Lactate infusions and panic attacks: Do patients and controls respond differently?

Ehlers, Anke; Margraf, Jürgen; Roth, Walton T.; Taylor, C. Barr; Maddock, Richard J.; Sheikh, Javaid I.; Kopell, Maya L.; McClenahan, Kristin L.; Gossard, Denis; Blowers, Geoffrey H.; Agras, W. Stewart; Kopell, Bert S.

doi:10.1016/0165-1781(86)90077-6

Cited by 80 publications

(18 citation statements)

References 20 publications

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“…24 We have also found these characteristics in our patients, who paid great attention to their bodies in order to avoid being surprised by an ICD discharge (Table IV). Our results are consistent with the data of Pauli et al,12 who reported that patients with ICD with high anxiety levels have increased catastrophic fears compared with healthy controls.…”

Section: Catastrophic Fears-a Possible Risk Factor In the Developmentsupporting

confidence: 60%

Panic disorders and agoraphobia: Side effects of treatment with an implantable cardioverter/defibrillator

Godemann

Butter

Lampe

et al. 2004

Clinical Cardiology

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SummaryBackground: Implantable cardioverter/defibrillator (ICD) treatment has reduced the mortality of patients with a high risk of sudden cardiac death. However, ICD discharges may cause anxiety with respect to new discharges and lead to preventive, for example, phobic, behavior. This study evaluated the frequency of panic disorders and agoraphobia in patients with ICD and assessed the risk factors in their development.Hypothesis: Treatment with ICD represents a risk factor in the development of anxiety disorders.Methods: Ninety patients with ICD were examined using a standardized lifetime Diagnostic Interview of Psychiatric Syndromes (DIPS). This interview makes it possible to estimate the incidence of panic disorders and agoraphobia. The impact of the severity of the underlying cardiac disease, the number of ICD discharges, and the subjective appraisal of the shock experience on the development of panic disorders and agoraphobia was assessed.Results: Fifteen patients (16.7%) developed anxiety disorders after ICD implantation. The incidence was 21% in patients with and 6.9% in patients without ICD discharge. In patients with two or more ICD discharges annually, the incidence of panic disorders and agoraphobia was higher than

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Section: Catastrophic Fears-a Possible Risk Factor In the Developmentsupporting

confidence: 60%

Panic disorders and agoraphobia: Side effects of treatment with an implantable cardioverter/defibrillator

Godemann

Butter

Lampe

et al. 2004

Clinical Cardiology

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“…In our own laboratory we recently completed a study that suggests the reactivity of patients and controls to lactate infusions may be the same (64). Subjects with the diagnosis of Panic Disorder or Agoraphobia with Panic Attacks had higher preinfusion subjective anxiety and heart rates than a control group, whereas both groups had equal increases in these measures during infusion.…”

Section: Influence Of Baseline Levels Of Anxiety and Arousalmentioning

confidence: 91%

Sodium lactate infusions and panic attacks: a review and critique.

Margraf¹,

Ehlers²,

Roth³

1986

Psychosomatic Medicine

176

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Response to sodium lactate infusions has been proposed as an experimental model and a biologic marker for panic attacks. Several authors have claimed that patients suffering from panic attacks, but not normal controls, "panic" in response to lactate. A careful review of methods and results of 13 studies, however, reveals serious methodologic problems, lack of specificity and sensitivity, and a failure to consider cognitive variables. When baseline differences are ruled out, the responses of patients and controls may not differ. So far, response to lactate cannot be interpreted as a model and marker for panic attacks and does not provide evidence for their underlying biologic distinctness from other types of anxiety. Known biologic mechanisms do not sufficiently explain the effects of lactate. Instead, an interaction of peripheral physiologic changes, past experience, environmental cues, and their appraisal as threatening or dangerous seems to be a more appropriate model.

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“…Indeed, the demonstration that clinical and lactate-induced panics do not activate the hypothalamus-pituitaryadrenal (HPA) axis was a remarkable finding inasmuch as it differentiated clinical panic from stress-like reactions and common fear (Hollander et al, 1989a(Hollander et al, , 1989b(Hollander et al, , 1989cLevin et al, 1987;Woods, Charney, Goodman, & Heninger, 1988;Woods, Charney, McPherson, Gradman, & Heninger, 1987;). These studies also brought into question the cognitive hypothesis which equated clinical panic to the fear produced by the catastrophic evaluation of bodily symptoms (Clark et al, 1997;Ehlers et al, 1986;). The cognitive hypotheses were also challenged by studies showing that panic patients do not endorse somatic symptoms indiscriminately (Goetz et al, 1989).…”

Section: A Short Story Of Panic Disordermentioning

confidence: 99%

Towards a translational model of panic attack.

Schenberg

2010

Psychology & Neuroscience

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About 20 years ago, Deakin and Graeff proposed that whereas generalized anxiety disorder is produced by the overactivity of 5-HT excitatory projections from dorsal raphe nucleus to the areas of prefrontal cortex and amygdala which process distal threat, panic attacks are a dysfunction of 5-HT inhibitory projections from dorsal raphe nucleus to the dorsal periaqueductal gray matter, thereby releasing the responses to proximal threat, innate fear or anoxia. Besides, they suggested that the decrease in 5-HT1A neurotransmission in the hippocampus results in learned helplessness and depression. Accordingly, the Deakin Graeff hypothesis provided a unified frame to the widespread use of 5-HT selective reuptake inhibitors in generalized anxiety, panic disorder and depression. Competitor hypotheses implicate panic attacks with the abnormal functioning of locus coeruleus, basolateral amygdala, dorsomedial hypothalamus or an as-yet-unknown suffocation alarm system. Conversely, cognitive psychologists suggest that panic attacks result from the catastrophic (cortical) interpretation of bodily symptoms. In any event, translational models of panic attack are expected to reproduce the main features of clinical panic, namely, the patient's higher sensitivity to both lactate and CO2, the drug specific sensitivity, the lack of stress hormone responses during panic attacks, the higher vulnerability of women and the high comorbidity with agoraphobia, major depression and childhood separation anxiety. Therefore, here we review the main steps in the experimental approach to anxiety disorders which are paving the route towards a translational model of panic attack.

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Lactate infusions and panic attacks: Do patients and controls respond differently?

Cited by 80 publications

References 20 publications

Panic disorders and agoraphobia: Side effects of treatment with an implantable cardioverter/defibrillator

Panic disorders and agoraphobia: Side effects of treatment with an implantable cardioverter/defibrillator

Sodium lactate infusions and panic attacks: a review and critique.

Towards a translational model of panic attack.

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