Carbon Dioxide—Induced Anxiety

Woods, Scott W.; Charney, Dennis S.; Goodman, Wayne K.; Heninger, George R.

doi:10.1001/archpsyc.1988.01800250051007

Cited by 219 publications

(45 citation statements)

References 60 publications

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“…Novel to our approach was the employment of continuous (vs. retrospective) measurements of subjective suffocation levels during the Read's rebreathing procedure. Consistent with most earlier studies [3][4][5][6][7][8]24], though not all [9,20], we found that individuals with PD scored significantly higher than did healthy controls on subjective CO 2 challenge responses (e.g., panic attack rate and subjective suffocation), as well as respiratory-related CO 2 challenge responses (e.g., breath-holding CO 2 and ventilatory response). In doing so, our findings lend further weight to the idea that individuals with PD manifest CO 2 hypersensitivity characterized in part by elevated perceptions of suffocation.…”

Section: Discussionsupporting

confidence: 92%

“…Over the last several decades, many investigators have attempted to understand the pathophysiology of PD by studying patients during exposure, under controlled laboratory conditions, to known panicogenic agents (e.g., sodium lactate, bicarbonate, and carbon dioxide). The continuous rebreathing of 5% CO 2 [2][3][4], as well as a single-or double-breath inhalation of 35% CO 2 [5][6][7][8], has been found to initiate panic attacks significantly more often in individuals with PD than in individuals with other anxiety disorders or in healthy controls. Furthermore, individuals with PD experience CO 2 -induced panic attacks as being very similar to naturally occurring attacks [2,4 -6,9].…”

Section: Introductionmentioning

confidence: 99%

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Suffocation and respiratory responses to carbon dioxide and breath holding challenges in individuals with panic disorder

Rassovsky

Abrams

Kushner

2006

Journal of Psychosomatic Research

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Suffocation and respiratory responses to carbon dioxide and breath holding challenges in individuals with panic disorder

Rassovsky

Abrams

Kushner

2006

Journal of Psychosomatic Research

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“…Similarly, cortisol responses have been seen in some acute, high-dose CO 2 challenges [2,15,39], but not in chronic, low-dose challenges [20,31].…”

mentioning

confidence: 91%

“…Catecholamine production (noradrenaline with or without adrenaline) has been noted in some but not all studies [5,15,31,39]. Similarly, cortisol responses have been seen in some acute, high-dose CO 2 challenges [2,15,39], but not in chronic, low-dose challenges [20,31].…”

mentioning

confidence: 95%

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

et al. 2006

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Multiple system atrophy (MSA) and pure autonomic failure (PAF) represent distinct pathological models of autonomic failure in humans. We have investigated the neuroendocrine, behavioural and autonomic cardiovascular responses to the 35% CO2 challenge. Nine patients with MSA, nine with PAF and five control subjects received a single breath of 35% CO2. Peripheral autonomic failure (i.e., PAF) was associated with significantly lower resting noradrenaline levels. All groups demonstrated a significant pressor response to CO2. In controls, the mean pressor response was +60.2 mm Hg, which was significantly smaller in both the PAF (+26.8 mm Hg, P < 0.01) and MSA (+18.3 mm Hg, P < 0.001) patients. In addition, the onset of the response was significantly delayed in both MSA (140.2 s) and PAF (154.2 s) patients compared with controls (32.4 s, P = 0.04 and P = 0.03, respectively). Noradrenaline levels increased only in controls. Central autonomic impairment (i.e., MSA) was associated with lower cortisol release (+8.8% in MSA compared with +35.2% in control and +23.7% in PAF) and fewer somatic symptoms of emotional arousal. Both MSA and PAF exhibit marked sympathetic autonomic impairment, however, residual (albeit differing) sympathetic pathways can still maintain a partial cardiovascular response. A central autonomic lesion, however, also appears to be associated with blunting of both cortisol and emotional responses to this stress paradigm.

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“…As Klein has repeatedly indicated (Klein, 1993;Klein, 2002;Preter and Klein, 2008), although panic and fear share many characteristics they have important physiological distinctions such as the lack of HPA-axis activation in panic (Hollander et al, 1989;Kellner and Wiedemann, 1998;Levin et al, 1987;Woods et al, 1988), which is a common neuroendocrine response to fear-related stimuli like exposure to a predator (Blanchard et al, 1998), predator odor (Masini et al, 2005;Masini et al, 2006), or conditioned fear (Cordero et al, 1998), and the presence of dyspnea in panic, which rarely occurs in natural fear responses (Klein, 1993;Preter and Klein, 2008). Although a comprehensive theory of panic disorder is still being formulated, as we shall see next, there is unequivocal neuropsychological evidence for the dissociation of fear and panic.…”

Section: Introduction To Panic Disordermentioning

confidence: 99%

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

Paul

Johnson

Shekhar

et al. 2014

Neuroscience & Biobehavioral Reviews

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The Deakin/Graeff hypothesis proposes that different subpopulations of serotonergic neurons through topographically organized projections to forebrain and brainstem structures modulate the response to acute and chronic stressors, and that dysfunction of these neurons increases vulnerability to affective and anxiety disorders, including Panic Disorder. We outline evidence supporting the existence of a serotonergic system originally discussed by Deakin/Graeff that is implicated in the inhibition of panic-like behavioral and physiological responses. Evidence supporting this panic inhibition system comes from the following observations: 1) serotonergic neurons located in the ‘ventrolateral dorsal raphe nucleus (DRVL) as well as the ventrolateral periaqueductal gray (VLPAG) inhibit dorsal periaqueductal gray-elicited panic-like responses; 2) chronic, but not acute, antidepressant treatment potentiates serotonin’s panicolytic effect; 3) contextual fear activates a central nucleus of the amygdala-DRVL/VLPAG circuit implicated in mediating freezing and inhibiting panic-like escape behaviors; 4) DRVL/VLPAG serotonergic neurons are central chemoreceptors and modulate the behavioral and cardiorespiratory response to panicogenic agents such as sodium lactate and CO2. Implications of the panic inhibition system are discussed.

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Carbon Dioxide—Induced Anxiety

Cited by 219 publications

References 60 publications

Suffocation and respiratory responses to carbon dioxide and breath holding challenges in individuals with panic disorder

Suffocation and respiratory responses to carbon dioxide and breath holding challenges in individuals with panic disorder

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

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