Epilepsy: A Comprehensive Textbook
2nd Edition
© 2008 Lippincott Williams & Wilkins
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Chapter 203
Personality Disorders in Epilepsy
Orrin Devinsky
Charles Vorkas
William B. Barr
Bruce P. Hermann
Introduction
At the turn of the 20th century, most of the lay and professional communities believed that people with epilepsy had pathologic personality traits and psychopathologic disorders such as aggression, sociopathy, and psychosis. However, from the medical perspective, this was partly an artifact of the main setting from which epilepsy was viewed: Chronically institutionalized patients, many of whom suffered comorbid disorders (e.g., head trauma, neurosyphilis). The concept of an epileptic personality—a ubiquitous and characteristically negative set of behavioral changes in epilepsy patients—was already established in antiquity, but continued to evolve slowly and relentlessly. Simultaneously, more humanistic and balanced views evolved during the 19th century. Based on extensive experience with a private outpatient population with idiopathic epilepsy, Reynolds87 concluded that epilepsy does not invariably involve abnormal mental change, and Gowers42 also recognized that many epilepsy patients had normal personality and intellect, but that many others could develop intraparoxysmal behavioral changes. He suggested that these changes resulted from many factors, but mainly from epilepsy.
The early 20th century brought diverse views concerning people with epilepsy and their behaviors. Wilson121 offered a progressive psychosocial view: “On epileptic temperament inordinate stress has been laid. Life is difficult for these patients, and much that is attributed to temperament can with greater reason be assigned to chronic invalidism and unlucky circumstance.” Sjobring99 adhered to the negative, pervasive view: “A mental change of a specific nature takes place in individuals suffering from epileptic seizures. They become torpid and circumstantial, sticky and adhesive, effectively tense and suffer from explosive outburst of rage, anxiety, etc.” Kraepelin61 reported aggressiveness in some of his outpatient epilepsy patients: “Almost always an intensification of mental irritability occurs.” The adhesive or viscous personality traits in which the patient has difficulty in disengaging from interpersonal exchanges was reviewed by many observers in the European literature under various terminologies such as the “enechetic constitution,” “ixoid character,” and “glischroid trait.”
The Modern Era
Early in the 20th century, the term “epileptic personality” was used by psychoanalytic theorists to describe a set of character traits associated with epilepsy that focused on impulsivity, egocentricity, and affective viscosity.17 These features were considered to result from hereditary factors, directly from seizures or treatment, or a reaction to painful social situations associated with epilepsy. Others believed that these particular personality features, in individuals with or without seizures, were a direct expression of epilepsy itself. Two coincident developments in the middle of the century helped reintroduce the highly controversial concept of personality changes in epilepsy: Identifying the role of the limbic system in emotion and behavior and localizing the onset of many partial seizures to the temporal lobe.
Papez81 conceived a circuit of interconnected structures comprising the emotion system: Hippocampus—fornix—hy-pothalamus/mammillary bodies—mammillothalamic tract—anterior thalamic nuclei—thalamocingulate fibers—cingulate cortex—amygdala/hippocampus. This emotion circuit theory was based on anatomic connections, sham rage studies, and lesion studies. Yakovlev124 conceived a basolateral circuit modulating emotional behavior, including the amygdala, insula, orbitofrontal cortex, and dorsomedial thalamic nucleus. MacLean67 combined earlier ideas and conceived the limbic system with all the above regions, as well as the septum and nucleus accumbens.
The specific association of temporal lobe epilepsy (TLE) and psychopathology had its major genesis in the 1951 report by Gibbs40 that up to 33% of patients with “psychomotor seizures” of temporal lobe origin exhibited interictal behavioral changes. Gastaut et al.36 in 1954 reiterated common observations on the frequency of emotional viscosity, hyposexuality, hypoactivity, and aggressiveness in epilepsy patients, and first suggested that the stereotypic symptom complex was the antithesis of behaviors in the Kluver-Bucy syndrome (KBS). KBS is characterized by oral exploratory behavior, increased sexual appetite, decreased aggressivity, and continuous environmental exploration as a consequence of bilateral anterior temporal destructive lesions.59
Waxman and Geschwind117 proposed a distinct subset of nonpathologic behaviors associated with TLE, which included deepened emotions, circumstantiality, altered religious and sexual concerns, and hypergraphia. They coined the term “interictal behavior syndrome,” sometimes referred to as Geschwind syndrome or Gastaut-Geschwind syndrome.6 Bear and Fedio4 expanded this syndrome to include the 18 traits based on a literature review. They found an increased frequency of all 18 traits in patients with TLE compared with non-neurologic controls. The interictal behavioral traits described by Bear and Fedio are summarized in Table 1. Some of these traits associated with this syndrome are described below in more detail.
Table 1 Proposed Personality Traits by Bear and Fedio
Hypergraphia
Hypermoralism
Altered sexuality
Religiosity
Aggression
Obsessionalism
Paranoia
Guilt
Humorlessness
Sadness
Emotionality
Circumstantiality
Philosophical interest
Personal destiny
Viscosity
Dependence
Elation
Anger
Viscosity
Viscosity is a tendency for prolonged interpersonal contacts; talking repetitively, circumstantially; and pedantically; and not ending conversations and visits after a socially appropriate interval. Bear and Fedio4 reported viscosity to be significantly elevated in both right and left TLE compared to normal and neurologic controls. Brandt et al.10 found increased viscosity among left TLE and generalized epilepsy (GE) patients, with no difference between right TLE and controls. Hoeppner et al.51 presented the “cookie thief” picture from the Boston
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Diagnostic Aphasia Examination, which shows a drawing of a boy stealing a cookie, to TLE, GE, and control subjects. Taped responses were reviewed blindly and all four individuals with verbose responses, characterized by trivial, circumstantial, and subjective details, had left temporal foci. A ten-item viscosity scale revealed significantly higher scores in the self-reports of patients with left TLE compared to right or bilateral TLE, absence seizures, panic disorder, or normal subjects.86 Proxy raters reported a trend for increased viscosity scores in the left TLE group, endorsing items such as “when I have a phone conversation with him/her, I always find I am the one who wants to get off first.” Seizure duration and viscosity score were significantly correlated for patients with left TLE.
Viscosity may result from some combination of linguistic impairment, social cohesion, mental slowness, and psychological dependence. Language dysfunction associated with left temporal lobe seizure foci may contribute to a verbal style characterized by circumstantiality and excessive discourse. However, there may be independent effects of left temporal foci on social behavior. Viscosity, the personality trait, may also result from an increased desire for interpersonal closeness, a need for affiliation with another being. Discrete limbic lesions can profoundly alter how animals maintain contacts with other members of their own or other species.41,60,73 For example, rats with septal lesions will remain in contact with each other in an open field and, if left alone, will actively approach cats despite expressions of fear.73 It is possible that some biologic effects of the epileptogenic process or recurrent seizures in a minority of patients with temporolimbic epilepsy, especially in the dominant hemisphere, fosters the development of viscosity.
Hyposexuality
Various changes in interictal sexual behavior occur in patients with TLE. Hyposexuality is frequently reported,7,31,35,83,93,98,101,108 with anecdotal reports of hypersexuality38,98 and deviant sexual behavior including exhibitionism,7,52 transvestism,27,84 transsexualism,50 and fetishism.26,74 Isolated cases of unusual sexual behavior occurring in patients with epilepsy could be chance associations. However, some cases develop profound changes in adulthood, shortly after the onset of epilepsy, raising the possibility of an etiologic relationship. Hyposexuality, including decreased libido and impotence, occurs in approximately half of TLE patients without gender bias. In many cases, especially those with seizure onset before puberty, patients may not marry or regard hyposexuality as a problem. Complaints are more likely to come from the spouse or parent who observes lack of interest in the opposite sex. Much of the original literature on hyposexuality from 1954 to 1985 was based on self-report76 without detailed interviews to assess the relative roles of libido, arousal, erectile dysfunction, anorgasmia, and sexual satisfaction, as well as physiologic measures of endocrine and sexual function.
Most studies found higher rates of hyposexuality and sexual dysfunction in TLE than other epilepsy groups, although Fenwick et al.31 did not observe any significant difference in sexual activity related to seizure type, type of epilepsy, or seizure frequency. Among those with TLE, no laterality effects were found for sexual behavior in left- versus right-sided seizure foci.16 A well-designed study of six men with erectile dysfunction found abnormal nocturnal penile tumescence and rigidity in five.44 The pattern of abnormality was consistent with neurogenic, not vasogenic, erectile dysfunction. In a self-report survey of 116 women with epilepsy, partial epilepsy patients experienced more dyspareunia, vaginismus, arousal insufficiency, and sexual dissatisfaction, whereas primary generalized epilepsy (PGE) patients experienced more anorgasmia and sexual dissatisfaction.75 Sexual symptoms were not associated with seizure frequency, antiepileptic drug (AED) exposure, sexual experience, depression, or prepubertal seizure onset.
The pathogenetic role of temporal lobe seizures in hyposexuality is supported by animal models30 and observations that sexual activity can increase following successful seizure control with AEDs83 and temporal lobectomy.7 In some postlobectomy subjects, marked hypersexuality similar to the Kluver-Bucy syndrome can develop occasionally.9 However, AEDs modulate hypothalamic-pituitary-gonadal axis hormone activity and can directly inhibit sexual behavior.64 Barbiturates may cause the greatest decrease in libido and sexual dysfunction.70 Other hepatic enzyme–inducing AEDs are also associated with decreased testosterone levels and diminished libido and function.49 Valproic acid is associated with menstrual disorders, hyperandrogenism, and polycystic ovaries.54,78
Religiosity
The ancient association between epilepsy and mystical/religious phenomena is paradigmatic of the difficulty reconciling dramatic anecdotes and long-standing medical opinion with limited clinical studies. Hippocrates began his monograph On the Sacred Disease by refuting the association between epilepsy and the divine. Despite his modern insights, religious and magical treatments of epilepsy predominated throughout the Middle Ages and Renaissance.109 In the 19th century, psychiatrists stressed the religiosity of epilepsy patients and observed that Siberian medicine men preferred epileptic pupils.64 Classic monographs on religious mysticism noted that “among the dread diseases that afflict humanity there is only one that interests us quite particularly; that disease is epilepsy.”64 Intense religious experiences and beliefs are reported frequently by people with epilepsy. Many prominent religious figures allegedly had epilepsy, including prophets and founders of several religions.116 The evidence supporting epilepsy in these people varies. Intense religious experiences can occur in association with seizures.13,25,53,66,102
Dewhurst and Beard23 reported six TLE patients who underwent sudden religious conversions. There was a clear temporal
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relationship between conversion and increased seizure activity in five patients; one patient had a marked decrease in seizure frequency prior to conversion (she attributed her improved seizure disorder to the Almighty). Increased religious conviction and practice is not a consistent behavioral feature in patients with epilepsy. There is little evidence that epilepsy or TLE patients as a group are hyperreligious, although a subgroup may have unusually strong religious beliefs. Two studies with questionnaires on religion failed to differentiate patients with right versus left TLE, TLE versus GE, or epilepsy patients and controls.110,120 However, one study found that patients with smaller right hippocampi had significantly higher ratings on a religiosity scale.123
Hypergraphia
Hypergraphia is not characteristic of interictal behavior among TLE or GE patients. However, several studies support that the subgroup manifesting this behavior most intensely are those with temporal lobe foci. Waxman and Geschwind116 reported seven TLE patients with hypergraphia, which is a tendency toward extensive and sometimes compulsive writing. There was a striking preoccupation with detail—words were defined and redefined and underlined, parentheses were used to make word meaning absolutely clear—and the writers accorded great importance to their material. In four patients, the writings focused on moral and religious concerns. Hypergraphia was viewed as a component of the deepened emotions and especially viscosity of interictal behavioral changes.
Utilizing a mailed standard questionnaire, Sachdev and Waxman92 demonstrated that TLE patients responded frequently and extensively (mean 1,301 words) as compared to other epilepsy patients (mean 106 words). Hermann et al.47 replicated the higher response rates and longest letters in the TLE group, but they did not find that the average response was longer in TLE patients compared to other seizure patients. Duration of epilepsy, hypomania, and number of significant life events during the past year positively correlated with hypergraphia.47,48 Hypergraphia occurs in 7% to 10% of TLE patients.47,48
Dostoyevsky was the most famous hypergraphic TLE patient,39 although his prolific writing also reflected his pay per page and financial troubles. As a person, he was deeply emotional, irritable, angered over minor provocations, guilt ridden, depressed, and tortured over the question of God’s existence. He described the relation between his writing and epilepsy in a letter to his brother (August 27, 1849): “Whenever formerly I had such nervous disturbances, I made use of them for writing; in such a state I could write much more and much better than usual.”24
Aggression
Interictal violence and aggression is a highly contentious topic, especially the relationship between TLE and aggression. There appears to be a relatively elevated incidence of interictal violence and hostility in patients with epilepsy as compared to healthy controls. The neurosurgical series of Serafetinides97 and of Taylor107 demonstrated rates of interictal aggression approaching 30% in TLE patients prior to temporal lobectomy. These studies were criticized for selection bias of refractory patients and those with psychiatric presentations. Rodin91 identified 5% of patients presenting to an epilepsy center as manifesting aggressive behavior. Seizure type did not distinguish aggressive from nonaggressive patients. Gunn and Fenton45 documented increased prevalence of epilepsy in British prisons relative to the general population. A study of the Illinois prison system documented a prevalence rate of epilepsy of 2.4%, elevated relative to the U.S. population at the time of the study. However, census of prisoners with epilepsy against matched nonepileptic controls did not reveal more serious violent crimes on the part of the epilepsy group.118
Violence and hostility in epilepsy is likely a consequence of an interaction of neurophysiologic as well as social factors. Male sex is a risk factor for violence and epilepsy, and Serafetinides noted that aggressiveness as a personality trait in TLE patients was more likely in those with seizure onset prior to age 10 years. Other risk factors identified in the TLE group include premature interruption of formal schooling, lower intellectual quotient, and lower socioeconomic status. These risk factors are associated with a greater risk of aggression in nonepileptic patients as well. Several studies found that ictal and interictal aggression appear to be more common in children than adults with TLE.43,80,106 More specific neurobiologic factors were identified in a quantitative magnetic resonance imaging (MRI) analysis of mesial temporal structures in epilepsy patients with and without a history of interictal aggression.112 Those with interictal aggression had less hippocampal atrophy. Two subgroups of those with aggression were identified: Those with severe amygdala atrophy and a history of encephalitis and those with left temporal lesions affecting the amygdala or periamygdaloid regions.112
Problems of Definition and Methodology
Defining specific personality traits and aberrations in patients with epilepsy is difficult and controversial. From a psychiatric standpoint, studies on interictal behavioral changes in epilepsy have not been “discipline neutral.”2 Over the past decades, stereotyped notions of personality attributes in patients with chronic seizures have been dominated by psychoanalysts and those performing trait analyses within the psychometric tradition of self-report methodologies and multivariate statistics. Debates in the literature center on complex personality concepts (e.g., hyperreligiosity) rather than attempt to integrate “first order” biologic variables that underlie the causality of complex behaviors (vide infra).
Considering the variety of epilepsy syndromes and their many etiologies, correlation of interictal behavior with a specific physiologic process or anatomic locus is difficult. Many studies on behavior and epilepsy were done before video-electroencephalographic (V-EEG) confirmation of a specific ictal onset zone and without high-resolution MRI. Many authors simplistically approach “TLE” as a monolithic entity primarily involving mesiotemporal structures. Analyses and speculations thereby focus exclusively on limbic-affective states. However, subdural grid electrode recordings frequently document TLE seizure onsets from neocortical extralimbic regions in isolation or together with mesial structures.58,68 Even when invasive monitoring documents a temporal lobe “focus,” there often is associated extratemporal glucose hypometabolism as defined by positron emission tomography (PET).57 In patients with TLE, as an illustration, prefrontal metabolic asymmetry is associated with cognitive impairment and depression.12,57
Identifying behavioral changes confined to the interictal period is another methodologic challenge. Preictal (premonitory), postictal, and interictal behavioral alterations are less well circumscribed temporally than ictal changes. In the extreme case of partial status epilepticus, cognitive impairments form a continuum despite EEG evolution from discrete seizures to periodic discharges and finally re-emergence of normal EEG background.88 For isolated seizures, transitions between ictal, preictal, postictal, and interictal behavioral states can be fluid,
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and clinical distinctions made may be artificial. These behavioral changes may morph over time and extend from their initial extent during the postictal period to more continuous disorders that fill the interictal periods.105
Studies from the pre-MRI/pre–V-EEG era are limited by methodologic issues, including the diagnosis of epilepsy (e.g., nonepileptic events), syndromic diagnosis (e.g., benign rolandic epilepsy vs. TLE in a child), and localization of the seizure focus (e.g., frontal vs. temporal), which may all be more problematic in older than more recent studies. Before high-resolution MRI, structural lesions such as cortical dysplasias, vascular malformations, and low-grade neoplasms were not identified. Studies of TLE patients in the pre-MRI era likely included patients with erroneous localization and lateralization.
Finally, past behavioral analysis of the population with ep-ilepsy focused on personality structure rarely assessed lifetime developmental, antiepileptic drug, or other variables.14,79,96,104
Interictal Behavioral Changes in Other Epilepsy Syndromes
Personality Changes in Primary Generalized Epilepsy
Personality changes in epilepsy are not restricted to patients with partial epilepsy; they also occur in patients with PGE syndromes such as juvenile myoclonic epilepsy (JME)55 and absence epilepsy.100 In JME, reported traits included irresponsibility and impaired impulse control, neglect of duties, self-interest, emotional instability, exaggeration, inconsiderateness, quick temper, and distractibility. Janz55 found that many JME patients repeatedly exposed themselves to sleep deprivation and often failed to comply with AEDs, taking their illness lightly. They denied problems and conflicts, or often yielded to temptation against better judgment. There was limited support for Janz’s clinical impression,5 although scientific evidence is sparse and some of these behaviors may reflect adolescence, not JME. Other studies found high rates of psychiatric disorders among patients with JME.82,113 Gelisse et al.37 reported 45 (26.5%) of 170 consecutive JME patients with psychiatric disorders. Twenty-four of these 45 patients had personality disorders, including borderline (11 cases), dependent (five cases), histrionic (two cases), obsessive-compulsive (one case), and not otherwise specified (five cases).
Absence epilepsy, long considered one of the most benign forms of epilepsy, recently has been associated with significant behavioral changes in a very well-controlled study. Wirrell et al.122 compared all children in Nova Scotia with typical absence epilepsy or juvenile rheumatoid arthritis (JRA) diagnosed between 1986 and 1997, who were aged 18 years or older at follow-up (mean age 23 years). Remission occurred in 32 (57%) of the patients with typical absence epilepsy but in only 17 (28%) of the patients with JRA. Five categories of outcome were studied: Academic-personal, behavioral, employment-financial, family relations, and social-personal relations. Patients with typical absence epilepsy had greater difficulties in the academic-personal and in the behavioral categories (p <0.001) than those with JRA. Those with ongoing seizures had the least favorable outcome. Most seizure-related factors showed minimal correlation with psychosocial functioning. Even patients whose epilepsy had remitted had significantly poorer outcomes than the JRA patients in the academic-personal and behavioral domains. Another recent study found that 54% of pediatric patients with PGE had psychiatric disorders.12 Early age of onset and poor seizure control were significantly associated with the severity of illogical thinking in these children. Thus, the recent literature strongly supports prior research that PGE is a risk factor for cognitive and behavioral problems.
Personality Changes in Patients with Frontal Lobe Epilepsy
The frontal lobes are important in personality, as highlighted by the effects of prefrontal surgeries. Thus, as limbic disorders can alter emotion- and drive-related behavior (e.g., sex and aggression), frontal dysfunction can alter personality, judgment, and executive functions. Further, the posterior orbitofrontal cortex and anterior cingulate gyrus, two critical limbic (paralimbic) areas, are located within the frontal lobe. Patients with anterior cingulate seizure foci can develop interictal psychosis, aggression, sociopathic behavior, sexual deviancy, irritability, obsessive-compulsive disorder, and poor impulse control.3,19,21,71 Orbitofrontal lesions can cause hyperphagia, failure to use autonomic cues to guide behavior, aberrant emotional responsiveness, increased aggression, dysfunctional social behavior (e.g., case of Phineas Gage16,97), behavioral disinhibition, and confabulation.20 Systematic studies on interictal behavior in patients with orbitofrontal seizure foci are lacking; however, behavioral disorders such as attention deficit hyperactivity disorder can occur.85 Given the critical role of this limbic cortex in social and emotional behavior, epileptic foci in this site could cause prominent interictal behavioral changes.
In the Vietnam Head Injury Study,103 patients with tonic–clonic seizures had a higher frequency of psychiatric treatment than those with complex partial seizures, possibly reflecting greater frontal lobe involvement. The role of the frontal lobe in the personality and behavior of epileptic patients deserves greater attention. Functional imaging studies suggest that, even among patients with temporal lobe seizure foci, frontal dysfunction contributes to affective, personality, and cognitive disorders.11,82,94
Characterizing the Interictal Behavior Syndrome
The Bear Fedio Inventory
In the original study using this measure, all 18 self-rated traits were significantly higher in the TLE group than in neurologic and healthy controls. The most significant differences (p <0.0001) were humorlessness, circumstantiality, dependence, and sense of personal destiny. Proxy raters (i.e., family or friends) identified TLE patients as significantly different from controls on 14 traits, most strongly (p <0.0001) for circumstantiality, obsessionalism, and dependence. Patients with right temporal foci reported more emotional traits and minimized their behavioral changes (i.e., polished their image), whereas patients with left temporal foci had more ideational traits and often tarnished their image on self-report relative to proxy reports. The previously reported associations of right hemisphere lesions with denial and neglect syndromes and left hemisphere lesions with depression33,34,89,90 were consistent with the right/left:polish/tarnish correlation.
Replication studies using the Bear Fedio Inventory (BFI) have produced mixed results.11,22,46,77 Use of the BFI generally reveals increased rates of these behavioral traits in patients with epilepsy (TLE and GE) in comparison to healthy controls or some medical patients, but it does not distinguish epilepsy (TLE or GE) from psychiatric patients. Findings from TLE
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versus GE patient comparisons are inconsistent. When differences are present, the TLE group usually has higher scores than the GE group. Left–right differences in TLE are typically minor.
The complicating issue of frontal lobe seizure foci or frontal lobe involvement (e.g., seizure spread or interictal hypometabolism/neuronal dysfunction) should also be considered in patients with TLE. Although personality disorders are highlighted in the literature as elements of TLE, they would be expected to be features of frontal lobe epilepsy (FLE) as well. Indeed, in the literature on the BFI, the study by Wieser119 was the only one to use invasive electrodes for localization and lateralization, and failed to replicate any laterality effects found by Bear and Fedio.5 Interestingly, Wieser found a significant increase in humorlessness in the FLE group and a nonsignificant trend for an increase in all BFI behavioral traits in the FLE group.
The studies with the BFI nearly vanished after 1990, just as high-resolution MRI and V-EEG monitoring allowed more confident anatomic and physiologic diagnoses. As the BFI fell out of favor, so did much of the research on personality in epilepsy patients. Consequently, the subject of personality changes in epilepsy warrants further study.
The Neurobehavioral Inventory (NBI) is a more recent tool to specifically assess interictal psychopathology in epilepsy patients.8 There has been relatively little use of the NBI, but it may prove valuable. In one study, patients with high ratings on the NBI religiosity scale had smaller hippocampi, while in another study, hyposexuality and hypergraphia were associated with bilateral hippocampal atrophy.111
Mazzini et al.72 evaluated 143 patients with traumatic brain injury (TBI), of which 27 developed posttraumatic epilepsy (PTE), using another measure—the Neurobehavioral Rating Scale (NBHRS)—along with the Minnesota Multiphasic Personality Inventory (MMPI), Overt Aggression Scale, Back Depression Inventory (BDI), and Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) definitions for personality disorders. Patients with epilepsy showed a significantly higher incidence of severe personality disorders. Disinhibited behavior, irritability, and agitated and aggressive behavior were significantly more frequent and severe in PTE patients.
Feddersen et al.29 examined 37 TLE patients, 38 with idiopathic generalized epilepsy with absence and generalized tonic–clonic seizures and 25 healthy controls using the Freiburg Personality Inventory/Form A (FPI-A-H)28 and the Index of Personality Characteristics (IPC).62 Patients with left TLE had increased emotional dependency, less externally judged composedness, increased depressive drive and mood, increased nervousness, increased search for information and exchange of disease experience, and greater tendency to persevere (p <0.05). This study supported the differentiation made by Bear and Fedio4 that patients with left TLE are more rational and tarnish their image, whereas patients with right TLE are more emotional and polish their image.
One study with the Millon Behavioral Health Inventory (MBHI) found that epilepsy patients have deficient coping styles.115 Patients with epilepsy obtained higher scores on scales assessing inhibition and sensitivity and lower scores on scales evaluating sociability and confidence.
Table 2 Rate of Personality Disorders in Epilepsy
Schwartz and Cummings (1988)95 38% (4% controls)
Fiordelli et al. (1993)32 21% (0% controls)
Victoroff (1994)114 18%
Manchanda et al. (1996)69 18%
Arnold and Privitera (1996)1 18%
Lopez-Rodriguez et al. (1999)65 21%
Krishnamoorthy et al. (2001)63 47%
Koch-Stoecker (2002)59a 61%
Galimberti et al. (2003)33a 38%
DSM Axis II Disorders
Another approach to examining personality disorder in epilepsy is to turn to formal DSM-IV Axis II diagnoses. By definition, personality disorders are characterized by long-lasting patterns of thought and behavior that deviate from cultural expectations, inflexible and pervasive in nature, that result in impairment of function. To receive a diagnosis of personality disorder, the pattern of behavior must result in significant distress or impairment in personal, social, or occupational situations. Several criteria must be met in addition to the specific criteria for individually named personality disorders. These include the following:
  • Experience and behavior that deviates markedly from the expectations of the individual’s culture. This pattern is manifested in two (or more) areas including cognition, affectivity, interpersonal functioning, and impulse control.
  • The enduring pattern is inflexible and pervasive across a broad range of personal and social situations.
  • The enduring pattern leads to clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • The pattern is stable and of long duration and its onset can be traced back at least to adolescence or early adulthood.
  • The enduring pattern is not better accounted for as a manifestation or consequence of another mental disorder.
  • The enduring pattern is not due to the direct physiologic effects of a substance or a general medical condition such as head injury.
There are ten specific personality disorders in DSM-IV, which are grouped into three clusters: Cluster A (odd or eccentric disorders) includes paranoid personality disorder, schizoid personality disorder, and schizotypal personality disorder; cluster B (dramatic, emotional, or erratic disorders) includes antisocial personality disorder, borderline personality disorder, histrionic personality disorder, and narcissistic personality disorder; and cluster C (anxious or fearful disorders) includes avoidant personality disorder, dependent personality disorder, and obsessive-compulsive personality disorder. Finally, personality disorder NOS is a category for behavior patterns that do not match these ten disorders but have the characteristics of a personality disorder.
A series of investigations have assessed Axis II disorders (not including mental retardation) in patients with epilepsy using contemporary diagnostic procedures. As can be seen in Table 2, the rate of Axis II disorders range from 18% to 61% across studies, with a mean of 31% (median = 21%). Only two studies incorporated controls. These rates are elevated overall and investigations that examined the distribution of clusters A through C reveal that most individuals with epilepsy with Axis II disorders exhibit cluster C disorders. Even biologically oriented researchers recognize that problems associated with living with epilepsy, particularly early-onset epilepsy, may lead to dependant and avoidant personality traits, although this contention has not been examined empirically.
Table 3 Distribution of Specific Personality Disorders in Epilepsy
Authors N A B C Procedure
Lopez-Rodriguez et al. 1999 52 0.0% 5.8% 15.4% SCID-II
Galimberti et al. 2003 69 1.4% 10.1% 26.0% SCID-II
Koch-Stoecker et al. 2002 100 6.0% 15.0% 24.0% DSM-III-R
Krishnamoorthy et al. 2001 35 17.1% 2.9% 22.9% SAP
SCID-II Structured Clinical Interview for DSM-IV-TR
DSM-III-R Diagnostic and Statistical Manual of Mental Disorders-III-R
PSE Present State Examination
A Cluster A; odd or eccentric disorders
B Cluster B; dramatic, emotional, or erratic disorders
C Cluster C; anxious or fearful disorders
Axis II disorders are probably underrecognized and incompletely addressed in the traditional clinic setting (Table 3). There is little information regarding their consequences, but
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the evidence available suggests that they are of consequence. Koch-Stoecker examined the predictors of postoperative psychiatric complications in 100 patients who underwent anterior temporal lobectomy (ATL).59a Patients were assessed for Axis I and II disorders preoperatively. Fourteen percent of their surgical patients were hospitalized for psychiatric reasons postoperatively and all these patients exhibited Axis II disorders preoperatively, either alone of in combination with Axis I disorders. No patients with just an Axis I disorder underwent postoperative psychiatric hospitalization.
Another indication of the maladaptive consequences associated with adverse personality features is demonstrated by Derry et al., who examined the impact of neuroticism on postoperative course in 45 individual ATL patients.18 Those who were high in preoperative neuroticism exhibited significantly worse postoperative psychosocial adjustment and quality of life.
Summary and Conclusions
Personality disorders and other, less pathologic personality changes are common and often unrecognized in epilepsy patients. These disorders likely result from biologic factors such as structural and physiologic abnormalities as well as social and emotional factors. The specificity of certain personality traits or clusters and anatomic seizure foci (e.g., TLE or FLE) and epilepsy syndromes (e.g., partial vs. generalized) remains controversial, mired in methodologic issues and limited by a literature that often predated MRI and V-EEG studies. However, traits such as hypergraphia, although present in <10% of TLE patients, appear to be much more common in this form of epilepsy than others. Patients with FLE and idiopathic generalized epilepsy can also develop behavioral changes and personality disorders that can significantly impact their lives. The area remains ripe for additional studies using modern psychiatric and neurologic diagnostic tools.
References
1. Arnold LM, Privetera MD. Psychopathology and trauma in epileptic and psychogenic seizure patients. Psychosomatics. 1996;37:438–443.
2. Barratt ES, Kent T, Stanford MJ. Biologic variables defining and measuring personality. In: Rately JJ, ed. Neuropsychiatry of Personality Disorders. Oxford: Blackwell Science; 1995:36–37.
3. Bear D, Levin K, Blumer D, et al. Interictal behavior. I. Hospitalized temporal lobe epileptics: relationship to idiopathic psychiatric syndrome. J Neurol Neurosurg Psychiatry. 1982;45:481–488.
4. Bear DM, Fedio P. Quantitative analysis of interictal behavior in temporal lobe epilepsy. Arch Neurol. 1977;34:454–467.
5. Bech P, Pedersen KK, Simonsen N, et al. Personality in epilepsy. Acta Neurol Scand. 1976;54:348–358.
6. Benson DF. The Geschwind syndrome. Adv Neurol. 1991;55:411–421.
7. Blumer D, Walker EA. Sexual behavior in temporal lobe epilepsy. Arch Neurol. 1967;16;37–43.
8. Blumer D. The neurobehavioral inventory: personality disorders in epilepsy. In: Ratey JJ, ed. Neuropsychiatry of Personality Disorders. Boston: Blackwell Science; 1995:230–263.
9. Blumer D. Hypersexual episodes in temporal lobe epilepsy. Am J Psychiatry. 1970;126:1099–1106.
10. Brandt J, Seidman LJ, Kohl D. Personality characteristics of epileptic patients: a controlled study of generalized and temporal lobe cases. J Clin Exp Neuropsychol. 1985;7:25–38.
11. Bromfield EB, Altshuler L, Leiderman DB, et al. Cerebral metabolism and depression in patients with complex partial seizures. Epilepsia. 1990;31:625–626.
12. Caplan R, Arbelle S, Guthrie D, et al. Formal thought disorder and psychopathology in pediatric primary generalized and complex partial epilepsy. J Am Acad Child Adolesc Psychiatry. 1997;36:1286–1294.
13. Cirignotta F, Todesco CV, Lugaresi E. Temporal lobe epilepsy with ecstatic seizures (so-called Dostoyevsky epilepsy). Epilepsia. 1980;21:705–710.
14. Csernansky JG, Leiderman DB, Mandabach M, et al. Psychopathology and limbic epilepsy: relationship to seizure variables and neuropsychological function. Epilepsia. 1990;31:275–280.
15. Damasio H, Grabowski T, Frank R, et al. The return of Phineas Gage: clues about the brain from the skull of a famous patient. Science. 1994;264:1102–1105.
16. Daniele A, Azzoni A, Bizzi A, et al. Sexual behavior and hemispheric laterality of the focus in patients with temporal lobe epilepsy. Biol Psychiatry. 1997;42:617–624.
17. Delay J, Pichot P, Lemperiere T, et al. The Rorschach and the Epileptic Personality. New York: Logos Press; 1958.
18. Derry PA, Rose KJ, McLachlan RS. Moderators of the affect of seizure symptoms on MMPI-2 clinical interpretation. J Clin Psychol. 2002;58:817–826.
19. Devinsky O, Abramson H, Alper K, et al. Postictal psychosis: a case control series of 20 patients and 150 controls. Epilepsy Res. 1995;20:247–253.
20. Devinsky O, D’Esposito M. The Neurology of Cognition and Behavior. New York: Oxford University Press; 2004:330–317.
21. Devinsky O, Morrell M, Bogt B. Contribution of anterior cingulate cortex to behavior. Brain. 1995;118:279–306.
22. Devinsky O, Theodore WH, eds. Epilepsy and Behavior. New York: Wiley-Liss; 1991.
23. Dewhurst K, Beard AW. Sudden religious conversions in temporal lobe epilepsy. Br J Psychiatry. 1970;117:497–507.
24. Dostoyevsky FM. Letters of Fyodor Michailovitch Dostoevsky to His Family and Friends. Mayne EC, translator. New York: Macmillan; 1915.
25. Dostoyevsky FM. The Idiot. Magarshack D, translator. London: Penguin Books; 1955.
26. Epstein AW. Fetishism: a study of its psychopathology with particular reference to a proposed disorder in brain mechanisms as an etiologic factor. J Nerv Ment Dis. 1960;23:247–249.
27. Epstein AW. Relationship of fetishism and transvestism to brain and particularly to temporal lobe dysfunction. J Nerv Ment Dis. 1961;133:247–253.
28. Fahrenberg J, Selg H, Hempel R. Das Freiburger Personlichkeitsinventar FPI. Gottingen: Hogrefe Verlag; 1973.
29. Feddersen B, Herzer R, Hartmann U, et al. On the psychopathology of unilateral temporal lobe epilepsy. Epilepsy Behav. 2005;6:43–49.
30. Feeney DM, Gullotta FP, Gilmore W. Hyposexuality produced by temporal lobe epilepsy in the cat. Epilepsia. 1998;39:140–149.
31. Fenwick PBC, Toone BK, Wheeler MJ, et al. Sexual behavior in a centre for epilepsy. Acta Neurol Scand. 1985;71:428–435.
32. Fiordelli E, Beghi E, Boglium G, et al. Epilepsy and psychiatric disturbance. Brit J Psychiatry. 1993;163:446–460.
33. Gainotti G. Emotional behavior and hemispheric side of lesion. Cortex. 1972;8:41–45.
P.2111

33a. Galimberti CA, Ratti MT, Murelli R, et al. Patients with psychogenic nonepileptic seizures, alone or epilepsy-associated, share a psychological profile distinct from that of epilepsy. J Neurol. 2003;250:338–346.
34. Galin D. Implications for psychiatry of left and right cerebral specialization. Arch Gen Psychiatry. 1974;31:572–583.
35. Gastaut H, Collomb H. Etude du comportement sexuel chez les epileptiques psychomoteurs. Ann Med Psychol (Paris). 1954;112:657–696.
36. Gastaut H, Morin G, Leserve N. Etude du comportement des épileptiques psycho-moteurs dans l’intervalle de leurs crises. Ann Medico-Psychol. 1955;113:1–27.
37. Gelisse P, Genton P, Samuelian JC, et al. Psychiatric disorders in juvenile myoclonic epilepsy. Rev Neurol. 2001;157:2907–2302
38. Geschwind N, Shader RI, Bear D, et al. Behavioral changes with temporal lobe epilepsy: assessment and treatment. J Clin Psychiatry. 1980;41:89–95.
39. Geschwind N. Dostoyevsky’s epilepsy. In: Blumer D, ed. Psychiatric Aspects of Epilepsy. Washington, DC: American Psychiatric Press, 1984:325–334. (Dosteyevsky letter, August 27, 1849.)
40. Gibbs FA. Ictal and non-ictal psychiatric disorders in temporal lobe epilepsy. Nerv Ment Dis. 1951;113:522–528.
41. Glendenning KK. Effects of septal and amygdaloid lesions on social behavior of the cat. J Comp Physiol Psychol. 1972;80:199–207.
42. Gowers WR. Epilepsy and Other Chronic Convulsive Disorders. New York: William Wood & Co.; 1885:101.
43. Guimaraes CA, Franzon RC, Souza EA, et al. Abnormal behavior in children with temporal lobe epilepsy and ganglioglioma. Epilepsy Behav. 2004;5:788–791.
44. Guldner GT, Morrell MJ. Nocturnal penile tumescence and rigidity evaluation in men with epilepsy. Epilepsia. 1996;37:1211–1214.
45. Gunn J, Fenton G. Epilepsy in prisons: a diagnostic survey. BMJ. 1969;4:326–328.
46. Hermann BP, Reil P. Interictal personality and behavioral traits in temporal lobe and generalized epilepsy. Cortex. 1981;17:125–128.
47. Hermann BP, Whitman S, Arnston P. Hypergraphia in epilepsy: is there a specificity to temporal lobe epilepsy? J Neurol Neurosurg Psychiatry. 1983;46:848–853.
48. Hermann BP, Whitman S, Wyler AR, et al. The neurological, psychosocial and demographic correlates of hypergraphia in patients with epilepsy. J Neurol Neurosurg Psychiatry. 1988;51:203–208.
49. Herzog AG, Fowler KM. Sexual hormones and epilepsy: threat and opportunities. Curr Opin Neurol. 2005;18:167–172.
50. Hoenig J, Kenna JC. EEG abnormalities and transsexualism. Br J Psychiatry. 1979;134:293–300.
51. Hoeppner JB, Garron DC, Wilson RS, et al. Epilepsy and verbosity. Epilepsia. 1987;28:35–40.
52. Hooshmand H, Brawley BW. Temporal lobe seizures and exhibitionism. Neurology. 1969;19:1119–1124.
53. Howden JC. The religious sentiments in epileptics. J Ment Sci. 1872–1873;18:491–497.
54. Isojarvi JI, Laatikainen TJ, Pakarinen AJ, et al. Polycystic ovaries and hyperandrogenism in women taking valproate for epilepsy. N Engl J Med. 1993;329:1383–1388.
55. Janz D. Die epilepsien. Stuttgart: Georg Thieme; 1969.
56. Jensen I, Larsen JK. Mental aspects of temporal lobe epilepsy. J Neurol Neurosurg Psychiatry. 1979;42:256–265.
57. Jokeit H, Seitz RJ, Markowitsch HJ, et al. Prefrontal asymmetric interictal glucose hypometabolism and cognitive impairment in patients with temporal lobe epilepsy. Brain. 1997;120:2283–2294.
58. Jung WY, Pacia SV, Devinsky O. Neocortical temporal lobe epilepsy: intracranial EEG features and surgical outcome. J Clin Neurophysiol. 1999;16:419–425.
59. Kluver H, Bray PC. Preliminary analysis of functions of the temporal lobe in monkeys. Arch Neurol Psychiatry. 1939;42:979–1002.
59a. Koch-Stoecker S. Personality disorders as predictors of severe postsurgical psychiatric complications in epilepsy patients undergoing temporal lobe resections. Epilepsy Behav. 2002;3:526–531.
60. Kolb B, Nonneman AJ. Frontolimbic lesions and social behavior in the rat. Physiol Behav. 1974;13:637–643.
61. Kraepelin E. Lectures on Clinical Psychiatry. 3rd ed. New York: William Wood & Col.; 1913.
62. Krampen G. IPC-Fragebogen zu Kontrollueberzeugungen. Gottingen/Toronto/Zurich: Verlag fur Psychologie; 1981.
63. Krishnamoorthy EA, Brown RJ, Trimble MR. Personality and psychopathology in nonepileptic attack disorder and epilepsy. Epilepsy Behav. 2001;2:418–422.
64. Leuba JH. The Psychology of Religious Mysticism. London: Kegan Paul, Trench, Trubner & Co.; 1925:204.
65. Lopez-Rodriguez F, Altschuler L, Kay J, et al. Personality disorder among medically refractory epileptic patients. J Neuropsych Clin Neurosci. 1999;11:464–469.
66. Mabille H. Hallucinations religieuses et delire religieux transitoire dans l’epilepsie. Ann Medico-Psychol. 1899;9/10:76–81.
67. MacLean PD. The Evolution of the Triune Brain. New York: Plenum; 1990.
68. Maillard L, Vignal JP, Gavaret M, et al. Semiologic and electrophysiologic correlations in temporal lobe seizure subtypes. Epilepsia. 2004;45:1590–1599.
69. Manchanda R, Schaefer B, McLachlan RS, et al. Psychiatric disorders in candidates for surgery for epilepsy. J Neurol Neurosurg Psychiatry. 1996;61:82–89.
70. Mattson RH, Cramer JA, Collins JF, et al. Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures. N Engl J Med. 1985;313:145–151.
71. Mazars G. Criteria for identifying cingulate epilepsies. Epilepsia. 1970;11:41–47.
72. Mazzini L, Cossa FM, Angelino E, et al. Posttraumatic epilepsy: neuroradiologic and neuropsychological assessment of long-term outcome. Epilepsia. 2003;44(4):569–574.
73. Meyer DR, Ruth RA, Lavond DG. The septal social cohesiveness effect: its robustness and main determinants. Physiol Behav. 1978;21:1027–1029.
74. Mitchell W, Falconer MA, Hill D. Epilepsy with fetishism relieved by temporal lobectomy. Lancet. 1954;2:626–630.
75. Morrell MJ, Guldner GT. Self-reported sexual function and sexual arousability in women with epilepsy. Epilepsia. 1996;37:1204–1210.
76. Morrell MJ. Sexual dysfunction in epilepsy. Epilepsia. 1991;32[Suppl 6]:S38–S45.
77. Mungas D. Interictal behavior abnormality in temporal lobe epilepsy: a specific syndrome or nonspecific psychopathology. Arch Gen Psychiatry. 1982;39:108–111.
78. Murialdo G, Galimberti CA, Magri F, et al. Menstrual cycle and ovary alterations in women with epilepsy on antiepileptic therapy. J Endocrinol Invest. 1997;20:519–526.
79. Nielsen H, Kristensen O. Personality correlates of sphenoidal EEG foci in temporal lobe epilepsy. Acta Neurol Scand. 1981;64:289–300.
80. Ounstead C. Aggression and epilepsy: rage in children with temporal lobe epilepsy. J Psychosom Res. 1969;13:237–242.
81. Papez JW. A proposed mechanism of emotion. Arch Neurol Psychiatry. 1937;38:725–743.
82. Perini GI, Tosin C, Carraro C, et al. Interictal mood and personality disorders in temporal lobe epilepsy and juvenile myoclonic epilepsy. J Neurol Neurosurg Psychiatry. 1996;61:601–605.
83. Peters UH. Sexualstorungen bei psychomotorischer Epilepsie. J Neurovis Relat. 1971;[Suppl 10]:491–497.
84. Petritzer BK, Foster J. A case study of a male transvestite with epilepsy and juvenile diabetes. J Nerv Ment Dis. 1955;121:557–563.
85. Powell AL, Yudd A, Zee P, et al. Attention deficit hyperactivity disorder associated with orbitofrontal epilepsy in a father and a son. Neuropsychiatry Neuropsychol Behav Neurol. 1997;10:151–154.
86. Rao SM, Devinsky O, Grafman J, et al. Viscosity in complex partial seizures: relationship to cerebral laterality and seizure duration. J Neurol Neurosurg Psychiatry. 1992;55:149–152.
87. Reynolds JR. Epilepsy: Its Symptoms, Treatment, and Relation to Other Chronic Convulsive Disorders. London: Churchill; 1861:39–77.
88. Ritaccio AL, March GR. The significance of BIPLEDS in complex partial status epilepticus. Am J Electroencephalogr Technol. 1993;33:27–34.
89. Robertson MM, Trimble MR, Townsend HRA. The phenomenology of depression in epilepsy. Epilepsia. 1987;28:364–372.
90. Rodin E, Schmaltz S. The Bear-Fedio personality inventory and temporal lobe epilepsy. Neurology. 1984;34:591–596.
91. Rodin EA. Psychomotor epilepsy and aggressive behavior. Arch Gen Psychiatry. 1973;28:210–213.
92. Sachdev HS, Waxman SG. Frequency of hypergraphia in temporal lobe epilepsy: an index of interictal behavior syndrome. J Neurol Neurosurg Psychiatry. 1981;44:358–360.
93. Saunders M, Rawson M. Sexuality in male epileptics. J Neurol Sci. 1970;10:577–583.
94. Schmitz EB, Moriarty J, Costa DC, et al. Psychiatric profiles and patterns of cerebral blood flow in focal epilepsy: interactions between depression, obsessionality, and perfusion related to the laterality of the epilepsy. J Neurol Neurosurg Psychiatry. 1997;62:458–463.
95. Schwartz, J, Cummings JL. Psychopathology and epilepsy: an outpatient consultation-liaison experience. Psychosomatics. 1988;29:295–300.
96. Seidman L. Lateralized cerebral dysfunction, personality, and cognition in temporal lobe epilepsy. Ph.D. thesis, University of Michigan, University Microfilms International, Ann Arbor, MI, 1980.
97. Serafetinides EA. Aggressiveness in temporal lobe epileptics and its relation to cerebral dysfunction and environmental factors. Epilepsia. 1965;6:33–42.
98. Shukla GD, Hrivastava ON, Katiyar BC. Sexual disturbances in temporal lobe epilepsy: a controlled study. Br J Psychiatry. 1979;134:288–292.
99. Sjobring H. Ixophreni. In: Psykologisk-pedagogisk uppslagsbok. Bd. 2. Stockholm; 1944. Quoted and translated by Gudmundsson.
100. Small JG, Milstein V, Stevens JR. Are psychomotor epileptics different? A controlled study. Arch Neurol. 1962;7:187–194.
101. Spark RF, Wills CA, Royal H. Hypogonadism, hyperprolactinemia, and temporal lobe epilepsy in hyposexual men. Lancet. 1984;1:413–416.
102. Spratling WP. Epilepsy and Its Treatment. New York: WB Saunders; 1904:473–474.
103. Swanson SJ, Rao SM, Grafman J, et al. The relationship between seizure type and interictal personality. Results from the Vietnam Head Injury Study. Brain. 1995;118:91–103.
P.2112

104. Swinkels WAM, Duijsens IJ, Spinhoven Ph. Personality disorder traits in patients with epilepsy. Seizure. 2003;12:587–594.
105. Tarulli A, Devinsky O, Alper K. Progression of postictal to interictal psychosis. Epilepsia. 2001;42:1468–1471.
106. Tassinari CA, Tassi L, Calandra-Buonaura G, et al. Biting behavior, aggression, and seizures. Epilepsia. 2005;46:654–663.
107. Taylor DC. Aggression and epilepsy. J Psychosom Res. 1969;13:229–236.
108. Taylor DC. Sexual behavior and temporal lobe epilepsy. Arch Neurol. 1979;21:510–516.
109. Temkin O. The Falling Sickness. 2nd ed. Baltimore: Johns Hopkins University Press; 1971.
110. Tucker DM, Novelly RA, Walker PJ. Hyperreligiosity in temporal lobe epilepsy: redefining the relationship. J Nerv Ment Dis. 1987;175:181–184.
111. van Elst LT, Krishnamoorthy ES, Baumer D, et al. Psychopathological profile in patients with severe bilateral hippocampal atrophy and temporal lobe epilepsy: evidence in support of the Geschwind syndrome? Epilepsy Behav. 2003;4:291–297.
112. van Elst LT, Woermann FG, Lemieux L, et al. Affective aggression in patients with temporal lobe epilepsy: a quantitative MRI study of the amygdala. Brain. 2000;123:234–243.
113. Vazquez B, Devinsky O, Luciano D, et al. Juvenile myoclonic epilepsy: clinical features and factors related to misdiagnosis. J Epilepsy. 1993;6:233–238.
114. Victoroff J. DSM-III-R psychiatric diagnoses in candidates for epilepsy surgery: lifetime prevalence. Neuropsych Neuropsych Behav Neurology. 1994;7(2):87–97.
115. Watten VP, Watten RG. Psychological profiles in patients with medically refractory epilepsy. Seizure. 1999;8(5):304–309.
116. Waxman SG, Geschwind N. Hypergraphia in temporal lobe epilepsy. Neurology. 1974;24:629–631.
117. Waxman SG, Geschwind N. The interictal behavior syndrome in temporal lobe epilepsy. Arch Gen Psychiatry. 1975;32:1580–1586.
118. Whitman S, Coleman TE, Patmon C, et al. Epilepsy in prison: elevated prevalence and no relationship to violence. Neurology. 1984;6:775–782.
119. Wieser HG. Selective amygdalohippocampectomy: indications, investigative technique and results. Adv Tech Stand Neurosurg. 1986;13:39–133.
120. Willmore LJ, Heilman KM, Fennell E, et al. Affects of chronic seizures on religiosity. Trans Am Neurol Assoc. 1980;105:85–87.
121. Wilson SAK. Neurology. Baltimore: Williams & Wilkins; 1940:1486.
122. Wirrell EC, Camfield CS, Camfield PR, et al. Long-term psychosocial outcome in typical absence epilepsy. Sometimes a wolf in sheep’s clothing. Arch Pediatr Adolesc Med. 1997;151:152–158.
123. Wuerfel J, Krishnamoorthy ES, Brown RJ, et al. Religiosity is associated with hippocampal but not amygdala volumes in patients with refractory epilepsy. J Neurol Neurosurg Psychiatry. 2004;75:640–642.
124. Yakovlev PI. Motility, behavior and the brain: stereodynamic organization and neural coordinates in behavior. J Nerv Ment Dis. 1948;107:313–335.
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