Irritable bowel syndrome (IBS) is a chronic gastrointestinal disorder with no identifiable physiological cause that affects 10-15% of the population (Brandt, et al 2002
, Saito, et al 2002
). IBS is characterized by abdominal pain or discomfort associated with altered bowel habits (i.e., constipation and/or diarrhea) and is often accompanied by sensations of distention, urgency, or incomplete evacuation (Longstreth, 2005
). Also, IBS is associated with significant disability and high cost from both health care utilization and loss of productivity (Longstreth, et al 2003
, Pare et al 2006
). IBS patients show an increased risk for a variety of psychiatric conditions, primarily anxiety disorders, depression, and somatization disorder (Whitehead, 2002). IBS may be most strongly associated with panic disorder and generalized anxiety disorder (Lydiard, 1992
Patients with IBS show hypervigilance and hypersensitivity to visceral sensations and increased autonomic arousal to visceral events (Naliboff et al., 1997
; Verne et al., 2001
; Tillisch et al., 2005
). While peripheral GI factors may play a role in subsets of patients with IBS (e.g., post-infectious IBS), converging clinical and neurobiological data suggest that enhanced central stress responsiveness involving anxiety may provide a specific mechanism for enhanced visceral sensitivity (Mayer et al., 2001
). GI symptom-specific anxiety may be an especially important variable leading to increased pain sensitivity, hypervigilance, and poor coping responses (Labus et al 2004
; Hazlett-Stevens et al., 2003
). Consequently, visceral anxiety is seen as a primary affective disturbance in IBS and as the mediating variable between other risk factors (e.g., neuroticism, trait anxiety, worry) and IBS symptom severity (Labus et al., 2005
Existing psychological treatments for IBS include psychodynamic psychotherapy, hypnotherapy, and cognitive-behavioral stress management therapy. Most of these approaches share the assumption that stress or anxiety is a critical feature that needs to be addressed during treatment, and suggest that stress acts to increase IBS symptoms or that increased stress reactivity (or neuroticism) results in IBS symptoms. For example, multicomponent cognitive-behavioral treatments (Blanchard, Schwarz, Suls, Gerardi, Scharff, Greene, Taylor, Berreman, & Malamood, 1992; Greene & Blanchard, 1994; Payne & Blanchard, 1995; Vollmer & Blanchard, 1998, Drossman et al, 2003
, Lackner et al, 2008
) aim to increase awareness of the association among stressors, thoughts, and IBS symptoms, identify and modify cognitive appraisals of situations and behaviors, and change depressive and/or anxiety-based schema (Vollmer & Blanchard, 1998). Several reviews and a meta-analysis generally support the efficacy of these interventions for decreasing IBS symptom severity and associated anxiety and depression when compared to no treatment or standard medical care (Lackner et al., 2004
; Blanchard & Scharff, 2002
; Lackner et al., 2008
). However, findings regarding differences from attention control conditions, such as patient education, are mixed (Drossman et al., 2003
; Creed et al., 2003
). As mentioned, these treatments focus on general stress management, and do not directly address the specific hypervigilance and hypersensitivity to visceral sensations observed in IBS. Outcomes may be improved with such a direct focus of treatment. In support, hypnotherapy for IBS, which has shown successful symptomatic outcomes, focuses on specific suggestions for calming the digestive system and normalizing GI function (Palsson, et al, 2002
The hypersensitivity and hypervigilance to gut sensations observed in IBS is analogous to the sensitivity to bodily sensations observed in panic disorder, in which anxiety becomes acutely focused on somatic sensations associated with panic attacks. For example, individuals with panic disorder become anxious during procedures that elicit sensations similar to ones experienced during panic attacks, such as hyperventilation (Antony, Ledley, Liss, & Swinson, 2006; Gorman et al., 1994; Perna et al., 1995), fear signals that ostensibly reflect heightened arousal in false physiological feedback paradigms (Craske, Lang, Rowe et al., 2002; Ehlers, Margraf, Roth et al., 1988), and preferentially attend to heartbeat stimuli and panic-related verbal stimuli (Kroeze & van den Hout, 2000; Pauli et al., 2005; Teachman, Smith-Janik, & Saporito, 2007). This sensitivity to bodily sensations has been attributed to conditional fear of internal cues (such as elevated heart rate) due to their association with intense fear/distress (Razran, 1961; Bouton et al., 2001) and catastrophic appraisals of bodily sensations as causing physical or mental harm (Clark, 1986; Clark et al., 1988). Consequently, low-level bodily sensations produce anxiety (via conditioning and/or catastrophic appraisals) and the resultant anxiety-induced autonomic arousal intensifies the sensations that are feared, thus creating a reciprocating cycle of fear and sensations that builds into a panic attack (Barlow, 1988, 2002). In turn, anxiety increases the likelihood of panic attacks, by directly increasing the availability of, and/or attentional vigilance to, sensations that have become cues for panic. Finally, avoidance behaviors are believed to maintain catastrophic beliefs about bodily sensations and interrupt natural extinction of conditional fear of bodily sensations.
The corresponding treatment involves cognitive skills for misappraisals of bodily sensations and repeated exposure to feared bodily sensations and situations where panic attacks are expected to occur, in order to extinguish conditional fear responding and provide further evidence to dispute catastrophic misappraisals (e.g., Barlow & Craske, 1994). This treatment has proven to be highly effective for panic disorder (e.g., Barlow et al., 1989; Craske et al., 1997). This model and treatment of panic disorder can be easily translated to a model of treatment for IBS. That is, the fear of gut sensations may contribute to pain intensity and acute IBS episodes. The anxiety about future IBS symptoms and associated vigilance to visceral sensations are likely to provide low level somatic cues that elicit a conditional distress/pain response due to prior experiences; and avoidance of visceral cues is likely to maintain anxiety about them.
The primary aim of the current study was to evaluate the efficacy of a treatment for IBS that directly targets hypervigilance and hypersensitivity to visceral sensations, modeled on the methods used for the treatment of panic disorder. The CBT approach for panic disorder was modified to target IBS by addressing threat-laden appraisals of visceral sensations and anxiety about IBS sensations through cognitive (e.g., cognitive restructuring) and behavioral (i.e., interoceptive and in vivo exposure) exercises. It was hypothesized that those receiving CBT focused on interoceptive cues (IE) would show significantly greater reductions in pain, pain vigilance, and bowel symptoms, and greater improvement in quality of life compared to CBT focused on stress management (SM) and an attention control (AC), with SM outperforming AC.