تغییرات در تغییرات واسطه ای دستگاه تنفس در ترس از احساسات جسمانی در اختلال پانیک
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31638||2009||12 صفحه PDF||سفارش دهید||7854 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 43, Issue 6, March 2009, Pages 634–641
The purpose of the study was to examine whether changes in pCO2 mediate changes in fear of bodily sensation (as indexed by anxiety sensitivity) in a bio-behavioral treatment for panic disorder that targets changes in end-tidal pCO2. Thirty-five panic patients underwent 4 weeks of capnometry-assisted breathing training targeting respiratory dysregulation. Longitudinal mediation analyses of the changes in fear of bodily symptoms over time demonstrated that pCO2, but not respiration rate, was a partial mediator of the changes in anxiety sensitivity. Results were supported by cross lag panel analyses, which indicated that earlier pCO2 levels predicted later levels of anxiety sensitivity, but not vice versa. PCO2 changes also led to changes in respiration rate, questioning the importance of respiration rate in breathing training. The results provide little support for changes in fear of bodily sensations leading to changes in respiration, but rather suggest that breathing training targeting pCO2 reduced fear of bodily sensations in panic disorder.
Abnormalities that may maintain panic disorder (PD) include low levels of carbon dioxide partial pressure (pCO2), which is the defining characteristic of hyperventilation, instabilities in blood gas regulation, and oversensitivities of chemoreceptors (oversensitive “suffocation alarm system”; Klein, 1993). There are several experimental studies that support this association: lowering pCO2 into the hypocapnic range or increasing pCO2 into the hypercapnic range often results in panic-like symptoms in PD patients ( Dager et al., 1995, Maddock and Carter, 1991, Wilhelm et al., 2001 and Gorman et al., 2004; but see Beck et al., 1999). Furthermore, sustained hypocapnic levels have been observed in PD ( Papp et al., 1995, Salkovskis et al., 1986 and Meuret et al., 2008; but see also, Garssen et al., 1996). The nature of the pCO2 dysregulation has been outlined in two theories of PD. Klein (1993) postulated a hypersensitive suffocation alarm system that triggers panic attacks when pCO2 rises; consequently PD patients keep levels of pCO2 low. Ley (1985a) emphasized the panicogenic effects of acute hyperventilation by which a vicious circle of chronic and acute levels of hypocapnia (low pCO2 levels) causes feared bodily sensations (in particular, dyspnea), which leads to more hyperventilation. This cycle may ultimately culminate in full-blown panic ( Ley, 1985a, Ley, 1985b and Ley, 1987). If respiratory dysregulation is a central feature of PD, then interventions specifically targeting respiratory dysregulation may be effective in treating it. We tested this idea by devising a capnometry-assisted breathing training therapy that uses immediate feedback to teach patients how to raise their pCO2 over a series of training and practice sessions. The treatment led to sustained increases in pCO2 levels and decreases in respiratory rate and was successful in substantially reducing panic severity and frequency ( Meuret et al., 2008). However, the mechanism by which this treatment worked remains unknown. The purpose of this study was to examine the causal and temporal relationships between pCO2, respiration rate, and self-reported changes in fearful symptom interpretation in a respiratory treatment for PD. We chose anxiety sensitivity (AS) as a measure of fear of bodily symptoms. This construct is conceptualized as a disposition that determines the tendency to respond fearfully to anxiety symptoms such as heart racing or shortness of breath ( Reiss and McNally, 1985). These (feared) physical symptoms are closely related to symptoms triggered by hypocapnia. We predicted that by reducing hypocapnia, a reduction of fear of bodily sensations, and thereby the fearful interpretation of those symptoms, would be achieved. Thus, changes in pCO2 would mediate and precede changes in fearful interpretation of symptoms measured by the anxiety sensitivity index (ASI).