SYSTEMATIC REVIEW article

Front. Psychol., 19 March 2019

Sec. Cognition

Volume 10 - 2019 | https://doi.org/10.3389/fpsyg.2019.00346

Gender and Hemispheric Asymmetries in Acquired Sociopathy

  • 1. Department of Neurology and Neuropsychiatry, D'Or Institute for Research and Education, Rio de Janeiro, Brazil

  • 2. Departments of Neurology and Psychiatry, Federal University of the State of Rio de Janeiro, Rio de Janeiro, Brazil

  • 3. School of Medicine, Federal University of the State of Rio de Janeiro, Rio de Janeiro, Brazil

  • 4. Shirley Ryan AbilityLab, Department of Physical Medicine, Rehabilitation, and Psychology, Neurology, Cognitive Neurology and Alzheimer's Center, Feinberg School of Medicine, Weinberg College of Arts and Sciences, Northwestern University, Chicago, IL, United States

Abstract

The emergence of enduring antisocial personality changes in previously normal individuals, or “acquired sociopathy,” has consistently been reported in patients with bilateral injuries of the ventromedial prefrontal cortex. Over the past three decades, cases of acquired sociopathy with (a) bilateral or (b) unilateral sparing of the ventromedial prefrontal cortex have been reported. These cases indicate that at least in a few individuals (a') neural structures beyond the ventromedial prefrontal cortex are also critical for normal social behavior, and (b') the neural underpinnings of social cognition may be lateralized to one cerebral hemisphere. Moreover, researchers have presented evidence that lesion laterality and gender may interact in the production of acquired sociopathy. In the present review, we carried out a comprehensive literature survey seeking possible interactions between gender and hemispheric asymmetry in acquired sociopathy. We found 85 cases of acquired sociopathy due to bilateral (N = 48) and unilateral (N = 37) hemispheric injuries. A significant association between acquired sociopathy and right hemisphere damage was found in men, whereas lesions were bilateral in most women with acquired sociopathy. The present survey shows that: (i) the number of well-documented single-cases of acquired sociopathy is surprisingly small given the length of the historical record; (ii) acquired sociopathy was significantly more frequent in men after an injury of the right or of both cerebral hemispheres; and (iii) in most women who developed acquired sociopathy the injuries affected both cerebral hemispheres. These findings may be especially valuable to neuroscientists and to functional neurosurgeons in particular for the planning of tumor resections as well as for the choice of the best targets for therapeutic neuromodulation.

Introduction: Acquired Sociopathy and Frontotemporoinsular Damage

Eslinger and Damasio coined the expression “acquired sociopathy” to describe the changes in personality of evr, a comptroller in a home-building firm who underwent a lasting change in personality following the surgical removal of an olfactory groove meningioma. evr's normal cognitive performance contrasted with his severe loss of social tact and comportment, which culminated in bankruptcy and abandonment by his wife and friends. In contrast to individuals with developmental psychopathy, who “never learn socially acceptable patterns of behavior” (Eslinger and Damasio, 1985, p. 1737), evr had learned and engaged in such patterns for most of his life; however, after his brain damage he failed to behave accordingly in real-life situations. The report by Eslinger and Damasio gave breath to the study of the neural underpinnings of human social behavior and its drastic changes following damage to the vmPFC (Barrash et al., 2000).

Pari passu with the renewed interest in the antisocial changes of personality due to vmPFC damage, investigators have documented the emergence of acquired sociopathy in lesions outside the vmPFC, more specifically, in dorsolateral prefrontal cortex (Eslinger et al., 1999; Eslinger and Biddle, 2000), rostrobasal forebrain (Poeck and Pilleri, 1965; Gorman and Cummings, 1992), ventromedial hypothalamus (Flynn et al., 1988), anterior temporal lobes (Relkin et al., 1996; Miller et al., 1999), anterior cingulate (Tow and Whitty, 1953; Angelini et al., 1980), medial thalamus (Sandson et al., 1991), basal ganglia (Richfield et al., 1987; Mendez et al., 1989), and rostral brainstem (Omar et al., 2007). In most cases, the behavioral changes were enmeshed in a fabric of more elementary symptoms, such as somnolence and hyperphagia, which usually reflect damage to functionally heterogeneous neural systems (Alpers, 1937). Conversely, sociopathy was surprisingly absent in patients with even extensive bilateral prefrontal (PF) damage (Penfield and Evans, 1935; Rylander, 1939; Hebb and Penfield, 1940; Nichols and Hunt, 1940; Ghosh et al., 2014; Plaza et al., 2014); still in others the brain damage had little if any impact on socio-occupational status (Tranel et al., 2005), exerting even a paradoxically beneficial effect in some (e.g., Labbate et al., 1997; cases of and eb, Storey, 1970; King et al., 2017). These discrepancies raise the possibility that in at least some cases the laterality of the hemispheric lesion may be decisive for the development of sociopathy; in other words, damage to one cerebral hemisphere might be sufficient to produce sociopathy in at least a few previously normal individuals. A reliable prediction of whom these individuals are might bear important theoretical and practical implications.

Despite the aforementioned clues on a possible asymmetric representation of acquired sociopathy in the cerebral hemispheres, few researchers have pursued this line of inquiry. The most consistent studies on lesion laterality and acquired sociopathy have been carried out by Tranel and colleagues, who additionally investigated a possible interaction between lesion laterality and gender. In four thoroughly matched cases, they found that acquired sociopathy in one man resulted from damage to the right vmPFC, while in one woman it was caused by damage to the left vmPFC; the reverse match was not attended by changes in personality (Tranel et al., 2005). These findings were later extended to four patients suffering from pharmacoresistant epilepsy who underwent unilateral ablation of the right or the left anterior temporal lobe. The anterior temporal lobes encompass a collection of neural structures which sustain profuse bidirectional connections with the ventromedial, orbitofrontal and insular cortices as well as with the amygdala (Pascalau et al., 2018). As in the vmPFC cases, sociopathy was associated with left lobectomy in one woman and with right lobectomy in one man (Tranel and Hyman, 1990). Thus, besides lesion laterality, the Tranel et al. studies imply that gender should likewise be considered critical for the production of acquired sociopathy (Tranel and Bechara, 2010).

Gender asymmetry has been supported by studies which have consistently found higher rates of antisocial behavior among men relative to women. This “gender gap,” which is already noticeable at an early age, remains stable from childhood to adulthood (with the exception of a discrete period limited to adolescence), and has been documented in different cultures (Choy et al., 2017). Although the male-to-female ratio of lifelong antisocial conduct is 10:1, research has also shown that boys and girls with persistent antisocial behavior are identical in terms of poor discipline, family adversity, pattern of cognitive deficits, undercontrolled temperament, hyperactivity, and rejection by peers; the relaxation of diagnostic criteria of conduct disorder for girls did not substantially change these conclusions (Moffitt et al., 2004). Therefore, the weight of the evidence indicates that men are referred more often than women to psychiatric treatment and to the justice system because of differences that are intrinsic to gender, the cultural milieu playing an adjunctive role by either enhancing or curbing the overt expression of antisocial acts.

A growing body of neuroscientific research has otherwise shown that the aforementioned differences largely reflect the aspects of the cerebral organization that underpin differences in men and women (Cahill, 2006). A representative instance of the interplay between gender biology and culture was provided by Fumagalli et al. (2010), who studied the performance of 100 right-handed adults (50 men and 50 women) on a moral judgment task; volunteers were further sorted into Catholics and non-Catholics according to their stated religious belief systems. They found that only gender predicted the kind of moral judgements by men and women, men producing a significantly higher proportion of utilitarian responses than women; religious belief and education played no role in differentiating the styles of moral decisions of men and women. The authors concluded that cultural factors exerted little, if any, influence on moral judgments, suggesting that the significant factor was gender-specific differences in neural organization. Functional neuroimaging studies concur with this view. For example, in a study on the cerebral correlates of judgments of procedural justice, the overall volume of cerebral activations in women were asymmetrical (total volume of activations = 7,449 mm3) with a leftward preponderance (left hemisphere activations exceeding right hemisphere activations = 1,698 mm3); activations in men were also asymmetric (total volume of activations = 10,082 mm3), but with a clear rightward preponderance (right hemisphere activations exceeding left hemisphere activations = 5,334 mm3); qualitatively similar results were obtained for judgments of distributive justice (Dulebohn et al., 2016). Recently, the ingenious application of neuroimaging methods to criminal cases with focal brain damage collected from the literature has been done with remarkable success (Darby et al., 2018). In this study, Darby et al. did not investigate if the neural networks that they found to underpin criminal behavior differed between men and women or between the cerebral hemispheres.

To test the gender/laterality interaction in acquired sociopathy we searched the literature for clinically-defined cases in which an enduring antisocial change in personality had been caused by a circumscribed, non-degenerative, brain lesion. Our main goals were to investigate (i) whether unilateral hemispheric lesions are sufficient to cause acquired sociopathy, and (ii) whether gender and lesion laterality interact to modulate the final emergence of acquired sociopathy.

Materials and Methods

Inclusion and Exclusion Criteria

An extensive literature search was conducted using the electronic databases PubMed, ISI Web of Science, and PsycInfo to identify articles published until April 2018. We used the following search terms in title, abstract or keywords: (“sociopath*” or “psychopathy” or “acquired” or “frontal lobe” or “damag*” or “injur*”) and (“imaging” or “magnetic resonance imaging” or “computed tomography” or “positron emission tomography” or “brain”). Additional papers were retrieved by checking the literature cited in the articles identified by the electronic database search as well as from the authors' personal archives. We retained all single cases or case series of previously normal children, adolescents or adults who developed a persistent antisocial change in personality following an injury of the frontal lobes with or without extension into the insula, temporal pole, and neighboring subcortical regions. The reason for extending the anatomical boundaries beyond the frontal lobes is the fact that patients with sole or predominantly temporopolar injury may also present severe antisocial personality changes (Miller et al., 1999). Note that the cases included in the present survey were selected solely on the basis of the behavioral criterion of persistent antisocial changes in personality, not on anatomical criteria such as lesion location or type. By definition, cases of developmental psychopathy fell outside the scope of the present review.

For the purposes of the present study, sociopathy was operationally defined as (a) a chronic, recurrent and pervasive pattern of disregard for, and violation of, the rights of others (American Psychiatric Association, 2000), which (b) broadly overlaps Factor 2, but not necessarily Factor 1, of the Hare Psychopathy Checklist (Hart et al., 1995). As extensively discussed elsewhere, virtually all individuals with a diagnosis of psychopathy meet a diagnosis of antisocial personality disorder, or sociopathy, but the converse is not necessarily true (Lykken, 2018). However, no attempt was made in this review to differentiate sociopathy from psychopathy sensu stricto because only recently have researchers begun to differentiate acquired from developmental psychopathy (Moll et al., 2003; Mitchell et al., 2006a). With a few notable exceptions (Karpman, 1947), the earlier authors used the terms sociopathy and psychopathy interchangeably, thus overlooking the essential personality traits that distinguish psychopathy from the sociopathic behavior of other neuropsychiatric disorders (Koenigs and Tranel, 2006). We were also careful to exclude patients with antisocial changes in personality secondary to a mood disorder (Thorneloe and Crews, 1981; Bakchine et al., 1989; Tyrer and Brittlebank, 1993) and dementia (Mendez et al., 2011). In the absence of formal measures of intelligence, evidence that overt dementia or mental retardation were not part of the clinical picture were obtained from the report, otherwise the case was excluded from further analysis. A history of seizures or loss of consciousness were not a reason for exclusion, but patients with delusions, hallucinations, or both (Malloy and Richardson, 1994; Harrington et al., 1997) as well as cases with solely deep subcortical (e.g., Richfield et al., 1987; Mendez et al., 1989), or brainstem (e.g., Omar et al., 2007) lesions were excluded. Cases of sociopathy following psychosurgery were allowed in if they met the preceding criteria. Only cases in which a causal nexus between the cerebral damage and acquired sociopathy could be inferred were selected. A causal nexus was primarily provided by evidence of (i) a normal premorbid personality, and (ii) a temporal relationship between the cerebral injury and the advent of the antisocial personality change (Vann, 1972). For our purposes, “normal” was operationally defined as the capacity to be productive in the chief domains of social and interpersonal life, especially in those niches represented by family, parental/marital, school/work, and extrafamilial life (Endicott et al., 1976). Due to the considerable interindividual variation in cytoarchitectonics (Zilles and Amunts, 2012) and the less than optimal neuroanatomical accuracy of several reports prior to the 1980's, no attempt was made at this time to chart the lesions on standard cytoarchitectonic maps; for similar reasons, we did not attempt to infer the topography of the cerebral lesions based on cranial landmarks as was usual before the advent of modern neuroimaging (e.g., Jarvie, 1954). In view of the fragmentary and heterogeneous nature of the available material, no attempt was made either to sort the personality changes into subordinate domains (Barrash et al., 2018) or to perform a formal meta-analysis. Finally, we accepted as valid four cases of vmPFC dysplasia (Table 1: cases U-8 and U-10; Table 2: cases B-32 and B-47) and one case of orbital pachygyria (Table 2: case B-15). Although not strictly “acquired”, we retained these cases because the lesions in each were circumscribed to frontotemporal regions known to produce acquired sociopathy in typical cases. A similar line of reasoning has been followed by other authors (Trebuchon et al., 2013).

Table 1

CodeSideaIdentificationSexbAge at injurycHandednessdReferences
U-1LHNRMNRNRSullivan, 1911
U-2LHCase 5M48RMiller et al., 1986
U-3LHJZM33RMeyers et al., 1992
U-4LHDT/D1W7REslinger et al., 1992; Anderson et al., 2006
U-5LHMr. A/Spyder CystkopfMcongenital or early infancyRParadis et al., 1994; Relkin et al., 1996
U-6LHBMMcongenitalRFine et al., 2001
U-7LH2748W30RTranel et al., 2005
U-8LHDKM26RMitchell et al., 2006b
U-9LH3310W49RTranel and Bechara, 2009
U-10LHBWMcongenitalRBoes et al., 2011
U-11LHNRM48NRGilbert and Vranič, 2015
U-12RHHFM53NRPilleri, 1963
U-13RHKWM20NRFaust, 1966
U-14RHCharles WhitmanMNRNRde Chenar, 1966; Martinius, 1983
U-15RHFLM56NRLesniak et al., 1972
U-16RHRNMBirth traumaNRMartinius, 1983
U-17RHPLM4RMarlowe, 1992
U-18RHCase 11.3M27NRBenson, 1994
U-19RHNRM33NRCohen et al., 1999
U-20RHMGSM20RDimitrov et al., 1999
U-21RHSubject B/ML/SB-2046/D2M3 monthsLAnderson et al., 1999, 2000, 2006; Tranel et al., 2002
U-22RHCase 2M65RMendez et al., 2000
U-23RHNRM14RCrucian et al., 2000
U-24RHNRM13RNyffeler and Regard, 2001
U-25RHCB-2310W71RTranel et al., 2002
U-26RHDV-1589M32RTranel et al., 2002
U-27RHRW-1768M54RTranel et al., 2002
U-28RHNRM24RBurns and Swerdlow, 2003
U-29RHCase 1M5NRNakaji et al., 2003
U-30RHCase 2M3.5NRNakaji et al., 2003
U-31RHD3M3AAnderson et al., 2006
U-32RHD4MBirth defectRAnderson et al., 2006
U-33RHPF1M3 daysLAnderson et al., 2007
U-34RH2713M46RTranel and Bechara, 2009
U-35RHNRM39RDevinsky et al., 2010
U-36RHPatient BMUncertainNRJonker et al., 2011
U-37RHCase 2M±60RScarpazza et al., 2018

Acquired sociopathy due to Unilateral (U) hemispheric damage (mania, mental retardation, and dementia excluded).

a

LH, left hemisphere; RH, right hemisphere.

b

M, man; NR, not reported; W, woman.

c

Age expressed in years unless stated otherwise.

d

A, ambidextrous; L, left-handed; NR, not reported; R, right-handed.

Table 2

CodeIdentificationSexaAge at injurybHandednesscReferences
B-1Franz BinzM32NRWelt, 1888
B-2Case 1M25NRvan Gehuchten, 1913
B-3JAM41NRBrickner, 1939, 1952
B-4KMM16RHebb and Penfield, 1940
B-5JPM4NRAckerly, 1964
B-6ALMadulthoodNRGoldar and Outes, 1972
B-7ABM±50NRRegestein and Reich, 1978
B-8EVRM35REslinger and Damasio, 1985
B-9Case 1M39RMiller et al., 1986
B-10GKM7 daysRPrice et al., 1990
B-11SG 1208M71RDamasio et al., 1990
B-12DM 1336MadulthoodRDamasio et al., 1990
B-13SNM11NRWilliams and Mateer, 1992
B-14Mrs. CW39ROrtego et al., 1993
B-15MGMcongenitalNRBenítez et al., 1996
B-16Case 1M21NRJurado and Junqué, 2000
B-17JSM56RBlair and Cipolotti, 2000
B-18NRM36RFrohman et al., 2002
B-19CDM26NRCato et al., 2004
B-20318MadulthoodRAnderson et al., 2006
B-211106MadulthoodRAnderson et al., 2006
B-221445MadulthoodRAnderson et al., 2006
B-231584MadulthoodRAnderson et al., 2006
B-241643MadulthoodRAnderson et al., 2006
B-25CLM14RMitchell et al., 2006a,b
B-26Case 1M36RKoenigs et al., 2007
B-27Case 2M48RKoenigs et al., 2007
B-28Case 6M59RKoenigs et al., 2007
B-29HNM53NRNamiki et al., 2008
B-30Patient 8M56NRMendez et al., 2011
B-31Patient AMadulthoodNRJonker et al., 2011
B-32Case 2McongenitalNRTrebuchon et al., 2013
B-33Case 3MuncertainNRTrebuchon et al., 2013
B-34NRM32RFumagalli et al., 2015
B-35NRM62NRSartori et al., 2016
B-36MHW4APrice et al., 1990
B-37FL 1164WadulthoodRDamasio et al., 1990
B-38HS 1065WadulthoodRDamasio et al., 1990
B-39SALW38RCicerone and Tanenbaum, 1997
B-40FDW15 monthsAAnderson et al., 2000
B-41Case 1W35NRJurado and Junqué, 2000
B-421164WadulthoodRAnderson et al., 2006
B-431942WadulthoodRAnderson et al., 2006
B-44Case 3W33RKoenigs et al., 2007
B-45Case 4W50RKoenigs et al., 2007
B-46Case 5W53RKoenigs et al., 2007
B-47Case 1WcongenitalRTrebuchon et al., 2013
B-48GCWearly developmentalRIbáñez et al., 2018

Acquired sociopathy due to Bilateral (B) hemispheric damage (mania, mental retardation, and dementia excluded).

a

M, man; NR, not reported; W, woman.

b

Age expressed in years unless stated otherwise.

c

A, ambidextrous; L, left-handed; NR, not reported; R, right-handed.

Statistical Analysis

Because most variables of interest were categorical, they were analyzed with the χ2 and related statistics. A significance threshold of 0.05, two-tailed, was set for all tests. Statistical power and effect sizes were computed with Cramér's V and classified as small (0.10), medium (0.30) or large (0.50) following Cohen's guidelines (Cohen, 1992).

Results

Tables 14 present the main results of the literature survey. Duplicate cases are also indicated in the tables. The main features leading to a diagnosis of acquired sociopathy in each case are presented in Tables 3 and 4 for the unilateral and bilateral cases, respectively. Readers may thus judge for themselves the appropriateness of the present analysis.

Table 3

CodeFeatures supportive of a diagnosis of sociopathy
U-1Excellent premorbid moral conduct. Arrested twice for robbery. Apathetic and indifferent to the disgrace and discomfort of imprisonment. More irritable than used to be.
U-2The patient developed subtle changes in personality and displayed poor financial judgment. He began to make sexual proposals toward his 7-year-old daughter and her friends. Arrested for propositioning children in his neighborhood.
U-3Honest and reliable as a worker and husband prior to brain injury. Thereafter, he became emotionally unstable, disinhibited and impulsive. Developed irresponsible behavior at work and at home. Unable to reassume regular jobs. Bankruptcy. Divorce.
U-4Normal social and emotional development. Personality changes included impairment of emotional expression and in the establishment of meaningful relationships. Sexually promiscuous up to seven boyfriends at a time. Unable to hold a job for more than a few weeks despite intact operational learning. At work, poor interpersonal skills, inability to execute the required activities, and failure to learn from mistakes.
U-5The subject was a college graduate who had a successful career as an advertising executive. He was involved in gambling activities. Strangled his wife and threw her body out of the window of a 13th floor apartment. He systematically arranged the crime scene in order to make it look like she committed suicide. An insanity defense was presented but the subject was convicted of manslaughter and sentenced to 7–21 years in prison.
U-6Childhood marked by social isolation and aggression. The subject was convicted of murder and rape. Exhibited profound difficulties in representing the mental states of others.
U-7Worked as a responsible bookkeeper before surgery. Soon thereafter, became impulsive and unpredictable. Impairments of social conduct, emotional processing, and decision-making. Discharged due to unreliability in her work attendance. Unable to hold other jobs.
U-8The subject exhibited deviant sexual behavior. Convicted multiple times of sexual attacks.
U-9After left temporal lobectomy, the patient developed prominent difficulties in emotional functioning and personality, marked especially by emotional lability and irritability. She was dismissed from her job due to inability to perform her duties. Disinhibition, impulsivity and perseveration were also observed during neuropsychological examination.
U-10Normal developmental milestones. Parents reported uncharacteristic behavior including stealing, lying, aggression, rage, rude language, and disobedience. Lack of response toward punishment. Impulsivity and disrespect for authority. Hypersexual behavior. Arson.
U-11Sentenced to 1 year in prison for a pedophilia-related offense, namely, physical assault and sexual harassment of his pubescent stepdaughter. Also exhibited depression, apathy and mild aggressive behavior. No premorbid history of sexual deviancy. A large tumor in the left frontal lobe on MRI.
U-12Evaded school since an early age. Known in his birthplace as the “Original” and the “Failure.”
U-13Came from a highly industrious family and worked as a baker. After suffering a traumatic occipital head injury, he developed transient loss of vision, after which he feigned severe visual loss, and became sexually promiscuous. Had numerous (heterosexual) affairs outside his marriage, often slept in the streets and did not care for his family. Alcoholic. Increasingly reported for neglect, loitering and begging. Known by his relatives as “the scoundrel of K.”
U-14Killed 16 people, including his mother and wife, and wounded other 32.
U-15Charged for assaulting and having incestuous intercourse with his 14-year-old daughter as well as for stripping himself naked and exhibiting his penis to two teenage girls. Caught several times by his wife in the cowshed having sex with cows and calves.
U-16Complicated birth. The patient exhibited destructive play behavior and inability to adjust to peer group at kinder garden. In school, he frequently engaged in fights for minor reasons and became offensive toward women. Murdered an 8-year-old boy by beating, strangling and stabbing him after being insulted. In a psychiatric unit he became easily irritated and displayed hostile attitude toward staff members. Overall intellectual capacities were slightly below average.
U-17Normal premorbid history. Aggressiveness, emotional lability and restlessness. Reacted violently with kicking, hitting and cursing at anyone who attempted to curb his bad behaviors without remorse afterward. The patient was suspended from school in the first grade for refusing to attend classes and assaulting the vice-principal as she attempted to restrain him from escaping school.
U-18Attained the rank of captain in the U.S army; regarded as a strict and evenhanded officer. After the lesion, he started to exhibit tendencies toward poorly controlled hedonic acts including sexual advances. His conversation was blatant, frank, often caustic and unpleasant to those around. Fired from his last job due to verbal dysdecorum. Behavior described as impulsive and self-serving.
U-19Worked for 10 years as a test driver. Married. No medical or psychiatric history prior to injury. Compulsive urge to “borrow” cars after the stroke. Arrested several times. Unable to hold a job for more than a few weeks owing to his compulsion. Over the years borrowed around 100 cars.
U-20Before the injury, he had been honored with more than 10 medals in the army. After his head injury during the Vietnam War, he was demoted of rank due to ineptitude. Unable to handle jobs. Divorced three times after returning from Vietnam. His third wife was a prostitute. Arrested for shoplifting. His parents reported moodiness, sarcasm, lack of social tact, emotional blunting, remoteness of rapport, social withdrawal, inability to make and keep friends and to handle money. The probation officer had to handle his finances once he started to give large amounts of money to people on the streets.
U-21Normal birth and developmental milestones. Impulsiveness and poor judgment since early childhood. Records from the school years indicated that he was disruptive in class and usually failed to turn in assignments on time despite high IQ scores. Unable to manage finances. Fired from several jobs. No realistic planning for the future. His parents described him as showing little or no worry, guilt, empathy, remorse and fear.
U-22Child molestation and hypersexuality.
U-23Normal development and average student at high school with age-appropriate social skills. After surgery, frequent outbursts of verbal and physical aggression. Reduced tolerance to frustration, poor control of impulses. Outbursts described as extreme and out of proportion to the triggering context.
U-24Unremarkable premorbid history. Kleptomania and pathologic gambling following brain surgery.
U-25Following an hemorrhagic stroke, this retired secretary underwent personality changes characterized by depression, anxiety, impulsivity, dependency, and loss of social adequacy, judgment and tact.
U-26Worked as a minister and counselor prior to stroke. Thereafter, severe impairment in behavioral organization, judgment, planning, social conduct and decision-making. No longer able to maintain a job or meet the basic exigencies of everyday life.
U-27Permanent and severe changes in personality and social conduct. Abulia, blunted affect and difficulty seeing tasks to fruition were reported. Unable to work.
U-28The OF injury likely exacerbated a preexisting interest in pornography, sexual deviancy and pedophilia. During a neurologic exam, he solicited sexual favors from female team members. Could not refrain from acting on his pedophilia despite awareness that this behavior was inappropriate, stating that “the pleasure principle overrode” his urge restraint. Symptoms remitted after excision of the tumor.
U-29Aggressive and violent behavior ranging from impulsive physical abuse of other children to an attempt to drop a brick on the head of an adult. Multiple suicide attempts. Frequently tried to ride his skateboard in the freeway. Antisocial behavior resolved after surgery.
U-30Aggressive behavior composed of unprovoked screaming fits and episodic attacks of rage and violence against other children. Dismissed from 2 preschools due to his antisocial behavior.
U-31Poor tolerance to frustration, emotional lability, irritability, apathy, poor judgment, social inappropriateness and impulsivity.
U-32Poor tolerance to frustration, emotional lability, irritability, apathy, poor judgment, social inappropriateness and impulsivity.
U-33Normal pregnancy and delivery. Difficulties in regulating the expression of disparate emotions (joy, approach, anger) in controlled laboratory settings. Absence of fear to strangers in new settings.
U-34Notable changes in personality and emotional processing after right anterior temporal lobectomy. The patient exhibited marked emotional lability and irritability as reported by his wife. Impulsive and perseverative tendencies were observed during neuropsychological testing. Unable to return to his job.
U-35Postsurgical hyperphagia with coprolalia, hypersexuality with de novo interest in pornography. Arrested at home for downloading child pornography.
U-36Dramatic change of personality after car accident. Charged with multiple criminal offenses thereafter.
U-37Sexually-inappropriate verbal comments during military service that never reached a physical approach. Arrested after forcing a child to touch his penis; seen masturbating close to a school. Pedophilic urges were disorganized and risky. A CT revealed a bulky meningioma over the right frontal and parietal lobes.

Antisocial features in acquired sociopathy due to Unilateral Hemispheric Damage (U).

Table 4

CodeFeatures supportive of a diagnosis of sociopathy
B-1Before the accident, Binz worked as a furrier who loved telling jokes and amusing stories; benevolent, outgoing, and always in a good mood. After falling from a window 100 ft. high without losing consciousness, became quarrelsome, mean, smug and deceitful. During his hospital stay, he took pleasure in frightening and torturing the other patients, sometimes even the medical staff and his close relatives.
B-2Family reported an “impossible, devastating and breaking character.” He threatened other patients with a knife and was eventually discharged from the hospital due to insubordination.
B-3Worked as a stockbroker before undergoing bilateral lobectomy. Cheerful mood with occasional angry tantrums, poor judgment and lack of initiative. No appreciation of the gravity of his situation.
B-4The patient exhibited childish, violent, stubborn and destructive behavior. Neighbors were terrified of him.
B-5Normal development throughout infancy and early childhood. During school years, defined as disobedient, truant, and a poor helper at home. Heartily disliked by peers and lonesome. Sent to a clinic after repeated incidents of masturbation and theft at school. Stealing and running away from home were frequent.
B-6Prior to the accident he was an effective employee; correct, calm and generous with good relations with friends. Following injury, became complainant, petty and aggressive. Forced his wife to have sexual intercourse in front of relatives; masturbated in public.
B-7Previously a normal musician, underwent significant personality changes after a right frontal craniotomy for removal of a meningioma. Used to awakening his wife at night demanding sexual intercourse. Caught in a woodshed engaging in sexual activity with a 5-year-old girl, solicited sexual favors from a 14-year-old boy and repeatedly raped his 8-year-old nephew over a 2-year period. Displayed lack of initiative, spontaneity, emotional lability and impoverished affect.
B-8Normal development. Following surgery, exhibited impaired decision-marking, drifted through several jobs being fired from all, and declared bankruptcy. Divorced twice. Indecisiveness (e.g., could take hours to decide where to dine).
B-9Masturbated and attempted to have intercourse with his wife and female nurses in public.
B-10Serious behavioral difficulties first identified at the age of 8. Did not respond to parental discipline, always sought gratification of his immediate needs, never developed adequate friendships, and blamed his difficulties on others. Dishonorably discharged 6 weeks after joining the Marine Corps. Hospitalized 27 times in psychiatric institutions over the ensuing 10 years; imprisoned 8 times on charges of assault, forgery, grand larceny, drug involvement and lewd behavior. Masturbated in public and was a suspect in the rape of 2 female ward patients. Showed little insight or empathy, felt victimized by others. He was given multiple diagnosis, including antisocial or borderline personality, atypical psychosis and paranoid schizophrenia.
B-11Severe deficits in social conduct, judgment, and planning.
B-12Severe deficits in social conduct, judgment, and planning.
B-13Unremarkable premorbid history. He exhibited tantrum behavior, aggressiveness, social inappropriateness, poor judgment and a tendency to be argumentative. A lack of consideration for others and stubbornness were also reported.
B-14Arrested after seducing and engaging in sexual activity with her son's girlfriend. Offered sex to other minors and requested that her son and his girlfriend engaged in sexual intercourse while she watched. No premorbid history of paraphilic behavior. Sexually inactive during the years that preceded the changes in conduct. Eventually convicted on all counts of child molestation.
B-15Known as a violent man in his neighborhood. Involved in multiple criminal acts. Stole and murdered a person.
B-16Sociable and respected at work prior to injury. Afterwards, engaged in thievery and other criminal activities which were performed with little or no planning: robbed a gas station without covering his face; stole caviar from the supermarket in which he was working at the time disregarding the cameras that would catch him. Except for hyperactivity, no abnormal social behavior was registered during the first years after the accident. The antisocial behavior emerged when his wife left him and under bad influences.
B-17Premorbid normal behavior. The subject exhibited irritability and aggressiveness. Episodes of property damage and violence were frequent and elicited after little provocation. Recklessness regarding others personal safety. Lack of remorse. Failure to plan ahead. Unable to sustain consistent work behavior.
B-18Unremarkable psychological history before the onset of aberrant sexual behavior. Approached and asked sexually explicit questions to strangers; masturbated 10–12 times a day. Reached and touched women breasts, recognizing his wrongdoings, but stating that he acted under irresistible urges.
B-19Straight-A student in high school and promoted several times in the US army. After the injury, became disinhibited, jocular with a parallel decline in social and occupational functioning. Divorced three times and rejected two of his three children.
B-20Behavioral changes included dampening of emotional experience, poorly modulated emotional reactions, defective decision making, especially in the social realm, impaired goal-directed behavior, and striking lack of insight.
B-21Emotional blunting, poorly modulated emotional reactions, defective decision making, especially in the social realm, impaired goal-directed behavior, and striking lack of insight.
B-22Behavioral changes included dampening of emotional experience, poorly modulated emotional reactions, defective decision making, especially in the social realm, impaired goal-directed behavior, and striking lack of insight.
B-23Behavioral changes included dampening of emotional experience, poorly modulated emotional reactions, defective decision making, especially in the social realm, impaired goal-directed behavior, and striking lack of insight.
B-24Behavioral changes included dampening of emotional experience, poorly modulated emotional reactions, defective decision making, especially in the social realm, impaired goal-directed behavior, and striking lack of insight.
B-25Normal development. After his injury, he became socially isolated. His work history was sporadic, and he was routinely dismissed from jobs within weeks or even days. He was first arrested as a young adult when he sexually assaulted and murdered a middle-aged woman. The diagnosis of “post-traumatic psychopathic disorder” was made. During custody, CL was reported to behave in an abrasive, domineering and confrontational manner, lacking insight into his offense and holding an unrealistically high self-opinion. Interpersonal relations are characterized by high rates of poor behavioral controls, sexual promiscuity, grandiosity, glibness, and shallow affect. PCL-R score of 26.3 (77th percentile).
B-26Striking defects in social emotion but intact intellect and normal baseline mood. Severely diminished empathy, embarrassment, guilt and impaired autonomic activity in response to emotionally charged pictures.
B-27Striking defects in social emotion but intact intellect and normal baseline mood. Severely diminished empathy, embarrassment, guilt and impaired autonomic activity in response to emotionally charged pictures.
B-28Striking defects in social emotion but intact intellect and normal baseline mood. Severely diminished empathy, embarrassment, guilt and impaired autonomic activity in response to emotionally charged pictures.
B-29Graduated from high school and ran his own company, working as a highly skilled crane operator. After injury he became apathetic and indifferent. The subject urinated in inappropriate places and displayed anger against his family. Unable to hold finances. Signed contracts without understanding their content. Marked disturbance recognizing facial emotions.
B-30Poor decision making in business; uncharacteristic sexual promiscuity with many recent affairs. Accused of indecent exposure. Poor impulse control during clinical examination.
B-31The subject was prosecuted more than 20 times for multiple offenses. He exhibited aggressiveness, impulsiveness and mood changes. His last conviction was due to shoplifting.
B-32Considered in school as a clever boy with no behavioral problems. During adolescence, disruptive behavior began, and the subject was expelled from school. Impulsive, hyperactive and aggressive displays of violent verbal and physical behavior. Pathological drinking and gambling. Pathological diagnosis: Taylor's dysplasia.
B-33No social disturbances were reported before the onset of the seizures. His career as a football player ended due to social behavior disturbances. The subject exhibited irritability and aggressiveness toward his family, displaying repeated physical assaults which led to 10 locked ward psychiatric admissions. Showed impulsivity with episodes of self-harm, including self-induced bleeding. Expressed no regret for his actions.
B-34Began to manifest pedophilic tendencies persuading 2 boys of 6 and 3 years to perform oral sex on him; displayed exhibitionism, frotteurism and voyeurism.
B-35Unremarkable medical history before the onset of antisocial behaviors. Arrested after being caught enacting sexually inappropriately toward a little girl in his office. While traveling with his wife, stole postcards from exhibitors in museum shops; watched adult pornography on the web, completely worriless of being caught. Pathological crying, easy irritability, childish and obsessive-compulsive behaviors and impairments in emotion attribution, moral reasoning and abstract thinking. MRI revealed compression of the orbitofrontal cortex, optic chiasm and hypothalamus by a clivus chordoma.
B-36Normal development until age 4, when she was struck by an automobile and remained unconscious for 48 h. Thereafter, she developed a low tolerance to frustration indicated by short-lived verbal and physical assaults against others. No sustained friendships. Poor academic performance. Sexually promiscuous. Neglected her 2.5-month-old daughter who was sent to a foster home. Her relatives lived in constant terror; they once called the police when she threatened them at knife point. Frequent outbursts against coworkers and customers in temporary jobs. Two nonplanned suicide attempts.
B-37Severe deficits in social conduct, judgment, and planning.
B-38Severe deficits in social conduct, judgment, and planning.
B-39Graduated from college before the injury. Following discharge from hospital, her husband became concerned about her episodes of abrupt crying and laughing, rigid and obsessive behaviors during daily homemaking activities. Frequent difficulties due to indecisiveness and perplexity by minor changes in her environment, poor judgement and empathy, impulsivity, disinhibition, and self-centeredness.
B-40Normal psychomotor development until age 3, when she was noted to be largely insensitive to punishment. Lied blatantly and frequently, failed to comply with school assignments and was often tardy or absent. Reprimanded for theft, intimidation, violations, destruction of property, and possession of contraband. Pregnant at the age of 18; dangerous insensitivity to infant's needs. Emotions described by relatives and caretakers as labile and poorly matched to context. Unable to articulate plans for the future.
B-41Normal premorbid background. Drastic changes in conduct and personality after the lesion. Unconcerned about personal care. Drug abuse, gambling, and theft became frequent. More irritable, aggressive; did not plan for the future.
B-42Emotional blunting, poorly modulated emotional reactions, defective social decision making and goal-directed behavior; striking lack of insight.
B-43Emotional blunting, poorly modulated emotional reactions, defective social decision making and goal-directed behavior; striking lack of insight.
B-44Striking impairment of social emotions, especially empathy, embarrassment and guilt, but normal baseline mood. Impaired autonomic reactivity to emotionally charged pictures.
B-45Striking impairment of social emotions, especially empathy, embarrassment and guilt, but normal baseline mood. Impaired autonomic reactivity to emotionally charged pictures.
B-46Striking impairment of social emotions, especially empathy, embarrassment and guilt, but normal baseline mood. Impaired autonomic reactivity to emotionally charged pictures.
B-47Described as a “model pupil” in school. At the age of 16, she started to exhibit egocentric and impulsive behavior, frequently directing physical aggression or threats against others. Unfit to work due to seizures and social conduct problems. Served a term in prison for drug abuse and disruptive behavior. Showed no evident remorse. Pathological diagnosis: Taylor's dysplasia.
B-48Disinhibition, impulsivity and disruption of social norms. Expelled from school due to impulsive behavior and recurrent aggression against peers.

Antisocial features in acquired sociopathy due to Bilateral Hemispheric Damage (B).

Acquired Sociopathy From Circumscribed Brain Damage

The main findings of this survey are presented in Table 5 and in Figure 1. There were 37 cases of acquired sociopathy due to unilateral hemispheric damage and 48 cases due to bilateral hemispheric damage; therefore, unilateral lesions leading to sociopathy were almost as frequent as bilateral lesions (binomial test: p = 0.27). There were more men than women in both the uni and the bilateral groups (binomial tests: p < 0.0001), as there were more cases with unilateral right hemisphere damage in the uni and the bilateral groups (binomial tests: p < 0.02). Information on handedness was available for 55 cases, 51 of which were right-handed, two were left-handed, and two were ambidextrous. The age of patients at the time of injury ranged from birth to 71 years (x = 28.8 ± 21.7 years), no statistically significant difference on age at injury being noted between men and women in either the uni or the bilateral groups (Mann-Whitney: U = 505, p > 0.37).

Table 5

WomenMen
Unilateral (N = 37)Right Hemisphere (N = 26)125
Left Hemisphere (N = 11)38
Bilateral (N = 48)1434

Distribution of cases of acquired sociopathy according to gender and lesion laterality.

Figure 1

There was a significant correlation between gender and the uni/bilaterality of brain damage (χ2 = 6.1, df = 1, p < 0.04; Cramér's V = 0.23) as well as between gender and unilateral lesions (χ2 = 4.4, df = 1, p < 0.04) corresponding to medium effect sizes (Cramér's V = 0.35). When only men were considered, the number of cases with uni (N = 37) and bilateral (N = 34) damage did not significantly differ (χ2 = 0.13, df = 1, p > 0.72); however, the number of men with a left hemisphere injury (N = 8) was significantly lower than those with an injury of the right (N = 25) or of both (N = 34) hemispheres (χ2 = 16.4, df = 2, p < 0.0001). When only women were considered, the number of cases with bilateral damage (N = 14) was significantly higher than those with a unilateral (N = 4) lesion (χ2 = 5.6, df = 1, p < 0.02); moreover, there were more cases with bilateral than either with unilateral right (N = 1) or left (N = 3) damage (χ2 = 16.3, df = 2, p < 0.0001). Ordinal regression revealed a significant association between acquired sociopathy and right hemisphere damage in men (OR = 10.3, p < 0.02). No equivalent associations were seen for women regardless of the laterality or bilaterality of damage (OR = 1.1, p > 0.90). The inclusion of handedness and age at which the brain injury was acquired in the regression model did not qualitatively change these results.

Finally, it may seem surprising not to find the case of Phineas Gage in the Tables. The reason for this is the dispute regarding the bilaterality (Damasio et al., 1994) or the unilaterality (Ratiu and Talos, 2004) of Gage's injury, which remains speculative because no postmortem exam was performed on Gage's brain. In addition, the details of Gage's case have often been embellished, distorted, or inferred beyond what is justified by the first-hand reports by Harlow and Bigelow (Macmillan, 2008).

Discussion

The present survey came to some intriguing and unexpected results which may be thus summarized: (i) unilateral lesions are almost as frequent as bilateral lesions leading to acquired sociopathy; (ii) there are relatively few well-documented cases of acquired sociopathy in the medical literature, especially when we consider the length of the historical record; (iii) acquired sociopathy was significantly more common in men after an injury of the right or of both cerebral hemispheres; (iv) in most women who developed acquired sociopathy the lesions affected both cerebral hemispheres; and (v) men outnumbered women in both the unilateral and bilateral groups.

As stated in the Material and Methods section, the point of departure of the present analyses was clinical, not anatomical. The logical next step is to follow the reverse course of case selection beginning with the collection of cases with lesions of the right and the left frontotemporoinsular cortices, and investigate their clinical manifestations according to gender and lesion laterality. These two approaches are not comparable, and the anatomical approach may lead to quite different conclusions.

Gaps in Need of Further Research

Owing to the limitations of the material herein surveyed, the present review should be considered cautiously. These limitations have to do with missing data in several reports, including the handedness of participants, the age at which the brain damage occurred, and when the manifestations of sociopathy were first noted; however, the most important gap is the fact that the anatomical descriptions are often too vague to allow in-depth clinicoanatomical deductions.

Besides the aforementioned gaps in knowledge, the present survey reveals that the number of well-documented cases of acquired sociopathy is surprisingly small, especially in view of the popularity that it has long enjoyed both among scholars and in the lay media (de Oliveira-Souza and Moll, 2019). This partly unfounded popularity has given breadth to the assumption that we know more about the cerebral underpinnings of acquired sociopathy than we actually do. Indeed, one of the main purposes of the present work was to gather these gaps in knowledge in a single communication. There is a pressing need to revive the clinicoanatomical tradition of studying single cases or case series with modern behavioral and neuroimaging methods. Despite its limitations, the postmortem exam remains the gold standard for increasing our knowledge of neural structures and pathways (Goetz, 2010). This assertion is bolstered by the exemplary studies that make up the body of the present survey (e.g., Dimitrov et al., 1999; Cato et al., 2004; Eslinger et al., 2004; Anderson et al., 2007).

Gender and Lesion Asymmetries in Acquired Sociopathy

Acquired sociopathy was significantly more common in men after an injury of the right or of both cerebral hemispheres. A corollary of this finding is that the left hemisphere in men who develop acquired sociopathy due to bi-hemispheric injuries probably plays a minor, if any, role in the genesis of the antisocial personality changes, a finding that is in line with Tranel et al. observations (see Introduction). In most women with acquired sociopathy, in contrast, injuries of both hemispheres were significantly more common than lesions of either hemisphere alone, a finding that is partially in line with Tranel et al. observations.

Despite the wealth of research on cerebral asymmetries and on the differences between the brains of men and women (Cahill, 2006), the neural underpinnings of the interactions between asymmetry and gender have been less studied. The gender and lateral asymmetries in acquired sociopathy revealed by the present survey provide converging evidence that the neural organization of sociomoral conduct in women has a more symmetrical organization in the cerebral hemispheres than in men, in whom the right hemisphere seems to play a dominant role. This conclusion, however provisional, is supported by the broader issue of gender differences in sociopathy (Moffitt et al., 2004) and by the cerebral organization of moral cognition and behavior in men and women (Dulebohn et al., 2016).

In most of the cases herein reviewed, the lesions were in a position to either directly destroy or impinge upon the uncinate fascicle (UF), the ventral amygdalofugal pathway, and the medial forebrain bundle. The UF is a hook-shaped association tract that interconnects the anterior temporal lobe, the insula, and the orbitofrontal and ventromedial prefrontal cortices (Ebeling and von Cramon, 1992). It is composed of five smaller, partially overlapping, fascicles with different origins, trajectories, and terminations (Hau et al., 2017); a remarkable rightward asymmetry of the UF, both in volume and number of fibers, has consistently been noted by researchers (Highley et al., 2002). The UF integrates a collection of cortical areas which play an essential role in the regulation of higher-order social behavior, as shown in extreme form by the human Klüver-Bucy syndrome (Hayman et al., 1998). This functional unity is also profusely interconnected with the amygdala and the basal forebrain bidirectional fiber systems that are responsible for the basic drives and the regulation of the internal milieu of the organism (Livingston and Escobar, 1971), thus allowing the reciprocal interaction between complex social and fundamental organic behaviors (Mogenson and Yang, 1991). For the most part, the frontotemporoinsular cortices fall within the projection fields of the UF, the ventral amygdalofugal pathway (Kamali et al., 2016), the stria terminalis (Baydin et al., 2017), and the inferomedial leaflet of the medial forebrain bundle (Edlow et al., 2016). These tracts funnel through the temporal stem toward the temporal pole and amygdala, a critical region of the white matter in which relatively small injuries may produce major disturbances in moral conduct and social behavior (Kling et al., 1993). The right UF has been shown to be reduced in individuals with psychopathy (Sobhani et al., 2015), but the integrity of other white matter pathways may be disrupted as well (Waller et al., 2017). Thus, there are good reasons to suppose that the UF and neighboring tracts also play a critical role in the manifestations of acquired sociopathy (van Horn et al., 2012).

The Male Preponderance in Acquired Sociopathy: Fact or Artifact?

When we began this project, we had no a priori expectations regarding the relative prevalence of men to women in acquired sociopathy. Neither do we now have a definitive explanation for the higher male-to-female preponderance either in the unilateral (7.2:1) or bilateral (2.3:1) groups. The most parsimonious explanation is provided by epidemiological studies, which indicate that the male preponderance of the present survey is a particular instance of a general phenomenon shared by common neurological illnesses such as stroke, head injury, and epilepsy (Braun et al., 2002). For example, men are three times more likely to suffer a traumatic brain injury than women (Gardner and Zafonte, 2018). The unequal proportion of genders in the literature should not divert us from the possibility that, as far as can be judged from the available cases, the occurrence of acquired sociopathy in injuries of the cerebral hemispheres seems to be strongly modulated by gender and lesion laterality. This hypothesis concurs with a growing body of evidence indicating that gender differences in various aspects of normal social and antisocial behavior mainly reflect neurobiological mechanisms rather than cultural modeling.

Final Remarks

Over a century ago, van Gehuchten (1913) and Agostini (1914) entertained the possibility that the laterality of a lesion in the frontal lobes played a critical role in the determination of acquired sociopathy. At that time, and for the ensuing seven decades, the means to test this possibility relied on postmortem exams, which usually reflect the final stages of the pathological process and often lay distant in time from the clinical and behavioral manifestations of interest. Such drawbacks can now be circumvented by the use of current neuroimaging techniques in the assessment of social cognition (Duclos et al., 2018). The differential neural underpinnings of social cognition between men and women should systematically be considered in the design of experiments on social cognition and behavior. They may be especially valuable to neurosurgeons, and to functional neurosurgeons in particular, in the planning of interventions for tumor resections as well as the choice of the best targets for therapeutic neuromodulation (Darby and Pascual-Leone, 2017). A more precise understanding of the neurobiology of acquired and developmental sociopathy may be closer than ever before.

Statements

Author contributions

RdO-S, TP, JG, and JM contributed to the conception and design of the study. RdO-S and TP collected and organized the database. RdO-S performed the statistical analysis and wrote the first drafts of the manuscript. All authors contributed to manuscript revision, read, and approved the submitted version.

Acknowledgments

RdO-S is indebted to Professor Omar da Rosa Santos (Gaffrée e Guinle University Hospital) for his unwavering institutional support, and to Mr. José Ricardo Pinheiro and Mr. Jorge Baçal (in memoriam) of the Library of the Oswaldo Cruz Institute, Rio de Janeiro, for the retrieval of the rare books and articles.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  • 1

    AckerlyS. S. (1964). A case of paranatal bilateral frontal lobe defect observed for thirty years, in The Frontal Granular Cortex and Behavior, eds WarrenJ. M.AkertK. (New York, NY: McGraw-Hill), 192218.

  • 2

    AgostiniC. (1914). Tumori dei lobi frontali e criminalità. Archivio di Antropologia Criminale Psichiatria Medicina Legale e Scienze Affini35, 544558.

  • 3

    AlpersB. J. (1937). Relation of the hypothalamus to disorders of personality: a case report. Arch. Neurol. Psychiatry38, 291303. 10.1001/archneurpsyc.1937.02260200063005

  • 4

    American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edn., Text Revision (DSM-IV-TR).Washington, DC: American Psychiatric Association.

  • 5

    AndersonS. W.AksanN.KochanskaG.DamasioH.WisnowskiJ.AfifiA. (2007). The earliest behavioral expression of focal damage to human prefrontal cortex. Cortex43, 806816. 10.1016/S0010-9452(08)70508-2

  • 6

    AndersonS. W.BarrashJ.BecharaA.TranelD. (2006). Impairments of emotion and real-world complex behavior following childhood- or adult-onset damage to ventromedial prefrontal cortex. J. Int. Neuropsychol. Soc.12, 224235. 10.1017/S1355617706060346

  • 7

    AndersonS. W.BecharaA.DamasioH.TranelD.DamasioA. R. (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nat. Neurosci.2, 10321037.

  • 8

    AndersonS. W.DamasioH.TranelD.DamasioA. R. (2000). Long-term sequelae of prefrontal cortex damage acquired in early childhood. Dev. Neuropsychol.18, 281296. 10.1207/S1532694202Anderson

  • 9

    AngeliniL.MazzucchiA.PicciottoF.NardocciN.BroggiG. (1980). Focal lesion of the right cingulum: a case report in a child. J. Neurol. Neurosurg. Psychiatry43, 355357.

  • 10

    BakchineS.LacomblezL.BenoitN.ParisotDChainF.LhermitteF. (1989). Manic-like state after bilateral orbitofrontal and right temporoparietal injury efficacy of clonidine. Neurology39, 777891. 10.1212/WNL.39.6.777

  • 11

    BarrashJ.StussD. T.AksanN.AndersonS. W.JonesR. D.ManzelK.et al. (2018). “Frontal lobe syndrome”? Subtypes of acquired personality disturbances in patients with focal brain damage. Cortex106, 6580. 10.1016/j.cortex.2018.05.007

  • 12

    BarrashJ.TranelD.AndersonS. W. (2000). Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal region. Dev. Neuropsychol.18, 355381. 10.1207/S1532694205Barrash

  • 13

    BaydinS.GungorA.TanrioverN.BaranO.MiddlebrooksE. H.RhotonA. L. (2017). Fiber tracts of the medial and inferior surfaces of the cerebrum. World Neurosurg.98, 3449. 10.1016/j.wneu.2016.05.016

  • 14

    BenítezI.MonteroL. O.AffanniJ. M. (1996). Alteraciones de la corteza orbitaria anterior en un sujeto con grave comportamiento antisocial. Alcmeon5: 117.

  • 15

    BensonD. F. (1994). The Neurology of Thinking.New York, NY: Oxford University Press.

  • 16

    BlairR. J. R.CipolottiL. (2000). Impaired social response reversal: a case of “acquired sociopathy”. Brain123, 11221141. 10.1093/brain/123.6.1122

  • 17

    BoesA. D.GrafftA. H.JoshiC.ChuangN. A.NopoulosP.AndersonS. W. (2011). Behavioral effects of congenital ventromedial prefrontal cortex malformation. BMC Neurol.11:151. 10.1186/1471-2377-11-151

  • 18

    BraunC. M. J.Montour-ProulxI.DaigneaultS.RouleauI.KuehnI.PiskoposM.et al. (2002). Prevalence, and intellectual outcome of unilateral focal cortical brain damage as a function of age, gender and etiology. Behav. Neurol.12, 112.

  • 19

    BricknerR. M. (1939). Bilateral frontal lobectomy: Follow-up report of a case. Arch. Neurol. Psychiatry41, 580583. 10.1001/archneurpsyc.1939.02270150154014

  • 20

    BricknerR. M. (1952). Brain of patient “A” after bilateral frontal lobectomy; status of frontal lobe problem. Arch. Neurol. Psychiatry68, 293313.

  • 21

    BurnsJ. M.SwerdlowR. H. (2003). Right orbitofrontal tumor with pedophilia and constructional apraxia sign. Arch. Neurol.60, 437440. 10.1001/archneur.60.3.437

  • 22

    CahillL. (2006). Why sex matters for neuroscience. Nat. Rev. Neurosci.7, 477484. 10.1038/nrn1909

  • 23

    CatoM. A.DelisD. C.AbildskovT. J.BiglerE. (2004). Assessing the elusive cognitive deficits associated with ventromedial prefrontal damage: a case of a modern-day Phineas Gage. J. Int. Neuropsychol. Soc.10, 453465. 10.1017/S1355617704103123

  • 24

    ChoyO.RaineA.VenablesP. H.FarringtonD. P. (2017). Explaining the gender gap in crime: the role of heart rate. Criminology55, 465487. 10.1111/1745-9125.12138

  • 25

    CiceroneK. D.TanenbaumL. N. (1997). Disturbance of social cognition after traumatic orbitofrontal brain injury. Arch. Clin. Neuropsychol.12, 173188. 10.1093/arclin/12.2.173

  • 26

    CohenJ. (1992). A power primer. Psychol. Bull.112, 155159. 10.1037/0033-2909.112.1.155

  • 27

    CohenL.AngladetteL.BenoitN.Pierrot-DeseillignyC. (1999). A man who borrowed cars. Lancet353, 34. 10.1016/S0140-6736(98)09047-3

  • 28

    CrucianG. P.FennellE. B.MariaB. L.QuislingR. G. (2000). Neuropsychological sequelæ of a pituitary germinoma: a case study. Neurocase6, 6572. 10.1080/13554790008402759

  • 29

    DamasioA. R.TranelD.DamasioH. (1990). Individuals with sociopathic behavior caused by frontal damage fail to respond autonomically to social stimuli. Behav. Brain Res.41, 8194. 10.1016/0166-4328(90)90144-4

  • 30

    DamasioH.GrabowskiT.FrankR.GalaburdaA. M.DamasioA. R. (1994). The return of Phineas Gage: clues about the brain from the skull of a famous patient. Science264, 11021105. 10.1126/science.8178168

  • 31

    DarbyR. R.HornA.CushmanF.FoxM. D. (2018). Lesion network localization of criminal behavior. Proc. Natl. Acad. Sci. U.S.A.115, 601606. 10.1073/pnas.1706587115

  • 32

    DarbyR. R.Pascual-LeoneA. (2017). Moral enhancement using non-invasive brain stimulation. Front. Hum. Neurosci.11:77. 10.3389/fnhum.2017.00077

  • 33

    de ChenarC. (1966). Report to the Governor. Medical aspects. Charles Joseph Whitman catastrophe. Austin, TX.

  • 34

    de Oliveira-SouzaR.MollJ. (2019). Moral conduct and social behavior, in Handbook of Clinical Neurology, Third Series: The Frontal Lobes, eds D'EspositoM.GrafmanJ. (New York, NY: Elsevier).

  • 35

    DevinskyJ.SacksO.DevisnkyO. (2010). Klüver-Bucy syndrome, hypersexuality and the law. Neurocase16, 140145. 10.1080/13554790903329182

  • 36

    DimitrovM.PhippsM.ZahnT. P.GrafmanJ. (1999). A thoroughly modern Gage. Neurocase5, 345354. 10.1080/13554799908411987

  • 37

    DuclosH.DesgrangesB.EustacheF.LaisneyM. (2018). Impairment of social cognition in neurological diseases. Rev. Neurol. (Paris) 174, 190198. 10.1016/j.neurol.2018.03.003

  • 38

    DulebohnJ. H.DavisonR. B.LeeS. A.ConlonD. E.McNamaraG.SarinopoulosI. C. (2016). Gender differences in justice evaluations: evidence from fMRI. J. Appl. Psychol.101, 151170. 10.1037/apl0000048

  • 39

    EbelingU.von CramonD. (1992). Topography of the uncinate fascicle and adjacent temporal fiber tracts. Acta Neurochir. Wien, 115, 143148. 10.1007/BF01406373

  • 40

    EdlowB. L.McNabJ. A.WitzelT.KinneyH. C. (2016). The structural connectome of the human central homeostatic network. Brain Connect.6, 187200. 10.1089/brain.2015.0378

  • 41

    EndicottJ.SpitzerR. L.FleissJ. L.CohenJ. (1976). The global assessment scale: a procedure for measuring overall severity of psychiatric disturbances. Arch. Gen. Psychiatry33, 766771. 10.1001/archpsyc.1976.01770060086012

  • 42

    EslingerP. J.BiddleK. R. (2000). Adolescent neuropsychological development after early right prefrontal cortex damage. Dev. Neuropsychol.18, 297329. 10.1207/S1532694203Eslinger

  • 43

    EslingerP. J.BiddleK. R.PenningtonB.PageR. B. (1999). Cognitive and behavioral development up to 4 years after early right frontal lobe lesion. Dev. Neuropsychol.75, 157191. 10.1080/87565649909540744

  • 44

    EslingerP. J.DamasioA. R. (1985). Severe disturbance of higher cognition after bilateral frontal lobe ablation: patient, E. V. R. Neurology35, 17311741. 10.1212/WNL.35.12.1731

  • 45

    EslingerP. J.Flaherty-CraigC. V.BentonA. L. (2004). Developmental outcomes after early prefrontal cortex damage. Brain Cogn.55, 8410310.1016/S0278-2626(03)00281-1

  • 46

    EslingerP. J.GrattanL. M.DamasioH.DamasioA. R. (1992). Developmental consequences of childhood frontal lobe damage. Arch. Neurol.49, 764769. 10.1001/archneur.1992.00530310112021

  • 47

    FaustC. I. (1966). Different psychological consequences due to superior frontal and orbito-basal lesions. Int. J. Neurol.5, 410421.

  • 48

    FineC.LumsdenJ.BlairR. J. R. (2001). Dissociation between ‘theory of mind' and executive functions in a patient with early left amygdala damage. Brain124, 287298. 10.1093/brain/124.2.287

  • 49

    FlynnF.CummingsJ. L.TomiyasuU. (1988). Altered behavior associated with damage to the ventromedial hypothalamus: a distinctive syndrome. Behav. Neurol.1, 4958. 10.1155/1988/291847

  • 50

    FrohmanE. M.FrohmanT. C.MoreaultA. M. (2002). Acquired sexual paraphilia in patients with multiple sclerosis. Arch. Neurol.59, 10061010. 10.1001/archneur.59.6.1006

  • 51

    FumagalliM.FerrucciR.MameliF.MarcegliaS.Mrakic-SpostaS.ZagoS.et al. (2010). Gender-related differences in moral judgments. Cogn. Process.11, 219226. 10.1007/s10339-009-0335-2

  • 52

    FumagalliM.PravettoniG.PrioriA. (2015). Pedophilia 30 years after a traumatic brain injury. Neurol. Sci.36, 481482. 10.1007/s10072-014-1915-1

  • 53

    GardnerA. J.ZafonteR. (2018). Epidemiology of traumatic brain injury, in Handbook of Clinical Neurology, Vol. 138 third series: Neuroepidemiology, eds RosanoC.IkramM. A.GanguliM. (Amsterdam: Elsevier), 207223.

  • 54

    GhoshV. E.MoscovitchM.ColellaB. M.GilboaA. (2014). Schema representation in patients with ventromedial PFC lesions. J. Neurosci.34, 1205712070. 10.1523/JNEUROSCI.0740-14.2014

  • 55

    GilbertF.VraničA. (2015). Paedophilia, invasive brain surgery, and punishment. Bioeth. Inq.12, 521526. 10.1007/s11673-015-9647-3

  • 56

    GoetzC. G. (2010). Jean-Martin Charcot and the anatomo-clinical method of neurology, in: Handbook of Clinical Neurology, Vol. 96 (third series): History of Neurology, eds FingerS.BollerS.TylerK. L. (Amsterdam: Elsevier), 203212.

  • 57

    GoldarJ. C.OutesD. L. (1972). Fisiopatología de la desinhibición instintiva. Acta Psiq. Psicol. Amer. Lat.18, 177185.

  • 58

    GormanD. G.CummingsJ. L. (1992). Hypersexuality following septal injury. Arch. Neurol.49, 308310. 10.1001/archneur.1992.00530270128029

  • 59

    HarringtonC.SallowayS.MalloyP. (1997). Dramatic neurobehavioral disorder in two cases following bilateral anteromedial frontal lobe injury: delayed psychosis and marked change in personality. Neurocase3, 137149. 10.1080/13554799708404047

  • 60

    HartS. D.CoxD. N.HareR. D. (1995). The Hare Psychopathy Checklist: Screening Version.Toronto, ON: Multi-Health Systems.

  • 61

    HauJ.SarubboS.HoudeJ. C.CorsiniF.GirardG.DeledalleC.et al. (2017). Revisiting the human uncinate fasciculus, its subcomponents and asymmetries with stem-based tractography and microdissection validation. Brain Struct. Funct.222, 16451662. 10.1007/s00429-016-1298-6

  • 62

    HaymanL. A.RexerJ. L.PavolM. A.StriteD.MeyersC. A. (1998). Klüver-Bucy syndrome after bilateral selective damage of amygdala and its cortical connections. J. Neuropsychiatry Clin. Neurosci.10, 354358. 10.1176/jnp.10.3.354

  • 63

    HebbD. O.PenfieldW. (1940). Human behavior after extensive bilateral removal from the frontal lobes. Arch. Neurol. Psychiatry44, 421428. 10.1001/archneurpsyc.1940.02280080181011

  • 64

    HighleyJ. R.WalkerM. A.EsiriM. M.CrowT. J.HarrisonP. J. (2002). Asymmetry of the uncinate fasciculus: a post-mortem study of normal subjects and patients with schizophrenia. Cereb. Cortex12, 12181224. 10.1093/cercor/12.11.1218

  • 65

    IbáñezA.ZimermanM.SedeñoL.LoriN.RapacioliM.CardonaJ. F.et al. (2018). Early bilateral and massive compromise of the frontal lobes. Neuroimage Clin.18, 543552. 10.1016/j.nicl.2018.02.026

  • 66

    JarvieH. F. (1954). Frontal lobe wounds causing disinhibition. A study of six cases. J. Neurol. Neurosurg. Psychiatry17, 1432. 10.1136/jnnp.17.1.14

  • 67

    JonkerC.MatthaeiI.SchouwsS. N. T. M.SickensE. P. K. (2011). Twee verdachten met hersenletsel en crimineel gedrag. De bijdrage van de neuroloog aan forensisch psychiatrische diagnostiek. Tijdschr. Psychiatr.53, 181187.

  • 68

    JuradoM. A.JunquéC. (2000). Conducta delictiva tras lesiones prefrontales orbitales. Estúdio de dos casos. Actas Esp. Psiquiatr.28, 337341.

  • 69

    KamaliA.SairH. I.BlitzA. M.RiascosR. F.MirbagheriS.KeserZ.et al. (2016). Revealing the ventral amygdalofugal pathway of the human limbic system using high spatial resolution diffusion tensor tractography. Brain Struct. Funct.221, 35613569. 10.1007/s00429-015-1119-3

  • 70

    KarpmanB. (1947). Moral agenesis. Towards the delimitation of the problem of psychopathic states. Psychiatr. Q.21, 361398. 10.1007/BF01562009

  • 71

    KingM. L.ManzelK.BrussJ.TranelD. (2017). Neural correlates of improvements in personality and behavior following a neurological event. Neuropsychologia.10.1016/j.neuropsychologia.2017.11.023

  • 72

    KlingA. S.TachikiK.LloydR. (1993). Neurochemical correlates of the Klüver-Bucy syndrome by in vivo microdialysis in monkey. Behav. Brain Res.56, 161170. 10.1016/0166-4328(93)90034-N

  • 73

    KoenigsM.TranelD. (2006). Pseudopsychopathy: a perspective from cognitive neuroscience, in The Orbitofrontal Cortex, eds ZaldD. H.RauchS. L. (New York, NY: Oxford University Press), 597619.

  • 74

    KoenigsM.YoungL.AdolphsR.TranelD.CushmanF.HauserM.et al. (2007). Damage to the prefrontal cortex increases utilitarian moral judgements. Nature446, 908911. 10.1038/nature05631

  • 75

    LabbateL. A.WardenD.MurrayG. B. (1997). Salutary change after frontal brain trauma. Ann. Clin. Psychiatry9, 2730. 10.3109/10401239709147771

  • 76

    LesniakR.SzymusikA.ChrzanowskiR. (1972). Multidirectional disorders of sexual drive in a case of brain tumour. Forensic Sci.1, 333338. 10.1016/0300-9432(72)90031-3

  • 77

    LivingstonK. E.EscobarA. (1971). Anatomical bias of the limbic system concept. A proposed reorientation. Arch. Neurol.24, 1721. 10.1001/archneur.1971.00480310045003

  • 78

    LykkenD. T. (2018). Psychopathy, sociopathy, and antisocial personality disorder. in Handbook of Psychopathy, 2nd. Edn., ed PatrickC. J. (New York, NY: The Guilford Press), 2232.

  • 79

    MacmillanM. (2008). Phineas gage—unravelling the myth. Psychologist21, 828831.

  • 80

    MalloyP. F.RichardsonE. D. (1994). The frontal lobes and content-specific delusions. J. Neuropsychiatry Clin. Neurosci.6, 455466. 10.1176/jnp.6.4.455

  • 81

    MarloweW. B. (1992). The impact of a right prefrontal lesion in the developing brain. Brain Cogn.20, 205213. 10.1016/0278-2626(92)90070-3

  • 82

    MartiniusJ. (1983). Homicide of an aggressive adolescent boy with right temporal lesion: a case report. Neurosci. Biobehav. Rev.7, 419422. 10.1016/0149-7634(83)90048-9

  • 83

    MendezM. F.AdamsN. L.LewandowskiK. S. (1989). Neurobehavioral changes associated with caudate lesions. Neurology39, 349354. 10.1212/WNL.39.3.349

  • 84

    MendezM. F.ChowT.RingmanJ.TwitchellG.HinkinC. H. (2000). Pedophilia and temporal lobe disturbances. J. Neuropsychiatry Clin. Neurosci.12, 7176. 10.1176/jnp.12.1.71

  • 85

    MendezM. F.ShapiraJ. S.SaulR. E. (2011). The spectrum of sociopathy in dementia. J. Neuropsychiatry Clin. Neurosci.23, 132140. 10.1176/jnp.23.2.jnp132

  • 86

    MeyersC. A.BermanA. S.ScheibelR. S.HaymanA. (1992). Acquired antisocial personality disorder associated with unilateral left orbital frontal lobe damage. J. Psychiatry Neurosci.17, 121125.

  • 87

    MillerB. L.CummingsJ. L.MclntyreH.EbersG.GrodeM. (1986). Hypersexuality or altered sexual preference following brain injury. J. Neurol. Neurosurg. Psychiatry49, 867873. 10.1136/jnnp.49.8.867

  • 88

    MillerB. L.HouC.GoldbergM.MenaI. (1999). Anterior temporal lobes: social brain, in The Human Frontal Lobes. Functions and Disorders. eds MillerB. L.CummingsJ. L. (New York, NY: The Guilford Press), 557567.

  • 89

    MitchellD. G. V.AvnyS. B.BlairR. J. R. (2006a). Divergent patterns of aggressive and neurocognitive characteristics in acquired versus developmental psychopathy. Neurocase12, 164178. 10.1080/13554790600611288

  • 90

    MitchellD. G. V.FineC.RichellR. A.NewmanC.LumsdenJ.BlairK. S.et al. (2006b). Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex. Neuropsychology20, 280289. 10.1037/0894-4105.20.3.280

  • 91

    MoffittT. E.CaspiA.RutterN.SilvaP. A. (2004). Sex Differences in Antisocial Behavior. Conduct Disorder, Delinquency, and Violence in the Dunedin Longitudinal Study.Cambridge: Cambridge University Press.

  • 92

    MogensonG. J.YangC. R. (1991). The contribution of basal forebrain to limbic-motor integration and the mediation of motivation to action. Adv. Exp. Med. Biol.295, 267290. 10.1007/978-1-4757-0145-6_14

  • 93

    MollJ.de Oliveira-SouzaR.EslingerP. J. (2003). Morals and the human brain: a working model. NeuroReport14, 299305. 10.1097/00001756-200303030-00001

  • 94

    NakajiP.MeltzerH. S.SingelS. A.AlksneJ. F. (2003). Improvement of aggressive and antisocial behavior after resection of temporal lobe tumors. Pediatrics112, e430e433. 10.1542/peds.112.5.e430

  • 95

    NamikiC.YamadaM.YoshidaH.HanakawaT.FukuyamaH.MuraiT. (2008). Small orbitofrontal traumatic lesions detected by high resolution MRI in a patient with major behavioural changes. Neurocase14, 474479. 10.1080/13554790802459494

  • 96

    NicholsI. C.HuntJ. M. (1940). A case of partial bilateral frontal lobectomy. A psychopathological study. Am. J. Psychiatry96, 10631087. 10.1176/ajp.96.5.1063

  • 97

    NyffelerT.RegardM. (2001). Kleptomania in a patient with a right frontolimbic lesion. Neuropsychiatry Neuropsychol. Behav. Neurol.14, 7376.

  • 98

    OmarR.WarrenJ. D.RonM. A.LeesA. J.RossorM. N.KartsounisL. D. (2007). The neuro-behavioural syndrome of brainstem disease. Neurocase13, 452465. 10.1080/13554790802001403

  • 99

    OrtegoN.MillerB. L.ItabashiH.CummingsJ. L. (1993). Altered sexual behavior with multiple sclerosis: a case report. Neuropsychiatry Neuropsychol. Behav. Neurol.6, 260264.

  • 100

    ParadisC. M.HornL.LazarR. M.SchwartzD. W. (1994). Brain dysfunction and violent behavior in a man with a congenital subarachnoid cyst. Hospital Commun. Psychiatry45, 714716. 10.1176/ps.45.7.714

  • 101

    PascalauR.StănilăR. P.SfrângeuS.SzaboB. (2018). Anatomy of the limbic white matter tracts as revealed by fiber dissection and tractography. World Neurosurg.113, e672e689. 10.1016/j.wneu.2018.02.121

  • 102

    PenfieldW.EvansJ. (1935). The frontal lobes of man: a clinical study of maximum removals. Arch. Neurol. Psychiatry58, 115133. 10.1093/brain/58.1.115

  • 103

    PilleriG. (1963). Über einen fall von psychopathischer persönlichkeit mit cholesteatom der orbitalgegend. Arch. Psychiatr. Nervenkr. Z. gesamte Neurol. Psychiatr.204, 349352. 10.1007/BF00341606

  • 104

    PlazaM.du BoullayV.PerraultA.ChabyL.CapelleL. (2014). A case of bilateral frontal tumors without “frontal syndrome”. Neurocase20, 671683. 10.1080/13554794.2013.826696

  • 105

    PoeckK.PilleriG. (1965). Release of hypersexual behavior due to lesion in the limbic system. Acta Neurol. Scand.41, 233244. 10.1111/j.1600-0404.1965.tb04295.x

  • 106

    PriceB. H.DaffnerK. R.StoweR. M.MesulamM-M. (1990). The comportmental learning disabilities of early frontal lobe damage. Brain113, 13831393. 10.1093/brain/113.5.1383

  • 107

    RatiuP.TalosI-F. (2004). The tale of phineas gage, digitally remastered. N. Engl. J. Med.351:e21. 10.1056/NEJMicm031024

  • 108

    RegesteinQ. R.ReichP. (1978). Pedophilia occurring after onset of cognitive impairment. J. Nerv. Ment. Dis.166, 794798.

  • 109

    RelkinN.PlumF.MattisS.EidelbergD.TranelD. (1996). Impulsive homicide associated with an arachnoid cyst and unilateral frontotemporal cerebral dysfunction. Semin. Clin. Neuropsychiatry1, 172183.

  • 110

    RichfieldE. K.TwymanR.BerentS. (1987). Neurological syndrome following bilateral damage to the head of the caudate nuclei. Ann. Neurol.22, 768771. 10.1002/ana.410220615

  • 111

    RylanderG. (1939). Personality changes after operations on the frontal lobes. Acta Psychiatr. Scand.14 (Suppl. 20), 7327.

  • 112

    SandsonT. A.DaffnerK. R.CarvalhoP. A.MesulamM. M. (1991). Frontal lobe dysfunction following infarction of the left-sided medial thalamus. Arch. Neurol.48, 13001303. 10.1001/archneur.1991.00530240106031

  • 113

    SartoriG.ScarpazzaC.CodognottoS.PietriniP. (2016). An unusual case of acquired pedophilic behavior following compression of orbitofrontal cortex and hypothalamus by a clivus chordoma. J. Neurol.263, 14541455. 10.1007/s004150168143-y

  • 114

    ScarpazzaC.PennatiA.SartoriG. (2018). Mental insanity assessment of -pedophilia: the importance of the trans-disciplinary approach. Reflections on two cases. Front. Neurosci.12:335. 10.3389/fnins.2018.00335

  • 115

    SobhaniM.BakerL.MartinsB.TuvbladC.Aziz-ZadehL. (2015). Psychopathic traits modulate microstructural integrity of right uncinate fasciculus in a community population. Neuroimage8, 323810.1016/j.nicl.2015.03.012

  • 116

    StoreyP. B. (1970). Brain damage and personality change after subarachnoid haemorrhage. Br. J. Psychiatry117, 129142. 10.1192/S0007125000192815

  • 117

    SullivanW. C. (1911). Note on two cases of tumour of prefrontal lobe in criminals; with remarks on disorders of social conduct in cases of cerebral tumour. Lancet178, 10041006. 10.1016/S0140-6736(01)69483-2

  • 118

    ThorneloeW. F.CrewsE. L. (1981). Manic depressive illness concomitant with antisocial personality disorder: six case reports and review of the literature. J. Clin. Psychiatry42, 59.

  • 119

    TowP. M.WhittyC. W. M. (1953). Personality changes after operations on the cingulate gyrus in man. J. Neurol. Neurosurg. Psychiatry16, 186193. 10.1136/jnnp.16.3.186

  • 120

    TranelD.BecharaA. (2009). Sex-related functional asymmetry of the amygdala: preliminary evidence using a case-matched lesion approach. Neurocase15, 217234. 10.1080/13554790902775492

  • 121

    TranelD.BecharaA. (2010). Sex-related functional asymmetry in the limbic brain. Neuropsychopharmacol. Rev.35, 340341. 10.1038/npp.2009.122

  • 122

    TranelD.BecharaA.DenburgN. L. (2002). Asymmetric functional roles of right and left ventromedial prefrontal cortices in social conduct, decision-making, and emotional processing. Cortex38, 589612. 10.1016/S0010-9452(08)70024-8

  • 123

    TranelD.DamasioH.DenburgN. L.BecharaA. (2005). Does gender play a role in functional asymmetry of ventromedial prefrontal cortex?Brain128, 28722881. 10.1093/brain/awh643

  • 124

    TranelD.HymanB. T. (1990). Neuropsychological correlates of bilateral amyg dala damage. Arch. Neurol.47, 349355. 10.1001/archneur.1990.00530030131029

  • 125

    TrebuchonA.BartolomeiF.McGonigalA.LaguittonV.ChauvelP. (2013). Reversible antisocial behavior in ventromedial prefrontal lobe epilepsy. Epilepsy Behav.29, 367373. 10.1016/j.yebeh.2013.08.007

  • 126

    TyrerS. P.BrittlebankA. D. (1993). Misdiagnosis of bipolar affective disorder as personality disorder. Can. J. Psychiatry38, 587589. 10.1177/070674379303800903

  • 127

    van GehuchtenA. (1913). Deux cas de lésion grave du lobe frontal: Tumeurs volumineuse du lobe frontal droit et abcès volumineux du lobe frontal gauche par anomalie des sinus. Bull. l'Acad. R. Méd. Belgique27, 536544.

  • 128

    van HornJ. D.IrimiaA.TorgersonC. M.ChambersM. C.KikinisR.TogaA. W. (2012). Mapping connectivity damage in the case of Phineas Gage. PLoS ONE7:e37454. 10.1371/journal.pone.0037454

  • 129

    VannD. (1972). Interval between sustaining brain damage and development of personality change. Med. J. Aust.2, 15071508.

  • 130

    WallerR.HaileyLDottererH. K.MurrayL.MaxwellA. M.HydeL. W. (2017). White-matter tract abnormalities and antisocial behavior: a systematic review of diffusion tensor imaging studies across development. Neuroimage14, 201215. 10.1016/j.nicl.2017.01.014

  • 131

    WeltL. (1888). Ueber charakterveränderungen des menschen infolge von läsionen des stirnhirns. Deutsch. Arch. Klin. Med.42, 339390.

  • 132

    WilliamsD.MateerC. A. (1992). Developmental impact of frontal lobe injury in middle childhood. Brain Cogn.20, 196204. 10.1016/0278-2626(92)90069-X

  • 133

    ZillesK.AmuntsK. (2012). Architecture of the cerebral cortex, in The Human Nervous System, 3rd Edn. eds MayJ. K.PaxinosG. (New York, NY: Elsevier), 836895.

Summary

Keywords

acquired sociopathy, frontal lobe syndromes, hemispheric asymmetry, morality, orbitofrontal syndrome, psychopathy, ventromedial prefrontal cortex

Citation

de Oliveira-Souza R, Paranhos T, Moll J and Grafman J (2019) Gender and Hemispheric Asymmetries in Acquired Sociopathy. Front. Psychol. 10:346. doi: 10.3389/fpsyg.2019.00346

Received

09 July 2018

Accepted

04 February 2019

Published

19 March 2019

Volume

10 - 2019

Edited by

Mattie Tops, VU University Amsterdam, Netherlands

Reviewed by

Nicola Canessa, Istituto Universitario di Studi Superiori di Pavia (IUSS), Italy; Arielle Ryan Baskin-Sommers, Yale University, United States; Jens Foell, Florida State University, United States

Updates

Copyright

*Correspondence: Ricardo de Oliveira-Souza

This article was submitted to Cognition, a section of the journal Frontiers in Psychology

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All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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