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Psychiatry Journal
Volume 2014 (2014), Article ID 296862, 6 pages
Clinical Study

Brain Circulation during Panic Attack: A Transcranial Doppler Study with Clomipramine Challenge

1Psychiatry Unit, Careggi University Hospital, Largo Brambilla 3, 50100 Florence, Italy
2Neurology Unit, Careggi University Hospital, Largo Brambilla 3, 50100 Florence, Italy
3Section of Psychology and Psychiatry, Department of Health Sciences, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy

Received 31 October 2013; Revised 23 January 2014; Accepted 11 February 2014; Published 16 March 2014

Academic Editor: Jayne Bailey

Copyright © 2014 Francesco Rotella et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Introduction. Cerebral blood flow has been well studied in patients with panic disorder, but only few studies analyzed the mechanisms underlying the onset of a panic attack. The aim of the present study was to monitor the cerebral hemodynamics modifications during a panic attack. Materials and Methods. 10 panic disorder patients with recent onset, fully drug naïve, were compared to 13 patients with panic disorder with a previous history of treatment and to 14 controls. A continuous bilateral monitoring of mean flow velocities in right and left middle cerebral arteries was performed by transcranial Doppler. Clomipramine was chosen as challenge. Results. Eight out of 10 patients drug naïve and 6 control subjects out of 13 had a full blown panic attack during the test, whereas none of the patients with a history of treatment panicked. The occurrence of a panic attack was accompanied by a rapid decrease of flow velocities in both right and left middle cerebral arteries. Discussion. The bilateral acute decrease of mean flow velocity during a panic attack suggests the vasoconstriction of the microcirculation of deep brain structures perfused by middle cerebral arteries and involved in the so-called “fear circuitry,” thus suggesting that cerebral homeostatic dysfunctions seem to have a key role in the onset of a panic attack.