Psychophysiological Correlates of Mental Disorders

Lapierre, Yvon D.; Knott, Vernon J.

doi:10.1007/978-1-4615-9775-9_15

Cited by 3 publications

(9 citation statements)

References 69 publications

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“…Both strategies have been followed in practice [e.g. Lapierre et al (38), strategy 1; Freedman et al (41), strategy 2]. Table 5 gives the results on psychologic measures reported in eight studies.…”

Section: Psychophysiologic Measuresmentioning

confidence: 94%

“…in separate sessions. In these studies, subjects and experimenters or observers were generally "blind" to which solution was being given on a specific day (25,38,(44)(45)(46)(47). Thus, these studies generally were double blind.…”

Section: Methodologic Overviewmentioning

confidence: 99%

“…This correlation could indicate a publication bias in that small samples are only published when rates are high, or that the experimenters give more personal attention to subjects in small studies and select them for more severe illness or create stronger implicit demands on them to panic during infusion. The only double-blind study relying entirely on automatized (noninteractive) self-report of panic symptoms as criterion for panic attacks found a clearly lower proportion of attacks in patients than all other studies, namely 2'6% (38). Although this lower proportion could also be due to the 500-ml limit that Lapierre et al imposed on their infusion (0.5 molar sodium lactate, 10 ml/kg/20 min), the average panic attack is reported to occur at doses well below 500 ml of 0.5 molar so- Table 3).…”

Section: Incidence Of Lactate-and Placebo-induced Panic In Patients Amentioning

confidence: 96%

“…The scores on the psychometric STAI are within one standard deviation of the mean of Spielberger et al's (51) general sample of neuropsychiatric patients (Tscores of 55 and 43, compared to an undergraduate sample 66 and 55). Lapierre et al (38) reported scores of about 5 on the 10-point numeric transformation of their visual analog anxiety scale for the subgroup of patients who panicked (nonpanickers averaged 0). Thus, although lactate induces a considerable number of self-reported symptoms in patients and (to a lesser degree) in controls, much lower levels of subjective anxiety were reached than one would expect for "panic attacks.…”

Section: Self-reported Symptoms and Subjective Anxietymentioning

confidence: 98%

“…Recently, Klein and his colleagues in a number of publications stated that they have confirmed Pitts and McClure's (25) finding that lactate infusions provoke panic attacks in most panic patients 1 but in very few control subjects (26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36). Currently several other centers are working in this area (37)(38)(39)(40)(41). Contemporary researchers focus more narrowly on Panic Disorder instead of considering sodium lactate as the biochemical substrate of anxiety in general (42).…”

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confidence: 98%

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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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Section: Psychophysiologic Measuresmentioning

confidence: 94%

Section: Methodologic Overviewmentioning

confidence: 99%

Section: Incidence Of Lactate-and Placebo-induced Panic In Patients Amentioning

confidence: 96%

Section: Self-reported Symptoms and Subjective Anxietymentioning

confidence: 98%

mentioning

confidence: 98%

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

Margraf¹,

Ehlers²,

Roth³

1986

Psychosomatic Medicine

176

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Angiotensin II's role in sodium lactate-induced panic-like responses in rats with repeated urocortin 1 injections into the basolateral amygdala

Johnson

Sajdyk

Fitz

et al. 2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Rats treated with three daily urocortin 1 (UCN) injections into the basolateral amygdala (BLA; i.e., UCN/BLA-primed rats) develop prolonged anxiety-associated behavior and vulnerability to panic-like physiological responses (i.e., tachycardia, hypertension and tachypnea) following intravenous infusions of 0.5 M sodium lactate (NaLac, an ordinarily mild interoceptive stressor). In these UCN-primed rats, the osmosensitive subfornical organ (SFO) may be a potential site that detects increases in plasma NaLac and mobilizes panic pathways since inhibiting the SFO blocks panic following NaLac in this model. Furthermore, since SFO neurons synthesize angiotensin II (A-II), we hypothesized that the SFO projects to the BLA and releases A-II to mobilizing panic responses in UCN/BLA-primed rats following NaLac infusions. To test this hypothesis, rats received daily bilateral injections of UCN or vehicle into the BLA daily for 3 days. Five to seven days following the intra-BLA injections, we microinjected either the nonspecific A-II type 1 (AT1r) and 2 (AT2r) receptor antagonist saralasin, or the AT2r-selective antagonist PD123319 into the BLA prior to the NaLac challenge. The UCN/BLA-primed rats pre-injected with saralasin, but not PD123319 or vehicle, had reduced NaLac-induced anxiety-associated behavior and panic-associated tachycardia and tachypnea responses. We then confirmed the presence of AT1rs in the BLA using immunohistochemistry which, combined with the previous data, suggest that A-II’s panicogenic effects in the BLA is AT1r dependent. Surprisingly, the SFO had almost no neurons that directly innervate the BLA, which suggests an indirect pathway for relaying the NaLac signal. Overall these results are the first to implicate A-II and AT1rs as putative neurotransmitter-receptors in NaLac induced panic-like responses in UCN/BLA-primed rats.

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Modelling Anxiety in Humans for Drug Development

Siepmann

Joraschky²

2007

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Animal behavioural profiles are commonly employed to investigate new therapeutic agents to treat anxiety disorders as well as to investigate the mechanism of action of anxiolytic drugs. However, many clinically important symptoms of anxiety can not be modelled directly in animals. Human models of anxiety should bridge between animal models and anxiety disorders. Experimental anxiety states in humans can be induced by either pharmacological means such as CO(2) inhalation or psychological means such as aversive conditioning of skin conductance responses to tones. Investigation of these models may contribute to a better understanding of anxiety disorders, both from a biological and behavioural point of view. In a comprehensive review existing models of human experimental anxiety states are summarized and validity is discussed.

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Psychophysiological Correlates of Mental Disorders

Cited by 3 publications

References 69 publications

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

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

Angiotensin II's role in sodium lactate-induced panic-like responses in rats with repeated urocortin 1 injections into the basolateral amygdala

Modelling Anxiety in Humans for Drug Development

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