Clinical Study Brain Circulation during Panic Attack: A Transcranial Doppler Study with Clomipramine Challenge Francesco Rotella, 1 Marinella Marinoni, 2 Francesca Lejeune, 1 Fabiana Alari, 2 Daniela Depinesi, 1 Fiammetta Cosci, 3 and Carlo Faravelli 3 1 Psychiatry Unit, Careggi University Hospital, Largo Brambilla 3, 50100 Florence, Italy 2 Neurology Unit, Careggi University Hospital, Largo Brambilla 3, 50100 Florence, Italy 3 Section of Psychology and Psychiatry, Department of Health Sciences, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy Correspondence should be addressed to Francesco Rotella; docrot@gmail.com 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. his 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 low has been well studied in patients with panic disorder, but only few studies analyzed the mechanisms underlying the onset of a panic attack. he aim of the present study was to monitor the cerebral hemodynamics modiications during a panic attack. Materials and Methods. 10 panic disorder patients with recent onset, fully drug na¨ ıve, were compared to 13 patients with panic disorder with a previous history of treatment and to 14 controls. A continuous bilateral monitoring of mean low velocities in right and let middle cerebral arteries was performed by transcranial Doppler. Clomipramine was chosen as challenge. Results. Eight out of 10 patients drug na¨ ıve 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. he occurrence of a panic attack was accompanied by a rapid decrease of low velocities in both right and let middle cerebral arteries. Discussion. he bilateral acute decrease of mean low 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. 1. Introduction Cerebral blood low (CBF) abnormalities have been reported in panic disorder (PD). hese CBF modiications have been studied using diferent imaging techniques: positron emission tomography (PET) [1–3], single photon emission computed tomography (SPECT) [4, 5], and functional mag- netic resonance imaging (fMRI) [6, 7], without a clear identiication of the structures involved. In these studies the central hypothesis was that blood low is coupled to brain activation/deactivation and, therefore, authors chose to use techniques with a greater spatial resolution in order to map these events in the brain at the expense of temporal resolution. Few studies [8–11] could observe PD patients during a panic attack (PA) and, of these, only two [10, 11] managed to describe cerebral activity, using fMRI. Pleiderer et al. [10] found a signiicant increase of activity in the right amygdala during the onset of a spontaneous PA, whereas Dresler and colleagues [11] observed that the neuronal dynamics of the structures involved in the fear network (i.e., amygdala, insula, and prefrontal cortex) mirrored the description of the attack made by a patient that experienced a full blown, spontaneous PA while performing fMRI. he study of cerebral hemodynamics during the onset of a PA would be crucial as a certain evidence of diferent mechanisms underlying PAs is emerging. However, studying cerebral hemodynamics during a PA is diicult because of three factors: (a) it is diicult to pinpoint an occurring PA; (b) the techniques commonly used to assess brain circulation are not sensitive to the real time variations; (c) the challenges commonly used to elicit a PA inluence the brain circulation. Hindawi Publishing Corporation Psychiatry Journal Volume 2014, Article ID 296862, 6 pages http://dx.doi.org/10.1155/2014/296862