CO2 vulnerability in panic disorder

Griez, Eric; Lousberg, H.; Hout, Marcel A. van den

doi:10.1016/0165-1781(87)90001-1

Cited by 192 publications

(66 citation statements)

References 18 publications

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“…Supporting this assumption, lactateinduced panic is associated with hyperventilation (Gorman 1988b; Klein 1993); moreover, in panic disorder patients, as well as in patients with premenstrual dysphoria, panic attacks can be elicited not only by sodium lactate, but also by CO 2 exposure (Gorman et al 1988aGriez et al 1987;Harrison et al 1989;Kent et al 2001;Papp et al 1997;Perna et al 1994;Woods et al 1986). …”

Section: Discussionmentioning

confidence: 97%

“…Supporting this concept, an anxiety-provoking effect similar to that of lactate has been observed after inhalation of CO 2 in panic disorder subjects and in women with premenstrual dysphoria (Gorman et al , 1988aGriez et al 1987;Harrison et al 1989;Kent et al 2001;Papp et al 1997;Perna et al 1994;Woods et al 1986). …”

Section: In Patients With Panic Disorder or Premenstrual Dysphoria Amentioning

confidence: 90%

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Respiratory Responses to Intravenous Infusion of Sodium Lactate in Male and Female Wistar Rats

Olsson

Annerbrink

et al. 2002

Neuropsychopharmacology

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In patients with panic disorder or premenstrual dysphoria, anxiety attacks can be triggered by intravenous administration of sodium lactate. Since respiratory symptoms, such as hyperventilation and shortness of breath, are characteristic features of spontaneous as well as lactate-induced panic, an involvement of central or peripheral chemoreceptors in this reactionIn patients with panic disorder (Liebowitz et al. , 1985Pitts and McClure 1967) or premenstrual dysphoria (Facchinetti et al. 1992;Sandberg et al. 1993), but not in healthy controls, intravenous (i.v.) administration of sodium lactate elicits an anxiety reaction strongly resembling spontaneous panic attacks. The anxiogenic effect of sodium lactate has been attributed to changes in calcium concentrations (Pitts and McClure 1967), pH (Grosz andFarmer 1972), redox activity (Carr et al. 1986), pCO 2 (Gorman et al. 1988a), and osmolarity (Jensen et al. 1991;Peskind et al. 1998). However, all these theories and findings have also been questioned, and the mechanism by which sodium lactate elicits panic attacks hence is as yet unexplained.Likewise, the reason why patients with panic disorder or premenstrual dysphoria differ from controls with respect to sensitivity to lactate is a matter of controversy. Notably, a more rapid and substantial rise in brain lactate has been observed in panic patients as compared with control subjects (Dager et al. 1999), but the difference between patients and controls may also be due to different responsiveness to a given concentration (Pohl et al. 1994;Rifkin et al. 1981).Panic attacks are almost always associated with hyperventilation and respiratory discomfort, such as shortness of breath; it has thus been suggested that lactate-induced as well as spontaneous panic attacks may be due to an activation of a hyperresponsive suffocation alarm system involving activation of central or peripheral chemoreceptors (Klein 1993). Supporting this concept, an anxiety-provoking effect similar to that of lactate has been observed after inhalation of CO 2 in panic disorder subjects and in women with premenstrual dysphoria (Gorman et al. , 1988aGriez et al. 1987;Harrison et al. 1989;Kent et al. 2001;Papp et al. 1997;Perna et al. 1994;Woods et al. 1986).We have previously reported that intravenous administration of sodium lactate to Wistar rats, but not to rats of the Sprague-Dawley strain, elicits an increase in blood pressure and variable effects on heart rate (Wikander et al. 1995). Such cardiovascular response is in line with the assumption that lactate induces a stimulation of central or peripheral chemoreceptors. In the present study, the effect of sodium lactate on respiratory rate and tidal volume in freely moving, unrestrained male and female rats of the Wistar strain was explored. Given the previous reports suggesting that spontaneous panic attacks are menstrual cycle-dependent (Basoglu et al. 2000;Breier et al. 1986;Cameron et al. 1988;Cook et al. 1990;Klein 1993), that panic disorder may improve during pregnancy (Hertzberg and Wa...

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Section: Discussionmentioning

confidence: 97%

Section: In Patients With Panic Disorder or Premenstrual Dysphoria Amentioning

confidence: 90%

Respiratory Responses to Intravenous Infusion of Sodium Lactate in Male and Female Wistar Rats

Olsson

Annerbrink

et al. 2002

Neuropsychopharmacology

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“…(4,6) An alternative method of CO 2 challenge involves a single vital capacity inhalation of a gas mixture containing 35% CO 2 and 65% oxygen. (6) Under these conditions, healthy subjects present with brief but pronounced respiratory stimulation accompanied by neurovegetative symptoms that largely overlap with those reported by panic patients. In panic disorder patients, the same intervention also induces a sharp, transitory rise in anxiety that has been equated with a real life panic attack.…”

Section: Co 2 Challengementioning

confidence: 99%

“…Klein (5) proposed the existence of an evolved "false suffocation alarm" system that triggers spontaneous panic attacks when the brain erroneously signals a lack of useful air and activates maladaptive autonomic responses to suffocation. Sensitivity to CO 2 might play a role in this hypersensitive suffocation detector, (5) and various respiratory tests, such as carbon dioxide inhalation, (6) hyperventilation (7) and breathholding, (8) have been fruitful in generating hypotheses about panic disorder. (3,5) Panic disorder patients exhibit behavioral and physiological abnormal responses to respiratory challenge tests that are very similar to those experienced during spontaneous panic attacks.…”

Section: Introductionmentioning

confidence: 99%

Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications

et al. 2009

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Multiple respiratory abnormalities can be found in anxiety disorders, especially in panic disorder (PD). Individuals with PD experience unexpected panic attacks, characterized by anxiety and fear, resulting in a number of autonomic and respiratory symptoms. Respiratory stimulation is a common event during panic attacks. The respiratory abnormality most often reported in PD patients is increased CO 2 sensitivity, which has given rise to the hypothesis of fundamental abnormalities in the physiological mechanisms that control breathing in PD. There is evidence that PD patients with dominant respiratory symptoms are more sensitive to respiratory tests than are those who do not manifest such symptoms, and that the former group constitutes a distinct subtype. Patients with PD tend to hyperventilate and to panic in response to respiratory stimulants such as CO 2 , triggering the activation of a hypersensitive fear network. Although respiratory physiology seems to remain normal in these subjects, recent evidence supports the idea that they present subclinical abnormalities in respiration and in other functions related to body homeostasis. The fear network, composed of the hippocampus, the medial prefrontal cortex, the amygdala and its brain stem projections, might be oversensitive in PD patients. This theory might explain why medication and cognitive-behavioral therapy are both clearly effective. Our aim was to review the relationship between respiration and PD, addressing the respiratory subtype of PD and the hyperventilation syndrome, with a focus on respiratory challenge tests, as well as on the current mechanistic concepts and the pharmacological implications of this relationship.Keywords: Panic disorder; Anxiety; Respiration; Hyperventilation; Carbon dioxide. ResumoMúltiplas anormalidades respiratórias podem ser encontradas em pacientes com transtornos de ansiedade, particularmente no transtorno de pânico (TP). Indivíduos com TP experimentam ataques de pânico inesperados, caracterizados por ansiedade, medo e diversos sintomas autonômicos e respiratórios. A estimulação respiratória é um fenômeno comum durante os ataques de pânico. A anormalidade respiratória mais citada em pacientes com TP é a sensibilidade aumentada para o CO 2 , que originou a hipótese de uma disfunção fundamental nos mecanismos fisiológicos de controle da respiração no TP. Há evidências de que pacientes com TP com sintomas respiratórios predominantes são mais sensíveis a testes respiratórios do que aqueles sem a manifestação de tais sintomas, representando um subtipo distinto. Pacientes com TP tendem a hiperventilar e a reagir com pânico como resposta a estimulantes respiratórios como o CO 2 , gerando uma ativação de um circuito de medo hipersensível. Apesar de a fisiologia respiratória desses pacientes permanecer normal, algumas evidências recentes apontam a presença de disfunções subclínicas na respiração e em outras funções relacionadas à homeostase corporal. O circuito do medo, composto pelo hipocampo, córtex pré-frontal medial, amígd...

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“…That led to the conclusion that the 35% CO 2 challenge might be a safe and simple method to provoke PAs and a potential laboratory model for the study of PD. In the same year, Griez et al 9 exposed 12 PD patients to the 35% CO 2 challenge and compared their response to that of 11 control subjects. Confirming the panicogenic effects of the test, the authors noted that the provoked PAs were reported by PD patients to be very similar to spontaneous PAs, and pointed to a biological susceptibility of PD patients to the concentration of CO 2 in a breathed air mixture.…”

Section: The 1980smentioning

confidence: 99%

The carbon dioxide challenge test in panic disorder: a systematic review of preclinical and clinical research

Amaral

Spadaro

Pereira³

et al. 2013

Rev. Bras. Psiquiatr.

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This systematic review assesses the current state of clinical and preclinical research on panic disorder (PD) in which the carbon dioxide (CO 2 ) challenge was used as a trigger for panic attacks (PAs). A total of 95 articles published from 1984 to 2012 were selected for inclusion. Some hypotheses for PD evolved greatly due to the reproducibility of PAs in a controlled environment using the safe and noninvasive CO 2 test. The 35% CO 2 protocol was the method chosen by the majority of studies. Results of the test report specific sensitivity to hypercapnia in PD patients of the respiratory PD subtype. The CO 2 challenge helped assess the antipanic effects of medication and nonpharmaceutical approaches such as physical exercise and cognitive behavioral therapy. The test was also used in studies about the genetic component of PD, in which twins and relatives of PD patients were analyzed.

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CO2 vulnerability in panic disorder

Cited by 192 publications

References 18 publications

Respiratory Responses to Intravenous Infusion of Sodium Lactate in Male and Female Wistar Rats

Respiratory Responses to Intravenous Infusion of Sodium Lactate in Male and Female Wistar Rats

Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications

The carbon dioxide challenge test in panic disorder: a systematic review of preclinical and clinical research

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