Panic induced by carbon dioxide inhalation and lack of hypothalamic–pituitary–adrenal axis activation
Psychiatry ResearchPublished 1 May 1999Open access
Smit S. Sinha, Jeremy D. Coplan, Jack M. Gorman, Daniel Pine, José Antônio Baddini Martínez, Donald F. Klein
Citations95
SJR quartileQ1
SJR score1.61
SNIP1.29
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TL;DR
Results lend support to the hypothesis that the pathophysiological mechanism underlying CO2-induced panic is different from that underlying general or anticipatory anxiety.
Abstract
It has been hypothesized that spontaneous panic is distinct from anticipatory anxiety, which activates the hypothalamic-pituitary-adrenal (HPA) axis. Panic attacks characterized by prominent respiratory symptoms, such as those induced by sodium lactate, are not associated with increases in cortisol. We examined blood cortisol responses to CO2-induced panic. Cortisol levels did not increase and actually decreased significantly in 10 panicking subjects with panic disorder. No reductions were noted after 20 min of CO2 inhalation in either eight normal comparison subjects or six non-panicking panic disorder patients. These results lend support to the hypothesis that the pathophysiological mechanism underlying CO2-induced panic is different from that underlying general or anticipatory anxiety.
Keywords
PsychologyNeuroscience
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