Physiologic instability in panic disorder and generalized anxiety disorder

Wilhelm, Frank H.; Trabert, Werner; Roth, Walton T.

doi:10.1016/s0006-3223(00)01000-3

Cited by 156 publications

(123 citation statements)

References 36 publications

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“…13 PD patients also have exaggerated endogenous lactate responses to a variety of metabolic challenges [14][15][16][17] and demonstrate abnormal respiratory patterns. 18,19 Both abnormal respiratory patterns and exaggerated endogenous lactate responses persist after clinical remission, suggesting they reflect a trait feature of patients with PD. 16,19 Understanding the mechanism of exaggerated brain lactate responses to metabolic challenges in PD may provide important clues about an underlying metabolic disturbance in this disorder.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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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 panic disorder appears to support this model, although the mechanism of this effect is not understood. Several mechanisms have been proposed to account for elevated brain lactate responses in panic disorder, including (1) brain hypoxia due to excessive cerebral vasoconstriction, and (2) a metabolic disturbance affecting lactate metabolism. Recent studies have shown that neural activation (for example, sensory stimulation) causes local lactate accumulation in the presence of increased oxygen availability. The current study used proton magnetic resonance spectroscopic measures of visual cortex lactate changes during visual stimulation in 15 untreated patients with panic disorder and 15 matched volunteers to critically test these two proposed mechanisms of elevated brain lactate responses in panic disorder. Visual cortex lactate/N-acetylaspartate increased during visual stimulation in both groups. The increase was significantly greater in the panic patients than in the comparison group. There were no group differences in end-tidal pCO 2 . The finding that visual stimulation leads to significantly greater visual cortex lactate responses in panic patients is not predicted by the hypoxia model. These results suggest that a metabolic disturbance affecting the production or clearance of lactate is the cause of the elevated brain lactate responses consistently observed in panic disorder and provide further support for metabolic models of vulnerability to this illness.

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Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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“…26 In individuals with generalized anxiety disorder, the irregularity of breathing is less pronounced than in those with PD. 41 Various studies have shown that, in individuals with PD, there is a strong correlation between the degree of respiratory irregularity and the frequency of panic attacks, as well as between such irregularity and CO 2 vulnerability.…”

Section: -18mentioning

confidence: 99%

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder

Sikter¹,

Frecska

Braun

et al. 2007

Rev. Bras. Psiquiatr.

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The role of hyperventilation -hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação -a hipocapnia no patomecanismo do distúrbio de pânico A b s t r a c t Objective: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. Method: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. Discussion: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO 2 ) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase. Conclusion: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.Descriptors: Acidosis; Catecholamines; Hyperventilation; Hypocapnia; Panic disorder Resumo Objetivo: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventilação crônica representa um mecanismo protetor contra os ataques de pânico. Método: Revisão seletiva da literatura a partir da base de dados Medline. Foram selecionados relatos referentes à inter-relação entre transtorno do pânico, hiperventilação, acidose, alcalose, liberação de catecolaminas e sensibilidade a catecolaminas, sendo os achados estruturados de modo a formar um modelo integrado. Discussão: Os ataques de pânico do transtorno do pânico desenvolvem-se com base numa acidose metabólica, que é uma resposta compensatória à hiperventilação crônica. Os ataques são desencadeados por um súbito aumento da pressão parcial de dióxido de carbono (pCO 2 ), quando a acidose (metabólica) latente se manifesta pela acidose hipercápnica. A condição acidótica induz liberação de catecolaminas. A simpaticotonia não pode manifestar-se durante...

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“…Quantified as the van Neuman statistic of breath-by-breath variation over 1-min periods. Elevated at baseline in panic disorder (Wilhelm et al, 2001f) (continued on next page)…”

Section: Vivologic Physiologic Data Analysis and Displaymentioning

confidence: 99%

Continuous electronic data capture of physiology, behavior and experience in real life: towards ecological momentary assessment of emotion

Wilhelm

Pfaltz

Grossman

2006

Interacting with Computers

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Emotions powerfully influence our physiology, behavior, and experience. A comprehensive assessment of affective states in health and disease would include responses from each of these domains in real life. Since no single physiologic parameter can index emotional states unambiguously, a broad assessment of physiologic responses is desirable. We present a recently developed system, the LifeShirt, which allows reliable ambulatory monitoring of a wide variety of cardiovascular, respiratory, metabolic, motor-behavioral, and experiential responses. The system consists of a garment with embedded inductive plethysmography and other sensors for physiologic data recording and a handheld computer for input of experiential data via touch screen. Parameters are extracted offline using sophisticated analysis and display software. The device is currently used in clinical studies and to monitor effects of physical and emotional stress in naturalistic settings. Further development of signal processing and pattern recognition algorithms will enhance computerized identification of type and extent of physical and emotional activation. q

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Physiologic instability in panic disorder and generalized anxiety disorder

Cited by 156 publications

References 36 publications

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

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

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder

Continuous electronic data capture of physiology, behavior and experience in real life: towards ecological momentary assessment of emotion

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