Brain regions showing increased activation by threat-related words in panic disorder

Stanford University, Palo Alto, California, United States
Neuroreport (Impact Factor: 1.52). 04/2003; 14(3):325-8. DOI: 10.1097/01.wnr.0000059776.23521.25
Source: PubMed


Threat-related stimuli consistently activate the posterior cingulate cortex in normal subjects and have exaggerated effects on memory in patients with panic disorder. We hypothesized that panic patients would show increased response to threat-related stimuli in the posterior cingulate cortex. While undergoing fMRI, six panic patients and eight healthy volunteers made valence judgements of threat-related and neutral words. Both groups showed threat-related activation in the left posterior cingulate and left middle frontal cortices, but the activation was significantly greater in panic patients. Panic patients also had more right>left asymmetry of activation in the mid-parahippocampal region. The increased responsivity observed in the posterior cingulate and dorsolateral prefrontal cortices is consistent with the hypothesis that panic disorder patients engage in more extensive memory processing of threat-related stimuli.

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    • "In agreement, PD patients show a deficit in discrimination learning by presenting an enhanced startle potentiation response to the learned safety cue rather than abnormal reactivity to the danger cue (Lissek et al., 2009). On the other hand, the hypoactive response of the anterior cingulate cortex when emotionally negative or conflictive information has to be processed (but see Maddock et al. (2003)) seems to translate into a disinhibition of the amygdala and increased fear expression in PD patients. Another potential area with abnormal functioning in PD is the orbitofrontal cortex. "
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    ABSTRACT: Fear is an ancestral emotion, an intrinsic defensive response present in every organism. Although fear is an evolutionarily advantageous emotion, under certain pathologies such as panic disorder it might become exaggerated and non-adaptive. Clinical and preclinical work pinpoints that changes in cognitive processes, such as perception and interpretation of environmental stimuli that rely on brain regions responsible for high-level function, are essential for the development of fear-related disorders. This review focuses on the involvement of cognitive function to fear circuitry disorders. Moreover, we address how animal models are contributing to understand the involvement of human candidate genes to pathological fear and helping achieve progress in this field. Multidisciplinary approaches that integrate human genetic findings with state of the art genetic mouse models will allow to elucidate the mechanisms underlying pathology and to develop new strategies for therapeutic targeting. Copyright © 2015. Published by Elsevier B.V.
    European journal of pharmacology 03/2015; 759. DOI:10.1016/j.ejphar.2015.03.039 · 2.53 Impact Factor
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    • "Cerebral blood flow (CBF) abnormalities have been reported in panic disorder (PD). These CBF modifications have been studied using different imaging techniques: positron emission tomography (PET) [1] [2] [3], single photon emission computed tomography (SPECT) [4] [5], and functional magnetic resonance imaging (fMRI) [6] [7], without a clear identification of the structures involved. In these studies the central hypothesis was that blood flow 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. "
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    ABSTRACT: 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.
    03/2014; 2014:296862. DOI:10.1155/2014/296862
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    • "Increased activity in the dorsolateral and dorsomedial prefrontal cortex (PFC), inferior frontal gyrus, hippocampus , anterior cingulate cortex (ACC), posterior cingulate cortex, orbitofrontal cortex and left middle frontal cortices has been reported in PD (Bystritsky et al., 2001; Ball et al., 2013; Dresler et al., 2012). A right-left asymmetry of the activity of the parahippocampal regions has also been found (Maddock et al., 2003), confirming the findings from earlier PET studies. However, some work reports less amygdala and cingulate cortex activation in PD patients during a fearful faces task (Pillay et al., 2006; Ottaviani et al., 2012). "
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    ABSTRACT: Models of the neuroanatomy of panic disorder (PD) have relied on both animal work on fear and on clinical data from neuroimaging. Early work hypothesised a network of brain regions involved in fear processing (e.g. the amygdala), but more recent work has also pointed to the involvement of other cortical areas and other brain circuitry (e.g. the insula and anterior cingulate cortex). Studies investigating functional and structural brain connectivity in PD may ultimately shed light on the extent to which the neuroanatomy of PD is localised versus distributed, and on how current treatments alter this neuroanatomy. Copyright © 2013 John Wiley & Sons, Ltd.
    Human Psychopharmacology Clinical and Experimental 11/2013; 28(6). DOI:10.1002/hup.2349 · 2.19 Impact Factor
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