panic disorder/hypoxia

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Novel hypothesis for the cause of panic disorder via the neuroepithelial bodies in the lung.

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Panic disorder (PD) is a complex condition that is further complicated by its numerous inducers, which include hypercapnia, hypoxia, sodium lactate, caffeine and cholecystokinin. It seems unlikely that there are specific suffocation receptors for each of these inducers in the brain. The pulmonary

Nitric oxide in the dorsal periaqueductal gray mediates the panic-like escape response evoked by exposure to hypoxia.

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Exposure of rats to an environment with low O₂ levels evokes a panic-like escape behavior and recruits the dorsal periaqueductal gray (dPAG), which is considered to be a key region in the pathophysiology of panic disorder. The neurochemical basis of this response is, however, currently

Translational approach to studying panic disorder in rats: hits and misses.

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Panic disorder (PD) patients are specifically sensitive to 5–7% carbon dioxide. Another startling feature of clinical panic is the counterintuitive lack of increments in ‘stress hormones’. PD is also more frequent in women and highly comorbid with childhood separation anxiety (CSA). On the other

The lactic acid response to alkalosis in panic disorder : an integrative review.

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Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive

Exaggerated anxiety is not unique to CO2 in panic disorder: a comparison of hypercapnic and hypoxic challenges.

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Current biological models of panic disorder (PD) assert that this disorder is maintained by hypersensitivity to carbon dioxide (CO2) and related asphyxia cues, which is manifested as an exaggerated suffocation alarm (D. Klein, 1993). Because suffocation can result from both increased CO2

Elevated brain lactate responses to neural activation in panic disorder: a dynamic 1H-MRS study.

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Converging evidence suggests that patients with panic disorder have a metabolic disturbance that may influence the regulation of arousal systems and confer vulnerability to 'spontaneous' panic attacks. The consistent finding of elevated brain lactate responses to various metabolic challenges in

Serotonin in the dorsal periaqueductal gray inhibits panic-like defensive behaviors in rats exposed to acute hypoxia.

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It has been proposed that spontaneous panic attacks are the outcome of the misfiring of an evolved suffocation alarm system. Evidence gathered in the last years is suggestive that the dorsal periaqueductal gray (dPAG) in the midbrain harbors a hypoxia-sensitive suffocation alarm system. We here

Panic-like escape response elicited in mice by exposure to CO2, but not hypoxia.

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Exposure to elevated concentrations of CO2 or hypoxia has been widely used in psychiatric research as a panic provoking stimulus. However, the use of these respiratory challenges to model panic-like responses in experimental animals has been less straightforward. Little data is available, from

The integrative role of the sigh in psychology, physiology, pathology, and neurobiology.

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"Sighs, tears, grief, distress" expresses Johann Sebastian Bach in a musical example for the relationship between sighs and deep emotions. This review explores the neurobiological basis of the sigh and its relationship with psychology, physiology, and pathology. Sighs monitor changes in brain

Highlights of the annual meeting of the International Society for the Advancement of Respiratory Psychophysiology and the 14th International Symposium on Respiratory Psychophysiology.

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This article provides a review of selected presentations and events that highlighted the annual meeting of the International Society for the Advancement of Respiratory Psychophysiology (ISARP) and the 14th International Symposium on Respiratory Psychophysiology, Toronto, Ontario, Canada, October

Evidence of a suffocation alarm system sensitive to clinically-effective treatments with the panicolytics clonazepam and fluoxetine.

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Dyspnea, 'hunger for air', and the urge to flee are the cardinal symptoms of respiratory-type panic attacks. Patients also show baseline respiratory abnormalities and a higher rate of comorbid and antecedent respiratory diseases. Panic attacks are also precipitated by both the infusion of 0.5 M

Evidence of a suffocation alarm system within the periaqueductal gray matter of the rat.

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Dyspnea, hunger for air, and urge to flee are the cardinal symptoms of panic attacks. Patients also show baseline respiratory abnormalities and a higher rate of comorbid and antecedent respiratory diseases. Panic attacks are also precipitated by infusion of sodium lactate and inhalation of 5% CO₂ in

Hemodynamic Characteristics of Postural Hyperventilation: POTS with Hyperventilation vs Panic vs Voluntary Hyperventilation.

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Upright hyperventilation occurs in approximately 25% of our patients with postural tachycardia syndrome (POTS). Poikilocapnic hyperventilation alone causes tachycardia. Here we examined changes in respiration and hemodynamics comprising cardiac output (CO), systemic vascular resistance (SVR) and

High altitudes, anxiety, and panic attacks: is there a relationship?

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People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to

Panic, hyperventilation and perpetuation of anxiety.

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1. Studies on the pathogenesis of panic disorder (PD) have concentrated on panic attacks. However, PD runs a chronic or episodic course and panic patients remain clinically unwell between attacks. Panic patients chronically hyperventilate, but the implications of this are unclear. 2. Provocation of

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