Henk Pols

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.

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.

Hypercarbia versus hypocarbia in panic disorder

In order to compare the panicogenic effects of hypercarbia and hypocarbia in panic disorder (PD), 12 PD patients and 11 healthy controls underwent a 35% CO2 challenge as well as a hyperventilation provocation test in a random cross-over design. Both anxiety and anxiety symptoms proved to be significantly higher during the 35% CO2 challenge in PD patients as compared to the response during 35% CO2 in normals and during hyperventilation in both patients and normals. The results suggest that PD patients are specifically hypersensitive to an increase in pCO2.

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.

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.

Breath-holding in Panic Disorder

In earlier studies, it was found that exogenous carbon dioxide administration provoked high anxiety in panic disorder (PD) patients, whereas healthy normals and patients suffering from other anxiety disorders were hardly affected. Breath-holding provides a simple method to induce endogenous CO2 accumulation. Fourteen PD patients, 14 patients suffering from other anxiety disorders, and 14 healthy controls were asked to hold their breath as long as possible. Apnea times appeared to be longer in the normal control group than in the other two groups. Using a one-tailed t test, a trend for a difference was found between the PD subjects and other anxiety patients, the PD patients having slightly lower values. No differences were found with respect to increase in anxiety during breath-holding or the ratio of apnea times before and after hyperventilation.

Ventilatory response to CO2 in panic disorder

The Read rebreathing technique was used to measure the ventilatory response to inhalation of carbon dioxide in 15 panic disorder patients, 15 obsessive-compulsive disorder patients, and 15 healthy control subjects. No significant differences in ventilatory response were found among the three groups. The tidal volume and frequency components of the ventilatory response also did not differ among the groups. The hypothetical pCO2 value corresponding with zero ventilation was significantly lower in the panic disorder patients than in normal control subjects.

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.

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.

The role of life events in the onset of panic disorder

Twenty-five panic disorder patients and fifteen obsessive-compulsive patients are compared with regard to a number of Life Events over the last 12 months prior to onset of the disorder and additionally over the total life course up until onset of the disorder. Panic Disorder patients do not differ from obsessive-compulsive disorder patients in terms of the number of life events, they experience during the last year prior to onset of their disorder. However, over the total life course, Panic Disorder patients do seem to be exposed to more Life Events than obsessive-compulsive disorder patients. The findings are discussed in light of the existing literature.