No chronic hyperventilation in panic disorder patients

Zandbergen, J.; Aalst, Vera van; Loof, Cathrien de; Pols, Henk; Griez, Eric

doi:10.1016/0165-1781(93)90050-q

Cited by 17 publications

(4 citation statements)

References 20 publications

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“…Assuming a functional equivalence at the subjective level between a hyperventilation episode and CO 2 inhalation, the present results may shed light on the finding that in some anxiety or somatoform disorders, psychosomatic complaints similar to those of hyperventilation can be registered (4) in the absence of hypocapnia (8,4,11). Because anxiety states in general are associated with a decreased Pco 2 level (38), occasional hyperventilation episodes are likely to occur during which situations or events may become CSs for conditioned physiologic re-…”

Section: Learning To Have Psychosomatic Complaintsmentioning

confidence: 64%

“…Klein (6) and Papp et al (7) suggested that panic patients hyperventilate as a consequence of a hypersensitive respiratory control mechanism, which is initially triggered by a central buildup of CO 2 . However, recent evidence suggests that hyperventilation may be grossly overstated as a mechanism that produces these complaints, because similar complaints may be present in the absence of a reduced Pco 2 level (8)(9)(10)(11). In addition, normal subjects who score themselves higher on questionnaires measuring negative affective states (12) and subjects reporting more psychosomatic symptoms (3,13) tend to have lower Pco 2 levels.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Learning to have Psychosomatic Complaints

Bergh

Stegen

Woestijne

1997

Psychosomatic Medicine

130

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Section: Learning To Have Psychosomatic Complaintsmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Learning to have Psychosomatic Complaints

Bergh

Stegen

Woestijne

1997

Psychosomatic Medicine

130

View full text Add to dashboard Cite

show abstract

“…Such assessment has been done by very few studies in panic disorder and findings have been mixed. Evidence for chronic hyperventilation using measurements of acid-base balance was found in studies by Gorman et al (1986) and Papp et al (1989), but not Zandbergen et al (1993). Studies assessing end-tidal measures of PCO 2 are more numerous and provide evidence for differences in baseline levels between patients suffering from panic disorder compared to non-panic patients and healthy controls.…”

Section: Hypocapnia In Panic Disordermentioning

confidence: 99%

Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies

Meuret

Ritz

2010

International Journal of Psychophysiology

105

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Sustained or spontaneous hyperventilation has been associated with a variety of physical symptoms and has been linked to a number of organic illnesses and mental disorders. Theories of panic disorder hold that hyperventilation either produces feared symptoms of hypocapnia or protects against feared suffocation symptoms of hypercapnia. Although the evidence for both theories is inconclusive, findings from observational, experimental, and therapeutic studies suggest an important role of low carbon dioxide (CO 2 ) levels in this disorder. Similarly, hypocapnia and associated hyperpnia are linked to bronchoconstriction, symptom exacerbation, and lower quality of life in patients with asthma. Raising CO 2 levels by means of therapeutic capnometry has proven beneficial effects in both disorders, and the reversing of hyperventilation has emerged as a potent mediator for reductions in panic symptom severity and treatment success.

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“…This has however not been replicated in all studies (Zandbergen et al 1993), and there is evidence to suggest that only PD patients of the respiratory subgroup hyperventilate chronically (Moynihan and Gevirtz 2001), but also evidence that chronic hyperventilation is not diagnostically specific to PD but occurs in non-PD anxiety patients as well (van den Hout et al 1992).…”

Section: Panic Disorder and Respirationmentioning

confidence: 99%

Paroxetine influences respiration in rats: implications for the treatment of panic disorder

Olsson¹,

Annerbrink²,

Bengtsson³

et al. 2004

European Neuropsychopharmacology

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SwedenPrinted by Chalmers Reproservice, Göteborg, Sweden Previously published papers were reproduced with kind permission from the publishers. Background and aims: Panic disorder is a psychiatric disorder characterized by sudden attacks of intense anxiety. It displays a lot of features suggesting that it may be associated with an underlying aberration in the autonomic regulation of heart activity and respiration: i) the attacks are often characterized by respiratory symptoms and symptoms from the heart, ii) the attacks can be elicited by respiratory stimulants, iii) between attacks, patients with panic disorder often display enhanced respiratory variability and reduced heart rate variability, and iv) patients with panic disorder display enhanced prevalence of respiratory disorders and enhanced mortality in cardiovascular disease. Addressing the reasons for these physiological aberrations may help in elucidating the pathophysiology underlying panic disorder, and shed light on why this disorder is associated with enhanced mortality in cardiovascular disease. Serotonin is believed to be a neurotransmitter of great importance for panic disorder, as well as for the regulation of respiration: one main purpose of the animal studies presented in this thesis hence was to increase our knowledge regarding the role of serotonin in respiratory regulation, the hypothesis being that aberrations in respiration may cause the anxiety attacks, and that serotoninmodulating drugs may prevent panic attacks partly by stabilizing the regulation of respiration. In the first part of the thesis, data is presented on the effects on respiration in freely moving rats of various serotonergic compounds. The second part of this thesis is focused on genetic variations that may be associated with panic disorder. Orexin is a neuropeptide of suggested importance for both respiratory regulation and arousal. We investigated two polymorphisms in the orexin receptors 1 and 2, HCRTR1 Ile408Val and HCRTR2 Val308Iso, in panic disorder patients and healthy controls. Catechol-O-methyltransferase (COMT) is an enzyme that degrades catecholamines such as dopamine and noradrenaline, and may thus be of importance for both autonomic control and psychiatric symptoms. The functional Val158Met polymorphism in this gene has been associated with panic disorder in several studies; in an attempt to replicate this finding, we genotyped this polymorphism in the same group of panic disorder patients. In a separate cohort, we also explored if the same polymorphism is associated with risk factors for cardiovascular disease. Observations: 1) Serotonin depletion with para-chlorophenylalanine decreased respiratory rate and increased respiratory variability. 2) Chronic treatment with serotonin reuptake inhibitors increased respiratory rate. 3) Acute treatment with serotonin reuptake inhibitors, as well as the serotonin releasing drugs d-fenfluramine and m-CPP, and the 5-HT1A antagonist WAY-100635, decreased respiratory rate. 4) The HCRTR2 Val308Iso polymorphism was significantly...

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No chronic hyperventilation in panic disorder patients

Cited by 17 publications

References 20 publications

Learning to have Psychosomatic Complaints

Learning to have Psychosomatic Complaints

Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies

Paroxetine influences respiration in rats: implications for the treatment of panic disorder

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