Panic Anxiety in Humans with Bilateral Amygdala Lesions: Pharmacological Induction via Cardiorespiratory Interoceptive Pathways
Abstract
We previously demonstrated that carbon dioxide inhalation could induce panic anxiety in a group of rare lesion patients with focal bilateral amygdala damage. To further elucidate the amygdala-independent mechanisms leading to aversive emotional experiences, we retested two of these patients (B.G. and A.M.) to examine whether triggering palpitations and dyspnea via stimulation of non-chemosensory interoceptive channels would be sufficient to elicit panic anxiety. Participants rated their affective and sensory experiences following bolus infusions of either isoproterenol, a rapidly acting peripheral β-adrenergic agonist akin to adrenaline, or saline. Infusions were administered during two separate conditions: a panic induction and an assessment of cardiorespiratory interoception. Isoproterenol infusions induced anxiety in both patients, and full-blown panic in one (patient B.G.). Although both patients demonstrated signs of diminished awareness for cardiac sensation, patient A.M., who did not panic, reported a complete lack of awareness for dyspnea, suggestive of impaired respiratory interoception. These findings indicate that the amygdala may play a role in dynamically detecting changes in cardiorespiratory sensation. The induction of panic anxiety provides further evidence that the amygdala is not required for the conscious experience of fear induced via interoceptive sensory channels.
Additional Information
© 2016 Khalsa, Feinstein et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution License Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. This article is freely available online through the J Neurosci Author Open Choice option. Received November 15, 2015. Revision received February 11, 2016. Accepted February 12, 2016. This work was supported by NIMH 3R01MH093535-02S2, by NIH/National Center for Advancing Translational Science UCLA CTSI UL1TR000124, from the David Wilder Trust, by NARSAD Young Investigator Awards to J.S.F and S.S.K., and from the William K. Warren Foundation. We thank Courtney Sheen for assistance with participant recruitment, Nahal Sabrkhani for assistance with data collection, Larissa Portnoff for assistance with data management, Kalyanam Shivkumar, and Olujimi Ajijola for assistance with EKG review and equipment support, Belinda Houston and Bill Hirokawa for assistance with isoproterenol preparation, and Eunah Park, Regina Olivas and the entire UCLA Clinical Translational Research Center staff for assistance with protocol implementation. Author contributions: S.S.K. and J.S.F. designed research; S.S.K., J.S.F., and R.H. performed research; S.S.K. and W.L. analyzed data; S.S.K., J.S.F., J.D.F., R.A., and R.H. wrote the paper. S.S.K. and J.S.F. contributed equally to this work. The authors declare no competing financial interests.Attached Files
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Additional details
- PMCID
- PMC4804013
- Eprint ID
- 65899
- Resolver ID
- CaltechAUTHORS:20160404-140752687
- National Institute of Mental Health (NIMH)
- 3R01MH093535-02S2
- National Center for Advancing Translational Science
- UL1TR000124
- David Wilder Trust
- Brain and Behavior Research Foundation
- William K. Warren Foundation
- Created
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2016-04-04Created from EPrint's datestamp field
- Updated
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2022-05-05Created from EPrint's last_modified field