Biomedical subjects
Publications and source records attributed to C de Loof.
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 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.
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.
Current and past frequencies of respiratory diseases were assessed in 30 patients with panic disorder, 30 patients with obsessive-compulsive disorder, and 30 patients with eating disorders. Lifetime prevalence of respiratory disorders was significantly higher in patients with panic disorder (47%) than in patients with either obsessive-compulsive disorder (13%) or eating disorder (13%). Point prevalences showed no differences.
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.
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.
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.
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.
In a double-blind randomized placebo-controlled cross-over design trial, the effects of a 4 week fluvoxamine versus a 4 week placebo treatment regimen on panic symptomatology were studied. Fluvoxamine seems to have specific antipanic properties, as a significant decrease in the number of panic attacks was observed. Other components of the disorder, like free-floating anxiety and avoidance behavior were not influenced during the short 4 week treatment period.