***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Thirteen healthy subjects with infrequent panic attacks and without agoraphobia who did not meet DSM-III-R criteria for panic disorder , 43 patients with panic disorder , and 43 healthy control subjects who never experienced panic attacks underwent one vital capacity inhalation of 35 % CO2 . Healthy subjects with infrequent panic attacks reacted similarly to patients with panic disorder and more strongly than healthy subjects who never experienced panic attacks . The results suggest that ( a ) subjects with sporadic unexpected panic attacks and patients with panic disorder belong to the same spectrum of vulnerability and ( b ) CO2 hypersensitivity might be a trait marker of panic attacks rather than of a clinical diagnosis of panic disorder OBJECTIVE Previous studies have indicated that patients with panic disorder are more likely than normal subjects to have acute panic attacks during inhalation of CO2 , but method ological objections have been raised . In this study the authors attempted to address three of these method ological problems by ensuring that raters who assessed whether panic attacks occurred were blind to subjects ' diagnoses , by r and omizing the order of administration of 5 % CO2 and hyperventilation , and by challenging a greater number of subjects with 7 % CO2 . METHOD Patients with panic disorder and normal subjects underwent 20-minute inhalations of 5 % CO2 and 7 % CO2 and 15 minutes of room-air hyperventilation . Ratings of panic/no panic during each condition were made separately by an assessor blind to diagnosis and by the subject . Scores on four panic rating scales were also recorded before and after each intervention . RESULTS Room-air hyperventilation caused panic attacks in a small number of patients ; the difference in panic rate between patients and comparison subjects was statistically significant by the subjects ' but not by the raters ' assessment . Panic rates during 5 % CO2 and 7 % CO2 were significantly greater among the patients by both assessment s ; the panic rate was greatest during 7 % CO2 . Order of administration did not significantly affect panic rates for hyperventilation and 5 % CO2 . CONCLUSIONS Panic patients were clearly more sensitive to the anxiogenic effects of CO2 than comparison subjects , and CO2 was a more potent anxiogenic stimulus than room-air hyperventilation . Seven percent CO2 discriminated best between patients and comparison subjects and should be the focus of further research BACKGROUND Panic disorder and generalized anxiety disorder ( GAD ) are both characterized by severe anxiety , but there is evidence that indicates a qualitative difference between these 2 anxiety disorders . To investigate the specificity of the association between carbon dioxide ( CO2 ) hypersensitivity and panic disorder and the possible relationships between panic disorder and GAD , the responses to inhalation of a gas mixture of 35 % CO2 and 65 % oxygen ( O2 ) were assessed . METHOD Fifteen patients with panic disorder , 13 patients with GAD , and 10 patients with comorbid GAD and panic disorder according to a consensus diagnosis using Diagnostic Interview Schedule Version III-R ( DIS-R ) and DSM-IV criteria , and 12 healthy controls inhaled 2 vital capacities : 1 of 35 % CO2 and 1 of compressed air . A double-blind , r and omized , crossover design was used . RESULTS GAD patients showed reactions to 35 % CO2  that were similar to those of healthy controls and significantly weaker than that of panic disorder patients . Patients with comorbid panic disorder and GAD had anxiogenic reactions similar to those of subjects with panic disorder . CONCLUSION The results of the present study support the idea that panic disorder and GAD are separate disorders that have at least some differences in pathogenetic mechanisms and suggest that the 35 % CO2 test might be a valid tool for discriminating between these 2 disorders There is now substantial evidence that an abnormal threshold for suffocation alarm underlies panic disorder . Because this disorder is highly familial , evidence of an abnormal suffocation threshold may be apparent in high-risk individuals before they develop clinical illness . To explore this possibility , we used a single inhalation of 35 % CO2 vs. air to evaluate 11 subjects who had at least one first-degree relative with DSM-III-R panic disorder , 13 who had at least two relatives treated for mania or for depression ( HR-AD ) , and 15 low-risk controls who had no family history of panic disorder , affective disorder , or alcoholism ( LR-C ) . All were aged 18 - 34 and had no history of panics or of any Research Diagnostic Criteria disorder . Five ( 45.5 % ) of the subjects at high risk for panic disorder , but none of the LR-C subjects ( p = .007 ) , nor any of the HR-AD subjects ( p = .011 ) , developed a panic attack following inhalation of the CO2 mixture The effects of a single inhalation of a 35 % CO2/65 % O2 gas mixture were examined in 71 patients with panic disorder with or without agoraphobia and 44 normal control subjects . Compared with the placebo condition , inhalation of air , the CO2/O2 mixture elicited a clear anxiety reaction only in panic disorder patients , who experienced a sudden rise of subjective anxiety as well as of several panic symptoms . Respiratory symptoms and the fear of dying best distinguished the patients from the control subjects . Baseline anxiety was not the key factor in explaining this differential reaction . The clinical features of panic disorder ( namely , frequency of panic attacks , agoraphobia , anticipatory anxiety , and duration of illness ) were not significantly related to the response to the challenge test , suggesting that CO2 reactivity might be a trait marker of panic disorder Among ethical concerns associated with biological challenge procedures is the risk of potentiating panic attacks in otherwise healthy persons who have no history of panic . The aim of the present study was to determine if repeated exposure to 20 % CO2 challenge increases the risk of developing panic attacks in a non clinical sample . One hundred and fifty-five ( 39.5 % ) of 392 participants who underwent a 20 % CO2 challenge procedure  and 51 ( 63.0 % ) of 81 controls who breathed only room air  were evaluated for panic attacks using the Panic Attack Question naire-Revised both at 6 and 12 months after the experiment . The percentage of participants who developed subsequent panic attacks did not differ significantly between the CO2 challenge group and the room air controls . High dose CO2 challenge does not increase the risk of subsequent panic attacks in non clinical population s ; it is a safe paradigm for use in psychopathology research with healthy individuals BACKGROUND Prospect i ve studies consistently find that smoking is a risk factor for the development of panic disorder ( PD ) . A possible explanation is that nicotine deprivation promotes heightened sensitivity to bodily sensations and /or arterial carbon dioxide ( CO2 ) . Abrams et al. ( 2011 ) previously found that , in response to a CO2 rebreathing challenge , smokers experiencing more ( vs. less ) intense nicotine withdrawal had more severe panic symptoms and a stronger urge to escape . However , participants were aware of the last time they smoked , leaving unclear the extent to which fear reactivity was influenced by the pharmacologic effects of nicotine deprivation versus beliefs regarding when nicotine was most recently used . The present study aim ed to ascertain whether nicotine deprivation , independent of beliefs regarding recent nicotine use , promotes fear reactivity among smokers . METHODS Moderate to heavy smokers without PD ( N = 25 ) participated in a placebo-controlled , double-blind study consisting of two sessions spaced 1 week apart . Participants abstained from nicotine for 2 hr prior to sessions . During one session participants were given a 21 mg nicotine replacement patch and , during the other , a placebo patch , with the order counterbalanced . For both sessions , after a 3-hr absorption period , participants underwent a 10-min CO2 rebreathing challenge . RESULTS Wearing a nicotine ( vs. placebo ) patch increased self-reported panic reactivity among participants , but did not significantly affect physiological and behavioral measures of reactivity . CONCLUSIONS In smokers without a history of PD , nicotine deprivation attenuates subjective panic reactivity . Possible explanations for the contrast between theory and laboratory findings as well as clinical implication s are discussed 1 . The authors investigated the psychological and biochemical factors associated with challenge by 5 % CO2 - 95 % O2 inhalation for 20 min . While fifteen healthy people were used as control , thirteen cases who were diagnosed by DSM-III-R as suffering from panic disorder were used as subjects .  CO2 inhalation induced panic in 38 % of the panic disorder patients , but did not cause panic in any of the control cases ( 0 % ) . 2 . Acute panic inventory ( API ) , heart rate and breathing rate of the panic group increased significantly after CO2 inhalation compared with the values in the control and non-panic groups . 3 . Heart rates and systolic blood pressure were significantly higher those in the panic disorder and non-panic groups than in the control group prior to CO2 inhalation . The cortisol values in the panic and non-panic groups also were significantly higher than those in the control group before and after CO2 inhalation . 4 . These results suggest elevated activity of the sympathetic nervous system during panic . The significantly higher heart rate , systolic blood pressure and cortisol values of the panic disorder subjects relative to the control before CO2 inhalation may have been due to circumstantial factors . The present findings of convincing evidence for behavioral , physiological , and biochemical hypersensitivity to CO2 in patients with panic disorders are consistent with a model of interoceptive conditioning in these patients OBJECTIVE The authors assessed the substance and diagnostic specificity of carbon-dioxide-induced panic since , in addition to the specific biochemical effects of inhaled carbon dioxide ( CO2 ) , simple physiologic distress is also frequently implicated as a panicogenic factor during respiratory challenge studies with CO2 in patients with anxiety disorders . METHOD Eighteen patients with panic disorder , 20 with social phobia , and 23 psychiatrically normal subjects  inhaled a mixture of 35 % CO2 and 65 % O2 for 30 seconds through a face mask . They also breathed for 30 seconds through a valve reducing the diameter of the airway . A double-blind , counterbalanced , r and omized design was used . RESULTS In spite of important similarities between the two interventions , including the induction of equal amounts of subjective respiratory distress , carbon dioxide inhalation was significantly more potent than increased airway resistance in provoking panic in the anxiety disorder patients . The patients with panic disorder were significantly more sensitive to CO2  than were the patients with social phobia or the normal subjects . CONCLUSIONS Carbon dioxide inhalation appears to have a specific panicogenic effect in panic patients that goes beyond simple breathlessness Introduction / Objective : The aim was to measure the lifetime prevalence of panic disorder ( PD ) in an Italian community sample , and to estimate the burden attributable to PD in compromising the quality of life ( QoL ) of people diagnosed with it . Methods : Community survey was conducted on a sample of 4,999 r and omly selected adult subjects . Instruments used were  semi-structured clinical interview Advanced Neuropsychiatric Tools and Assessment Schedule ( ANTAS ) , administered by clinicians and allowing diagnosis according to Diagnostic and Statistical Manual of Mental Disorder ( 4th ed . ; DSM-IV ) ; Short Form Health Survey ( SF-12 ) . Results : The lifetime prevalence of PD was 3.6 % ( 4.4 % in females , 2.5 % in males ; p = .002 ) . People with PD had a lower SF-12 score than the st and ardized community sample ( 35.5 ± 6.5 vs. 38.4 ± 5.9 ; p < .0001 ) with a mean difference ( attributable burden ) of 2.9 ± 0.7 , that is , lower than PD with agoraphobia ( AP ; 4.2 ± 2.4 ) . Wilson Disease ( WD ) , Multiple Sclerosis , Major Depressive Disorder and Eating Disorders ( ED ) show a higher attributable burden in impaired QoL than PD , while the attributable burden of PD with AP is not lower than in ED and WD . Conclusions : The burden attributable to the impairment of QoL following a lifetime diagnosis of PD was found to be not so great compared to the impairment caused by Major Depressive Disorder ( MDD ) or neurological conditions . The comorbidity of PD with AP worsens QoL significantly Background : Psychiatric disorders including anxiety , depression , somatization , obsessive compulsive , and bipolar disorders are recognized as causing the biggest burden of disease worldwide . Aim : In this study , we aim ed to assess the prevalence and burden of common mental disorders at Primary Health Care Centers ( PHCC ) using the World Health Organization Composite International Diagnostic Interview ( WHO-CIDI ) in the Qatari population , aged 18–65 who attended Primary Health Care ( PHC ) setting s. Design : A prospect i ve cross-sectional study conducted during November 2011 to October 2012 . Setting : Primary Health Care Centers of the Supreme Council of Health , Qatar . Subjects : A total of 2,000 Qatari subjects aged 18–65 years were approached ; 1475 ( 73.3 % ) agreed to participate . Methods : Prevalence and severity of International Classification of Disease-10 disorders were assessed with the WHO-CIDI ( Version 3.0 ) . Results : Of the 1475 participants , 830 ( 56.3 % ) were females 
    Output:
    
There is an increased sensitivity of carbon dioxide inhalation in patients with PD and their healthy first-degree relatives .