Abstract
Exposure-based cognitive-behaviour therapy (CBT) for anxiety disorders is an effective intervention, but the brain mechanisms driving recovery are largely unknown. In this experimental medicine study, we investigated to what degree CBT affects neural markers of anxiety at an early stage of treatment, to identify dynamic mechanistic changes which might be crucial in the process of recovery as opposed to those seen following full treatment completion. In a randomised controlled trial, unmedicated patients with panic disorder either received four weekly sessions of exposure-based CBT (N = 14) or were allocated to a waiting group (N = 14). Symptom severity was measured before and after the intervention. During functional magnetic resonance imaging (fMRI), patients performed an emotion regulation task, either viewing negative images naturally, or intentionally down-regulating negative affect using previously taught strategies. Four-session CBT led to marked reductions in symptoms and 71% of patients reached recovery status (versus 7% in the control group). This intervention normalised brain hyperactivation previously seen in panic disorder, particularly in areas linked to threat monitoring, fear memory, and maladaptive emotion regulation, such as amygdala, dorsomedial and dorsolateral prefrontal cortex, and temporal gyrus. Our findings suggest that optimal treatment doses for panic disorder might be much lower than previously thought. Furthermore, this is the first study to show that neural markers of anxiety change very early during CBT, highlighting potential neural mechanisms that might drive clinical recovery. Such knowledge is important for the development of more compact combination treatments targeting these mechanisms more effectively. (Neural Effects of Cognitive-behaviour Therapy in Panic Disorder; clinicaltrials.gov; NCT03251235)
Highlights
Exposure-based cognitive-behaviour therapy (CBT) for anxiety disorders—the human equivalent to fear extinction in animal models involving exposure to fearprovoking situations to dispute catastrophic expectations—is an effective first-line treatment[1]
During 4-week CBT, there was a significant reduction of trait anxiety and depression (HADS), fear of physical sensations (BSQ), and agoraphobic cognitions (ACQ) in treated patients, leading to significant group differences compared to the waiting group on all these measures at retest
We found that a brief treatment altered activation in limbic, paralimbic and prefrontal brain areas in patients with panic disorder
Summary
Exposure-based cognitive-behaviour therapy (CBT) for anxiety disorders—the human equivalent to fear extinction in animal models involving exposure to fearprovoking situations to dispute catastrophic expectations—is an effective first-line treatment[1]. It is already well known that anxiety disorders are associated with a distinctive pattern of altered responsivity in a network of limbic and prefrontal-cortical brain regions. Anxiety is associated with increased activation in a range of ventral and lateral prefrontal-cortical regions known to be implicated in emotional control[5]. Most importantly, these patterns of hyperactivation in limbic and prefrontal areas have been shown to resolve with recovery after conventional long-term courses of CBT in phobia, OCD and social anxiety[6,7,8,9,10], reinforcing the idea
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