15 research outputs found
Amiloride-sensitive cation channel 2 genotype affects the response to a carbon dioxide panic challenge
Book reviews
Till saknadens lov (Mikael Enckell, 1988) is reviewed by Inge Jonsson.Judiskt liv i Norden (eds. G. Broberg, H. Runblom & M. Tydén, 1988) is reviewed by Karl-Johan Illman.Multiethnic studies in Uppsala. Essays presented in honour of Sven Gustavsson June 1, 1988 (1988) is reviewed by Karl-Johan Illman.The wandering Jew. Essays in the interpretation of a Christian legend (eds. Hasan-Rokem & A. Dundes, 1985) is reviewed by Ulrika Wolf-Knuts and Nils Martola.Jude i Finland (Boris Grünstein, 1988) is reviewed by Karmela Bélinki
Book reviews
Till saknadens lov (Mikael Enckell, 1988) is reviewed by Inge Jonsson.Judiskt liv i Norden (eds. G. Broberg, H. Runblom & M. Tydén, 1988) is reviewed by Karl-Johan Illman.Multiethnic studies in Uppsala. Essays presented in honour of Sven Gustavsson June 1, 1988 (1988) is reviewed by Karl-Johan Illman.The wandering Jew. Essays in the interpretation of a Christian legend (eds. Hasan-Rokem & A. Dundes, 1985) is reviewed by Ulrika Wolf-Knuts and Nils Martola.Jude i Finland (Boris Grünstein, 1988) is reviewed by Karmela Bélinki
Therapygenetics: 5-HTTLPR genotype predicts the response to exposure therapy for agoraphobia
35% CO2 sensitivity in social anxiety disorder
The 35% carbon dioxide (CO(2)) challenge is a well-established model of panic. This study aimed to investigate 35% CO(2) sensitivity in patients with social anxiety disorder (SAD) compared with patients with panic disorder (PD) and normal controls. First, a 35% CO(2) challenge was conducted including 16 patients with generalized SAD, 16 with PD and 16 normal subjects. Outcome was assessed by a Visual Analogue Scale for Fear (VAS-F) and the Panic Symptom List (PSL). Second, meta-analyses of fear and panic scores were performed, including data from the present experiment and from previous 35% CO(2) challenge studies in patients with SAD. The present 35% CO(2) challenge found equal increases in VAS-F and PSL in patients with SAD compared with normal controls, whereas the CO(2) response in patients with PD was significantly stronger than in controls. The meta-analyses confirmed the experimental data from this study, and in addition showed an intermediate panic rate in SAD patients, in between that of normal controls and patients with PD. In conclusion, neither our experiment nor the meta-analyses found evidence for a similarly exaggerated 35% CO(2) sensitivity in SAD and PD, suggesting that the pathogenesis of SAD is different from PD, although patients with SAD may be slightly more sensitive than non-anxious controls.status: publishe
Brainstem response to hypercapnia: A symptom provocation study into the pathophysiology of panic disorder
Background: The biological basis of uncued panic attacks is not yet understood. An important theory concerning the nature and cause of panic disorder is the 'suffocation false alarm theory'. This alarm is supposed to be over-sensitive in panic disorder patients and can be triggered by CO2. No neurobiological substrate has been identified for such an alarm. The present study investigates differences in brain activation in panic patients, healthy individuals and experienced divers in response to CO2, representing three groups with descending sensitivity to CO2. Method: Brain activation was measured with functional magnetic resonance imaging. Subjects breathed through a mouthpiece delivering a continuous flow of 100% oxygen for two minutes, followed by a hypercapnic gas mixture (7% CO2) for the next two minutes. Statistical analysis was performed using SPM8. Results: There was a significant main effect of group in response to the CO2. Patients show increased brainstem activation in response to hypercapnia compared to controls and divers. Subjective feelings of breathing discomfort were positively correlated with brain activation in the anterior insula in all groups. Conclusion: This is the first study showing that the behavioural response to CO2 that characterises panic disorder patients is likely due to increased neural sensitivity to CO2 at brainstem level