دانلود مقاله ISI انگلیسی شماره 32732
عنوان فارسی مقاله

علائم اختلال نقص توجه/بیش فعالی در بزرگسالان: رابطه با سیستم رویکرد رفتاری گری

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
32732 2006 12 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Attention-Deficit/Hyperactivity Disorder symptoms in adults: Relationship to Gray’s Behavioral Approach System
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Personality and Individual Differences, Volume 40, Issue 4, March 2006, Pages 749–760

کلمات کلیدی
اختلال نقص توجه/بیش فعالی؛ نظریه حساسیت تقویت؛ سیستم رویکرد رفتاری؛ سیستم بازداری رفتاری
پیش نمایش مقاله
پیش نمایش مقاله علائم اختلال نقص توجه/بیش فعالی در بزرگسالان: رابطه با سیستم رویکرد رفتاری گری

چکیده انگلیسی

Disinhibition has received considerable recognition as a primary deficit in Attention-Deficit/Hyperactivity Disorder (AD/HD). The goal of the present study was to investigate claims that Gray’s Behavioral Approach System (BAS) is linked to a disinhibitory deficit and can account for hyperactive-impulsive AD/HD behaviors. A sample of 184 undergraduates responded to measures of Gray’s and other personality dimensions. BAS scores were positively related to and were significant predictors of hyperactive-impulsive symptoms, and also appeared to be related to inattentive AD/HD symptoms in females. Behavioral Inhibition System (BIS) scores did not predict hyperactive-impulsive symptoms, suggesting that it is not a primary deficit for hyperactive-impulsive behaviors. Other disinhibitory pathways along Gray’s model, such as a response modulation deficit, were supported. Overactive BAS functioning is offered as a contributor to hyperactive-impulsive symptoms in adults.

مقدمه انگلیسی

Attention-Deficit/Hyperactivity Disorder (AD/HD) is a developmental disability with three core symptoms, they are inattention, hyperactivity, and impulsivity (American Psychiatric Association, 2000). Those diagnosed with AD/HD are categorized into Predominantly Inattentive, Predominantly Hyperactive-Impulsive, or Combined subtypes. Follow-up studies of children diagnosed with AD/HD report persistence of the disorder into adulthood (see Faraone et al., 2000, for a review). One of the proposed primary deficits in AD/HD is a failure to inhibit goal irrelevant behavior. These disinihibition theories emphasize hyperactive-impulsive symptoms as the core symptom in AD/HD (Nigg, 2001). However, before a resolution can be reached whether disinhibition is a primary cause, it must first be defined. In a review of disinhibitory AD/HD accounts, Nigg (2001) provided a conceptual framework of inhibitory processes and a distinction between types: executive inhibition and motivational inhibition. Executive inhibition processes refer to withholding cognitive and motor responses so that a goal that is internally represented in working memory may be reached at a later time (Nigg, 2001). An example of this inhibitory model is Barkley, 1997a and Barkley, 1997b theory which claims that AD/HD individuals are more likely to fail to suppress responses that are not directed towards an internally represented goal. The motivational account refers to the inhibition of cognitive or behavioral responses to environmental cues of reward or punishment that redirect attention to an unanticipated stimulus (Nigg, 2001). Gray’s (1991) personality model is considered a motivational account and has a particularly long history of involvement in AD/HD deficit accounts (e.g., Quay, 1988 and Quay, 1997). A recent meta-analysis of the Stroop Task, an executive task, indicated performance between AD/HD and control groups does not differ (van Mourik, Oosterlaan, & Sergeant, 2005). Also, alternative accounts to executive disinhibition (i.e., motivational), have not been adequately explored (Nigg, 2001). Additionally, poor motivational inhibition mediates executive inhibition (Avila & Parcet, 2001), indicating that these two disinhibition processes are not distinct and the motivational account should be better understood so that it may be considered in defining the disinhibition process within AD/HD. Therefore, the purpose of the current study was to investigate the relationship between Gray’s dimensions of personality and their relationship to AD/HD symptoms, particularly hyperactivity-impulsivity. 1.1. Reinforcement Sensitivity Theory Gray’s theory—Reinforcement Sensitivity Theory (RST)—emphasizes individual differences along the Behavioral Inhibition System (BIS) and the Behavioral Approach System (BAS) (Pickering & Gray, 1999). Individual differences result from a variation in sensitivity or reactivity along each dimension to specific reinforcing stimuli. The BAS responds to stimuli for reward or relief from punishment (Gray, 1991). The BAS activates the organism in response to cues of reward and is characterized by impulsivity (see Pickering & Gray, 1999, for a review). In past versions of RST, the BIS responds to conditioned stimuli for punishment and nonreward, as well as novelty and innate fear stimuli, to increase passive avoidance and extinction (Gray, 1991). For example, the BIS may cause an organism to stop any ongoing behavior, increase nonspecific arousal, and focus attention on environmental cues and lead to an orienting response. Recent updates emphasize the BIS is also responsible for the resolution of goal conflict in general, such as approach and avoidance conflict (see Corr, 2004, for a summary; Gray & McNaughton, 2000). The BIS is characterized by anxiety (Gray, 1991). 1.2. Application of RST to AD/HD Nigg (2001) provides a review of a motivational model applying RST to AD/HD. In short, a number of pathways to AD/HD within an RST-based framework have received consideration. These pathways include underactive BIS output (Quay, 1988 and Quay, 1997), overactive BAS output, and poor response modulation (Newman and Wallace, 1993 and Patterson and Newman, 1993). Nigg (2001) described another pathway, overactive BIS activity resulting in anxious impulsivity (Wallace, Newman, & Bachorowski, 1991), which seems specific to AD/HD with comorbid anxiety. According to an underactive BIS account (Quay, 1988 and Quay, 1997), passive avoidance is controlled by the BIS. Passive avoidance is the learned inhibition of behavior following a threat of punishment or nonreward. In AD/HD, the BIS provides little output, which leads to an extinction of behavioral inhibition following the cue to a threat and may manifest as hyperactive-impulsive AD/HD behaviors. For example, AD/HD individuals are less responsive to conditioned stimuli cues and indications that punishment or nonreward is likely to be contingent on making a particular response. However, comorbid internalizing disorders resulting from an overactive BIS are common in AD/HD (Biederman et al., 1993) and create conflicting accounts of BIS activity. Both overactive BAS and response modulation deficit accounts suggest hyperactive-impulsive AD/HD symptoms are related to the overactivation of the BAS. Overactive BAS accounts propose that response inhibition is difficult in the presence of cues to reward and results in characteristic hyperactive-impulsive AD/HD symptoms (Newman & Wallace, 1993). Rather than attributing hyperactive-impulsive behavior solely to an overactive BAS, the deficient response modulation model (Newman and Wallace, 1993 and Patterson and Newman, 1993) accounts for the dual role of the BIS. Impulsive behaviors emerge as a result of deficient response modulation between the BAS and BIS. Deficient response modulation involves a failure to suspend a dominant BAS response to receive environmental feedback. When cues to reward are present and activate the BAS in a person with deficient response modulation, the person may be more resistant to BIS activity. In other words, BAS activity is dominant and the BIS cannot interrupt despite the presence of cues to punishment. Instead, the person is overly-focused on goal-directed behavior and has difficulty shifting attention to the nondominant response set. Without response modulation, effortful evaluation and alteration of behavior (i.e., self-regulation) cannot occur (Newman & Wallace, 1993) and learning-impaired response repertoires occur because cues to punishment do not disrupt reward-seeking behavior (Pickering & Gray, 1999). Experimental tasks assessing AD/HD disinhibition within the RST framework provide the strongest support for the latter two accounts discussed above (see Nigg, 2001, for a review). These tasks involve assessing responsiveness to cues to rewards and punishments in laboratory settings. In addition to the evidence reviewed by Nigg (2001), recent studies support a response modulation deficit. For example, Gomez (2003) evaluated the impulsive responding of AD/HD children (Combined subtype) and controls in punishment-only, reward-only, and reward–punishment conditions on the go/no-go task. AD/HD participants displayed greater impulsivity when required to modify their behavior from reward to punishment-mediated cues. This suggests that hyperactive-impulsive AD/HD behaviors are related to BAS functioning, specifically a response modulation deficit. In a study of adult AD/HD Combined and Inattentive subtypes, self-report composite BIS and BAS scores revealed hyperactive-impulsive AD/HD symptoms were related to BAS activity (Kepley, 2002). The Combined subtype was identified with higher BAS scores than the Inattentive subtype. Thus, BAS scores differentiated those with and without hyperactive-impulsive AD/HD symptoms, suggesting BAS activity contributes to hyperactive-impulsive AD/HD symptoms. 1.3. Goals and hypotheses The purpose of the present study was to test the basic assumption of overactive BAS and response modulation deficit accounts that BAS output contributes to hyperactive-impulsive AD/HD symptoms. BAS scores were hypothesized to predict hyperactive-impulsive symptoms in a regression model. BIS scores were not expected to be a significant predictor since overactive BAS and response modulation deficit accounts suggest that BIS activity is not the primary cause of hyperactive-impulsive behaviors. Conduct Disorder (CD) and Anxiety symptoms were also considered as these disorders are proposed to result from BAS or BIS dysfunction, respectively (e.g., Quay, 1988), and can be comorbid with AD/HD symptoms (Faraone et al., 2000). These symptoms may create a spurious relationship between AD/HD symptoms and BIS or BAS as they are also proposed to relate to BIS–BAS dysfunction.

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