Panic disorder patients show decrease in ventilatory response to CO2 after clomipramine treatment.
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Adult↗
Biomedical subjects
H Lousberg
Publications and source records attributed to H Lousberg.
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↗
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↗
[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↗
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.
Adult↗
Effect of hypercapnia and other disturbances in the acid-base-balance on panic disorder.
Naturally occurring panic attacks and various interventions which trigger anxiety in panic patients are accompanied by disturbances in the acid-base balance. Carbon dioxide appears to play an important role in many experimental panic provoking conditions. The influence of respiratory and metabolic pH disturbances on cerebral physiology is discussed and speculations are made about the possible mechanisms underlying CO2-induced anxiety in panic disorder.
Acid-Base Equilibrium↗
Carbon dioxide chemosensitivity in panic disorder.
The ventilatory response to the inhalation of carbon dioxide was studied in 19 panic patients and 14 normal controls, using the Read rebreathing technique. The panic patients showed significantly higher ventilatory response compared with normal controls.
Adult↗
Serotonin antagonism in panic disorder: an open trial with ritanserin.
Eleven patients with panic disorder were administered ritanserin, a post-synaptic serotonin S2 antagonist, during a 4 week period at a daily dose of 10-20 mg. The treatment resulted in a decrease in the number of panic attacks, and a diminution of agoraphobic avoidance. The possible practical and theoretical signification of these findings is discussed.
Adult↗
Pulmonary carbon dioxide and panic-arousing sensations after 35% carbon dioxide inhalation: hypercapnia/hyperoxia versus hypercapnia/normoxia.
Experimental research has demonstrated that CO2 inhalation provides a valid laboratory model for acute panic. Earlier studies employed CO2/O2 mixtures that were not only hypercapnic but also hyperoxic, raising the question of the relative contribution of the hyperoxidity. A comparison between a hypercapnic/hyperoxic mixture (35% CO2/65% O2) and a hypercapnic/normoxic mixture (35% CO2/20% O2/45% N2) revealed no differences on self-reported panic symptoms or end tidal pCO2. It is concluded that findings from previous CO2/O2 inhalation studies should be attributed to the hypercapnic, rather than to the hyperoxic, nature of the mixtures.
Adult↗
CO2 vulnerability in panic disorder.
The immediate effects of a single inhalation of a 35% CO2 mixture in oxygen were examined in 12 patients with panic disorders and 11 normal control subjects. Compared to a placebo air inhalation, the CO2 inhalation provoked short-lived autonomic panic symptoms in both patients and normals; it also elicited high subjective anxiety in patients with panic disorders. The latter rated the overall CO2-induced state as very similar to a real-life panic attack.
Adult↗
Reduction of CO2-induced anxiety in patients with panic attacks after repeated CO2 exposure.
The authors compared the subjective reaction of 13 panic patients and eight control subjects to a 35% CO2 challenge, a treatment known to produce physical symptoms comparable to those of natural or lactate-induced panic, and to placebo treatment (inhalation of air). They found that patients had higher placebo scores than control subjects, patients tended to get highly anxious on CO2 and control subjects did not, and CO2-induced subjective anxiety in patients decreased as the number of CO2-induced exposures to interoceptive anxiety symptoms increased. The data support a behavioral account of the effects of anxiogenics.
Adolescent↗
Cognitive determinants of lactate-induced anxiety.
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Adult↗
Effects of low pulmonary CO2 on panic anxiety.
In order to investigate the possible role of hyperventilation in the pathogenesis of panic, 11 panic patients and eight normal controls underwent a hyperventilation provocation test. The word "hyperventilation" itself was not used; the subjects were told the test was meant to measure the amount of carbon dioxide in their expired air. End tidal pCO2 was reduced to less than half of its initial value, resulting in a significant increase in physical symptoms, both in patients and controls. However, there proved to be no significant increase in subjective anxiety. It is suggested, that hypocarbia alone is not sufficient to provoke anxiety in panic disorder patients.
Adult↗