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وبلاگ مقالات کامل روانشناسی مصطفی نجفی - اختلالات شخصيت

پنجشنبه 1 آذر1386

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  1. Personality Disorders, Behavioral Disinhibition, and Addiction: next term A Commentary
  2. Robert O. Pihl Corresponding Author Contact Information, a, E-mail The Corresponding Author

  3. aPsychology and Psychiatry, McGill University, Montreal, Quebec, Canada.
    Received 8 June 2007;  accepted 14 June 2007.  Available online 30 August 2007.



  4. Article Outline
  1. As chronic relapsing disorders, addictions seem to mirror the relatively enduring characteristics of a personality disorder. Indeed, the two readily co-occur. In particular, antisocial and borderline personality disorders (ASPD and BPD, respectively) and the adult antisocial behavior syndrome (AABS) (which is ASPD minus a history of conduct disorder) are frequent concomitants with addictions. Consistently, epidemiologic surveys have linked these disorders, with the most recent specific to alcohol problems, the National Epidemiologic Survey on Alcohol and Related Conditions being illustrative. In a U.S. representative sample of individuals with a lifetime diagnosis of alcohol use disorders, ASPD was found in 10.4% of men and 6.6% of women, and AABS was found in 30.3% of men and 26.4% of women ( 1). Regarding BPD, almost half the individuals with this diagnosis have been reported to display an alcohol use disorder at some time in their life ( 2). Not only are these co-occurring disorders relatively prevalent but they also signify increased severity and, in the case of BPD, increased risk for suicide. Greater comorbidity, of course, exists for other addictions, particularly illegal drugs, but as alcohol problems are the most prevalent, they are the primary focus of this commentary.
  2. Treatment of comorbid addiction and personality disorders has been particularly pessimistic ( 3). Treatments, with a few exceptions, remain generalized and are tied in formulary fashion to an overarching single DSM-IV-TR diagnosis. As DSM-IV disorders are fundamentally syndromes, there is thus a natural obfuscation of differential etiology. This results in a definite lack of the necessary discriminability for understanding mechanisms and thus developing and implementing interventions targeted to divergent and even contradictory etiologies in different individuals. Conrod et al. ( 4) have shown in a factor analysis of multiple trait measures of nontreated substance dependent women that the emergent four factors were related to differential drug dependencies and comorbid DSM-IV disorders. For example, impulsive women were co-diagnosed as ASPD and stimulant dependent, whereas anxiety sensitive individuals were labeled with a simple phobia, somatization, and/or generalized anxiety disorder and were dependent on drugs with an anxiolytic effect. Increasingly, therefore, research focus is shifting toward the search for underlying factors, where definition is reduced to the level of markers of putative mechanisms.
  3. The existence of a common underlying factor, or group of factors, must meet a number of criteria. These markers must first be present in individuals who develop and are at risk for the disorder and should correlate with factors such as severity and age of onset. Further, the characteristic cannot be a consequence of the disorder, which, for example, is the typical complication that occurs when studying individuals with a syndrome. When heritability is involved, the marker should also appear in unaffected relatives at a greater incidence than in nonaffected families. Also, importantly, the marker should provide specific biological manifestations. Finally and foremost, the marker should prospectively have predictive power. These requirements underscore the significance of an at-risk/longitudinal research approach. The study of at-risk individuals has the advantages of separating cause from consequence, clarifying predictive factors, allowing the delineation of the hetereogeneity of outcome, and even determining operative, interactive, and feedback mechanisms.
  4. One underlying factor common to some dependencies, and ASPD and BPD in particular, is disinhibitory behavior. However, often lacking is sufficient definitional clarity. Clinical symptoms used to define ASPD and BDP, such as "reckless disregard for safety of self or others" and "impulsivity or failure to plan ahead" (ASPD) and "impulsivity in two self-damaging areas" and "recurrent suicidal gestures" (BPD), are basic to the diagnosis of these disorders. Indeed, impulse control is one of the four enduring behavior patterns descriptive of a personality disorder. Unfortunately, what is reckless, impulsive, and recurrent can be very much in the eye of the beholder and/or influenced by the cultural/situational context, and thus diagnostic reliability suffers, a fact endemic to personality disorders. Hence, in part, is the current argument/movement for definitional improvement emphasizing that these disorders be considered as continuous rather than discreet phenomena ( 5).
  5. To address these clinical deficiencies and to provide a more operational definition of disinhibitory behavior, researchers have turned to paper and pencil and laboratory measures. Commonly used among the former are The Barrett Impulsiveness Scale, The Dickman Impulsiveness Scale, The Kipnis Scale, The Lifetime History of Impulsive Behavior Interview, and many specific scales drawn from popular personality as well as sensation-seeking scales. Regarding laboratory tasks, the go/no-go and stop-signal tasks have tended to become measures of choice. In the go/no-go paradigm, the subject is asked to respond to one set of stimuli and not respond to another, both often rapidly presented, while in the stop-signal task, on some trials, a stop-signal appears following a go signal and a response must be interrupted ( 6). Unfortunately, the level of agreement between rating scales and laboratory measures in the assessment of disinhibition is not robust ( 7). Hence, generalization between studies can be an issue.
  6. Even considering these significant definitional and measurement caveats, disinhibitory behavior and its co-occurring neural/biochemical response patterns, some genetically related, appear essential to understanding why some individuals develop certain addictions. Challenge studies in at-risk individuals where differential behavioral and physical responses to the drug in question are measured and assessed against baseline characteristics provide an optimal test of individual vulnerability.
  7. An exemplar population is sons of male alcoholics, who represent an increased risk of 4 to 9 times for developing the disorder. Numerous reviews have concluded that these individuals display an increased incidence of conduct disorder, attention-deficit disorder, lowered performance on cognitive tests, and differential brain electrophysiology. These characteristics have collectively been labeled as "impaired behavioral regulation," a synonym for disinhibition. However, even in this select risk group, heterogeneity is common. When challenged with an intoxicating dose of alcohol, it is mostly those sons from a multigenerational history of alcoholism who display a particular profile, which includes a heightened heart rate response to the drug, and it is this response that correlates with a history of impaired behavioral regulation. Further testing of these sons of alcoholics and others who also display this high heart rate response has shown that when compared with control subjects, they have, when sober, an increased frequency of problem gambling and risk taking, a history of deviancy, and reduced cognitive functioning. When intoxicated, they are more aggressive on laboratory tasks, show increased errors of commission and shorter reaction times on go/no-go tasks, and display even greater risk-taking behavior ( 8). These individuals also demonstrate higher levels of alcohol consumption; subjectively respond more positively to the drug, both on the rising and falling limb of the blood alcohol curve; retain positively learned material better if followed by drinking; and with positron emission tomography, have been shown to release more dopamine in the nucleus accumbens ( 9). Further, if dopamine depleted, they will work less than control subjects to obtain alcohol and their heart rate increase response can also be blocked with the drug naltrexone ( 10).
  8. Given the pattern of behavior, both sober and intoxicated, that individuals who display this high heart rate response to alcohol display, many but not all of the criteria stated previously of a marker of risk for addiction are established. This response and it would also appear the related disinhibitory behavior are at least, in part, explainable by a hyperresponsivity of a dopaminergic system, the presence of relative cognitive deficits, and the existence of a stimulating situation and/or drug effects that evoke cues of possible reward, the known functionality of this pathway.
  9. One final caveat is warranted, as addictions and disinhibiting behavior represent the ends of differential etiological pathways. The above example of individuals who display an overly excitatory response to a drug that correlates with a disinhibitory behavior and also are cascading toward addiction represents but one putative path. The multilevel study of these individuals, however, can represent a model for studying other groups at risk and delineating their differential pathways. ( 6). 

     
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  11. ROP reports no biomedical financial interests or potential conflicts of interest.
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  14. References
  15. 1 R. Goldstein, D. Dawson, T. Saha, J. Ruan, W. Compton and B. Grant, Antisocial behavioral syndromes and DSM-IV alcohol use disorders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions, Alcohol Clin Exp Res 31 (2007), pp. 814–828. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (1)
  16. 2 S. Wilson, E. Fertuck, A. Kwitel, M. Stanley and B. Stanley, Impulsivity, suicidality, and alcohol use disorders in adolescents and young adults with borderline personality disorder, Int J Adolesc Med Health 18 (2006), pp. 189–196. View Record in Scopus | Cited By in Scopus (1)
  17. 3 V. Sclafani, P. Finn and G. Fein, Psychiatric co-morbidity in long-term abstinent individuals, Alcohol Clin Exp Res 31 (2007), pp. 795–803.
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  20. 6 E. Congdon and T. Canli, The endophenotype of impulsivity: Reaching consilience through behavioral, genetic and neuroimaging approaches, Behav Cogn Neurosci Rev 4 (2005), pp. 262–281. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (4)
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  22. 8 J. Assaad, R. Pihl, J. Séguin, D. Nagin, F. Vitaro and R. Tremblay, Intoxicated behavioral disinhibition and the heart rate response to alcohol, Exp Clin Psychopharmacol 14 (2006), pp. 377–388. Abstract | PDF (141 K) | Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (1)
  23. 9 L. Boileau, J. Assaad, R. Pihl, C. Benkelfat, M. Leyton and M. Diksic et al., Alcohol promotes dopamine release in the human nucleus accumbens, Synapse 49 (2003), pp. 226–231.
  24. 10 J. Peterson, P. Conrod, J. Vassileva, C. Gianoulakis and  




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