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Biomedical subjects

E Griez

Publications and source records attributed to E Griez.

At least 19 recordsLinked to original sources
PubMed2000

Reactivity to a 35% CO2 challenge in healthy first-degree relatives of patients with panic disorder.

BACKGROUND: The effects of a 35% CO2 challenge were examined in healthy first-degree relatives of panic disorder patients and in healthy control subjects matched for age and gender. METHODS: One single inhalation of a 35% CO2/65% O2 challenge was administered to 50 first-degree relatives of panic disorder patients and 50 control subjects. RESULTS: The first-degree relatives were more reactive to the 35% CO2 challenge than the control subjects. CONCLUSIONS: These findings indicate that being a member of a family with a panic disorder patient is, in itself an important factor in CO2 hypersensitivity among subjects who have never experienced a panic attack. Both panic disorder patients and their first-degree relatives have a tendency to be more reactive to the CO2 challenge.

Adolescent↗
PubMed2000

Effects of tryptophan depletion on carbon dioxide provoked panic in panic disorder patients.

Results of an earlier study in healthy volunteers suggest that the serotonergic system is involved in anxiety-related mechanisms. We studied the influence of tryptophan depletion on the response to a 35% carbon dioxide challenge. Twenty-four panic disorder patients received a mixture of amino acids, either with or without tryptophan, under double-blind conditions. There was a significant increase in anxiety as well as in neurovegetative symptoms in the depletion group, compared to the placebo condition. Furthermore, when we compare the results of the placebo group with earlier panic provocation studies, it also seems that a balanced amino acid mixture might have a protective effect against a panic provocation. We conclude that the panic-enhancing effect of tryptophan depletion as well as the potential protective effect of tryptophan administration in panic disorder patients can be explained by the Deakin-Graeff theory of anxiety.

Adult↗
PubMed2000

10 microg CCK-4 premedication and 35% CO2 challenge in healthy volunteers.

1. The purpose of the study was to confirm whether a subthreshold dose of CCK-4 would enhance the vulnerability of healthy subjects to a 35% carbon dioxide challenge. 2. 40 subjects, with no prior or present psychiatric disorder and in good physical health were challenged with a vital capacity breath of a 35% carbon dioxide 65% oxygen mixture, immediately after an intravenous injection of 10 microg CCK-4 or placebo, according to a random order, double blind, separate group design. 3. Subjects reported significantly less anxiety and panic symptoms upon carbon dioxide after premedication with CCK-4 than after placebo. 4. CCK-4 and carbon dioxide seem to inhibit rather than enhance each other's effects, possibly through an effect on different neurobiological systems.

Adult↗
PubMed2000

Effects of low-dose cholecystokinin on respiratory function in healthy volunteers.

Injection of high doses of cholecystokinin tetrapeptide (CCK-4), a recent experimental model for panic, causes panic attacks and respiratory stimulation, a key feature of panic, in healthy volunteers. However, it has not yet been established whether respiratory stimulation is specifically linked to panic or merely an effect of arousal in general. Results of the present study show that respiratory stimulation is not merely linked to higher arousal and suggest a link between CCK-provoked panic and respiratory stimulation.

Anxiety↗
PubMed1999

Effect of CCK-4 on a 35% carbon dioxide challenge in healthy volunteers.

1. The purpose of this study was to determine whether a subthreshold dose of CCK-4 would enhance the vulnerability of healthy subjects to a 35% carbon dioxide challenge. 2. 27 subjects, with no prior or present psychiatric disorder and in good physical condition were challenged with a vital capacity breath of a 35% carbon dioxide mixture, immediately after an intravenous injection of 5 micrograms CCK-4 or placebo, according to a random order double blind crossover design. 3. Subjects reported significantly less panic symptoms upon carbon dioxide after premedication with CCK-4 than after placebo. 4. Both CCK-4 and carbon dioxide may act on the same neuronal pathways, but seem to inhibit rather than potentiate each other effects.

Adult↗
PubMed1998

Reliability of the 35% carbon dioxide panic provocation challenge.

The objective of this study was to determine the test-retest reliability of the 35% carbon dioxide (CO2) panic provocation challenge. Thirty patients with panic disorder were included in this study. Twenty-four patients were challenged twice, with 1 week between the two challenges. Six patients dropped out after the first test. The 35% CO2 challenge appeared to have a good test-retest reliability; both on induced subjective anxiety, measured on a Visual Analogue Scale for Anxiety (VAS-A), and induced panic symptoms, measured with a Panic Symptom List. Assessing the state of anxiety immediately after the challenge gave the most reliable results. Calculating increase in anxiety from the pre- and post-scores on the VAS-A rendered less reliable scores. This study completes a series of studies in which the criteria for an ideal model of panic are tested for the 35% CO2 challenge. Apart from an absolute specificity for panic disorder, the challenge meets these criteria.

Adult↗
PubMed1998

Effects of tryptophan depletion on anxiety and on panic provoked by carbon dioxide challenge.

Results of several studies suggest that anxiety is under serotonergic control. We studied the influence of tryptophan depletion on generalized anxiety and on the response to a 35% carbon dioxide (CO2) challenge. Fifteen healthy male volunteers received both a mixture of amino acids without tryptophan and a placebo mixture under double-blind conditions. The tryptophan-free mixture led to an 80% decrease in blood tryptophan levels compared to the placebo. There was a significant increase in anxiety on the Spielberger Anxiety Inventory and a trend towards more tension on the Profile of Mood States-'tension' items, both of which were interpreted as increased nervousness. Furthermore, a significant increase in neurovegetative panic symptoms occurred after the CO2 challenge. We conclude that the serotonergic system is causally involved in anxiety-related mechanisms and that it may be worth pursuing the role of tryptophan depletion on CO2-induced panic in patients with anxiety disorders.

Adult↗
PubMed1998

Experimental pathophysiology of panic.

In this article, we review how the knowledge of the pathophysiology of panic disorder has expanded, with special emphasis on laboratory models using lactate and carbon dioxide challenges. Experiments in the late 1960s revealed that lactate infusion can induce panic attacks. A prominent feature of these attacks is hyperventilation. Because lactate infusion induces a metabolic alkalosis, one would rather expect a compensatory hypoventilation. For years hyperventilation was thought to be causally linked to panic, but it has since been proven to be a symptom rather than a cause of panic attacks. Similarly, it is not hypocapnia but hypercapnia that has proven to be capable of provoking panic attacks. Carbon dioxide challenges are comparable to lactate infusion in the degree to which they meet the criteria for an ideal model of panic disorder. Experiments with carbon dioxide in first-degree relatives of panic disorder patients and in monozygotic twins support the idea of a constitutional predisposition to panic disorder. Of the various other agents that have been used to trigger panic attacks, cholecystokinin seems particularly promising as a valid laboratory model of panic disorder and may provide valuable data regarding the mechanism of panic attacks. The false suffocation alarm theory, proposed by Klein, is an integrative hypothesis that may account for a large number of the laboratory as well as clinical observations.

Carbon Dioxide↗
PubMed1998

Comorbid depressive disorder increases vulnerability to the 35% carbon dioxide (CO2) challenge in panic disorder patients.

BACKGROUND: The hypothesis of this study was that panic disorder patients with a comorbid depressive disorder would be less vulnerable to the 35% CO2 panic provocation challenge than panic disorder patients without a comorbid depressive disorder. This hypothesis was based on findings from ventilatory response studies in depressive patients. METHODS: Twelve panic disorder patients with and 23 panic disorder patients without a comorbid depressive disorder were challenged. RESULTS: Panic disorder patients with a comorbid depressive disorder scored significantly higher on ratings of subjective anxiety and panic symptoms induced by the challenge. CONCLUSIONS: A comorbid depressive disorder appeared to increase the vulnerability of panic disorder patients to this panic provocation. LIMITATION: We did find significant differences, but these differences did not confirm the original hypothesis. CLINICAL RELEVANCE: Our results support clinical data that show that a comorbid depressive disorder correlates with an increased severity of panic disorder.

Adult↗
PubMed1996

Alprazolam premedication and 35% carbon dioxide vulnerability in panic patients.

A group of 20 patients who met the DSM-III-R criteria for panic disorder with or without agoraphobia underwent a 35% carbon dioxide (CO2) challenge after either 1 mg alprazolam or placebo in a double-blind, randomized, cross-over design. Despite the anxiolytic potential of alprazolam, it produced no significant effects on CO2-induced anxiety and panic symptomatology when compared to placebo.

Adult↗
PubMed1995

Respiratory disorders as a possible predisposing factor for panic disorder.

150 consecutive anxiety patients completed a specially designed questionnaire which asked for the occurrence of respiratory and other somatic disorders before the onset of their anxiety disorder. The sample was divided into 82 panic disorder patients and 68 other anxiety patients serving as controls. Panic disorder patients had a significantly higher prevalence of respiratory diseases before the onset of their anxiety disorder than controls (42.7 vs. 16.2%). This higher prevalence was mainly due to a higher prevalence of bronchitis (26.8 vs. 8.8%). Differences in numbers of respiratory disorders mentioned appeared not to result from a tendency to hypochondria.

Adult↗
PubMed1995

Discrimination between panic disorder and generalized anxiety disorder by 35% carbon dioxide challenge.

OBJECTIVE: The authors' goal was to determine whether 35% carbon dioxide (CO2) challenge would discriminate between patients with panic disorder and patients with other anxiety disorders. METHOD: Nine patients with panic disorder and nine with generalized anxiety disorder underwent the 35% CO2 challenge. RESULTS: Patients with panic disorder experienced a significantly stronger increase in subjective anxiety than patients with generalized anxiety disorder. However, increases in panic symptom scores were high in both groups. CONCLUSIONS: These results suggest that a large increase in subjective anxiety due to the CO2 challenge is specific for patients with panic disorder but that an increase in panic symptoms is not.

Adult↗
PubMed1994

Yohimbine premedication and 35% CO2 vulnerability in healthy volunteers.

A group of 20 healthy volunteers underwent a 35% carbon dioxide/65% oxygen air-placebo controlled challenge test twice, premedicated 1 h before with either 20 mg yohimbine or placebo, following a double-blind randomized crossover design. Contrary to expectation the anxiety response to carbon dioxide was not higher when premedicated with yohimbine compared to premedication with placebo. Possible implications of this finding are discussed, with reference to general chemical models of panic.

Adolescent↗
PubMed1994

A 35% carbon dioxide challenge in simple phobias.

Twenty-eight subjects meeting the DSM-III-R criteria for simple phobia and 30 normal controls were subjected to a 35% carbon dioxide panic provocation challenge. Simple phobics were subdivided into two groups, animal phobics and situational or natural phenomena phobics. Animal phobics were not more vulnerable to carbon dioxide than normal controls. However, situational or natural phenomena phobics reacted significantly more strongly to the challenge than normal controls. The increase in anxiety in this group was comparable to the increase of anxiety of panic disorder patients from previous studies. Our results suggest the existence of a constitutional predisposition that may not only lead to panic disorder but also to the development of certain specific phobias.

Adolescent↗
PubMed1993

No chronic hyperventilation in panic disorder patients.

Arterial blood gases were measured and base excess calculated in 18 nonpanicking panic disorder (PD) patients, 12 subjects suffering from other anxiety disorders, and 18 normal control subjects. There was neither chronic nor clinically significant acute hyperventilation in either group.

Acid-Base Equilibrium↗