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Cognitive behavioral therapy-related increases in cortical inhibition in problematic perfectionists
Natasha Radhu1, Zafiris J Daskalakis, Crissa L Guglietti
1School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada.
Background:
Several lines of evidence suggest that cognitive behavioral therapy (CBT) is an effective treatment for depression and anxiety disorders. Evidence suggests that the therapeutic effects of CBT are related to neurophysiologic changes in the cortex, particularly γ-aminobutyric acid (GABA) potentiation. Transcranial magnetic stimulation (TMS) represents a noninvasive method of measuring cortical inhibition, which is a neurophysiologic mechanism associated with the pathophysiology of several psychiatric disorders.
Objective/Hypothesis:
To demonstrate the effectiveness of a 12-week CBT intervention compared with a wait list control group measuring cortical inhibition in participants with pathologic perfectionism. Participants within the CBT group would demonstrate increases in cortical inhibition and improvements on clinical outcomes relative to the wait list control group.
Methods:
Twenty-four right-handed perfectionists were randomly assigned to a 12-week CBT intervention or a wait list control group. Cortical inhibition was measured at pre- and postintervention with TMS paradigms specifically short-interval cortical inhibition and the cortical silent period, which index GABAA and GABAB receptor-mediated inhibitory neurotransmission, respectively.
Results:
The CBT group demonstrated a significant potentiation of the cortical silent period when compared with the wait list control group. The CBT group demonstrated a decrease in anxiety sensitivity and automatic thoughts relative to the control group.
Conclusions:
These findings demonstrate that CBT tailored for perfectionism is accompanied by an increase in cortical inhibition of the motor cortex and positive changes on clinical outcomes. These findings provide compelling evidence for an association between positive CBT effects and a potentiation of GABAergic inhibitory neurotransmission.
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