria. They were unable to find relevant anatomical lesions in their patients. However, their quest was limited by the histological methods of the times. In response to the absence of identifiable lesions, both men postulated physiological or 'dynamical' neurological disturbances to account for the functional disturbances and physical findings they observed in their patients.

As noted earlier, Charcot emphasized the importance of trauma in patients with hysteria. However, he focused upon the emotional trauma, or 'shock' rather than physical injury to the nervous system. Review of his cases fully substantiates the importance of shock and emotional trauma in these unfortunate individuals (Harris, 1991). However, his case reports also describe physical trauma, and in particular, head injury as well as debilitating illnesses in the vast majority of his cases. While Charcot described these physical insults, he did not postulate a causal relationship between head injury and hysteria, presumably because of the absence of neurological lesions in postmortem tissue.

Given the obvious presence of emotional trauma and psychological symptoms among hysterical patients and the failure to find neurological lesions, it was natural that subsequent clinical investigators, led by Janet and Freud, would focus upon psychodynamics. The success of psychological investigations and failure of biological investigations led neurologists to abandon the subject of hysteria. The primary interest of neurologists became limited to the differentiation of hysteria from 'true' neurological disorders.

Apart from recognizing the importance of emotional trauma in his patients, Charcot was unable to provide further insight into the aetiology of hysteria. However, he did provide extraordinarily useful descriptions of findings on neurological examination as well as vivid description of hysterical seizures. His extraordinarily detailed studies of the phenomenology of hysterical patients can be found in the lectures chronicled by his students (Charcot, 1879; Harris, 1991). Based on these observations, Charcot described four phases of the archetypal hysterical seizure: (1) a prodromal phase, (2) an epileptoid phase, (3) a phase characterized by bizarre postures and (4) an emotional phase. Less severe or elaborate seizures could occur. These modified attacks consisted of only parts of the full-blown archetypal seizures. The study of these phases was aided by drawings that captured the important details of hysterical seizures (see Figures 14.1 and 14.2). A large sample of these drawings was published in a book by Richer (1885). Richer's drawings captured the motor manifestations of pseudoseizures (for example, see Figure 14.1). Even more impressive was his success in rendering facial expressions which capture the intense emotional and experiential aspects of certain phases of the hysterical seizure. An example is illustrated in Figure 14.2.

The question arises as to whether today's patient with psychogenic pseudoseizures suffers from the same malady as the hysteria cases of Charcot's time. Given the

Figure 14.1. Reproduction of a drawing by Richer depicting a patient experiencing the epileptoid phase of a hysterical seizure (from Richer, 1885).

high incidence of nonepileptic seizures ('hystero-epilepsy') in hysterical patients of the nineteenth century, it seems reasonable to assume that Charcot was describing the same clinical entity as that underlying today's psychogenic pseudoseizure. Citing Briquet, Charcot stated that hysterical seizures occurred in all but 25% of patients with hysteria (Harris, 1991). Thus, nonepileptic seizures have been considered a typical manifestation of hysteria from the beginning of modern neurology. In the nineteenth century, hysteria was grouped along with other disorders which had no known anatomical lesion. Examples of such disorders included epilepsy and chorea, neither of which were associated with neuropathological lesions demonstrable with the histological techniques of the time. Disorders considered to be neurological, yet without a demonstrable lesion, were classified as 'neuroses'. Paradoxically, while the term 'neurosis' has persisted, its modern meaning, in contrast to that of nineteenth century clinical investigators, indicates psychological causation.

The modern vestige of this early attempt at classification is a tendency among many clinicians to consider nonepileptic seizures as 'functional' rather than

Postictal Psychosis
Figure 14.2. Reproduction of the 'period of passionate attitude' (the emotional phase), the fourth stage of a classical hysterical seizure.

'neurological' or 'organic' in aetiology. The implication is that nonepileptic pseudo-seizures do not have a biological substrate. However, careful reading of Charcot's lectures suggests that he used the term 'functional' to mean a disorder of the nervous system that is not associated with demonstrable lesions of the nervous system. Today, with knowledge gained from more powerful investigative tools, we have extended the concept of organic to include a number of toxic, metabolic, degenerative and genetic disorders that are not associated with physical lesions. In clinical practice today, the term 'functional', applied to a symptom or finding on examination, is taken to mean that the cause is 'psychological' as opposed to biological in nature. It is generally accepted that many disorders once considered to be 'functional' are due to biological causes (e.g. Gilles de la Tourette syndrome, schizophrenia, bipolar affective disorder). In an analogous manner, it is possible that a biological substrate for pseudoseizures will be identified, using today's sophisticated investigative tools.

Charcot meticulously applied the prevailing clinical-anatomical method, a method which he helped perfect, to the investigation of patients with hysteria. The clinical-anatomical method involved the correlation of clinical signs and symptoms to anatomical lesions in the nervous system. His application of this method to the study of the progressive muscular atrophies, amyotrophic lateral sclerosis, and multiple sclerosis resulted in major contributions to the understanding of those disorders. Such cases were classified as organic because they were associated with localized lesions of the nervous system. Such lesions were detectable by visual inspection of autopsy material. More detailed localization and description of these organic lesions was made possible by skilful use of the microscope, a tool that had been recently introduced into medical science.

In contrast to his success with the organic neurological disorders, Charcot was unable to unravel the mystery of hysteria through the application of the clinical-anatomical method. Hysterical patients presented a plethora of observable physical findings on neurological examination. In addition to seizures, these findings included blindness, diplopia, limb weakness, sensory loss, tremors and involuntary movements. However, these findings occurred in patterns that differed from those found in patients with observable anatomical lesions of the nervous system. In some cases, the pattern of visual disturbance, weakness, or sensory loss conflicted with the rules of functional neuroanatomy known at the time. More importantly, the profound clinical abnormalities were not associated with detectable lesions in the nervous system. Charcot was convinced that the clinical findings of hysterical patients were due to appropriately located anatomical abnormalities. However, in the absence of observable structural lesions, he referred to these lesions as 'dynamical' lesions (Harris, 1991).

Although the clinical findings in hysterical patients differed from those of the organic neurological disorders, Charcot was able to demonstrate classical clinical findings that have become the hallmark of hysteria. These findings include constricted visual fields, monocular diplopia, monoplegia, strange contractures and hemianaesthesia. The motor weakness observed in hysterics was not associated with the reflex abnormalities which were seen in patients with demonstrable lesions of the nervous system. Even today, such findings are taken as evidence for the presence of hysteria, although modern psychiatrists prefer to apply more modern terms, such as 'conversion disorder'.

Charcot preferred not to offer theories to explain neurological disorders, generally preferring to confine his discussions to empirical findings. However, his observations of the effects of hypnosis and suggestion in hysterics served as a stimulus for the subsequent development of the psychological theories pioneered by Janet and Freud (Goetz, 1987). The clinical histories he provided during his lectures frequently described neurological as well as psychiatric illness in family members. His comments suggest that he considered heredity an important factor in the development of hysteria. Although he did not speculate about this issue, his discussions indicate that various neurological symptoms appearing in the same family represented different clinical manifestations of an underlying hereditary predisposition (Harris, 1991).

Charcot's lectures included descriptions of traumatic events in his female patients with hysterical seizures (Charcot, 1879); however, we noted that it was in his male hysterics that he emphasized the history of antecedent trauma and previous illness (Harris, 1991). In his lectures on seven cases of male hysteria (in all of whom pseudoseizures figured prominently), he emphasized the history of antecedent trauma and its relationship to the onset of symptoms. During his lectures, his comments focused upon psychological trauma. However, our careful review of his lectures on seven male patients with hysteria reveals numerous references to significant closed head injuries. Indeed, he describes closed head injuries in four of the seven cases described. A fifth patient lost consciousness as a result of an accident that caused severe blood loss. Three were either physically abused or attacked. Antecedent debilitating illnesses occurred in five cases. Emotional trauma is described in all seven cases. Paternal alcohol abuse was described in four cases, but there is only one patient with a history of past alcohol abuse. Charcot's emphasis on the role of emotional trauma and not physical trauma is understandable, given the intolerable psychological and social stresses patients experienced. What is less clear is that he did not consider the impact of the physical trauma which was equally apparent in his patients.

Consistent with the historic heritage discussed in this chapter, a number of contemporary authors have rediscovered serious traumatic experiences in patients with psychogenic pseudoseizures (Alper et. al., 1993; Arnold and Privitera, 1996; Bowman, 1993; Cartmill and Betts, 1992; Gross, 1982; Harden, 1997; Kalogjera-Sackellares, 1995). This recurrent theme of trauma figured so prominently in the histories of pseudoseizure patients that it played a key role in the classification of pseudoseizure syndromes proposed by Kalogjera-Sackellares (1995). The continuity of historical and contemporary reference to trauma makes the study of trauma a natural starting point for investigations into the nature of pseudoseizures (Kalogjera-Sackellares and Sackellares, 1999). It must be considered relevant to the understanding of its causes and to the development of approaches to clinical management (Kalogjera-Sackellares, 1995).

Although psychic trauma is a dominant factor in most cases of psychogenic pseudoseizures, physical trauma, often involving closed head injuries also is a

Table 14.1. Demographics of 100 patients with psychogenic pseudoseizures referred to the neuropsychology programme at the University of Michigan

Source: Adapted with permission.

prominent part of the history in many patients. Several recent authors have commented on head injuries in their patients with psychogenic pseudoseizures. A high incidence of head trauma occurring during physical abuse or during accidents was reported by Bowman (1993). Similarly, Lancman et al. (1993) found many patients with head trauma associated with loss of consciousness. In addition, Westbrook et al. (1998) found that 32% of their patients with nonepileptic seizures had experienced an antecedent head trauma which was classified as minor in 91% of the cases.

Upon reviewing the histories of 100 patients with psychogenic pseudoseizures evaluated at the University of Michigan (Kalogjera-Sackellares and Sackellares, 1999), we found a documented history of significant closed head injury in 52% (see Table 14.1). In most instances, the trauma would have been categorized as mild head injury. These patients sustained head injury as a result of motor vehicle accidents, accidents on the job, falls or physical assault. Often, the physical assault was part of a chronic pattern of physical abuse. In many instances, these injuries occurred during childhood. However, there are some cases in which there was no history of significant head trauma until adulthood. As in many of Charcot's cases, in those cases with head trauma during adulthood, the injury preceded seizure onset by days to months and the patients usually ascribed a causal role to the head injury.

The high incidence of head trauma in patients with psychogenic pseudoseizures raises the question as to whether the head trauma may have played some role in the pathogenesis of the disorder. Is it possible that mild brain injury can render a patient more vulnerable to psychogenic pseudoseizures? In our sample, other potential causes of brain injury were reported. A history of drug or alcohol abuse was found in 13% of patients (Table 14.1). Approximately 29% (Table 14.1) were

Males Females Mean age

Pure pseudoseizures

Mixed epilepsy and pseudoseizures

Abnormal neurological examination

Structural brain abnormality on neuroimaging

History of closed head injury

History of substance abuse

found to have a prior or concurrent history of epilepsy. In another sample, we found evidence for active epilepsy in approximately 25% of patients with psychogenic pseudoseizures (Kalogjera-Sackellares and Sackellares, 1997«, b). In their case series, Wilkus et al. (1984) reported a high incidence of events that may have contributed to neurological impairment. Such events occurred in fully 80% of their sample. These events included head injury with loss of consciousness or other sequelae in 7 of their 25 cases; an infectious disorder with sequelae in 2 cases; prior brain surgery had occurred in 2 cases. Other events such as birth trauma, sun stroke, severe heat exhaustion, partial drowning or gas exposure also occurred in their patients.

Further evidence of impaired brain function in patients with psychogenic pseudoseizures comes from studies of cognitive and intellectual function in these patients. Neuropsychological test batteries are employed in clinical practice to detect evidence of organic brain dysfunction. Therefore, it is natural to expect that patients with a purely 'functional' disorder would perform normally on these tests. Alternatively, one might expect the pattern of test performance to differ from patients with 'organic' brain disorders. However, several investigators have reported impaired neuropsychological performances in patients with pseudoseizures. In fact, several studies, reported by different investigators, have produced very similar results (Kalogjera-Sackellares and Sackellares, 1999). Wilkus et al. (1984; Wilkus and Dodrill, 1989) reported results from administration of an intensive clinical neuropsychological test battery in 25 patients with psychogenic pseudoseizures evaluated at the University of Washington. These investigations revealed that their sample of patients performed in the impaired range on 51.2% of the tests. Sackellares et al. (1985) analysed a sample of patients evaluated at the University of Virginia and University of Michigan. The authors found that 'the cognitive performance of that group was less than would be expected for normal individuals of similar intelligence'. Binder et al. (1998) compared a group of patients with nonepileptic seizures with a group of patients with epilepsy and with normal control subjects on a battery of neuropsychological tests. They found that the two seizure groups performed significantly more poorly than normal controls. However, there were no significant differences between the two seizure groups on any items of the extensive test battery. They also found that performance on neuropsychological tests was more strongly correlated with measures on the MMPI/MMPI-2 in the nonepileptic seizure group. Based on these observations, the investigators concluded that neuropsychological tests do not discriminate between patients with epilepsy and those with nonepilep-tic seizures. These investigators concluded that impairment of neuropsychological performance was strongly related to emotional and psychosocial factors.

In a more recent study, we examined intellectual and neuropsychological test performance in 53 patients with psychogenic pseudoseizures (Kalogjera-

Sackellares and Sackellares, 1999). The group comprised 44 patients with pseudo-seizures who had no evidence of concomitant epilepsy, and no definitive historical data that would support the diagnosis of antecedent epilepsy. This subgroup was designated as the 'pure pseudoseizure' subgroup. In addition, there were nine patients with documented pseudoseizures and concomitant epilepsy, or a well-documented history of epileptic seizures. This subgroup was designated as the 'mixed pseudoseizures and epilepsy' subgroup. In both subgroups, there was a preponderance of women (77% in the pure subgroup and 78% in the mixed subgroup). Intellectual functioning had been measured, using the WAIS-R in each of these patients. The Halstead-Reitan Neuropsychological Test Battery (Boll, 1981) was administered to all but one. These tests were performed as a part of standard clinical evaluation which included medical and neurological history, physical and neurological examinations, routine EEG, neuroimaging, neuropsychological evaluations, and in most cases, long-term EEG-video monitoring. Interestingly, there were no statistically significant differences in the two subgroups with respect to WAIS-R scores. The group as a whole (pure and mixed subgroups combined) revealed an interesting pattern of scores (see Figure 14.3). The mean verbal IQ, performance IQ, and full scale IQ all fell in the average range. Scores were highly variable and ranged from the mentally deficient to the very superior. However, the overall distribution was skewed toward the low end of the average range. Scores on the Halstead-Reitan Neuropsychological Test Battery were not significantly different for the pure and mixed subgroups. Of particular importance is the finding that more than 50% of the group as a whole performed in the impaired range on more than half of individual subtests of the battery (based on published cutoff scores of Jarvis and Barth (1984). The percentage of patients scoring in the impaired range on each of the Halstead-Reitan tests for which cutoff scores are available is shown in Table 14.2. The Halstead Impairment Index (HII) is a summary score for the Halstead-Reitan Neuropsychological Test Battery. The mean HII for the entire sample and for each subgroup was in the impaired range. However, individual HII scores varied substantially (Figure 14.4). Scores ranged from 0.1 (normal) to 1.0 (impaired performance on all the constituent tests used to calculate the HII). The HII fell within the moderately to severely impaired range (0.7 and higher, based on the criteria of Jarvis and Barth (1984)) in nearly half (48.8%) of the pure pseudo-seizure group. This finding was particularly important given that this group had not been diagnosed with any defined neurological disorder and their symptoms had been assumed to result from purely psychological causes.

This study (Kalogjera-Sackellares and Sackellares, 1999) involved a large sample of patients with well-documented psychogenic pseudoseizures. The intellectual and neuropsychological findings of this study are consistent with those of previous studies. These studies together underscore the prevalence of measurable

Performance Range

60-69 70-79 80-89 90-99 100-109 110-119 120-129 130-139

IQ range

60-69 70-79 80-89 90-99 100-109 110-119 120-129 130-139

IQ range

— Verbal IQ WSHSSH Performance IQ ^^ Full scale IQ

Figure 14.3. Distribution of scores on the Wechsler Adult Intelligence Scale - Revised (WAIS-R) in a sample of 53 patients with psychogenic pseudoseizures. Scores range from the mentally deficient to the very superior range. However, the overall distribution was skewed toward the low end of the average range. (Adapted with permission.)

neuropsychological and cognitive deficits in patients with psychogenic pseudo-seizures. Although some investigators have attributed these deficits to emotional factors (Binder et al., 1998), an equally plausible explanation is that many patients with pseudoseizures, with or without concomitant epilepsy, have undiagnosed neurological abnormalities. In the vast majority of cases, structural abnormalities are not reported on MRI and CT scans. In the vast majority of cases, neurological examinations do not reveal focal or lateralized abnormalities that fit patterns that are seen with lesions of the nervous system. In fact, focal or lateralized neurological findings do not fit characteristic patterns associated with anatomical lesions of the nervous system. However, this does not exclude the possibility of biological disturbances affecting brain function. Not all such disturbances cause gross anatomical changes detectable by routine CT or MRI scans.

A surprising observation in our patient sample provides additional evidence that biological factors may play an important role in the pathogenesis of psychogenic

Table 14.2. Percentage of subjects scoring in the impaired range on Halstead-Reitan Neuropsychological Test Battery

Groups Pure Mixed pseudoseizures combined pseudoseizures and epilepsy


Groups Pure Mixed pseudoseizures combined pseudoseizures and epilepsy


Halstead Index




















Speech Sounds Perception Test




Seashore Rhythm Test




Trails A Time




Trails B Time




Finger tapping - dominant hand




Source: Reprinted with permission.

Source: Reprinted with permission.

pseudoseizures. We recently discovered the very interesting fact that approximately 30% of our patients with pure pseudoseizures are left-handed (Kalogjera-Sackellares and Sackellares, 2001). This is markedly increased in comparison with the 10% prevalence of left-handers reported in the general population (Hardyck and Petrinovich, 1977). This observation can be explained in one of three ways: (1) it is a chance observation, (2) left-handers are prone to developing psychogenic pseudoseizures, or (3) our sample contains pathological left handers. The probability of finding this high incidence of left-handers by chance alone is extremely low (P = 0.000381) (see Kalogjera-Sackellares and Sackellares, 2001). That normal lefthanders are predisposed to developing some sort of functional disorder characterized by seizure-like activity seems quite unlikely. Given the neuropsychological and cognitive difficulties observed in patients with pseudoseizures, it is more likely that the over-representation of left-handers in our sample is due to the presence of some pathological left-handers (see Kalogjera-Sackellares and Sackellares, 2001). Pathological left-handers are individuals who were destined to be right-handers, but developed left-hand dominance due to an insult to the left frontal lobe pre-natally, during infancy or early in childhood.

In summary, we traditionally consider psychogenic pseudoseizures to be a manifestation of a purely psychological disorder. This view stems largely from the absence of gross neuroanatomical lesions that can explain the seizures or associated neurological symptoms and signs. Further, these patients manifest a plethora of

Halstead Reitan Report Brain Damage

Figure 14.4 Distribution of the Halstead Impairment Index (HII), the summary score for the

Halstead-Reitan Neuropsychological Test Battery, administered to 52 of the same patients shown in Figure 14.3. A score of 0.1 is normal. Scores of 0.7 and above are in the moderately to severely impaired range. A score of 1.0 indicates performance in the pathological range on all constituent tests used to compute the HII. Note that individual scores ranged from normal to 1.0. However, 46.9% of patients in the entire group (pure pseudoseizures and mixed pseudoseizures and epilepsy subgroups combined) scored in the moderately to severely impaired range; and 48.8% of the pure group (n = 44) scored in the moderately to severely impaired range. (Adapted with permission.)

Figure 14.4 Distribution of the Halstead Impairment Index (HII), the summary score for the

Halstead-Reitan Neuropsychological Test Battery, administered to 52 of the same patients shown in Figure 14.3. A score of 0.1 is normal. Scores of 0.7 and above are in the moderately to severely impaired range. A score of 1.0 indicates performance in the pathological range on all constituent tests used to compute the HII. Note that individual scores ranged from normal to 1.0. However, 46.9% of patients in the entire group (pure pseudoseizures and mixed pseudoseizures and epilepsy subgroups combined) scored in the moderately to severely impaired range; and 48.8% of the pure group (n = 44) scored in the moderately to severely impaired range. (Adapted with permission.)

emotional and personality disturbances (Bowman, 1993; Cartmill and Betts, 1992; Kalogjera-Sackellares, 1995; Kalogjera-Sackellares and Sackellares, 1997«, b; Roy, 1979; Vanderzant et al, 1986) which direct the clinician toward psychiatric issues. The importance of psychological factors is further underscored by the prevalence of traumatic emotional experiences in these patients. Yet, a persistent question is why these traumatic experiences trigger pseudoseizures and other pseudoneuro-logical symptoms in some individuals, but not others. At least one possibility is that some individuals are biologically susceptible to the development of psychogenic pseudoseizures in response to traumatic emotional experiences.

We suggest that, at least in some individuals, the biological susceptibility may result from neurological impairment. As our previous discussion indicates, a number of investigators have reported a high incidence of closed head injury and other neurological insults in their patients. Several investigators have reported impaired performance on tests of neuropsychological and cognitive function. Finally, we have found an over representation of left-handers in our pseudo-seizure patient sample (Kalogjera-Sackellares and Sackellares, 2001). This over-representation of left-handers suggests one of two possibilities. First, it is possible that left-handers subjected to certain neurological insults or severe emotional trauma may be predisposed to psychogenic pseudoseizures. A second, and more plausible explanation is the presence of pathological left-handers in the sample. If the additional left-handers are pathological left-handers, it suggests that some patients may have experienced neurological insults to the left hemisphere prior to the establishment of hand dominance (Kalogjera-Sackellares and Sackellares, 2001).

Taken together, all of these observations suggest that biological factors play an important aetiological role in the development of psychogenic pseudoseizures. This possibility in no way negates the role of emotionally traumatic experiences or other environmental factors in the development of psychiatric disorders characterized by pseudoseizures. Nonetheless, it may help to explain why all individuals experiencing traumatic life events do not develop pseudoseizures.

We feel that it is extremely important to consider the strong possibility that psychobiological factors may play an important role in the pathophysiology of epilepsy. Because pseudoseizures have long been assumed to stem from purely 'functional' causes, there have been essentially no investigations into the neurobiology of this disorder.

This disorder causes as much disability as medically intractable epilepsy. Yet, little progress has been made in the exploration of new therapeutic interventions. Psychotherapy can be beneficial to many of these patients (Kalogjera-Sackellares, 1995). However, not all respond, and many do not have access to psychotherapy. To our knowledge, there have been no organized scientific investigations into the use of psychopharmacology in the treatment of this disorder.

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