Search PubMed⌕ Search

Biomedical subjects

E Griez

Publications and source records attributed to E Griez.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1991

Attenuation of carbon dioxide-induced panic after clonazepam treatment.

Ten patients meeting the DSM-III-R criteria for panic disorder were treated with clonazepam. Prior to clonazepam treatment and after a 5-week treatment period, patients underwent a 35% carbon dioxide challenge procedure. Following clonazepam treatment, a significant reduction in carbon dioxide vulnerability was observed.

Adult↗
PubMed1991

Low doses of clonazepam in the treatment of panic disorder.

In order to assess the efficacy of a high-potency benzodiazepine in the treatment of panic disorder, an open trial was conducted with clonazepam. Clonazepam was administered in relatively low doses and, after four weeks, was shown to be effective in reducing the number of panic attacks and associated features of the disorder.

Adult↗
PubMed1990

Clinical and non-clinical binges.

A study was conducted to determine if, and in what respects, clinical binges (reported by bulimic subjects) are different from non-clinical binges (reported by a non-clinical population). Furthermore, the study tested whether the DSM-III-R criteria and other variables that are retrospectively claimed to be defining characteristics indeed differentiate binges from non-binge eating episodes. Clinical binges appeared to differ from non-clinical binges as to amount of calories ingested and duration. With respect to subjective experience, clinical and non-clinical binges did not differ. The DSM-III-R criteria for binge eating discriminate clinical and non-clinical binges quite well from non-binges. With the addition of other seemingly important variables, binges are not discriminated better from non-binges than with the DSM-III-R variables alone. It is argued that the difference between pathological binge eating and non-clinical binge eating is mainly a matter of severity.

Adult↗
PubMed1990

Specific sensitivity of patients with panic attacks to carbon dioxide inhalation.

One inhalation of 35% CO2 in oxygen was administered to 36 patients with anxiety disorders and 14 healthy controls. Eighteen patients had a diagnosis of panic disorder (PD) and 18 of obsessive-compulsive disorder (OCD). As a placebo control for CO2, compressed air was administered in a double-blind design. Immediately before and after the inhalation, levels of anxiety and DSM-III-R symptoms of panic were assessed. CO2 elicited high levels of subjective anxiety in the PD group. Patients with OCD were hardly affected by the inhalation, and did not differ from healthy controls. These results suggest that CO2 challenge should be considered as a specific probe for subjects with panic-anxiety. It is speculated that CO2 may trigger some as yet undefined mechanisms, possibly linked to ventilation control, which demarcate panic from other types of pathological anxiety.

Administration, Inhalation↗
PubMed1990

Response to 35% CO2 as a marker of panic in severe anxiety.

One inhalation of 35% CO2 was administered to each of 32 patients with high anxiety ratings. Only patients with panic disorder had increases in reported anxiety upon CO2 intake. CO2-triggered anxiety appears specific for panic disorder and independent of baseline anxiety.

Adult↗
PubMed1990

[Experimental possibilities of biological provocation of panic attacks].

On the point of anxiety states, behavioural sciences have only recently been provided with sufficient operational definitions of clinical concepts to enable us to start working on the construction of valid models for the different disorders. Panic attacks are defined as attacks manifested by discrete periods of apprehension or fear, concomitant with at least four marked vegetative sensations, as described in the DSM-III. Several interventions have proved to be able to mimic experimentally such episodes in vulnerable patients, providing the researcher with valuable models for panic research such as the lactate infusion technique, the single CO2 inhalation model and, to a lesser extent, the hyperventilation provocationtest. The study of these models may be a major contribution to a better understanding of panic anxiety, both from a biological and behavioural point of view. Biological observations of those models point to pH changes and ionic shifts as a physiological concomitant in the genesis of experimentally induced panic, and suggests that hypersensitive chemoreceptive structures of the CNS may be implicated. As to the behavioural aspects of the models, there is strong evidence for the ancient phobophobia, or "fear of fear" idea, which may explain the invaldating recurrence of panic attacks.

Anxiety Disorders↗