اختلال اتونوم در اختلال شخصیت مرزی: مطالعه آزمایشگاهی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33107||2009||8 صفحه PDF||سفارش دهید||7375 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Brain and Cognition, Volume 71, Issue 3, December 2009, Pages 279–286
Recent research suggests that emotional dysfunction in psychiatric disorders can be reflected in autonomic abnormalities. The present study examines sympathetic and parasympathetic autonomic nervous system activity in individuals with Borderline Personality Disorder (BPD) before, during, and following a social stressor task. Data were obtained from an analogue sample of participants screening positive for BPD (n = 12) and healthy controls (n = 28). In general, BPD participants exhibited increased sympathetic activity (indexed by Cardiac Sympathetic Index, CSI; Toichi et al., 1997) and decreased parasympathetic activity (indexed by Respiratory Sinus Arrhythmia, RSA) compared to controls. During the stressful task, BPD and control participants exhibited different trajectories of sympathetic activation: estimates of sympathetic activity increased for BPD participants and decreased for controls. Furthermore, BPD participants reported the task (but not baseline or recovery phases) to be more frustrating than controls. Findings are interpreted in the context of Polyvagal theory.
Borderline Personality Disorder (BPD) is a complex and debilitating psychiatric disorder. According to the DSM-IV-TR, “the essential feature of [BPD] is a pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity that begins by early adulthood and is present in a variety of contexts” (APA, 2000, p. 706). Other indicators of BPD include extreme difficulties with emotion regulation, self-injurious behaviors, intense fears of abandonment, and occasionally the presentation of “psychotic-like” symptoms during times of stress (APA, 2000). BPD affects approximately 2–6% of the general population (APA, 2000, Grant et al., 2008, Torgersen et al., 2001 and Widiger and Weissman, 1991) and as many as 20% of the psychiatric inpatient population (APA, 2001 and Zanarini and Grankenbrug, 2001). Seventy-five percent of individuals diagnosed with BPD are female (APA, 2000). Studies indicate that BPD is frequently comorbid with other psychiatric disorders, particularly mood disorders (Skodol et al., 1999 and Zimmerman and Mattia, 1999) and eating disorders (APA, 2000). Between 70% and 75% of BPD individuals have a history of suicide attempts (Clarkin et al., 1993 and Cowdry et al., 1985), and as many as one in 10 will eventually complete suicide (McGlashan, 1986, Paris, 2002 and Stone, 1993), a rate 50 times higher than the general population (Skodol et al., 2002). In light of the disorder’s prevalence and pernicious course, research on factors that may cause and maintain BPD has increased in recent years. Research suggests that emotion dysregulation is a central, possibly core characteristic of BPD (Conklin et al., 2006, Glenn and Klonsky, 2009 and Linehan, 1993). Several BPD symptoms, including affective instability, inappropriate anger, and chronic emptiness, appear to reflect emotional dysregulation. Other BPD symptoms, such as self-injury, result from emotion dysregulation (Klonsky, 2007 and Klonsky, 2009). Moreover, research suggests that affective instability is the BPD symptom that best predicts the course of the disorder over time (Tragesser, Solhan, Schwartz-Mette, & Trull, 2007). Therefore, clarifying the nature of emotion dysregulation in BPD could enhance knowledge about the disorder’s etiology and treatment. Recently, research has examined how emotion dysregulation in BPD is reflected in central nervous system functioning. Deficits in frontolimbic circuitry, often broadly associated with difficulties inhibiting automatic emotional and behavioral response, have been identified in BPD (see Brendel, Stern, & Silbersweig, 2005 for a review), as has reduced cingulate gray matter, thought to contribute to decreased impulse control and difficulties with emotional processing (Hazlett et al., 2005). A number of studies have also reported increased activation of the amygdala and areas of visual cortex in response to emotional stimuli in BPD. Herpertz et al. (2001) reported increased bilateral activation in the amygdala and fusiform gyri in response to unpleasant compared to neutral images in individuals with BPD compared to controls. Donegan et al. (2003) found similar amygdala hyperactivity in individuals with BPD in response to emotional faces. These data have been interpreted as reflecting the emotional symptoms of BPD (e.g., affective instability, difficulty controlling anger). In contrast, other psychophysiological studies have not always found consistent patterns in how individuals with BPD respond to emotional stimuli. Findings for the eye-blink startle response have been mixed: some groups have found no differences between BPD and Non-BPD individuals in affective modulation of the startle response (Ebner-Priemer et al., 2005, Herpertz et al., 1999 and Herpertz et al., 2002), while others have demonstrated a greater increase in startle response following negative emotional stimuli in BPD (Hazlett et al., 2007). Additionally, as compared to healthy controls, BPD patients have comparable responses to emotional stimuli in terms of skin conductance and self-report ratings (Herpertz et al., 1999), and comparable responses to idiographic stressors in terms of heart rate, skin conductance, and blood pressure (Schmahl et al., 2004). These null results are somewhat surprising given the evidence for differences in central nervous system functioning in individuals with BPD (Donegan et al., 2003 and Herpertz et al., 2001), and the fact that the central and peripheral nervous systems are intertwined (Hagemann et al., 2003 and Thayer and Lane, 2000).