2006
DOI: 10.1001/archneur.63.12.1798
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Panic Attacks in an Individual With Bilateral Selective Lesions of the Amygdala

Abstract: To describe the unique case of a patient with panic attacks and bilateral selective amygdala lesions due to Urbach-Wiethe disease.

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Cited by 50 publications
(36 citation statements)
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“…Accordingly, the present study reviewed the translational approaches to the investigation of neural processing of PD. However, because fear-unresponsive Urbach-Wiethe disease patients with extensive bilateral calcifications of the amygdala develop panic both spontaneously (Wiest et al, 2006) and in response to a single deep inhalation of 35% CO 2 (Feinstein et al, 2013), the present study emphasised the likely mediation of PD by the PAG and, to a lesser degree, the DMH. This approach neither excludes the possible participation of PAGprojecting efferents of the ventromedial hypothalamus (VMH) in the non-respiratory type of panic (Wilent et al, 2010), nor does it exclude the eventual participation of the amygdala, the hippocampus and the prefrontal cortex in comorbid anticipatory anxiety and agoraphobia.…”
Section: Towards a Translational Model Of Panic Disordermentioning
confidence: 83%
See 1 more Smart Citation
“…Accordingly, the present study reviewed the translational approaches to the investigation of neural processing of PD. However, because fear-unresponsive Urbach-Wiethe disease patients with extensive bilateral calcifications of the amygdala develop panic both spontaneously (Wiest et al, 2006) and in response to a single deep inhalation of 35% CO 2 (Feinstein et al, 2013), the present study emphasised the likely mediation of PD by the PAG and, to a lesser degree, the DMH. This approach neither excludes the possible participation of PAGprojecting efferents of the ventromedial hypothalamus (VMH) in the non-respiratory type of panic (Wilent et al, 2010), nor does it exclude the eventual participation of the amygdala, the hippocampus and the prefrontal cortex in comorbid anticipatory anxiety and agoraphobia.…”
Section: Towards a Translational Model Of Panic Disordermentioning
confidence: 83%
“…Accordingly, although we cannot discard the involvement of angiotensin-II and orexin systems in anxious states accompanying thirst and hunger, LAC-induced behavioural effects in 'panic-prone' rats are unlikely to reproduce clinical panic. As mentioned, the hypothesised participation of the amygdala in panic attacks was also severely compromised by recent studies showing that patients with extensive bilateral calcifications of the amygdala develop panic attacks both spontaneously (Wiest et al, 2006) and in response to 35% CO 2 (Feinstein et al, 2013).…”
Section: Modelling the Lactate Vulnerability Of Panic Disorder Patientsmentioning
confidence: 99%
“…57 Remarkably, findings of greater amygdala activation in patients with panic disorder than in healthy controls are inconsistent, 9,58 and panic attacks have even been observed in patients with amygdala lesions. [59][60][61] Thus, the amygdala seems to be associated with relevance detection and salience processing, 62,63 initiating a cascade of panic-related activations without being necessarily involved in (all) full-blown panic attacks. 60 The thalamus, as a sensory relay station, is important for the fast processing of incoming visual input and weighing its relevance.…”
Section: Discussionmentioning
confidence: 99%
“…7 Subsequent medial temporal lobe architectural distortion with gliotic tissue and calcium accumulation can lead to a constellation of reported neurologic manifestations, which range from migraine, variable degrees of mental retardation, seizures, depression, anxiety, and panic attacks to disturbances in decision making, memory, and abnormal social interaction patterns. 8,9 These varied symptoms frequently lead to radiologic evaluation by CT or MR imaging, which, in unsuspected patients, may indicate the proper diagnosis.…”
Section: Patientmentioning
confidence: 99%