ظهور اختلالات فکری و روانی: پیامدها برای رویکرد نوروفیزیولوژیک به اختلالات رشد
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34310||2006||29 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Cognition, Volume 101, Issue 2, September 2006, Pages 414–442
In this paper, I am going to examine the disorder of psychopathy and consider how genetic anomalies could give rise to the relatively specific neuro-cognitive impairments seen in individuals with this disorder. I will argue that genetic anomalies in psychopathy reduce the salience of punishment information (perhaps as a function of noradrenergic disturbance). I will argue that the ability of the amygdala to form the stimulus–punishment associations necessary for successful socialization is disrupted and that because of this, individuals with psychopathy do not learn to avoid actions that will harm others. It is noted that this model follows the neuropsychological approach to the study of developmental disorders, an approach that has been recently criticized. I will argue that these criticisms are less applicable to psychopathy. Indeed, animal work on the development of the neural systems necessary for emotion, does not support a constructivist approach with respect to affect. Importantly, such work indicates that while environmental effects can alter the responsiveness of the basic neural architecture mediating emotion, environmental effects do not construct this architecture. However, caveats to the neuropsychological approach with reference to this disorder are noted.
The intellectual roots of psychopathy can be traced to Pritchard (1835); see (Pichot, 1978). Pritchard developed the concept of “moral insanity” to account for socially damaging or irresponsible behavior that was not associated with known forms of mental disorder. He attributed morally objectionable behavior to be a consequence of a diseased “moral faculty”. Psychiatric and legal classifications have followed this tradition; Antisocial Personality Disorder is a classification within the American Psychiatric Association’s DSM-IV. Unfortunately, the psychiatric diagnoses of Conduct Disorder (CD) and Antisocial Personality Disorder (APD: American Psychiatric Association, 1994) are seriously flawed. These diagnoses of CD and APD focus on the presence of antisocial behavior and tend to identify a highly heterogeneous sample. Indeed, DSM-IV acknowledges this heterogeneity by specifying two forms of CD: childhood- and adolescent- onset types. In childhood-onset type, onset of at least one criterion characteristic of CD must have occurred prior to 10 years of age. In adolescent-onset type there should be not be any criteria characteristic of CD prior to 10 years of age. Because of their lack of precision, the diagnostic rate of CD can reach 16% of boys in mainstream education (American Psychiatric Association, 1994) while the diagnostic rate of APD can reach over 80% in adult forensic institutions (Hart & Hare, 1996). Unsurprisingly, therefore, diagnoses of CD and APD are relatively uninformative regarding an individual’s prognosis. In sharp contrast, the classification of psychopathy, introduced by Hare, 1980 and Hare, 1991, is highly informative. The classification is a very useful predictor of a patient’s future behavior (Hare, 1991) and is at the basis of many recidivism risk assessments. The classification of psychopathy involves affective-interpersonal (e.g., such as lack of empathy and guilt) and behavioral components (e.g., criminal activity and poor behavioral controls); (Frick et al., 1994, Hare, 1980, Hare, 1991 and Harpur et al., 1989). It is a developmental disorder (Harpur & Hare, 1994). In childhood and adolescence, psychopathic tendencies are identified principally by either the use of the Antisocial Process Screening Device (Frick & Hare, 2001) or by the Psychopathy Checklist: Youth Version (Forth et al., 2003 and Kosson et al., 2002). In adulthood, psychopathy is identified though use of the Psychopathy Checklist – Revised (Hare, 1991). A remarkable feature of the behavioral profile of individuals with psychopathy is their excessive displays of instrumental aggression (Cornell et al., 1996 and Williamson et al., 1987). The term instrumental aggression (also referred to as proactive aggression) is used to distinguish aggression that is purposeful and goal directed. The aggression is used instrumentally to achieve a specific desired goal such as obtaining the victim’s possessions or to increase status within a group hierarchy (Berkowitz, 1993). Bullying is an example of instrumental aggression and, unsurprisingly, individuals who engage in bullying behaviors, frequently engage in other forms of instrumental antisocial behavior in other contexts (Roland & Idsoe, 2001). In contrast, reactive aggression (also referred to as affective aggression) occurs when a frustrating or threatening event triggers the aggressive act and frequently also induces anger (Barratt et al., 1999, Barratt et al., 1997, Berkowitz, 1993, Crick and Dodge, 1996 and Linnoila et al., 1983). Importantly, the aggression is initiated without regard for any potential goal. Elevated levels of reactive aggression are found in many disorders; e.g., psychopathy, depression, anxiety, bipolar disorder and post traumatic stress disorder (see, for a review, Blair, 2003a). However, only individuals with psychopathy show elevated levels of instrumental aggression. Instrumental aggression is, of course, a form of instrumental behavior. Whether an individual displays a particular instrumental behavior is a product of their developmental learning experiences and decision-making regarding the current context. The suggestion that will be made here is that the impairment seen in individuals with psychopathy disrupts their capacity for normal socialization such that antisocial behavior is more likely to be displayed (Blair, 1995, Lykken, 1957 and Trasler, 1973). The disorder of psychopathy should be of interest to developmental cognitive neuroscientists for at least two main reasons. First, psychopathy allows us to understand the cognitive mechanisms necessary for the development of morality, an issue that is of clear intrinsic interest. Second, and more importantly, psychopathy represents a developmental disorder which affects a relatively specific set of neuro-cognitive systems. The pathology seen in individuals with psychopathy does not lead to global deficits in the development of a variety of neuro-cognitive systems. Instead, the effects of the pathology influence a relatively specific series of systems. In this paper, I will consider why this is. However, first I will describe the functional impairment seen in individuals with psychopathy. 1.1. What is the functional impairment shown by individuals with psychopathy? Psychopathy is associated with a core set of empirically demonstrated behavioral difficulties. There are clear difficulties with emotional processing (Blair, 1995, Blair et al., 1997, Cleckley, 1976, Eysenck, 1964, Fowles, 1988, Gray, 1987, Lykken, 1995, Mealey, 1995, Patrick, 1994, Pichot, 1978, Trasler, 1978 and Trasler, 1973) and some indications of difficulty with some forms of attentional processing (Jutai and Hare, 1983 and Raine and Venables, 1988). I will concentrate on the difficulties with emotional processing as these have the clearest developmental implications. There is a considerable body of literature revealing that individuals with psychopathy are impaired in the processing of fear-related stimuli. Thus, individuals with psychopathy show impairment in: (1) aversive conditioning (Flor et al., 2002 and Lykken, 1957); (2) generating autonomic responses to anticipated threat (Hare, 1982 and Ogloff and Wong, 1990); (3) the augmentation of the startle reflex to visual threat primes (Herpertz et al., 2001 and Levenston et al., 2000); (4) passive avoidance learning (Lykken, 1957 and Newman and Kosson, 1986); and (5) response reversal (Mitchell et al., 2002 and Newman et al., 1987). In addition, individuals with psychopathy show clear difficulties in empathic responding. Thus, individuals with psychopathy show impaired processing of the sadness and fear of others (Aniskiewicz, 1979, Blair, 1999, Blair et al., 1997 and House and Milligan, 1976). In addition, individuals with psychopathy show impaired recognition of/autonomic responding to sad and fearful facial and vocal expressions (Aniskiewicz, 1979, Blair et al., 2002, Blair, Colledge et al., 2001, Blair, Colledge, Murray et al., 2001, Blair, Monson et al., 2001 and Blair et al., 1997). The fear-related data have led to repeated suggestions that individuals with psychopathy show impairment in the neuro-physiological systems modulating fear behavior (Cleckley, 1976, Eysenck, 1964, Fowles, 1988, Gray, 1987, Lykken, 1995, Mealey, 1995, Patrick, 1994, Pichot, 1978, Trasler, 1978 and Trasler, 1973). Developmentally, these positions all assume that moral socialization is achieved through the use of punishment (Eysenck and Gudjonsson, 1989 and Trasler, 1978). In essence, they assume that the healthy individual is frightened by punishment and associates this fear with the action that resulted in the punishment thus making the individual less likely to engage in the action in the future. They suggest that individuals with psychopathy, because they are less aversively aroused by punishment, make weaker associations and thus are more likely to engage in the punished action in the future than healthy individuals. However, several researchers have questioned the assumption that conditioned fear responses play a crucial role in moral socialization (Blackburn, 1988 and Blair and Morton, 1995). Thus, the developmental literature indicates that moral socialization is not achieved through the formation of conditioned fear responses but rather through the induction and fostering of empathy (Hoffman, 1984). Studies have shown, for example, that moral socialization is better achieved through the use of induction (reasoning that draws children’s attention to the effects of their misdemeanors on others and increases empathy) than through harsh authoritarian or power assertive parenting practices which rely on the use of punishment (Baumrind, 1971, Baumrind, 1983 and Hoffman and Saltzstein, 1967). Indeed, several researchers have suggested that while empathy may facilitate moral socialization, fear may actually obstruct it (Brody and Shaffer, 1982 and Hoffman, 1994). On a related note, if healthy individuals learn to avoid antisocial behavior because of fear of punishment, it must be assumed that the healthy child judge all rules/transgressions in a similar way. In other words, if we learn to avoid talking in class and hitting other individuals because we are punished when we commit these actions, there is no reason for us to distinguish between these two transgressions. However, healthy developing children make a distinction between moral (victim-based) and conventional (social order based) transgressions from the age of 36 months (Smetana, 1981, Smetana, 1985 and Smetana, 1993). In other words, children do not judge all transgressions in an identical fashion. Instead, they differentiate between those transgressions that result in harm to another from those that simply cause social disorder. The importance of empathy for moral socialization was one of the reasons for the development of the Violence Inhibition Mechanism model of psychopathy and moral development (Blair, 1995 and Blair et al., 1997). At its simplest, I argued that the Violence Inhibition Mechanism (VIM) was a system that when activated by distress cues (the sad and fearful expressions of others) results in increased autonomic activity, attention and activation of the brainstem threat response system (usually resulting in freezing); (Blair, 1995); see Fig. 1. I considered the VIM to be activated whenever distress cues are displayed rather than being reliant upon contextual information about ongoing violence for activation. In line with the model, the display of distress cues has been found to result in the inhibition of not only aggression (Perry & Perry, 1974) but also non-violent disputes over property ownership (Camras, 1977) and sexual activity (Chaplin, Rice, & Harris, 1995). Full-size image (11 K) Fig. 1. The Violence Inhibition Mechanism model. Key to Fig. 1: arrows indicate information flow. The broken arrow represents that transgression stimuli will only come to activate the VIM after learning has occurred; pairings of the transgression representations with distress cues. Boxes indicate putative mechanisms. Figure options The main focus of the model was to describe the cognitive prerequisites for moral development. According to the model, moral socialization occurs through the pairing of the activation of the mechanism by distress cues with representations of the act that caused the distress cues (Blair, 1995). Through association these representations of moral transgressions become triggers for the mechanism. The appropriately developing child thus initially finds the pain of others aversive and then, through socialization, the thoughts of acts that cause pain to others aversive. I proposed that individuals with psychopathy have had disruption to this system such that representations of acts that cause harm to others do not become triggers for the VIM (Blair, 1995). One early index of appropriate moral socialization, and thus the developmental integrity of the VIM, is the demonstration by the child of the moral/conventional distinction mentioned above. Children with psychopathic tendencies and adults with psychopathy show impairment in distinguishing moral and conventional transgressions (Blair, 1995, Blair, 1997, Blair, Jones et al., 1995, Blair, Sellers, et al., 1995, Blair, Colledge et al., 2001, Blair, Colledge, Murray et al., 2001 and Blair, Monson et al., 2001); see, for related work with children with Behavior Disorder and CD (Arsenio and Fleiss, 1996 and Nucci and Herman, 1982). In addition, and in line with the VIM position, psychopathic adults show reduced comprehension of situations likely to induce guilt although they show appropriate comprehension of happiness, sadness and even complex social emotions such as embarrassment (Blair, Jones et al., 1995 and Blair, Sellers, et al., 1995). Moreover, and a direct prediction of the model, children and adults with psychopathy show pronounced impairment in processing sad and fearful facial and vocal expressions (Aniskiewicz, 1979, Blair et al., 2002, Blair, 1999, Blair, Colledge et al., 2001, Blair, Colledge, Murray et al., 2001, Blair, Monson et al., 2001, Blair et al., 1997 and House and Milligan, 1976). However, while the original VIM model could provide an account of the emergence of instrumental antisocial behavior in individuals with psychopathy and while it did generate a variety of predictions that have been empirically confirmed, it faced a serious difficulty; it could not account for the data associated with the fear hypotheses. Moreover, it could not account for data on the interaction of temperament and socialization practice on the development of moral development/ conscience. Kochanska has stressed the role of fearfulness as the important temperamental factor (Kochanska, 1993 and Kochanska, 1997). Indeed, she and others have found fearful children to show higher levels of moral development/conscience using a variety of measures (Asendorpf and Nunner-Winkler, 1992, Kochanska, 1997, Kochanska et al., 1994 and Rothbart et al., 1994). In addition, Kochanska has stressed that different socialization practices may promote moral development in children with different temperaments (Kochanska, 1993 and Kochanska, 1997). In line with this, she found that for fearful children, maternal gentle discipline promoted moral/conscience development. In contrast, for “fearless” children, alternative socialization practices, presumably capitalizing on mother-child positive orientation (secure attachment, maternal responsiveness), promoted the development of conscience (Kochanska, 1997). Because of these difficulties for the VIM model, I recently expanded it at both the cognitive and neural levels (Blair, 2003a, Blair, 2003b, Blair, 2003c, Blair, 2004 and Blair and Charney, 2003); see below. 1.1.1. Summary Individuals with psychopathy are profoundly impaired in the processing of fear-related stimuli and in the processing of the fearful and sad expressions of others. The Violence Inhibition Mechanism (VIM) model provided an account of the impairment in the processing of sad and fearful expressions in individuals with psychopathy and the implications of this impairment for moral development in these individuals. However, the VIM model cannot be considered a complete model of psychopathy; notably, it could not account for the impairments in the processing of fear-related stimuli in individuals with psychopathy. In the following sections of this paper, I will consider a series of issues. First, I will consider whether there is a genetic basis to this disorder. Second, I will consider the neural and neuro-chemical systems on which I believe this genetic contribution may be operating (the systems which mediate the basic response to threat). Two options will be considered: (a) the genetic anomalies disrupt the functioning of the amygdala; and (b) the genetic anomalies disrupt the functioning of specific neurotransmitter(s) which are involved in specific aspects of amygdala functioning, in particular coding punishment information. Third, I will consider other neural systems that may be dysfunctional in psychopathy, in particular, the extent of orbital frontal cortex dysfunction in psychopathy. Within these second and third issues, I will develop a neuro-cognitive account of psychopathy, the Integrated Emotion Systems model. Fourth, I will consider the dissimilarities between psychopathy and another disorder linked to impairment in social cognition, autism. Fifth, I will consider psychopathy with respect to the neuropsychological approach to developmental disorders. I will point out the considerable benefit the study of psychopathy has gained from the neuro-psychological approach. However, I will also point out the limits of the neuro-psychological approach; specifically, the pathology associated with psychopathy is not equivalent to that seen subsequent to an amygdala lesion. 1.2. What is the ultimate cause of psychopathy? Growing evidence suggests a genetic contribution to psychopathy. Early twin, adoption, and family studies indicated that antisocial behavior was heritable (Rhee & Waldman, 2002). However, such studies are difficult to interpret. Much antisocial behavior is goal directed: the individual mugs the victim for their wallet, the individual steals the bag to obtain its contents, the individual engages in an elaborate sting operation to gain another person’s money. It is extremely unlikely that there is a direct genetic contribution to these behaviors or at least it is as likely as there is a direct genetic contribution to the use of a light switch to enable the navigation of a dark room. An individual might learn to use a light switch and under particular conditions, alternatively he/she might learn to mug people for their wallets. However, where genetics are likely to play a role is in determining the probability that the individual will learn an antisocial strategy to gain money (mugging other people) as opposed to a strategy sanctioned by society (using an ATM machine at the end of the workday). Many individuals have argued that the emotional dysfunction shown by individuals with psychopathy makes them more likely to learn antisocial strategies to reach goals ( Blair, 1995, Eysenck, 1964, Lykken, 1995 and Trasler, 1973). The argument developed here is that there may be a genetic contribution to the emotional dysfunction and that it is this which results in an apparent genetic contribution to antisocial behavior. Recent data suggests that this is indeed the case. Blonigen, Carlson, Krueger, & Patrick (2003) collected data from 353 adult male twins using the self-report Psychopathic Personality Inventory [PPI] (Lilienfeld & Andrews, 1996). The PPI includes 163 items and forms a global index of psychopathy with eight sub-scales. Most of these subscales showed moderate heritability (h2 = 0.29–0.56) and negligible shared environmental influence ( Blonigen et al., 2003). Moreover, in a considerably larger study, examining almost 3500 twin pairs within the Twins Early Development Study (TEDS), the callous and unemotional component of psychopathic tendencies was indexed at age 7 ( Viding, Blair, Moffitt, & Plomin, 2005). This study revealed a significant group heritability of View the MathML sourcehg2=.67 and no shared environmental influence on the callous-unemotional component; i.e., genetic factors account for two thirds of the difference between the callous-unemotional probands and the population. As yet, the roles of environmental influences on the emergence of psychopathy remain unclear. The genetics studies above suggested relatively little influence. However, there is a considerable literature indicating a relationship between socioeconomic status (SES) and antisocial behavior (Raine, 1993). With respect to psychopathy, it would be surprising if social variables did not impact on the probability of antisocial behavior; SES, for example, is likely to constrain the possibility of alternative behavioral choices to antisocial behavior as well as increase the salience of the money contained in a potential victim’s wallet. Indeed, in line with this, a relationship between SES and the antisocial behavior component of psychopathy has been reported (Hare, 2003). Thus, genetics would determine the level of emotional dysfunction while the environment would influence how this genetically determined emotion dysfunction was expressed. 1.2.1. Summary It is likely that there is a genetic contribution to psychopathy. I argue that this contributes to the emotional dysfunction that is the basis of the disorder. The emotional dysfunction, in turn, puts the individuals for learning antisocial behaviors to solve goals. Social environmental variables are likely to have an influence, most importantly constraining the possibility of alternative behavioral choices to antisocial behavior as well as potentially increasing the salience of the rewards the might accrue through antisocial behavior. In the following section, I will consider the neural and neuro-chemical architecture upon which this genetic contribution may be operating. 1.3. The basic threat response Three basic responses to threat are freezing, escape behaviors and reactive aggression (a rage attack at the threat); (Blanchard, Blanchard, & Takahashi, 1977). Which behavioral response is initiated is determined by the threat’s intensity and proximity. At low levels of intensity, from a distant threat, the animal will freeze. At higher levels, from a closer threat, the animal will attempt to escape the environment. At higher levels still, when the threat is very close and escape is impossible, the animal will display reactive aggression (Blanchard et al., 1977). These responses to threat are mediated by a neural circuit that is common to many mammalian species (Gregg and Siegel, 2001 and Panksepp, 1998). It runs from medial amygdaloidal areas downward, largely via the stria terminalis to the medial hypothalamus, and from there to the dorsal half of the periaqueductal gray (PAG). With respect to the basic response to threat, these systems function as a unitary entity. Stimulation of any of these systems may induce the basic threat responses. Which one is elicited is determined by the level of stimulation. An important neuro-chemical response to threat involves the noradrenergic system (Charney, 2003 and Francis and Meaney, 1999). When specific neurons in the central nucleus of the amygdala are activated by threat, they activate, in turn, the locus coeruleus, leading to an increase in noradrenaline release. Rogers and others have argued that noradrenaline influences the salience of aversive cues (Rogers, Lancaster, Wakeley, & Bhagwager, 2004); greater noradrenaline levels should allow faster learning about information associated with the aversive cues. With regards to psychopathy, I suggest that the genetic anomalies potentially present in individuals with psychopathy (Blonigen et al., 2003 and Viding et al., 2005), affect particularly a component of this circuit; the amygdala. I argue that this leads to an individual who is less responsive to aversive stimuli. I will consider here two possibilities regarding how this might occur. First, the genetic anomalies disrupt the functioning of the amygdala (Blair, 2001, Blair, 2002, Blair et al., 1999 and Patrick, 1994). Second, the genetic anomalies disrupt the functioning of specific neurotransmitter(s) which are involved in specific aspects of amygdala functioning, in particular coding punishment information (Blair et al., 2006a and Blair et al., 2006b). 1.3.1. Summary The mammalian basic response to threat is mediated by a circuit that runs from the amygdala to the hypothalamus and from there to the peri-aqueductal gray. An important neuro-chemical response to threat involves the noradrenergic system. In the following sections we will consider whether the genetic contribution to psychopathy disrupts the functioning of the amygdala or, perhaps, disrupts the functioning of specific neurotransmitter(s) which are involved in specific aspects of amygdala functioning.