Panic disorder and medical comorbidity: A review of the medical and psychiatric literature
ABSTRACT Epidemiological studies have found significant comorbidity between panic disorder and many medical illnesses. The authors discuss the accumulating psychiatric and medical literature addressing comorbidity between panic disorder and cardiac, respiratory, gastrointestinal, and neurological illnesses. Cardiac symptoms such as chest pain and palpitations, as well as certain disorders such as mitral valve prolapse, hypertension, and cardiomyopathy, share significant comorbidity with panic disorder. Researchers have also shown significant comorbidity between panic disorder and chronic obstructive pulmonary disease, irritable bowel syndrome, and migraine headache. Pathophysiological mechanisms that may explain the association between panic disorder and comorbid medical illnesses, such as autonomic dysregulation of cardiac activity and smooth muscle tone and dynamic abnormalities of the coronary microvasculature, are discussed as well.
- SourceAvailable from: Chia-Yih Liu
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- "For example, respiratory sensations such as breathlessness and chest tightness as well as ventilatory changes are diagnostic for anxiety disorders suggesting a close relationship between respiratory sensory processing and anxiety symptoms (American Psychiatric Association, 2013). Previous studies have demonstrated that negative affective states and traits including anxiety are related to over-perception of respiratory sensations irrespective of underlying ventilatory changes (Carr et al., 1994; Zaubler and Katon, 1996; Bogaerts et al., 2005; von Leupoldt and Dahme, 2007; von Leupoldt et al., 2013). However, few of the aforementioned studies used objective measures for respiratory perception, and the neural mechanisms that underlie the interrelationships between anxiety and increased perception of respiratory sensations are poorly understood (von Leupoldt et al., 2013). "
ABSTRACT: The perception of respiratory sensations plays an important role both in respiratory diseases and in anxiety disorders. However, little is known about the neural processes underlying respiratory sensory perception, especially in patient groups. Therefore, the present study examined whether patients with generalized anxiety disorder (GAD) would demonstrate altered respiratory sensory gating compared to a healthy control group. Respiratory-related evoked potentials (RREP) were measured in a paired inspiratory occlusion paradigm presenting two brief occlusion stimuli (S1 and S2) within one inspiration. The results showed a significantly greater S2/S1 ratio for the N1 component of the RREP in the GAD group compared to the control group. Our findings suggest altered respiratory sensory processing in patients with GAD, which might contribute to altered perception of respiratory sensations in these patients.Frontiers in Psychology 07/2015; 6:957. DOI:10.3389/fpsyg.2015.00957 · 2.80 Impact Factor
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- "However, respiration is usually not sensed unless ventilatory pattern changes or is attended to . Methods for measuring respiratory perception include not only subjective measurements such as self-reporting questionnaires   , but also objective measurements. For example, cortical neuronal activations elicited by inspiratory or expiratory loads can be measured by the respiratory-related evoked potential (RREP) in the electroencephalogram (EEG)  . "
ABSTRACT: The perception of respiratory sensations can be of significant importance to individuals for survival and greatly impact quality of life. Respiratory sensory gating, similar to somatosensory gating with exteroceptive stimuli, is indicative of brain cortices filtering out repetitive respiratory stimuli and has been investigated in adults with and without diseases. Respiratory gating can be tested with the respiratory-related evoked potential (RREP) method in the electroencephalogram with a paired inspiratory occlusion paradigm. Here, the RREP N1 component elicited by the second stimulus (S2) shows reduced amplitudes compared to the RREP N1 component elicited by the first stimulus (S1). However, little is known regarding the effect of development on respiratory sensory gating. The present study examined respiratory sensory gating in 22 typically developed school-aged children and 22 healthy adults. Paired inspiratory occlusions of 150-ms each with an inter-stimulus-interval of 500-ms were delivered randomly every 2-4 breaths during recording. The main results showed a significantly larger RREP N1 S2/S1 ratio in the children group than in the adult group. In addition, children compared to adults demonstrated significantly smaller N1 peak amplitudes in response to S1. Our results suggest that school-aged children, compared to adults, display reduced respiratory sensory gating.Neural Plasticity 01/2015; 2015:7. DOI:10.1155/2015/389142 · 3.60 Impact Factor
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- "Although somatic symptoms are noted across anxiety and affective disorders, panic disorder (PD) is the anxiety disorder most closely associated with physical distress. PD is a heritable disorder associated with physical (nonpsychiatric) disorders such as mitral valve prolapse, migraine headaches, asthma, and hypertension (see Muller et al., 2005; Zaubler & Katon, 1996 for review of medical comorbidity and Hettema et al., 2001 for a review of heritability). While respiratory symptoms are the most common symptom of panic attacks (PA; Barlow, 2002), they may also include a variety of gastrointestinal symptoms (Barlow, 2002; American Psychiatric Association, 1987, 1994). "
ABSTRACT: We explored the comorbidity between panic attacks (PA), whose symptoms can include gastrointestinal discomfort, and gastrointestinal disorders (GD). Structural equation modeling was used to analyze data from 1,874 MZ and 1,498 DZ male-male twin pairs from the Vietnam Era Twin Registry. PA and GD were associated (relative risk for GD = 2). The percentage of liability due to genetic factors was estimated to be 37% for PA and 31% for GD. There was significant correlation between the genetic risk factors for PA and GD (estimated r = .55, 95% CI of 34% to 82%) and no evidence of correlation between the environmental causes of PA and GD. Therefore, PA and GD comorbidity can be explained by overlapping genetic factors and not overlapping environmental factors. Although these data cannot identify a biological pathway for such a shared liability, it suggests the presence of GD may be informative for genetic studies of panic.Twin Research and Human Genetics 02/2011; 14(1):16-24. DOI:10.1375/twin.14.1.16 · 1.92 Impact Factor